Biological Psychology 168 (2022) 108245

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Biological Psychology
journal homepage: www.elsevier.com/locate/biopsycho

Prolonged NoGo P3 latency as a possible neurobehavioral correlate of

aggressive and antisocial behaviors: A Go/NoGo ERP study
Carl Delfin a, b, c, *, Märta Wallinius a, b, c, Malin Björnsdotter d, Emily Ruzich e, Peter Andiné b, f, g
a
Lund Clinical Research on Externalizing and Developmental Psychopathology, Child and Adolescent Psychiatry, Department of Clinical Sciences Lund, Lund University,
Lund, Sweden
b
Centre for Ethics, Law and Mental Health, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of
Gothenburg, Gothenburg, Sweden
c
Research Department, Regional Forensic Psychiatric Clinic, Växjö, Sweden
d
Department of Affective Psychiatry, Sahlgrenska University Hospital, Gothenburg, Sweden
e
MedTech West, Sahlgrenska University Hospital, Gothenburg, Sweden
f
Forensic Psychiatric Clinic, Sahlgrenska University Hospital, Gothenburg, Sweden
g
Department of Forensic Psychiatry, National Board of Forensic Medicine, Gothenburg, Sweden

A R T I C L E I N F O A B S T R A C T

Keywords: Aggressive and antisocial behaviors are detrimental to society and constitute major challenges in forensic mental
Aggression health settings, yet the associated neural circuitry remains poorly understood. Here, we investigated differences
Antisocial behaviors in aggressive and antisocial behaviors between healthy controls (n = 20) and violent mentally disordered of­
Event-related potentials
fenders (MDOs; n = 26), and examined associations between aggressive and antisocial behaviors, behavioral
Go/NoGo
inhibitory control, and neurophysiological activity across the whole sample (n = 46). Event-related potentials
were obtained using EEG while participants completed a Go/NoGo response inhibition task, and aggressive and
antisocial behaviors were assessed with the Life History of Aggression (LHA) instrument. Using a robust Bayesian
linear regression approach, we found that MDOs scored substantially higher than healthy controls on LHA
Aggression and Antisocial subscales. Using the whole sample and after adjusting for age, we found that scores on
the LHA Aggression and Antisocial subscales were robustly associated with longer NoGo P3 latency, and less
robustly with longer NoGo N2 latency. Post-hoc analyzes suggested that healthy controls and MDOs exhibited
similar associations. With several limitations in mind, we suggest that prolonged NoGo P3 latency, reflecting
decreased neural efficiency during the later stages of conflict monitoring or outcome evaluation, is a potential
neurobehavioral correlate of aggressive and antisocial behaviors.

1. Introduction
Antisocial behaviors, usually defined as actions and attitudes that
violate societal norms and the rights of others (Burt, 2012), exact a
tremendous toll on society, both financially (Scott, Knapp, Henderson, &
Maughan, 2001) and in terms of reduced quality of life and well-being
among those affected (Hanson, Sawyer, Begle, & Hubel, 2010; Tan &
Haining, 2016). Although the term ‘antisocial behavior’ is broad and
often parsed into overtly aggressive (such as fighting, bullying, and
threatening) and covertly aggressive (such as lying, stealing, and
vandalizing) behaviors (Burt, 2012; Tackett, Krueger, Iacono, & McGue,
2005), both forms appear to stem from a common latent factor, with
joint genetic and environmental influences (Niv, Tuvblad, Raine, &
Baker, 2013). Still, some important differences between the two forms
have been highlighted. Covertly aggressive forms of antisocial behav­
iors, for instance, appear more closely associated with impaired
behavioral control, whereas overtly aggressive forms may instead pri­
marily reflect affective dysregulation (Burt & Donnellan, 2008; Hop­
wood et al., 2009).
In forensic mental health settings, aggressive and antisocial behav­
iors represent both prime targets for therapeutic interventions as well as
risk factors for an unsafe treatment environment (Lane, Kjome, &
Moeller, 2011; Meyer, Cummings, Proctor, & Stahl, 2016; Trestman,
2017). The importance of aggressive and antisocial behaviors in this
context is underscored by research showing that between ~ 30% and ~
60% of forensic psychiatric inpatients commit at least one violent assault

* Correspondence to: Research Department, Regional Forensic Psychiatric Clinic, Johan Allgulins väg 1, Växjö, Sweden.
E-mail address: carl.delfin@med.lu.se (C. Delfin).

https://doi.org/10.1016/j.biopsycho.2021.108245
Received 11 October 2021; Received in revised form 29 November 2021; Accepted 22 December 2021
Available online 24 December 2021
0301-0511/© 2021 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
C. Delfin et al.
during their hospitalization (Broderick, Azizian, Kornbluh, & Warbur­
ton, 2015; Verstegen, de Vogel, de Vries Robbé, & Helmerhorst, 2017).
Recently, Klein Tuente, Bogaerts, and Veling (2021) found a staff-rated
prevalence as high as 86% for at least one occurrence of moderate
aggressive behavior, with a corresponding prevalence of 65% for severe
aggressive behavior and 37% for physical aggression, during 30 weeks
of monitoring of male forensic psychiatric patients. While patients with
at least one incident of physical aggression had a higher prevalence of
Cluster B personality disorders in the study by Klein Tuente et al. (2021),
there is, unfortunately, little to no systematic evidence of effective
treatment of aggressive and antisocial behaviors at the severe end of the
spectrum (Bateman, Gunderson, & Mulder, 2015; van den Bosch,
Rijckmans, Decoene, & Chapman, 2018). In fact, the aggressive aspects
of mental disorders appear notably understudied compared to other
emotional behaviors (Flanigan & Russo, 2019).
In light of the apparent lack of evidence of effective treatments,
developing novel interventions that can prevent aggressive outbursts
and antisocial tendencies remains a key objective in forensic mental
health research. For the development of novel interventions to succeed,
some researchers argue, a better understanding of the neural circuitry
associated with aggressive and antisocial behaviors is vital (Flanigan &
Russo, 2019), and using a combination of biological and behavioral
measures may be an especially effective strategy in this regard (Nelson &
Trainor, 2007). Indeed, such a “multimethod” approach aligns well with
recent initiatives calling for research across multiple “levels of analysis”,
including the Research Domain Criteria (RDoC; Cuthbert, 2014) and the
Hierarchical Taxonomy of Psychopathology (HiTOP; Perkins et al.,
2020).
Response inhibition — the ability to inhibit unwanted or inappro­
priate actions — is a core component of executive control (Friedman &
Miyake, 2017; Miyake et al., 2000) and an integral part of both the RDoC
and the HiTOP frameworks. Poor response inhibition has been robustly
associated with both aggressive and antisocial behaviors in the general
population (Dambacher et al., 2015; Madole, Johnson, & Carver, 2020)
as well as among mentally disordered offenders (MDOs) (Tonnaer, Cima,
& Arntz, 2016a, 2016b). Longitudinal studies have shown that poor
response inhibition in childhood and adolescence is predictive of a wide
range of externalizing behaviors later in life (Bohlin, Eninger, Brocki, &
Thorell, 2012; Nigg et al., 2006), and the association appears primarily
genetic in origin (Young et al., 2009), suggesting a shared liability.
Neurophysiological activity related to response inhibition can be
investigated using event-related potentials (ERPs) acquired with elec­
troencephalography (EEG). Two ERP components in particular, the N2
and the P3 — both typically elicited using variants of the Go/NoGo
response inhibition task (Luijten et al., 2014) — are believed to reflect
processes either directly or indirectly related to inhibition (Huster,
Enriquez-Geppert, Lavallee, Falkenstein, & Herrmann, 2013). Of the
two, the P3 component is probably the best known, and reduced P3
amplitude has long been envisioned as a neurobiological marker of
aggressive and antisocial behaviors (e.g., Patrick et al., 2006). Still, a
moderating effect of N2 (but not P3) amplitude on the relationship be­
tween inhibitory control and aggression has also been observed (Rawls,
Jabr, Moody, & Lamm, 2018), and that both components may be of
importance is further supported by two recent meta-analyses: Pasion
et al. (2019) found that severe manifestations of aggressive and anti­
social behaviors, including violence and antisocial personality disorder,
was associated with reduced N2 amplitude, ostensibly related to deficits
in response inhibition, and Pasion, Fernandes, Pereira, and Barbosa
(2018) found a clear relationship between reduced P3 amplitude and
antisocial behaviors.
Although most ERP research has focused on the amplitude of the N2
and P3, distinguishing between the amplitude and the latency, usually
defined as the time point where the amplitude peaks, of an ERP
component may be important, since the two might reflect different kinds
of neural activity. Specifically, amplitude is believed to be an index of
“neural power”, or the amount of allocated cognitive resources, whereas
2
Biological Psychology 168 (2022) 108245
latency is believed to be an index of “neural efficiency”, or processing
speed (van Dinteren, Arns, Jongsma, & Kessels, 2014). The
meta-analysis by Pasion et al. (2019) focused solely on amplitude, likely
reflecting a lack of research on N2 latency, and out of the 36 studies
included in Pasion et al. (2018) only nine analyzed latency effects on a
group level. Even fewer, a mere six studies, included latency in dimen­
sional analyses. Thus, in contrast to previous meta-analytic research
demonstrating delayed P3 latency in aggressive and antisocial in­
dividuals (Gao & Raine, 2009), the findings of Pasion et al. (2018) were
too inconsistent to draw firm conclusions. Similarly, while some studies
have observed delayed N2 latencies in individuals with poor response
inhibition (Falkenstein, Hoormann, & Hohnsbein, 1999) and alcohol
dependence (Porjesz, Begleiter, Bihari, & Kissin, 1987), others report no
delays in N2 latency in individuals with alcohol abuse (Pandey et al.,
2012) and ADHD (Woltering, Liu, Rokeach, & Tannock, 2013). The lack
of studies including latency analyses, in conjunction with the inconsis­
tent findings of available research, signals an apparent need for further
investigation of the role of ERP latency in aggressive and antisocial
behaviors.
To date, most ERP research has focused on the so-called P3a and P3b
components. The frontally distributed P3a component, also called the
“novelty P3”, is elicited by task-irrelevant infrequent stimuli, whereas
the more parietally distributed P3b component is believed to reflect the
detection of task-relevant infrequent stimuli. The frontally distributed
NoGo P3 (and the preceding NoGo N2), however, is elicited by infre­
quent stimuli that requires withholding a response, such as in response
inhibition tasks (Polich, 2007). Although still debated, the NoGo
component is generally believed to reflect processes associated with
monitoring and outcome evaluation (Gajewski & Falkenstein, 2013;
Huster et al., 2013). The NoGo component is also especially meaningful
in a forensic mental health context, since it may be used to examine the
“frontal dysfunction hypothesis”, which suggests that aggressive and
antisocial behaviors may be associated with weakened prefrontal ac­
tivity during response inhibition (Pasion et al., 2018; Rodman et al.,
2016).
Taken together, reduced amplitude and prolonged latency of the
NoGo N2 and P3 components may constitute transdiagnostic neuro­
behavioral correlates of aggressive and antisocial behaviors. So far,
however, few studies have investigated the NoGo N2/P3 components in
relation to aggressive and antisocial behaviors, and fewer still have
included latency in dimensional analyses. Here, we addressed this
knowledge gap using data from healthy controls and violent MDOs. We
first investigated differences in aggressive and antisocial behaviors be­
tween healthy controls and MDOs, and then, using the whole sample,
examined associations between aggressive and antisocial behaviors,
behavioral inhibitory control, and NoGo N2 and P3 amplitude and la­
tency. We hypothesized that MDOs would exhibit higher levels of
aggressive and antisocial behaviors, and that aggressive and antisocial
behaviors would be associated with decreased behavioral inhibitory
control, decreased NoGo N2 and NoGo P3 amplitude, and prolonged
NoGo N2 and NoGo P3 latency.
2. Methods
2.1. Ethics
The study was approved by the regional ethics review board in
Linköping, Sweden (2017/56-31, 2018/7-32, 2018/321-32) and was
conducted in accordance with the Declaration of Helsinki. All partici­
pants provided voluntary, informed consent prior to participation.
2.2. Participants
Inpatient MDOs were recruited from an ongoing research project at a
maximum security forensic psychiatric hospital in Sweden (details on
the project and the full cohort are available in Laporte, Ozolins,
C. Delfin et al.
Westling, Westrin, & Wallinius, 2021). Following participation in the
project, all male MDOs were approached and asked to participate in the
current study if they had, at some point in their life, been sentenced for a
violent crime, on the condition that they did not have a history of brain
damage with lasting effects and that the treating psychiatrist did not
deem participation unsuitable due to current psychiatric status or safety
concerns.
Out of 35 available and eligible MDOs, a total of 29 agreed to
participate, although two MDOs were omitted due to missing or
incomplete self-report and/or file data, and one MDO was omitted from
further analyzes due to having only two correct NoGo trials left after
EEG data preprocessing. Previous work has shown that the P3, when
elicited using a Go/NoGo task, reaches adequate internal consistency
after 8–14 trials, depending on which measure is used (Rietdijk,
Franken, & Thurik, 2014). More recently, it was demonstrated that the
P3 may reach adequate internal consistency with as few as 10 trials,
especially if averaging over multiple sensors and time points, as is the
case in the current study, whereas excellent internal consistency may be
achieved at 20 trials (Thigpen, Kappenman, & Keil, 2017). Although the
participant with only two NoGo trials was omitted, it should be noted
that two MDOs had 9 correct NoGo trials each, and two healthy controls
had 6 and 12 correct NoGo trials each. We decided to keep these par­
ticipants for subsequent analyzes in order to keep the sample size at a
reasonable level. Remaining participants (N = 42, 91.3%) had 14 or
more correct NoGo trials available for analysis, with the majority of
participants (N = 37, 80.4%) having 20 or more, and with an average of
28 trials (SD = 10.2) for MDOs and 28.2 trials (SD = 9.9) for healthy
controls. Thus, a total of 26 MDOs, aged 20–57 years (M = 37.2, SD =
9.5), were included in the current study. In one MDO approximately one
third of the EEG data was lost due to technical issues. All MDOs
participated while on their usual treatment plan, including medication,
and received a voucher (~ $10) for use either in the hospital’s kiosk or at
a local mall as reimbursement directly after participation.
Healthy controls were recruited among hospital staff and university
students using posters, e-mail, and verbal information. We aimed to
match control participants as closely as possible to MDOs with regards to
education and age, and thus having received a degree after three or more
years of higher education was an exclusion criteria, in addition to having
a history of brain damage with lasting effects, having a current major
mental disorder, and self-reported drug use within the last 6 months.
Although a total of 25 control group participants were recruited, five
had to be excluded after participation (but prior to data analysis) due to
self-reported drug use within the last 6 months and/or having a history
of brain damage with lasting effects, resulting in 20 healthy controls,
aged 20–58 years (M = 33.1, SD = 11.8), included in the current study.
All healthy controls received either a voucher (~ $10) for use at a local
mall or a movie ticket as reimbursement directly after participation.
With minor differences, the sample used in the current study has
been used in a previous publication, in which further details on partic­
ipant and clinical characteristics are available (Delfin, Ruzich, Wall­
inius, Björnsdotter, & Andiné, 2020).
2.3. Measures
2.3.1. Aggressive and antisocial behaviors
The Life History of Aggression (LHA; Coccaro, Berman, & Kavoussi,
1997) instrument, consisting of 11 items rated from 0 (has never
occurred) to 5 (has occurred an uncountable number of times), was used
to assess lifetime aggressive and antisocial behaviors. The 11 LHA items
are summed in a total score and divided into three separate subscales:
Aggression (LHAAGG), Consequences/Antisocial Behavior (LHAANTI),
and Self-directed Aggression. Here, only scores on the LHAAGG and
LHAANTI subscales were used. The LHAAGG subscale consists of 5 items
describing physical fights, physical assaults on people, animals, or
property, as well as temper tantrums and verbal aggression, with
possible scores ranging from 0 to 25. The LHAANTI subscale consists of 4
3
Biological Psychology 168 (2022) 108245
items depicting school disciplinary problems, problems with supervisors
at work, and antisocial behaviors both with and without police
involvement, with possible scores ranging from 0 to 20. The LHA may be
scored using either self-reports or clinical ratings. In the current study,
self-reports were used for healthy controls, and clinical ratings, per­
formed by one out of three research assistants with several years of
experience in forensic psychiatry and subsequently validated by a
licensed psychologist, were used for MDOs.
In line with current recommendations (Hayes & Coutts, 2020;
McNeish, 2018), the internal reliability of the included LHA subscales
was assessed separately for healthy controls and MDOs using McDo­
nald’s Omega total (ωt ). Both subscales demonstrated satisfactory reli­
ability, with ωt = 0.77 and ωt = 0.78 for LHAAGG in healthy controls and
MDOs, respectively, and ωt = 0.68 and ωt = 0.78 for LHAANTI in healthy
controls and MDOs, respectively.
2.3.2. Inhibitory control
A Go/NoGo task based on previous work (Kiehl, Liddle, & Hopfinger,
2000; Steele, Maurer, Bernat, Calhoun, & Kiehl, 2016) was implemented
using Presentation software (Neurobehavioral Systems, Inc.) in order to
assess inhibitory control and elicit ERPs. Participants were comfortably
seated approximately 60 cm from a 22-inch widescreen LCD TFT
monitor (1680 × 1050 resolution @ 60 Hz). With both oral and
on-screen instructions, participants were told to respond as quickly and
accurately as they could, by pressing the left mouse button, every time
the Go stimulus (a white “X”) appeared on-screen, but to withhold their
response every time a NoGo stimulus (a white “K”) appeared. Both Go
and NoGo stimuli were presented on-screen for 250 ms in white text
against a black background. A fixation point (+) located at the center of
the screen was shown between trials, and we used an inter-stimulus
interval pseudorandomly distributed between 1000 and 3000 ms at
500 ms increments. Participants completed 10 practice trials prior to
beginning the task, and had to answer correct on at least 50% of these
trials in order to proceed. The task then consisted of 326 trials, 264
(84%) of which were Go trials, in order to establish a dominant response,
and 52 (16%) of which were NoGo trials. These trials were divided into
two blocks of 162 trials each, and participants could rest for as long as
they wanted in between.
2.4. EEG data acquisition, preprocessing, and reliability
2.4.1. EEG data acquisition
A high-impedance NetStation NA400 amplifier (Electrical Geodesics,
Inc.) and a 128 Ag/AgCl electrode Hydrocel Geodesic sensor net was
used to record EEG signals. The EEG signals were recorded at 1000 Hz
while referenced to the midline vertex electrode (Cz), and we aimed to
keep impedances below 100 kΩ. Due to, for instance, time constraints,
this was not achieved for all relevant electrodes on all participants.
Although lower impedances are preferable, a study conducted by re­
searchers from the equipment manufacturer showed that impedances
below 200 kΩ still allow for accurate (less than 0.1% error) signal
acquisition (Ferree, Luu, Russell, & Tucker, 2001). We achieved im­
pedances below 100 kΩ for 84% of healthy controls and 94% of MDOs,
and impedances below 200 kΩ for 94% of healthy controls and 96% of
MDOs, with average impedances of 51.5 kΩ (SD = 143.9) for MDOs and
60.7 kΩ (SD = 70.6) for healthy controls (note that due to technical
errors during data collection, impedance data was missing for three
healthy controls). Furthermore, since all recordings were carried out in
cool and dry environments, and since we used state-of-the-art filtering,
artifact detection, and artifact rejection methods, any remaining high
impedances should have negligible impact on our results (Kappenman &
Luck, 2010). The entire EEG acquisition procedure, including an addi­
tional resting-state task, took approximately 45 min for each
participant.
C. Delfin et al.
2.4.2. EEG data preprocessing
All EEG data preprocessing was carried out using the MNE-Python
module, version 0.20.4 (Gramfort, 2013; Gramfort et al., 2014)
running on Python version 3.8.2. The preprocessing pipeline largely
adhered to recommended procedures (Jas et al., 2018) and was, with the
exception of the removal and interpolation of bad channels, independent
component analysis (ICA) components, and artifacts following visual
inspection, fully automated. Prior to the automated procedure all EEG
data was visually inspected and bad channels marked. Then, a bandpass
filter from 0.1 to 30 Hz was applied, bad channels interpolated, and ICA
was used to identify and remove artifacts. To circumvent issues related
to ICA being sensitive to low frequency drifts, we bandpass filtered a raw
copy of the data from 1 to 30 Hz and used that to find ICA components.
The ICA components were visually assessed, and components judged to
represent eye blinks, saccades, heartbeats, and other non-brain related
signals were marked and zeroed out from the raw data. Data was then
epoched around a stimulus-locked window of 1000 ms (− 200 to 800 ms
after stimulus presentation) as well as baseline corrected (− 200 to
0 ms). Finally, automated artifact rejection using Autoreject version
0.2.1 (Jas, Engemann, Bekhti, Raimondo, & Gramfort, 2017), with
default values for peak-to-peak thresholding, was applied in order to
interpolate artefactual channels and remove contaminated epochs. The
preprocessed data was then imported into R for further statistical
analysis.
Only non-subtracted, correct NoGo trials were used for further
analysis (Gajewski & Falkenstein, 2013). Since research suggests that
ERP-based measures may be more reliable when averaged across mul­
tiple electrode sites (e.g., Ribes-Guardiola, Poy, Patrick, & Moltó, 2020;
Baldwin, Larson, & Clayson, 2015), we based our ERP measures on a
frontocentral region of interest by averaging data from nine electrodes
(E20, E12, E5, E118, E13, E6, E112, E7, E106). We defined NoGo N2
amplitude as the mean amplitude in a 225–325 ms window post-stimuli
(NoGo N2WIN) and NoGo P3 amplitude as the mean amplitude in a
325–625 ms window post-stimuli (NoGo P3WIN). These time windows
are similar to windows used in previous studies on aggressive and
antisocial behaviors (e.g., Brennan & Baskin-Sommers, 2018; Guan
et al., 2015; Verona & Bresin, 2015), and were chosen to avoid overlap
between components. Latency was defined, using a fractional area
approach, as the time point before which 50% of the negative (for N2) or
positive (for P3) area of the waveform is observed (Luck, 2014). Finally,
moving window amplitudes (labeled NoGo N2MOV and NoGo P3MOV),
defined as the mean amplitude 50 ms before and 50 ms after the 50%
fractional area latency was observed, were calculated as complementary
measures in order to account for potential latency effects.
2.4.3. Reliability analysis
The reliability of Go/NoGo task performance and all ERP measures
was assessed using split-half robust correlations between the averages of
odd and even trials (Venables et al., 2018; Ribes-Guardiola et al., 2020),
corrected using the Spearman-Brown formula (de Vet, Mokkink, Mos­
muller, & Terwee, 2017). The Go/NoGo paradigm exhibited high reli­
ability, with ρSB = 0.79 [0.66, 0.89] for median NoGo response time and
ρSB = 0.90 [0.84, 0.94] for NoGo accuracy. NoGo N2 latency exhibited
moderate reliability, with ρSB = 0.59 [0.36, 0.77], and all remaining
ERP measurements exhibited high reliability, with ρSB = 0.76 [0.60,
0.88] for NoGo N2WIN, ρSB = 0.72 [0.53, 0.85] for NoGo N2MOV, ρSB
= 0.82 [0.70, 0.91] for NoGo P3WIN, ρSB = 0.84 [0.73, 0.92] for NoGo
P3MOV, and ρSB = 0.80 [0.67, 0.90] for NoGo P3 latency.
2.5. Statistical analysis
Statistical analysis was carried out using the R statistical language,
version 4.1.1 (R Core Team, 2021). Due to the relatively small sample
size, we opted for a fully Bayesian approach. All statistical models were
specified using the R package brms (Bürkner, 2017), bridging R with the
Stan probabilistic programming language (Carpenter et al., 2017).
4
Biological Psychology 168 (2022) 108245
Group differences were modeled using a robust simple linear
regression approach that allowed for unequal variances between the
groups, with LHAAGG and LHAANTI scores used as outcome variables and
a dummy coded group variable used as predictor variable. Similarly, a
robust multiple linear regression approach was used to model the as­
sociation between aggressive and antisocial behaviors and inhibitory
control and ERP measures. Specifically, LHAAGG and LHAANTI scores
were entered as predictor variables, with NoGo accuracy and ERP
measures entered as outcome variables. Due to its robust association
with both P3 amplitude and latency (e.g., Johnstone, Pleffer, Barry,
Clarke, & Smith, 2005), we included age as a covariate in these models.
Finally, a robust correlation approach was used for reliability analysis.
All variables were centered and scaled prior to analysis in order to
obtain standardized estimates, robustness was achieved by using a
Student’s T likelihood (Lange, Little, & Taylor, 1989), and all priors
were chosen to be weakly informative, with negligible impact on ob­
tained estimates, but still providing moderate regularization (Gelman,
Simpson, & Betancourt, 2017). Model sampling using Markov chain
Monte Carlo (MCMC) was carried out using 12 chains with 4000 itera­
tions each, after 1000 warm-up iterations were discarded. All models
converged well, with Gelman-Rubin diagnostics ( R)
̂ of 1.00 (Gelman &
Rubin, 1992) and number of effective samples well above 10,000 at the
tails for each parameter.
Results from Bayesian analyses are presented as median posterior
estimates along with 90% highest density intervals (HDIs) presented
within square brackets, which may be interpreted such that it has a 90%
probability of containing the actual estimate. Since there is no notion of
“statistical significance” in Bayesian statistics, we adopted guidelines
recommending that a probability of 90% or higher can be considered
“very likely” (Mastrandrea et al., 2011). Thus, findings were considered
as robust if the 90% HDI did not contain zero, and thus were very likely
different from zero. A Bayesian variant of the conventional R2 (Gelman,
Goodrich, Gabry, & Vehtari, 2019) was used to estimate the amount of
explained variance of the multiple linear regression models, and we used
the leave-one-out cross-validated information criterion (LOOIC; Vehtari,
Gelman, & Gabry, 2017) to assess whether adding group as an interac­
tion term increased model fit in post-hoc, exploratory analyses. The
LOOIC is a Bayesian analog of the Akaike Information Criterion often
used in frequentist statistics as a measure of model fit, with the added
benefit that the LOOIC does not make distributional assumptions and
includes prior information. Lower LOOIC values indicate better model
fit.
3. Results
MDOs scored substantially higher than healthy controls on both LHA
subscales, as detailed in Table 1 and Fig. 1.
Using the whole sample, and after controlling for age, we found that
NoGo P3 latency was robustly and positively associated with both
LHAAGG and LHAANTI scores. These estimates were very likely different
from zero, with corresponding Bayesian R2 values of 0.15 [0.02, 0.28]
and 0.16 [0.03, 0.29], respectively, indicating moderately strong linear
relationships. Back-transforming the standardized estimates to their
original scale, each point on the LHAAGG subscale was associated with a
1.21 millisecond increase in NoGo P3 latency, and each point on the
LHAANTI subscale was associated with a 1.33 millisecond increase in
NoGo P3 latency. We also saw a less robust, positive association between
NoGo N2 latency and LHAAGG, although the 90% HDI did contain zero.
Remaining associations were small and non-robust. Full details are
presented in Table 2 and visualized in Fig. 2. The ERP waveform as well
as predicted associations between LHAAGG and LHAANTI scores and
NoGo P3 latency, based on the posterior predictive distribution, are
visualized in Fig. 3.
C. Delfin et al. Biological Psychology 168 (2022) 108245

Table 1
Descriptive overview and estimated group differences in aggressive and antisocial behaviors.
Full sample (n = 46) HCs (n = 20) MDOs (n = 26)

Subscale Mean ± SD Range Mean ± SD Range Mean ± SD Range Est. diff. [90% HDI]

LHA Aggression 13.02 ± 6.97 1–25 8.4 ± 5.81 1–20 16.58 ± 5.63 4–25 8.49 [5.45, 11.42]
LHA Antisocial 8.57 ± 7.13 0–20 1.95 ± 2.72 0–8 13.65 ± 4.88 3–20 12.09 [10.06, 14.14]

Note. HCs, healthy controls; MDOs, mentally disordered offenders; LHA, Life History of Aggression; SD, standard deviation; HDI, highest density interval.

Fig. 1. Boxplots with individual data points showing group differences in (A) aggressive and (B) antisocial behaviors between healthy controls (n = 20) and mentally
disordered offenders (n = 26). LHA, Life History of Aggression; HCs, healthy controls; MDOs, mentally disordered offenders.

interaction term, respectively, and 135.14 (SE = 9.45) and 131.75

Table 2
(SE = 9.05) for LHAANTI with and without the interaction term,
Standardized estimates (β) from robust Bayesian regression models, using the
respectively. Thus, our findings suggest that both healthy controls and
whole sample (n = 46) and adjusted for age.
MDOs exhibit similar patterns of association between NoGo P3 latency
LHA Aggression LHA Antisocial and aggressive and antisocial behaviors.
β [90% HDI] β [90% HDI]

NoGo accuracy 0.01 [− 0.25, 0.27] 0.1 [− 0.16, 0.36] 4. Discussion

NoGo N2 latency 0.06 [− 0.19, 0.31] 0.19 [− 0.06, 0.45]
NoGo N2WIN 0.06 [− 0.17, 0.3] 0.07 [− 0.17, 0.31]
NoGo N2MOV 0.07 [− 0.17, 0.32] 0.09 [− 0.16, 0.34] The current study examined differences in aggressive and antisocial
NoGo P3 latency 0.28 [0.03, 0.52] 0.31 [0.07, 0.55] behaviors between healthy controls and MDOs, and then, using the
NoGo P3WIN -0.03 [− 0.21, 0.15] -0.05 [− 0.23, 0.12] whole sample and controlling for the effect of age, investigated whether
NoGo P3MOV 0.07 [− 0.19, 0.32] -0.08 [− 0.34, 0.17]
aggressive and antisocial behaviors were associated with behavioral
Note. LHA, Life History of Aggression; HDI, highest density interval. Estimates inhibitory control and associated neurophysiological activity. We found
where the 90% HDI does not contain zero are shown in bold. that MDOs, in line with our hypothesis, scored substantially higher than
healthy controls on both the LHAAGG and the LHAANTI subscales. Also in
3.1. Post-hoc examination of group interaction line with our hypothesis, we saw a robust, positive association between
LHAAGG and LHAANTI scores and NoGo P3 latency, and a positive yet
Following the above findings, and with the robust group difference in smaller and less robust association with NoGo N2 latency. Post-hoc
LHA scores in mind, we also wanted to explore whether there was a analyses revealed no effect of group, indicating that healthy controls
group effect on the association between NoGo P3 latency and aggressive and MDOs exhibit similar associations. Against our hypotheses, how­
and antisocial behaviors (i.e., whether healthy controls and MDOs ever, we saw no robust associations between LHAAGG or LHAANTI scores
demonstrated similar or different patterns of association). We re-ran the and NoGo N2/P3 amplitude or performance on the Go/NoGo task.
relevant regression models, but this time included a Group × LHAAGG/
LHAANTI interaction term. Adding the interaction did not result in
4.1. Group differences in aggressive and antisocial behaviors
improved model fit for either model, with LOOIC values of 136.54
(SE = 8.99) and 132.28 (SE = 8.32) for LHAAGG with and without the
That MDOs would score substantially higher than healthy controls on

Fig. 2. Standardized estimates (β) showing the

association between behavioral inhibitory con­
trol, event-related potentials, and (A) aggres­
sive and (B) antisocial behaviors in a combined
sample (n = 46) of healthy controls (n = 20)
and mentally disordered offenders (n = 26). All
estimates are adjusted for age. Dots represent
posterior medians and lines represent 90%
highest density intervals. Estimates where the
90% highest density interval does not contain
zero are highlighted in green. LHA, Life History
of Aggression.

5
C. Delfin et al.
Fig. 3. (A) The ERP waveform, with the NoGo N2 and P3 components marked by arrows. (B–C) The predicted association between NoGo P3 latency and (B)
aggressive and (C) antisocial behaviors, with age held constant at 35 years (the sample mean), in a combined sample (n = 46) of healthy controls (n = 20) and
mentally disordered offenders (n = 26). Scattered dots show the actual data whereas the dark green middle line shows the predicted regression line and the lighter
shaded green region shows the 90% highest density interval. LHA, Life History of Aggression; HC, healthy controls; MDO, mentally disordered offenders.
both the LHAAGG and LHAANTI subscales was expected, and falls in line
with previous research on Swedish psychiatric patients (including
MDOs) demonstrating that scores on both these subscales exhibit robust,
medium to large correlations (ρs between ~ 0.30 and ~ 0.70) with
several of the disorders and behaviors often observed among MDOs,
including childhood-onset problems such as attention deficits, hyper­
activity, and conduct problems, personality traits such as novelty
seeking, and externalizing behaviors such as alcohol and drug abuse
(Hofvander et al., 2011). Notably, however, while MDOs scored
approximately twice as high on the LHAAGG subscale as healthy controls
in the current study, their score on the LHAANTI scale was almost five
times higher than that of healthy controls. The LHAANTI scale taps be­
haviors that, to a certain extent, are more closely related to covertly
aggressive or rule-breaking aspects of antisociality, such as problems at
school and work and encounters with law enforcement. While the small
sample size prohibits firm conclusions to be drawn from this, the results
do seem logical given the criminological background of Swedish,
forensic psychiatric patients (Laporte et al., 2021; Swedish National
Forensic Psychiatric Register, 2020).
Since the more covertly aggressive, rule-breaking form of anti­
sociality seems primarily associated with impaired behavioral control
and personality traits such as low constraint (Burt, 2012), a potential
clinical implication, following the high LHAANTI scores among MDOs in
the current study, is that therapeutic interventions might benefit from
increased focus on improving self-control. Indeed, such improvements
seem especially important when bearing in mind recent research
observing reductions in self-control among prisoners after just three
months of imprisonment, possibly linked to the impoverished environ­
ment (i.e., a sedentary lifestyle, social isolation, lack of cognitive chal­
lenges) that imprisonment often entails (Meijers, Harte, Meynen,
Cuijpers, & Scherder, 2018). Although, as far as we can tell, relatively
few studies have been carried out, there is some evidence suggesting that
cognitive and self-control training might be effective in reducing overt
aggression (Denson, Capper, Oaten, Friese, & Schofield, 2011; Papalia,
Spivak, Daffern, & Ogloff, 2019; Wilkowski, Crowe, & Ferguson, 2015)
and other externalizing behaviors, such as problematic alcohol con­
sumption (Walters, 2000). Still, the exact mechanisms underlying
improved self-control remain poorly understood (Friese, Frankenbach,
Job, & Loschelder, 2017), and further research aimed specifically at
MDOs is warranted.
4.2. The association between aggressive and antisocial behaviors,
inhibitory control, and ERP measures
Using the whole sample, and after controlling for age, we found that
both aggressive and antisocial behaviors were robustly associated with
increased NoGo P3 latency, and to a certain extent also with increased
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Biological Psychology 168 (2022) 108245
NoGo N2 latency. Mindful of the scarcity of research on P3 latency
overall and NoGo P3 latency in particular, this finding is difficult to
interpret considering that we, contrary to our expectations, saw no as­
sociations with NoGo N2 or P3 amplitude. Since each point on the
LHAANTI scale, for instance, predicted an increase in NoGo P3 latency of
1.33 ms, and since MDOs scored an estimated 12.09 points higher on the
LHAANTI scale than healthy controls, the predicted difference in NoGo P3
latency between the two groups was 16.08 ms. The prediction is well in
line with the estimated 17.41 ms difference in NoGo P3 latency between
MDOs and healthy controls we have reported in previous work based on,
with minor differences, the same sample (Delfin et al., 2020). In addi­
tion, in our previous work, we found that NoGo P3 latency was associ­
ated with higher levels of self-reported disinhibition, whereas NoGo P3
amplitude was not. The results of the current study, focused specifically
on aggressive and antisocial behavior, thus seem to mirror our previous
findings in this regard.
The lack of a clear association between aggressive and antisocial
behaviors and NoGo N2 and particularly NoGo P3 amplitude, as well as
with behavioral inhibitory control, in the current study was unexpected
in light of the rather robust association between aggressive and antiso­
cial behavior and reduced P3 (including NoGo P3) amplitude reported
by Pasion et al. (2018). Differences in sample size and participant
characteristics, such as the combined sample of healthy controls and
MDOs, is a possible explanation. For instance, the pharmacological
treatment of MDOs in the current study often included multiple sub­
stances, primarily antipsychotics (for details, see Delfin et al., 2020).
Since NoGo P3 amplitude is modulated by dopamine D2 receptors, a
primary target of antipsychotics, this could have affected our results
(Beste, Stock, Epplen, & Arning, 2016; Beste, Willemssen, Saft, & Fal­
kenstein, 2010).
Another possible source of discrepancy is our choice of task. We used
a “cool” Go/NoGo task with neutral stimuli instead of a “hot” version,
with emotionally salient stimuli (e.g., Zelazo & Carlson, 2012). Casey
et al. (2011) used both a “cool” and a “hot” version of the Go/NoGo to
differentiate between adult individuals that had completed a delay of
gratification task in childhood. Measures from the “cool” version could
not reliably differentiate between low- and high-delay individuals,
whereas measures from the “hot” version could, suggesting that the
emotional valence of stimuli may be important. Recently, Sun et al.
(2020) used an emotional Go/NoGo task and observed lower NoGo P3
amplitude in participants with high compared to low levels of trait
aggression, and Madole et al. (2020) used an emotional Go/NoGo task
and found that behavioral inhibitory control was directly related to
higher levels of self-reported aggression. Neither of these two studies
included a neutral comparison task, however, so the effect attributable
specifically to the use of a “hot” task is difficult to evaluate. There is also
evidence suggesting that “cool” and “hot”, or neutral and emotional,
C. Delfin et al.
versions of the Go/NoGo actually capture the same basic neuropsy­
chological constructs (Littman & Takács, 2017; Schulz et al., 2007), and
it thus remains unclear whether our choice of a neutral Go/NoGo task
could explain the lack of association between aggressive and antisocial
behaviors and NoGo N2/P3 amplitude.
In addition to the difference between “cool” and “hot” tasks, the
meta-analysis by Pasion et al. (2019) suggests that reduced NoGo N2
amplitudes are consistently elicited when using the Stop Signal Task
(SST), but not when using the Go/NoGo. Although both tasks are
believed to tap inhibitory control, the SST reflects the ability to inhibit
an already ongoing response, while the Go/NoGo instead reflects the
ability to withhold a response altogether (Littman & Takács, 2017).
Importantly, while they are often used seemingly interchangeably to
capture individual differences in behavioral inhibitory control, they
nonetheless appear to operate through different neural mechanisms
(Raud, Westerhausen, Dooley, & Huster, 2020), and it is possible,
therefore, that aggressive and antisocial behaviors may be more closely
related to the stopping aspects of inhibitory control, rather than to
withholding. Whether this also applies to the P3 component remains
unclear, however.
4.2.1. A possible relationship between NoGo P3 latency and myelination
Finally, one interpretation is that our findings instead highlight the
importance of distinguishing between amplitude and latency. The NoGo
P3 component is believed to reflect processes related to the monitoring
evaluation of conflict and the outcome of actions (Gajewski & Falken­
stein, 2013; Huster et al., 2013). If NoGo P3 amplitude reflects “neural
power”, or the amount of allocated cognitive resources, and if NoGo P3
latency reflects “neural efficiency” (van Dinteren et al., 2014), then
perhaps it is not the magnitude of allocated resources but rather the speed
with which such allocation occurs that is relevant in aggressive and
antisocial behaviors. This speed of allocation has been linked to the
so-called “myelin hypothesis”, which suggests that increased thickness
of the brain’s myelin sheath leads to increased nerve conduction ve­
locities, in turn leading to reduced response times on inhibition tasks
and a general improvement of cognitive and behavioral inhibitory
control (Bartzokis, 2005; Tuch et al., 2005).
There is a close relationship between the degree of myelination and
P3 latency across the lifespan, indicating that the two are indeed closely
intertwined (van Dinteren et al., 2014), further corroborated by research
showing that individuals with multiple sclerosis, a disease characterized
by the destruction of the myelin sheath, exhibit delayed P3 latencies for
certain types of stimuli (Ivica, Titlic, & Pavelin, 2013). Decreased rates
of myelination during adolescence have also been associated with an
increased expression of psychopathology later in life (Vanes et al.,
2020). Substance use and impulse control problems, both closely related
to aggressive and antisocial behaviors (Alcorn et al., 2013; Krueger,
Markon, Patrick, Benning, & Kramer, 2007), may also play a role here,
since the use of alcohol (Bjork, Grant, & Hommer, 2003; McQueeny
et al., 2009), opioids (Velasco, Mohamed, & Sato-Bigbee, 2021),
cannabis (Bava et al., 2009), and cocaine (Bartzokis et al., 2002) is toxic
to the vulnerable myelination process, and may in turn exacerbate
already existing impulse control problems and contribute to poor out­
comes in individuals prone to substance abuse (Bartzokis, 2005). While
speculative, it is possible that aggressive and antisocial individuals
exhibit aberrant myelination, which in turn could manifest as decreased
NoGo P3 latency. Speaking against this interpretation is the fact that we
saw no association between aggressive and antisocial behaviors and
performance on the response inhibition task. If the positive association
between aggressive and antisocial behaviors and NoGo P3 latency
observed in the current study is in fact due to individual differences in
myelination, then a negative association between aggressive and anti­
social behaviors and performance on the Go/NoGo task would be ex­
pected. That we did not observe such an association could be due to the
task itself being too easy to detect meaningful variance in inhibitory
control (see discussion in Delfin et al., 2020), or that performance on a
7
Biological Psychology 168 (2022) 108245
single laboratory task does not fully capture the variance associated with
aggressive and antisocial behaviors (Young et al., 2009). Future studies
should further explore whether myelination, NoGo P3/N2 latency, and
aggressive and antisocial behaviors are indeed related, perhaps by
combining suitable techniques for probing the brain’s white-matter
structure with ERP measures.
4.2.2. Gray-matter regions involved in generating NoGo ERPs
Besides the putative role of white-matter alterations such as differ­
ences in myelination, several gray-matter regions have been implicated
in the generation of the NoGo N2/P3 components. Although likely the
sum of multiple neural networks acting in concert (Huster, West­
erhausen, Pantev, & Konrad, 2010), the midcingulate cortex (MCC) has
emerged as a particularly important region in the generation of the
NoGo N2/P3 (Baumeister et al., 2014; Beste, Saft, Andrich, Gold, &
Falkenstein, 2008; Hong, Wang, Sun, Li, & Tong, 2017; Huster et al.,
2010). Research into its functions is still ongoing, but the MCC, covering
what is sometimes also labeled the dorsal part of the anterior cingulate
cortex (ACC), appears to be a key region involved in the monitoring of
conflicts and outcomes of actions (Botvinick, 2007; Jahn, Nee, Alex­
ander, & Brown, 2014), which corresponds to the processes believed to
be reflected in the NoGo N2/P3 components (Gajewski & Falkenstein,
2013). It seems possible, therefore, that the positive association between
aggressive and antisocial behaviors and NoGo P3 latency (and, to some
degree, NoGo N2 latency) observed in the current study reflects
abnormal functioning of the MCC/ACC, which in turn would offer at
least partial support for the “frontal dysfunction hypothesis” (Rodman
et al., 2016). The lack of neuroimaging data prohibits us from drawing
firm conclusions about particular brain regions, however, and further
studies are required in order to elucidate the complex relationship be­
tween aggressive and antisocial behaviors, NoGo N2/P3 latency, and
brain structure and function.
4.3. Relevance in clinical settings
From a clinical point of view, and if NoGo latency is indeed related to
the degree of myelination, then longitudinally investigating whether
early interventions targeting substance abuse have an effect on white-
matter structure and, subsequently, NoGo latency would shed further
light on some of the questions arising from our findings. Another avenue
worth exploring more in-depth is whether it is possible to improve (i.e.,
shorten) NoGo latency using neuromodulation techniques. Some
promising results were recently presented by Sergiou et al. (2021), who
used high-definition transcranial direct current stimulation (tDCS) to
modulate activity in the ventromedial prefrontal cortex, and found that
tDCS could reduce aggression and alter electrophysiological responses in
a sample of male forensic patients. Studies targeting the MCC/ACC using
tDCS have observed improvements in cognitive function (Khan, Wang,
Ti, Tse, & Tong, 2020), but to the best of our knowledge, no study has
employed these techniques to target the ACC/MCC in a forensic psy­
chiatric sample.
4.4. Strengths and limitations
This study has some methodological strengths that should be noted.
The combination of dimensional assessments of aggressive and antiso­
cial behaviors, a behavioral response inhibition task, and neurophysio­
logical measures is in line with research along multiple “levels of
analysis” encouraged by emerging frameworks such as the RDoC
(Cuthbert, 2014) and HiTOP (Perkins et al., 2020). The Bayesian sta­
tistical approach has several advantages, such as allowing genuine
probabilistic statements that remain valid regardless of sample size
(Wagenmakers et al., 2018) and representing a move away from strict
reliance on p-values and associated interpretations of (statistical) sig­
nificance (Wasserstein, Schirm, & Lazar, 2019). Still, in order to facili­
tate interpretation for readers unaccustomed to the Bayesian approach,
C. Delfin et al.
we opted to use the 90% HDI as a heuristic for determining the
robustness of our findings; some readers may prefer different heuristics,
and our results should be interpreted in light of this. We also used
non-Gaussian likelihoods, which are robust to outliers (Lange et al.,
1989), and weakly informative priors centered around zero, which
ameliorates concerns of multiple comparisons.
Despite these strengths, the small sample size remains a concern.
From a statistical point of view, it makes it difficult to include additional
covariates, such as data on pharmacological treatment, in our models.
Thus, we opted to just include age, given its strong association with N2/
P3 amplitude and latency, but are cognizant of the fact that the inclusion
of additional covariates could have affected our results. The small
sample size also leads to relatively wide HDIs, limiting the precision of
our findings.
Another limitation is that aggression was only measured using a
single instrument; using a different, or a combination of several in­
struments, may also have rendered different results. Furthermore,
although it would be preferable to use the same method of obtaining
LHA scores for both MDOs and healthy controls, clinical ratings were
unfortunately not available for healthy controls. Previous research has
voiced some concern about socially desirable responding when obtain­
ing self-reported LHA scores in a psychiatric population (Dellazizzo et al.
2017). In particular, a lack of self-awareness may cause participants to
deny the extent of their own aggressiveness (Ramírez & Andreu, 2006).
Since very few – approximately 13% – of inpatient MDOs in Sweden are
assessed to have full insight into their own mental illness and the effect it
has on their behavior and experiences, with 52% being assessed to only
have partial insight (Swedish National Forensic Psychiatric Register,
2020), we chose to use clinically rated LHA scores for MDOs.1
One limitation is that the experimental paradigm used in the current
study did not counterbalance target (“K”) and non-target (“X”) letters
between participants, and we therefore cannot rule out that we did not
observe any letter-specific activity. Furthermore, behavioral inhibitory
control was also measured using a single task, which may not fully
capture the variance associated with aggressive and antisocial behav­
iors. Therefore, the use of multiple tasks is recommended (Young et al.,
2009), and a structural equation modeling approach using a combina­
tion of multiple tasks and instruments, along the lines of Venables et al.
(2018), is likely a more optimal approach. It should be noted, however,
that such an approach requires larger data set and more time spent on
participation, which may not be feasible in forensic mental health set­
tings given the many difficulties encountered when recruiting MDOs (e.
g., Pedersen, Bergman, Berlin, & Hartvigsson, 2021; Bergman et al.,
2020). To get around this limitation, we encourage multisite collabo­
rations. Finally, despite these limitations, it should be acknowledged
that small sample studies employing a “bivariate mapping” approach (i.
e., investigating the association between just two measures), as in the
current study, remain important both for continued validation of
emerging research frameworks and for discovering potential neuro­
behavioral correlates that may be further investigated (e.g., Perkins,
Latzman, & Patrick, 2020).
5. Conclusions
We found that MDOs presented with substantially higher levels of
aggressive and antisocial behaviors than healthy controls. In line with
prior work, this finding further highlights a need for effective treatment
of aggressive and antisocial behaviors in forensic mental health settings.
Using the entire sample, and controlling for the effect of age, we also
1
Following review, we re-analyzed group differences and associations using
self-reported LHA scores for MDOs. The LHA scores were lower, but overall,
results were very similar, and the association between LHAAGG and LHAANTI
scores and NoGo P3 latency remained virtually unchanged. Full details are
available in the Supplementary material.
8
Biological Psychology 168 (2022) 108245
observed a robust, positive association between NoGo P3 latency (and to
a lesser extent NoGo N2 latency) and aggressive and antisocial behav­
iors. We propose that this finding reflects decreased neural efficiency
primarily during the later stages of conflict monitoring and outcome
evaluation, and further speculate that this in turn could be related to
individual differences in myelination. These findings add to a scarce
literature on the role of the NoGo ERP overall and NoGo P3 latency in
particular, and may be used to guide further research aimed at early
interventions and the evaluation of novel treatment approaches.
Funding
This study was supported by grants from Region Kronoberg, Södra
Sjukvårdsregionen, the Swedish state under the agreement between the
Swedish Government and the county councils, the ALF-agreement
(432551 and 819681), and from the Swedish Research Council for
Health, Working Life and Welfare (2018-01409). The grant providers
had no role in study design, recruitment and data collection, analysis, or
in the interpretation of findings.
Software availability
All code used is publicly available at the Open Science Framework.
All code relevant to the Go/NoGo task and for EEG data preprocessing is
available at https://osf.io/yscdh/, and the code used for all statistical
analyses and the creation of figures and tables in the current study is
available at https://osf.io/3wzrx/.
Declaration of Competing Interest
None to disclose.
Acknowledgments
The authors are grateful to Natalie Laporte, Johan Berlin and Christel
Karlsson for their work with data collection and administration, and to
the Regional Forensic Psychiatric Clinic in Växjö, Sweden, the Rågården
Forensic Psychiatric Hospital in Gothenburg, Sweden, and Marie Tor­
stensson Levander and her colleagues at the Department of Criminology,
Malmö University, Sweden, for help and support during data collection.
Appendix A. Supporting information
Supplementary data associated with this article can be found in the
online version at doi:10.1016/j.biopsycho.2021.108245.
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