Personality Disorders: Theory, Research, and Treatment © 2017 American Psychological Association

2017, Vol. 8, No. 1, 2–13 1949-2715/17/$12.00 http://dx.doi.org/10.1037/per0000195

Using Personality Neuroscience to Study Personality Disorder

Samantha V. Abram and Colin G. DeYoung
University of Minnesota

Personality neuroscience integrates techniques from personality psychology and neuroscience to eluci-
date the neural basis of individual differences in cognition, emotion, motivation, and behavior. This
endeavor is pertinent not only to our understanding of healthy personality variation, but also to the
aberrant trait manifestations present in personality disorders and severe psychopathology. In the current
review, we focus on the advances and limitations of neuroimaging methods with respect to personality
neuroscience. We discuss the value of personality theory as a means to link specific neural mechanisms
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with various traits (e.g., the neural basis of the “Big Five”). Given the overlap between dimensional
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models of normal personality and psychopathology, we also describe how researchers can reconceptu-
alize psychopathological disorders along key dimensions, and, in turn, formulate specific neural hypoth-
eses, extended from personality theory. Examples from the borderline personality disorder literature are
used to illustrate this approach. We provide recommendations for utilizing neuroimaging methods to
capture the neural mechanisms that underlie continuous traits across the spectrum from healthy to
maladaptive.

Keywords: personality neuroscience, personality disorder, neuroimaging, personality

Personality neuroscience is concerned with the neural correlates
of individual differences in cognition, emotion, motivation, and
behavior (Allen & DeYoung, in press; DeYoung, 2010; Mar,
Spreng, & DeYoung, 2013; Whittle, Allen, Lubman, & Yücel,
2006; Zuckerman, 2005). At the intersection of two fields, person-
ality neuroscience blends perspectives and methodologies from
personality psychology and neuroscience. Researchers studying
personality have made considerably more progress in describing
how people differ than in explaining why they differ. Historically,
the emphasis on description was largely due to the pressing need
for a taxonomy to organize the great variety of personality traits (a
need that was effectively satisfied with the development of the
Five-Factor Model or “Big Five”). The paucity of research into the
underlying sources of personality also stemmed from the immatu-
rity of neuroscientific methodology. However, with recent ad-
vances in noninvasive techniques, such as neuroimaging, research-
ers now have the tools needed to investigate the biological
mechanisms that underlie individual differences. Although psy-
chosocial or cultural factors can shape the manifestation of indi-
vidual differences, such forces must influence persistent brain
function if they are to have lasting effects on personality, given
that the brain is the proximal generator of all behavior and expe-
rience (DeYoung, 2010; Kitayama & Uskul, 2011).
In the present review, we discuss the advances and limitations of
personality neuroscience research, with an emphasis on neuroim-
aging methodology. In addition to neuroimaging techniques like
Samantha V. Abram and Colin G. DeYoung, Department of Psychology,
University of Minnesota.
Correspondence concerning this article should be addressed to Colin G.
DeYoung, Department of Psychology, University of Minnesota, Twin
Cities, 75 East River Parkway, Minneapolis, MN 55455. E-mail:
cdeyoung@umn.edu
MRI and positron emission tomography (PET), neuroscience
methods used in personality research include electrophysiological
techniques (e.g., electroencephalography [EEG]), molecular genet-
ics, pharmacological manipulations, and assays of endogenous
psychoactive substances. This review focuses primarily on MRI,
which is currently the most popular of these techniques. Stemming
from dimensional models of personality and psychopathology, our
review considers neuroimaging research spanning the continuum
from healthy to maladaptive trait presentations. In what follows,
first, we provide an overview of the neuroimaging methods used to
study personality. Second, we discuss important methodological
considerations, emphasizing issues related to statistical power and
reliability that are critical for the study of individual differences.
Third, we address the strengths and weaknesses of neuroimaging
methods for elucidating the biological basis of maladaptive per-
sonality patterns (i.e., personality disorders). Throughout, we pro-
vide advice for researchers who wish to integrate cutting-edge
neuroimaging techniques with the study of personality and per-
sonality disorders.
Methods in Personality Neuroscience
Personality, defined as relatively stable patterns of emotion,
cognition, motivation, and behavior, is most often measured via
self-report questionnaires but collecting additional ratings from
peer informants typically yields incremental validity (Connelly &
Ones, 2010; Oh, Wang, & Mount, 2011). Personality traits can also
be assessed via behavioral and cognitive tasks, such as perfor-
mance tests or decision tasks; although, the test–retest reliability of
such tasks must be demonstrated to ensure that they are suffi-
ciently stable to be considered trait measures (DeYoung, 2011).
Compared with self-report questionnaires, performance measures
may be more susceptible to state-related influences (e.g., fatigue,
acute drug effects). Recent efforts to devise standardized comput-
erized batteries for the measurement of individual differences may

2
 PERSONALITY NEUROSCIENCE
help to identify such cognitive trait measures, while also improv-
ing consistency across sites (e.g., Gur et al., 2010).
As noted above, MRI is the most common neuroscience method
used to examine personality. MRI is a noninvasive approach that
produces three-dimensional brain images based on the properties
of different brain tissues. Structural MRI (sMRI) approaches gen-
erally fall into two categories. The first includes methods that
measure regional brain volume, shape/curvature, and thickness
(e.g., voxel-based morphometry [VBM]). VBM entails spatial
normalization of high-resolution structural images to match a
template brain that includes gray and white matter (Ashburner &
Friston, 2000). The gray matter portions are then segmented and
smoothed, with each voxel indicating the average concentration of
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gray matter within itself and the surrounding voxels. The second
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popular type of structural imaging is based on diffusion weighted
imaging (DWI). DWI methods are used to measure macrostruc-
tural white matter organization (e.g., using various tractography
software), microstructural white matter coherence (e.g., using tract
based spatial statistics) of white matter pathways, and, less com-
monly, subcortical gray matter (e.g., Bhagat & Beaulieu, 2004).
DWI is typically analyzed using a diffusion tensor imaging model
(DTI), which evaluates the direction of water propagation along
white matter pathways. The most common DTI-derived metric,
fractional anisotropy (FA), indicates the relative linearity of mo-
lecular diffusion along a principal white matter axis. This metric is
typically considered to reflect the health, integrity, and coherence
of white matter tracts (Mukherjee, Chung, Berman, Hess, &
Henry, 2008). In healthy samples, however, individual differences
in FA may be more likely to reflect differences in white matter
organization and/or fiber count, rather than differences in white
matter health or integrity (Jones, Knösche, & Turner, 2013).
Functional MRI (fMRI) measures changes in the relative con-
centrations of oxygenated blood in different brain regions (i.e.,
fluctuations in the blood-oxygen-level dependent (BOLD) signal.
BOLD signal is taken to indicate the amount of neural activity in
a given region. fMRI can be further subdivided into task and
resting-state methods. Task-based fMRI uses a regression model
to examine BOLD activation as a function of temporal events. For
example, researchers may be interested in activation related to
evocative stimuli, decisions, or other cognitive and emotional
events. Although task-based fMRI is useful for mapping specific
cognitive processes with neural functions, an inherent limitation of
this method is the need to contrast activation (or events) of interest
with resting periods or other events. In addition, neural findings
from task-based data may be confounded by individual differences
in attention or effort.
Resting fMRI is a powerful alternative (or complement) to
task-based approaches, whereby data collection occurs in the ab-
sence of a task (e.g., participant rests with eyes open or closed for
the scan duration). Researchers use resting fMRI to measure func-
tional connectivity, or patterns of temporal synchrony between
brain areas. More specifically, regions are considered functionally
connected if they exhibit comparable temporal patterns of activa-
tion and deactivation. Resting-state approaches may be particularly
valuable for characterizing individual differences in broad person-
ality domains, where mapping specific cognitive or emotional
processes may be less crucial than identifying relevant networks
(Abram et al., 2015). Indeed, it is possible that specific task
demands could obscure the association between personality and
3
neural function (Sutin, McCrae, & Costa, Jr., 2011). Resting fMRI
also circumvents the limitations of task-based fMRI in several
important ways. First, there is no need to implement specific
contrasts, as resting fMRI is processed using model-free ap-
proaches that do not make assumptions about temporal events
(e.g., independent components analysis, seed-based connectivity
analyses). Second, individual differences in effort, attention, or
comprehension are less likely to impact resting state data, partic-
ularly for neuropsychiatric samples (Greicius, 2008). Third, there
are fewer design constraints to impede cross-sample replications or
multisample meta-analyses. Fourth, functional networks derived at
rest show striking overlap with those observed during task perfor-
mance (Smith et al., 2009) Thus, resting connectivity approaches
may be especially useful for assessing the baseline network dy-
namics associated with personality traits. Although we also note
that the combination of task-based and functional connectivity
approaches may be especially powerful.
Similar to fMRI, PET is a functional imaging technique that
produces three-dimensional brain images. PET is unique in that it
measures neurotransmitter activity; however, this requires inva-
sive, radioactive injections that decay rapidly. As a result, PET is
limited to short acquisition periods. Both MRI and PET benefit
from strong spatial resolution and in turn, have become valuable
neuroimaging tools. Despite the advancements in these techniques,
several methodological considerations should influence their ap-
plication for personality neuroscience.
Methodological Considerations
Statistical Power
A fundamental constraint in personality neuroscience is the need
for large samples to adequately assess interindividual variability
(Mar et al., 2013). Small samples are unlikely to represent the full
range of any given distribution (i.e., range restriction) and often
have multivariate outliers that can obscure true effects. The cor-
relational methods necessary for studying individual differences
are especially susceptible to outliers (Mathalon & Ford, 2012).
Moreover, even when small samples yield large correlation coef-
ficients, they are typically accompanied by extremely wide confi-
dence intervals (Mathalon & Ford, 2012). Studies may need up-
ward of 250 subjects to achieve stable estimates of correlations in
the expectable range (Schönbrodt & Perugini, 2013).
Although it may be difficult to predict the size of expected
effects in a field as young as personality neuroscience, we can
draw on more general information about the distribution of signif-
icant effects reported in psychology, wherein one third are smaller
than r ⫽ .2, one third are between .2 and .3, and only one third are
larger than .3 (Hemphill, 2003). This is not surprising, given that
if a variable has more than 3 or 4 causal sources, the correlation of
that variable with any single source cannot be more than about .4
(Ahadi & Diener, 1989). In general, it seems likely that complex
psychological traits will be influenced by many neural parameters,
with the result that the correlation with any single parameter will
be moderate at most, and results from personality neuroscience
studies with reasonably large samples generally support this hy-
pothesis (Allen & DeYoung, in press; Kievit et al., 2012; Ritchie
et al., 2015; Sutin et al., 2011). Given the expense of neuroimaging
 4 ABRAM AND DEYOUNG
research, it is also not surprising that many studies fail to have
adequate power to detect expectable effects.
An extreme-groups design is one approach to achieving greater
statistical power, especially when funds are limited. This technique
entails recruiting participants who are very high or low on the trait
of interest, in order to produce a larger effect size (i.e., the
difference between the high and low groups on some variable
hypothesized to be associated with the trait). Although this method
can enhance power in smaller sample sizes, it has at least two
drawbacks. First, it is difficult to predict how much the effect size
will increase. Second, this approach typically precludes meaning-
ful analysis of other relevant traits or covariates (and critical
covariates should be balanced during the recruitment phase).
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Given these considerations, extreme-group designs may be best
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suited for scenarios where the researcher has a specific, clearly
defined hypothesis and a limited budget. We note that one should
never divide an existing dataset into extreme groups (excluding the
remaining participants despite their complete data) nor dichoto-
mize a continuous variable as if it were categorical, as both of
these techniques reduce power unnecessarily (MacCallum, Zhang,
Preacher, & Rucker, 2002).
Low statistical power not only increases Type II errors (failures
to detect true effects) but also increases the proportion of signifi-
cant results that are Type I errors (i.e., false positives) because
smaller sample sizes are associated with decreases in precision
when estimating effects (Green et al., 2008; Yarkoni, 2009, 2015).
Poor precision is especially problematic in MRI research where
statistical tests are typically performed in many voxels. In small
samples, significant nonzero effects may simply be chance fluc-
tuations due to imprecision (even with proper use of correction for
multiple tests). Further, even when the true effect is not zero, low
power still tends to artificially inflate effect sizes. Without suffi-
cient power to detect smaller effects, only voxels that overestimate
an effect are likely to achieve significance (Yarkoni, 2009). As a
result, such findings can produce false impressions that effects are
large and restricted to narrow brain regions, when the true effects
are likely to be weaker and more dispersed (Yarkoni, 2015).
Methodological Variability
Similar to low statistical power, methodological heterogeneity
can contribute to increases in Type I error rates. A recent review
of neuroimaging studies found that over 90% of the reviewed
studies used different methodological approaches (Carp, 2012).
Given the immense flexibility in designing an analytic pipeline,
researchers can test several methods before selecting the one that
yields the most significant findings or best supports their hypoth-
eses (Ioannidis, 2011). In effect, this increases the likelihood of
false positives through publication bias and selective reporting of
analyses (Button et al., 2013). Conversely, some methods may
actually obscure true effects and instead produce Type II errors
(Henley et al., 2010). Methodological variability can also cause
inconsistencies in the literature, as even the same MRI software
package on different computers can produce divergent findings
(Gronenschild et al., 2012). Even the specific preprocessing steps
(e.g., motion correction, detrending, spatial smoothing) can influ-
ence fMRI results, and establishing optimized preprocessing pipe-
lines may enhance fMRI reproducibility (Churchill, Oder, et al.,
2012; Churchill, Yourganov, et al., 2012; Della-Maggiore, Chau,
Peres-Neto, & McIntosh, 2002; LaConte et al., 2003; Zhang et al.,
2009).
Intertwined with issues of methodological variability is the fact
that certain methods are simply better than others. There is no
comprehensive account of the relative performance of neuroimag-
ing techniques. Nonetheless, emerging critiques can help guide
researchers in selecting and/or modifying techniques for person-
ality research. VBM is one example for which criticisms have
yielded key software advancements (Bookstein, 2001; Davatzikos,
2004). Flaws in the standard VBM procedure led to alternative
approaches that included nonlinear transformations to assess vol-
umetric differences, such as deformation- or tensor-based mor-
phometry (TBM). Recent updates of the VBM toolbox (available
through the Statistical Parametric Mapping software suite, or
SPM) introduced the TBM method under the label “modulation”
(http://dbm.neuro.uni-jena.de/vbm/segmentation/modulation/); we
recommend always selecting the nonlinear modulation option.
Another example is that resting fMRI connectivity methods are
sensitive to head motion confounds (Cole, Smith, & Beckmann,
2010). Head motion can decrease long-range connectivity esti-
mates and increase short-range connectivity estimates because
adjacent voxels are more likely to experience similar disruptions
from movement than are distal voxels (Power, Barnes, Snyder,
Schlaggar, & Petersen, 2012; Power, Schlaggar, & Petersen, 2015;
van Dijk, Sabuncu, & Buckner, 2012). There is also evidence that
motion is a stable within-subject characteristic or trait (van Dijk et
al., 2012). Studies of individual and group differences should,
therefore, carefully address the impact of motion, especially for
target groups that are likely to exhibit more movement. Fortu-
nately, many techniques have emerged to counteract motion-
related artifacts in resting fMRI, including the use of motion
regressors, global signal regression, time-point censoring, and
multiecho sequencing (for a thorough review, see Power et al.,
2015). Although the optimal strategy is not yet clear, this is a
burgeoning research area where we expect major developments
soon. Cardiovascular processes can also confound resting fMRI
data (van Buuren et al., 2009), and it is therefore recommended to
include related variables as covariates.
Reliability
Identifying relations between personality traits and neural sig-
natures depends not only on reliable psychological measures, but
also on neuroimaging methods that can detect reliable neural
differences between people (Wu, Samanez-Larkin, Katovich, &
Knutson, 2014). A recent review of the fMRI literature reveals
inconsistent test–retest results; some studies note almost perfect
reliability and others indicate relatively low reliability (Bennett &
Miller, 2010). Although differences in power and test–retest inter-
val length can yield differing estimates of reliability, there may
also be genuine differences in reliability (i.e., within-subject vari-
ability over time) for different neural parameters. For example,
studies have generally found greater reliability for parameters in
motor and sensory tasks than in tasks assessing higher cognitive
processes (Bennett & Miller, 2010). A broad range of reliability
values has also been detected in resting fMRI data, with values
ranging from poor to high depending on the specific networks
and/or methodologies used to derive metrics for reliability analysis
(Braun et al., 2012; Wisner, Atluri, Lim, & Macdonald, 2013).
 PERSONALITY NEUROSCIENCE
Ideally, the reliability of neural estimates should be considered
when designing studies of individual differences. Bennett and
Miller (2010) suggested that reliability may be increased by ac-
quiring more data to increase the signal-to-noise ratio. Addition-
ally, selecting brain regions where measurements are demonstrably
reliable helps to limit multiple testing while simultaneously in-
creasing the likelihood of detecting effects (Wu et al., 2014).
Group-level reliability (i.e., the consistency of fMRI results
across samples or scanners) is another important consideration,
particularly for multicenter collaborations. Personality neurosci-
ence is an ideal field for amalgamating datasets, as personality data
is easy to combine and does not need to be collected at the same
time that neuroimaging data acquisition occurs (Mar et al., 2013;
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Sutin et al., 2011). Although there are challenges in creating large
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neuroimaging databases, these types of initiatives are on the rise.
For example, the Human Connectome Project is a multicenter
project with a target N of 1,200 subjects (Van Essen et al., 2012).
A primary aim of this project is to evaluate intersubject variability
as opposed to average group-level connectivity, and various per-
sonality measures are being collected along with the neural data.
Longitudinal studies can help elucidate the reliability of neuro-
imaging measures, as well as the stability of associations between
traits and neural parameters to provide a better understanding of
changes in personality traits and their neural correlates. In turn,
such an account can help researchers parse replication failures
related to biological factors (e.g., maturation, aging) versus meth-
odological differences (e.g., different scanners, task parameters).
Researchers have begun to employ longitudinal designs for per-
sonality research (e.g., Kapogiannis, Sutin, Davatzikos, Costa, &
Resnick, 2013; Taki et al., 2013; Wu et al., 2014).
Identifying Regions of Interest
One crucial issue in personality neuroscience is the identifica-
tion of brain regions of interest (ROI) for analyses of association
with personality traits. Importantly, a single ROI can also be a
specific set of regions that form a functional network, without all
being spatially adjacent, and it may be useful to begin referring to
such ROI as “networks of interest” (NOI). NOI can be identified
through data-driven methods like independent components analy-
sis, or they can be based on prior attempts to map the brain’s
functional architecture in large samples (e.g., Yeo et al., 2011).
Whole brain analyses, in which one examines the association of a
trait variable with every brain voxel, do not require ROI selection,
but they exacerbate the problem of statistical power because one
must correct significance levels for conducting so many statistical
tests. Whenever a more specific hypothesis is possible, it is desir-
able to test the association of a trait with an ROI or NOI. One
benefit of aggregating across voxels in an ROI is that the reliability
of the resulting measurement is increased relative to individual
voxels, just as the reliability of a personality scale score is higher
than that of each constituent item.
An obvious approach to defining ROI is to use a priori anatom-
ical divisions. This is particularly effective for smaller, well-
delineated brain regions, such as subcortical structures. One can
assess the volume or activity of the amygdala, caudate nucleus, or
hippocampus, for example. In the cortex, however, it is harder to
delineate ROI boundaries effectively because standard anatomical
divisions may often be larger than the ROI that one wants to study
5
(based on prior research on the function of certain cortical re-
gions). In these cases, one may wish to use a variable other than
the trait of interest to select the ROI.
A standard strategy for identifying an ROI in task-based fMRI
is to use a group-level contrast and select a region that is signifi-
cantly activated by the task or event of interest. Unfortunately, this
approach is potentially problematic when studying individual dif-
ferences. This is because regions that are significantly active on
average in the whole sample are likely to be precisely those
regions where every subject shows a similarly high level of acti-
vation (i.e., regions of low variability). When considering the
association of a trait with neural activity, however, one is inter-
ested in regions where subjects show varying levels of activity. In
those regions, some subjects may show very little activity, or even
reductions in activity, relative to the baseline or control condition.
In turn, those regions are less likely to be selected based on a
criterion of significant group-level activation. One way to reduce
this problem is to use relatively lenient thresholds for selecting
ROI based on group-level activation. The point here is not to be
confident that the whole region is reliably activated by the task
(which would typically require a more stringent threshold), but
rather to select an ROI that is likely to be involved in the task and
yet may be differentially involved across subjects.
The problem of using average activation to identify ROI can be
circumvented entirely by using an individual-difference variable
rather than a group-level contrast to identify the ROI. For example,
to study the association between working memory-linked neural
activity and the personality trait Intellect, DeYoung, Shamosh,
Green, Braver, and Gray (2009) selected four ROI where neural
activity (based on the contrast of working memory task vs. rest)
was significantly correlated with working memory accuracy dur-
ing the scan. Although these regions were not necessarily signif-
icant at the group level, they were precisely those regions where
neural activity helped to differentiate subjects with better and
worse working memory ability, and two of them were significantly
correlated with intellect.
A Dimensional Approach to Personality Disorder
The methodological issues described above are not restricted to
investigations of normal personality variation, but rather apply to
any neuroimaging research on interindividual variation. They are
especially relevant for psychopathology research as the field shifts
away from categorical diagnostic models toward dimensional con-
ceptualizations of disorder that emphasize continuous traits or
symptoms. Considerable research indicates that psychopathology
is not neatly organized into categories, as initially proposed by the
American Psychiatric Association’s Diagnostic and Statistical
Manuals (DSMs). Instead, mounting empirical evidence supports
dimensional models of psychopathology (Carragher, Krueger, Ea-
ton, & Slade, 2015; Eaton, Rodriguez-Seijas, Carragher, &
Krueger, 2015; Markon, Chmielewski, & Miller, 2011; Wright &
Simms, 2015). Further, research demonstrates a strong correspon-
dence between normal and abnormal personality structure (e.g.,
detachment can be interpreted as the pathological variant of low
extraversion; Wright et al., 2012). Like personality traits, dimen-
sions of symptoms and risk for disorder are structured in a hier-
archy, such that broad risk factors, like internalizing and external-
izing, can be subdivided into lower-level constructs (e.g.,
 6 ABRAM AND DEYOUNG
detachment, antagonism, negative affect, etc.; e.g., Wright et al.,
2012). This hierarchical structure is likely to reflect how distinct
aspects of psychopathology are interrelated via shared psycholog-
ical and biological factors; in this framework, some processes
influence broad tendencies, and others influence more specific
behaviors at lower levels of the hierarchy (Krueger & DeYoung,
2016). For example, serotonin may impact all externalizing behav-
iors, whereas other biological mechanisms may help differentiate
lower-level externalizing traits like antagonism and disinhibition
(Carver, Johnson, & Joormann, 2008; DeYoung, Peterson, Séguin,
& Tremblay, 2008; Lee & Coccaro, 2001).
Compared with traditional case versus control designs, a
hierarchical-dimensional approach may be better suited to eluci-
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date the neurobiological parameters involved in psychopathology.
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Case– control designs treat both groups as if they are homoge-
neous. Although this may enable them to detect fairly general
deficits (e.g., subjects with schizophrenia commit more working
memory errors on average when compared with controls), such
designs are poorly suited to discovering the underlying processes
that lead to those deficits. This is because (a) cases typically differ
from controls along multiple trait dimensions and (b) various
combinations of traits/symptoms can lead to the same diagnosis. In
contrast, a hierarchical-dimensional approach in more extended
samples lends itself to multivariate methods that can identify the
relevant dimensions more effectively. For example, one study
linked parameters of brain morphology with externalizing traits in
a large community sample (N ⫽ 297) via multivariate regression
(Ameis et al., 2014). Another study demonstrated associations
between resting insula connectivity and externalizing traits also
using a large community sample (N ⫽ 244; Abram et al., 2015). In
this study, we showed differential effects for different externaliz-
ing components (e.g., disinhibition vs. aggression), as well as
specificity for insula– externalizing associations versus the contri-
butions from other frontal or limbic networks. Note that these two
studies benefited from reasonable power, which is often lacking in
case– control neuroimaging studies.
As with other forms of psychopathology, discrete diagnostic
categories do not accurately reflect the heterogeneity of individu-
als with personality disorders (Eaton, Krueger, South, Simms, &
Clark, 2011; Widiger & Trull, 2007), which are conceptualized as
patterns of persistent maladaptive personality traits that cause
impairment or distress (Krueger & Markon, 2014). It follows that
combining dimensional-hierarchical models with neuroimaging
techniques could advance our understanding of the biological basis
of personality disorders. We illustrate this point with a specific
example from the personality disorder literature.
An Example: Borderline Personality Disorder
Borderline personality disorder (BPD) is estimated to affect
roughly 1% to 3% of the population and is the most common
personality disorder diagnosis encountered in a clinical setting
(Lenzenweger, Lane, Loranger, & Kessler, 2007). Severe affective
dysregulation is a hallmark feature of BPD that contributes to
impairments in interpersonal, cognitive, behavioral, and emotional
functioning (Lieb, Zanarini, Schmahl, Linehan, & Bohus, 2004;
Skodol et al., 2002). Per DSM–IV and DSM⫺5, a diagnosis of
BPD is assigned to an individual who meets five of nine criteria,
including impulsivity, self-injury, unstable self-image, and so forth
(American Psychiatric Association, 2000, 2013). Thus, 256 unique
combinations of symptoms can yield a BPD diagnosis (even with-
out taking into account further gradations of symptom severity).
This variety would be less problematic if all nine symptoms were
indicative of a single underlying dimension; however, the symp-
toms are multidimensional (Eaton, Krueger, Keyes, et al., 2011)
and come from at least three major dimensions of psychopathology
(i.e., negative affect, disinhibition, and antagonism). Unsurpris-
ingly, this clinical heterogeneity has posed challenges for research
targeting BPD (Trull, Distel, & Carpenter, 2011). No single bio-
logical mechanism or system is likely to be identified as the cause
of BPD; rather, multiple factors should contribute (O’Neill &
Frodl, 2012).
Neuroimaging investigations of BPD began over 20 years ago,
with the first studies employing computed tomography (CT) to
examine whole brain and ventricle volumetric differences (Lucas,
Gardner, Cowdry, & Pickar, 1989; Schulz et al., 1983). Although
initial CT studies did not reveal gross abnormalities in BPD, sMRI
studies have indicated reduced amygdala and hippocampal vol-
umes as candidate endophenotypes for BPD (O’Neill & Frodl,
2012; Rosenthal et al., 2008; Ruocco, Amirthavasagam, & Zakza-
nis, 2012; Schmahl & Bremner, 2006). Additionally, fMRI studies
have found reduced engagement of regulatory control regions
(e.g., dorsolateral prefrontal cortex, anterior cingulate cortex), and
heightened activation in limbic structures (e.g., amygdala, insula),
particularly in response to negative emotions (Krause-Utz, Winter,
Niedtfeld, & Schmahl, 2014; New, Goodman, Triebwasser, &
Siever, 2008; O’Neill & Frodl, 2012). However, other studies have
found that individuals with BPD exhibited less amygdala activa-
tion during negative emotion conditions (Ruocco, Amirthava-
sagam, Choi-Kain, & McMain, 2013). Recent studies have also
shown aberrant functional connectivity in BPD, particularly within
the default-mode network (DMN; Kluetsch et al., 2012; Krause-
Utz et al., 2014; Wolf et al., 2011), a network associated with
self-directed thought and emotional control (Andrews-Hanna,
Smallwood, & Spreng, 2014).
Despite apparent advances in identifying the neural correlates of
BPD, we note three methodological problems in this literature.
First, the majority of BPD neuroimaging studies have used small
samples (typically 30 subjects or less), with considerable variabil-
ity in gender ratios and psychiatric comorbidities. Thus, low power
and sample-heterogeneity limit the conclusions that may be drawn.
Some researchers have sought to overcome this limitation through
meta-analysis (Ruocco et al., 2013; Schulze, Schmahl, & Niedt-
feld, 2015). Unfortunately, the use of different tasks across studies
is a likely source of noise for fMRI meta-analyses (Ruocco et al.,
2013). Moreover, publication bias and the likely prevalence of
false positives due to massively underpowered samples cannot be
adequately corrected through standard meta-analysis (Simonsohn,
Nelson, & Simmons, 2014); garbage in, garbage out, as the saying
goes. Second, there is a paucity of longitudinal data on BPD-
associated brain changes (O’Neill & Frodl, 2012). Longitudinal
studies could help disentangle the impact of brain maturation on
adolescent BPD, as well as long-term neural progressions associ-
ated with BPD versus normal aging. Third, BPD studies predom-
inantly entail between-groups designs that do not address within-
group heterogeneity. Multivariate analyses would be better able to
uncover associations between neural markers and specific symp-
toms or symptom dimensions (Brendel, Stern, & Silbersweig,
 PERSONALITY NEUROSCIENCE
2005). Further, personality neuroscientific theories that connect
biological systems with psychological traits may provide an on-
ramp for elucidating the specific neural correlates of trait/symp-
toms that underlie clinically heterogeneous disorders like BPD.
The Importance of Theory for
Personality Neuroscience
A staggering number of neural parameters can be investigated
using neuroimaging and other neuroscience techniques. The task
of linking these parameters to the traits or symptom dimensions of
personality disorders is daunting if not hopeless without guiding
theories. A promising approach for developing neurobiological
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
hypotheses is to link psychological functions with the so-called
This document is copyrighted by the American Psychological Association or one of its allied publishers.
“Big Five” trait dimensions that are common to both normal and
abnormal personality variation (DeYoung, Carey, Krueger, &
Ross, 2016; Krueger & Markon, 2014; Markon, Krueger, & Wat-
son, 2005; Widiger & Trull, 2007). We will label these dimensions
by their standard names from normal personality research, but first
we list them with their pathological counterparts from the DSM–5:
extraversion versus detachment, neuroticism or negative affectiv-
ity, agreeableness versus antagonism, conscientiousness versus disin-
hibition, and openness/intellect or psychoticism (the correspondence
of psychoticism with openness/intellect is more complicated than the
other four dimensions; DeYoung, 2015; DeYoung et al., 2016).
Several theories have been proposed to specify the psychological
mechanisms associated with each of the Big Five (e.g., Denissen &
Penke, 2008; DeYoung, 2015; Nettle, 2006; Van Egeren, 2009), and
they are reasonably consistent with each other. In the following
discussion, we rely on DeYoung’s (2015) cybernetic big five theory
(CB5T) because it is the most thoroughly elaborated and has been
used to organize a recent review of the field of personality neurosci-
ence (Allen & DeYoung, in press). It has also been integrated with
the new measurement system for personality disorder in DSM–5
(DeYoung et al., 2016).
Cybernetics is the study of the principles governing goal-
directed, adaptive systems. CB5T describes personality traits as
relatively stable patterns of behavior and experience that reflect
variation in the parameters of evolved cybernetic mechanisms (i.e.,
biologically instantiated psychological mechanisms). These mech-
anisms carry out the processes that allow people to identify goals,
properly motivate and orient toward goals, and interpret feedback
to represent their environments and maintain goal-pursuit (DeYoung,
2015). (“Goals” are defined broadly as any desired state of the
organism and need not necessarily be conscious.) In this framework,
extraversion reflects sensitivity to rewards, leading to approach and
exploratory behavior as well as positive affect; neuroticism reflects
defensive emotional responses to uncertainty, threat, and punishment;
openness/intellect reflects variation in processes of cognitive explo-
ration and engagement with information; conscientiousness reflects
controlled processes that prevent impulsive disruption in the pursuit of
nonimmediate or abstract goals; agreeableness reflects altruism and
cooperation, involving the coordination of goals, interpretations, and
strategies with those of others. This theory relates psychological
processes to each dimension and thus enables the effective develop-
ment of hypotheses regarding their neural correlates. Progress has
been made in linking all of the Big Five traits with neurobiological
substrates; however, we focus the current review on findings related
to neuroticism, conscientiousness, and agreeableness, given their
7
implications for reconceptualizing BPD (for a more comprehensive
review see Allen & DeYoung, in press). We present these findings
from a systems neuroscience perspective that considers how brain
areas interact to produce trait dimensions, rather than assuming traits
are isolated to specific regions.
Of the Big Five, neuroticism has received the most attention
from neuroscience, likely because it is such a major risk factor for
psychopathology (Lahey, 2009). Individuals high in neuroticism
often engage in avoidant or defensive behaviors in response to
stress (e.g., anxiety, irritability, panic). Evidence indicates that the
neurotransmitters serotonin and noradrenaline are key contributors
to neuroticism (Gray & McNaughton, 2000). Serotonergic drugs
are often used to treat clinical disorders that reflect extreme neu-
roticism, such as anxiety and depression, and reductions in neu-
roticism following treatment have been found to accompany suc-
cessful treatment (Du, Bakish, Ravindran, & Hrdina, 2002; Quilty,
Meusel, & Bagby, 2008; Tang et al., 2009). Several PET studies
have linked individual differences in neuroticism with serotonin
receptor or transporter binding (Frokjaer et al., 2008; Takano et al.,
2007; Tauscher et al., 2001). Evidence from fMRI and sMRI
studies implicate the amygdala, consistent with its role in negative
affectivity and response to threat, and a region of medial prefrontal
cortex involved in emotion regulation through its connection to the
amygdala (Barrós-Loscertales et al., 2006; Holmes et al., 2012;
Hyde, Gorka, Manuck, & Hariri, 2011; Iidaka et al., 2006; Koel-
sch, Skouras, & Jentschke, 2013; Schuyler et al., 2014; Somerville,
Whalen, & Kelley, 2010). Functional connectivity between the
amygdala and other limbic and prefrontal areas also appears linked
to neuroticism (Adelstein et al., 2011; Mujica-Parodi et al., 2009;
Servaas et al., 2015; Servaas et al., 2013). Finally, neuroticism shows
robust negative associations with the integrity of white matter tracks
connecting cortical and subcortical areas (Bjørnebekk et al., 2013;
Taddei, Tettamanti, Zanoni, Cappa, & Battaglia, 2012; Westlye,
Bjørnebekk, Grydeland, Fjell, & Walhovd, 2011; Xu & Potenza,
2012). These connectivity reductions may help to explain the poor
emotion regulation associated with neuroticism, as they could
suggest that cortical processes exert less control over the subcor-
tical generators of negative affect.
Conscientiousness and agreeableness have received less exten-
sive attention in neuroscience research, but findings are beginning
to emerge regarding both dimensions. Several neuroimaging stud-
ies have implicated the dorsolateral prefrontal cortex in conscien-
tiousness (DeYoung et al., 2010; Forbes et al., 2014; Jackson,
Balota, & Head, 2011; Kapogiannis et al., 2013), which is consis-
tent with the prefrontal cortex’s role in goal-oriented behaviors
(Miller & Cohen, 2001). The larger network encompassing the
ventral attention and salience networks, which includes portions of
the lateral prefrontal cortex, may be especially important for con-
scientiousness (Allen & DeYoung, in press; DeYoung, 2015; Yeo
et al., 2011). This network is involved in redirecting attention away
from distractions and toward stimuli needed to attain goals (Fox,
Corbetta, Snyder, Vincent, & Raichle, 2006). Other regions in this
network, such as the anterior insula and anterior cingulate cortex,
have also been linked with conscientiousness (or impulsivity as
assessed by the Barratt Impulsivity Scale; Adelstein et al., 2011;
Brown, Manuck, Flory, & Hariri, 2006; Churchwell & Yurgelun-
Todd, 2013; Farr, Hu, Zhang, & Li, 2012; Liu et al., 2013; Matsuo
et al., 2009).
 8 ABRAM AND DEYOUNG
The centrality of altruism and cooperation for agreeableness
suggests that empathy, the ability to understand the mental state
of others, should be an important source of the trait. Indeed,
agreeableness has been found to predict this ability (Nettle &
Liddle, 2008). DMN areas are key candidates for neural sub-
strates of empathy, given their involvement in perspective tak-
ing (Andrews-Hanna et al., 2014). Two resting functional con-
nectivity studies revealed positive associations between DMN
connectivity and agreeableness (Adelstein et al., 2011; Sam-
paio, Soares, Coutinho, Sousa, & Gonçalves, 2013). Although
brain structure studies have been somewhat inconsistent, two
studies have reported negative associations of agreeableness
with a DMN region that is involved in interpreting the actions
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
and intentions of others by decoding biological motion (i.e., the
This document is copyrighted by the American Psychological Association or one of its allied publishers.
posterior superior temporal gyrus; DeYoung et al., 2010; Ka-
pogiannis et al., 2013). Another crucial component of agree-
ableness is the suppression of aggressive impulses (Meier,
Robinson, & Wilkowski, 2006), and an sMRI study found that
amygdala volume at age 26 was negatively associated with both
current aggression and history of aggression (Pardini, Raine,
Erickson, & Loeber, 2014).
Implications for Research on Borderline
Personality Disorder
Given the robust overlap between normal and abnormal per-
sonality dimensions, researchers can extend CB5T to develop
neural hypotheses about personality disorders. In effect, re-
searchers can reconceptualize personality disorders as extreme
variants of normal personality traits and formulate biological
hypothesis regarding the sources of those traits. Returning to
the example of BPD, meta-analyses reveal that BPD is most
consistently associated with high neuroticism, low conscien-
tiousness, and low agreeableness (Samuel & Widiger, 2008;
Saulsman & Page, 2004). Within the hierarchical-multivariate
framework, we can develop hypotheses both regarding biolog-
ical sources that these dimensions share and regarding biolog-
ical sources specific to each dimension. The shared variance of
conscientiousness, agreeableness, and low neuroticism forms
one of the two broadest dimensions at the top of the Big Five
personality hierarchy and has been labeled stability (DeYoung,
2015). Perhaps not coincidentally, the suggestion was made
decades ago that BPD should be relabeled “unstable personality
disorder,” a more usefully descriptive term (Spitzer, Endicott,
& Gibbon, 1979). Based on research implicating serotonin in
conscientiousness and agreeableness, as well as neuroticism,
CB5T hypothesizes that serotonin is an important neurobiolog-
ical factor influencing stability (Allen & DeYoung, in press),
making serotonergic dysfunction a likely contributor to BPD.
Moving down the trait hierarchy to the level of the Big Five,
we can devise specific neural hypotheses for each of the three
traits in question. Rather than treating BPD diagnosis as a
unified disorder, this approach recognizes that BPD may have
quite different etiologies given different levels of symptoms
within these three dimensions. Weak connections from medial
prefrontal cortex to the amygdala may play a key role in the
affective dysregulation that underlies the high levels of neurot-
icism associated with BPD. In contrast, however, if the finding
that BPD is associated with reduced amygdala volume proves
robust (O’Neill & Frodl, 2012; Rosenthal et al., 2008; Ruocco
et al., 2012; Schmahl & Bremner, 2006), this would be incon-
sistent with findings that amygdala volume is positively corre-
lated with neuroticism (Holmes et al., 2012), but it would be
consistent with the finding that aggression (low agreeableness)
is negatively associated with amygdala volume (Pardini et al.,
2014). This illustrates how a multivariate approach can some-
times make sense of superficially contradictory findings. Also
in relation to low agreeableness, one might hypothesize that the
DMN substrates of empathy and perspective-taking abilities are
likely to be disrupted in BPD. Finally, with respect to consci-
entiousness, we might anticipate disruptions in lateral prefron-
tal cortex functionality to contribute to poor impulse control.
The salience network may additionally underlie impaired goal-
direction and attentional deficits related to conscientiousness
versus disinhibition, as this network both directs attention to-
ward salient stimuli and helps to switch between the DMN and
central executive network to maintain focus on task-relevant
goals (Uddin, 2015). The approach outlined in this section
shows that we can formulate hypotheses about the neural basis
of specific maladaptive traits that are crucial for the problems
captured by the BPD diagnosis, while avoiding the limitations
associated with the reification of categorical diagnoses.
Conclusions and Future Directions
Personality neuroscience is a rapidly advancing field with the
capacity to inform our understanding of the neural mechanisms
that support continuous trait dimensions ranging from healthy to
maladaptive. In the current review, we show how researchers can
use hierarchical-dimensional approaches and personality theory to
devise specific neural hypotheses regarding both normal person-
ality variation and the aberrant trait presentations observed in
personality disorders. Although neuroimaging methods have cre-
ated immense possibilities for exploring the biological basis of
personality, we discuss several methodological issues that endan-
ger research on personality disorders, including statistical power,
reliability, and ROI selection methods. Our strongest recommen-
dation is a shift toward larger samples (preferably of 200 or more);
however, acquiring clinical samples of this size is a considerable
challenge. Researchers should, therefore, consider the value of (a)
large nonclinical samples that capture a range of personality pa-
thology in the general population, and (b) recruitment of treatment-
seeking individuals without selection for particular disorders.
Large samples will help to limit Type I and Type II errors, and
enable the use of multivariate methods to parse the contributions of
various trait dimensions that underlie heterogeneous clinical dis-
orders.
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Correction to Hecht et al. (2016)

In the article “Parsing the Heterogeneity of Psychopathy and Aggression: Differential Associa-
tions Across Dimensions and Gender” by Lisa K. Hecht, Joanna M. Berg, Scott O. Lilienfeld, and
Robert D. Latzman (Personality Disorders: Theory, Research, and Treatment, 2016, Vol. 7, No.
1, pp. 2–14. http://dx.doi.org/10.1037/per0000128), there was an error in Table 3 and in the fifth
paragraph of the Results.

The first row of Table 3, “Step 3” results were switched for “Primary ⫻ Gender” and “Second-
ary ⫻ Gender” under the “Reactive aggression” column. The correct data for “Primary ⫻
Gender” under the “Reactive aggression” column are: ␤: ⫺.07; t: ⫺1.00. The correct data for
“Secondary ⫻ Gender” under the “Reactive aggression” column are: ␤: .16; t: 2.41ⴱ.

The fifth paragraph of the “Results” section, “Explaining Reactive and Proactive Aggression
From Dimensions of PPI-R Psychopathy” reflected the error in Table 3. The paragraph should
read as follows:

After accounting for demographic variables, LSRP psychopathy contributed an additional 4.7%
of the variance for RA (see Table 3). Primary Psychopathy was negatively (␤ ⫽ ⫺.12, t ⫽ ⫺2.95,
p ⬍.001) and Secondary Psychopathy positively (␤ ⫽.26, t ⫽ 7.39, p ⬍.001) associated with RA.
In addition, the association between LSRP Secondary Psychopathy and RA was significantly
moderated by gender (␤ ⫽ .16, t ⫽ 2.41, p ⬍.05). As shown in Figure 1, examination of simple
slopes revealed that the association between Secondary Psychopathy and RA was significantly
stronger for women (␤ ⫽ .30, p ⬍ .001) than for men (␤ ⫽ .15 p ⬍ .05). Thus, although higher
levels of Secondary Psychopathy predicted higher levels of RA in both men and women, the
magnitude of this association was stronger for women.

http://dx.doi.org/10.1037/per0000225