BPD Minzenberg 08

A neurocognitive model of borderline
personality disorder: Effects of childhood

sexual abuse and relationship to adult social
attachment disturbance
MICHAEL J. MINZENBERG,
a
JOHN H. POOLE,
b,c
AND
SOPHIA VINOGRADOV
b,c
a
University of California, Sacramento;
b
University of California, San Francisco; and
c
San Francisco Veterans Affairs Medical Center
Abstract
Borderline personality disorder (BPD) is a paradigmatic disorder of adult attachment, with high rates of antecedent
childhood maltreatment. The neurocognitive correlates of both attachment disturbance and maltreatment are both
presently unknown in BPD. This study evaluated whether dimensional adult attachment disturbance in BPD is related to
specific neurocognitive deficits, and whether childhood maltreatment is related to these dysfunctions. An outpatient BPD
group (n 43) performed nearly 1 SD below a control group (n 26) on short-term recall, executive, and intelligence
functions. These deficits were not affected by emotionally charged stimuli. In the BPD group, impaired recall was related
to attachmentanxiety, whereas executive dysfunction was related to attachmentavoidance. Abuse history was correlated
significantly with executive dysfunction and at a trend level with impaired recall. Neurocognitive deficits and abuse
history exhibited both independent and interactive effects on adult attachment disturbance. These results suggest that
(a) BPD patients reactivity in attachment relationships is related to temporallimbic dysfunction, irrespective of the
emotional content of stimuli, (b) BPD patients avoidance within attachment relationships may be a relational strategy to
compensate for the emotional consequences of frontal-executive dysregulation, and (c) childhood abuse may contribute to
these neurocognitive deficits but may also exert effects on adult attachment disturbance that is both independent and
interacting with neurocognitive dysfunction.
The role of psychobiological factors in adult dis-
orders of social attachment has been to date lar-
gely unaddressed. Consequently, the influence
of antecedent developmental experiences, such
as maltreatment, on this relationship in adult-
hood remains unknown. Borderline personality
disorder (BPD) is a prototypical disorder of
adult social attachment (Agrawal, Gunderson,
Holmes, & Lyons-Ruth, 2004; Gunderson, 1996;
Levy, 2005; Melges &Swartz, 1989), and is as-
sociated with high rates of childhood maltreat-
ment (Zanarini, 2000). Thus, studying indi-
viduals with this disorder may provide insight
into how adult attachment disturbance is related
to psychobiological factors, and how this rela-
tionship may be influenced by childhood expe-
rience.
A Dimensional Model of Adult Social
Attachment
Phillip Shaver and colleagues (Crowell, Fraley, &
Shaver, 1999) have articulated an influential
model of adult social attachment, under the
Address correspondence and reprint requests to: Mi-
chael Minzenberg, Imaging Research Center, UC-Davis
School of Medicine, 4701 X Street, Sacramento, CA
95817; E-mail: michael.minzenberg@udcmc.ucdavis.edu.
We acknowledge the assistance of Uyen Huynh, NiVonne
Thompson, and Nami Kim with the study procedures.
A portion of this work was presented at the 59th annual
meeting of the Society for Biological Psychiatry in 2004.
Development and Psychopathology 20 (2008), 341368
Copyright
#2008 Cambridge University Press
Printed in the United States of America
DOI: 10.1017/S0954579408000163
341
guiding principle that attachment theoryis a life-
span developmental theory. They offer a dimen-
sional perspective on what has traditionally been
referred to as attachment style, characterized as
The systematic pattern of relational expecta-
tions, emotions, and behavior that results fromin-
ternalization of a particular history of attachment
experiences and consequent reliance on a particu-
lar attachment-related strategy of affect regula-
tion (Mikulincer, Shaver, & Pereg, 2003, p. 79).
In this model, neurobehavioral attachment
systems activate proximity-seeking behavior to
mitigate negative emotional states arising from
stressors that can be either physiological (e.g., ill-
ness) or psychological (e.g., absence of a parent
or mate) in nature (Mikulincer et al., 2003). Ro-
mantic relationships are of particular interest be-
cause the relationships among adults that exhibit
all four defining features of attachment relation-
ships (proximity maintenance, safe haven, se-
cure base, and separation distress) are primarily
romantic in nature (Hazan & Diamond, 2000),
and when queried about important attachment
relationships, adults tend to nominate romantic
relationships (Fraley & Davis, 1997). The rela-
tionship of adult romantic attachment to early
attachment experiences remains unclear, as
longitudinal studies are presently unavailable
(discussed in Fraley & Shaver, 2000). Their
two-dimensional measure of adult attachment,
the Experiences in Close Relationships Scale
(ECR), is derived from factor analysis of the en-
tire corpus of self-report adult attachment mea-
sures existing at one point in time (Brennan,
Clark, & Shaver, 1998). One dimension, attach-
mentanxiety, refers to reactive negative affect
that individuals may experience with attachment
partners, particularly the fear of rejection and
abandonment that are a clinical hallmark of
BPD(Gunderson, 1996). Asecond, independent
dimension, attachmentavoidance, refers to
emotional and behavioral strategies for attaining
interpersonal distance from attachment part-
ners. Along this second dimension, BPDpatients
appear to oscillate between intimacy seeking
and relational withdrawal, suggesting a particu-
lar form of approachavoidance conflict within
attachment relationships (Melges & Swartz,
1989). Among nonclinical populations, variation
in attachmentavoidance is related to cognitive
(Fraley & Shaver, 1997) and behavioral (Fraley
& Shaver, 1998) strategies for managing the
negative emotional effects of attachment-related
thoughts, or separations. On a neurocognitive
level, these observations represent the implemen-
tation of control processes to regulate reactivity.
In light of this observation, the cyclic relational
pattern that is typical of BPDpatients may reflect
the adoption of a strategy for emotion regulation
that cannot be achieved internally (intrapsychi-
cally). Fraley and Waller (1998) have argued
for the reliability and validity of a dimensional
approach to adult social attachment, and suggest
that a dimensional approach facilitates the task
of addressing underlying mechanisms. This
includes potential convergence with the di-
mensional approach to the psychobiology of per-
sonality disorders (Siever & Davis, 1991).
The Functional Neuroanatomy
of Attachment
The functional neuroanatomy underlying nor-
mal social attachment behavior has been ad-
dressed in animal models. The separation dis-
tress call, a behavior linked to infantmaternal
attachment across mammalian species, has
been related to a distributed limbic network
that includes the amygdala and situates the
anterior cingulate cortex (ACC) at the apex, in
both rodent and primate models (Hofer, 1996;
MacLean, 1985). Motherinfant attachment in
rodents also depends on the development of a
preference of each for the others odors. In
this process, the amygdala encodes the salience
of sensory stimuli and subsequently exerts in-
fluence on memory consolidation effected by
the hippocampus (Fleming, ODay, & Krae-
mer, 1999). In addition, advantageous infant
care (occurring naturally) by maternal rats is
associated with enhancements in both hippo-
campal synaptogenesis and related learning
and memory performance in the infants (Liu,
Diorio, Day, Francis, & Meaney, 2000). Fur-
thermore, pair bonding in the adult prairie
vole requires the presence in the limbic system
(including an ACC homolog) of oxytocin re-
ceptors in the female, and vasopressin receptors
in the male (Insel & Young, 2001).
Among nonhuman primates, the ACC,
amygdala (Bauman, Lavenex, Mason, Capito-
nito, & Amaral, 2004), and dorsolateral
M. J. Minzenberg, J. H. Poole, and S. Vinogradov 342
prefrontal cortex (dorsolateral PFC; Rilling
et al., 2001) mediate infant responses to mater-
nal separation. The hippocampus and orbito-
frontal cortex (OFC) have also been implicated
in affiliative behavior in primates and appear
to be involved in attachment-related behavior
in primates as well (Beauregard, Malkova, &
Bachevalier, 1995; Leckman & Herman, 2002;
Raleigh & Steklis, 1981).
Functional neuroimaging studies of healthy
adult humans have found activation of the
ACC, OFC, and other PFC areas while mothers
were exposed to their infants pictures (Bartels &
Zeki, 2004; Leibenluft, Gobbini, Harrison, &
Haxby, 2004; Nitschke et al., 2004) or cries
(Lorberbaum et al., 2002). Deactivation of the
amygdala was also observed in the mothers re-
sponse to their infant pictures (Bartels & Zeki,
2004). Reciprocal activation of the ACC and de-
activation of the amygdala is also found when
adults view pictures of their romantic partners
(Bartels & Zeki, 2000). Imaging studies of
healthy women who were grieving the death of
a first-degree family member (Gundel, OCon-
nor, Littrell, Fort, & Lane, 2003) or the breakup
of a romantic relationship (Najib, Lorberbaum,
Kose, Bohring, & George, 2004) showed
changes in activity in a number of brain regions,
including the ACC and temporal lobe, while the
subjects viewed pictures of the object of grieving.
Another study found that when healthy women
thought of negative romantic relationship out-
comes, activation was observed in the ACC and
the related adjacent medial PFC, as well as hippo-
campus andthe pole of the temporal lobe (Gillath,
Bunge, Shaver, Wendelken, & Mikulincer,
2005). Hippocampal activity was correlated
with attachmentanxiety scores from the ECR.
In addition, active suppression of these thoughts
was also associated with ACC activation, consis-
tent with the ACC roles in regulating emotion
(Ochsner & Gross, 2005), including the subjec-
tive experience of social rejection (Eisenberger,
Lieberman, &Williams, 2003), and hormonal re-
sponses tostress (Diorio, Viau, &Meaney, 1993).
This literature indicates that a widely distrib-
uted corticolimbic network subserves the many
behavioral, emotional, and cognitive features of
the social attachment system. Activity among
these regions may vary in complex patterns, de-
pending in part on the experimental paradigm
used to measure attachment. Allan Schore
(Schore, 1994, 2001) has integrated the empir-
ical literature on attachment together with that
addressing the development of emotion/moti-
vation, cognition, and behavioral control sys-
tems, to propose a model of the functional neu-
roanatomy that both mediates and is modified
by early attachment experiences. In this model,
the maturation of the brain proceeds as an expe-
rience-dependent process, in the context of the
infants relationship with the primary caregiver.
Hierarchical organization of the limbic system
is achieved as the later-maturing midline PFC
areas (particularly the right OFC and ACC)
begin to exert executive control over subcorti-
cal limbic areas. Relatively simple appraisals
of environmental stimuli attained in subcortical
limbic areas are then subject to top-down regu-
lation by the OFC and ACC, which generally
integrate social, emotional, and cognitive infor-
mation to guide complex cognition and behav-
ior (Bush, Luu, & Posner, 2000; Rolls, 2004).
This includes the joint attention, subjective
states and representations that are shared be-
tween dyads (Decety & Sommerville, 2003),
and the initiation and guidance of complex be-
havioral sequences in the interpersonal realm
(such as approach-related attachment behavior).
As emphasized by Schore (2001), attachment
functions may be particularly dependent on non-
conscious implicit information processing and
associated with nonlanguage-related functions
lateralized to the right hemisphere. Furthermore,
the midline OFC and ACC areas are ideally situ-
ated anatomically and functionally to implement
the control system of attachment posited by
Bowlby and subserve functions that can also be
considered fundamental to defining personality
(Cavada &Schultz, 2000). The effects of adverse
early attachment experiences are then understood
to be manifest inthe disruption of this experience-
dependent maturation of these higher order PFC
areas (Schore, 2002), a process described by
Hughlings Jackson as dissolution (Meares,
Stevenson, & Gordon, 1999).
Neurocognition and Temperament:
A Model for BPD
This distinction between the activity of sub-
cortical limbic areas, versus their descending
Neurocognition, attachment, and abuse in borderline 343
executive regulation by midline PFC areas, is
also fundamental to a neurocognitive model
that has particular importance for personality
and developmental disorders such as BPD
(Rothbart, Ahadi, & Evans, 2000; Posner &
Rothbart, 2000; Posner et al., 2003). In this
model, a Negative Affectivity factor is de-
scribed that includes negatively valenced and
reactive affectivity (Rothbart & Posner, 2005).
A second factor is Effortful Control, which
comprises traits indicating the voluntary and
willful regulation of attention and behavior (a
third factor, Extraversion/Surgency, is less
relevant to the authors corresponding model of
BPD, as outlined below). These authors suggest
that the Negative Affectivity factor may have a
basis in amygdala activity as well as the OFC
modulation of hippocampal function. The
Effortful Control factor is translated in the cog-
nitive domain as cognitive control, an executive
function that is postulated to have its substrate
in the ACC, adjacent medial PFC, and dorso-
lateral PFC and measured in the laboratory with
tasks such as the Stroop (Rothbart & Posner,
2005). Effortful control is found to undergo
rapid development in early childhood in concert
with the development of these brain areas (Pos-
ner & Rothbart, 2000). Although the construct
of temperament is typically understood to
have a rather fixed biological basis (typified
in the notion of genetic heritability), their the-
ory has been described as having a structural
similarity to attachment theory (Vaughn &
Bost, 1999), and temperament is identified as
one of several contributions of the individuals
state in the development of attachment
(Rothbart & Ahadi, 1994, p. 58). These investi-
gators emphasize that their model is dynamic
and interactive, and very resolvable in the
framework of social attachment, and with expe-
rience more generally (Rothbart & Ahadi,
1994). For instance, the development of effort-
ful control and its neural substrate is observed to
be dependent on interactions with the caregiver.
In addition, with brief training experiences,
children are able to improve performance on
some laboratory measures of effortful control
(Rothbart & Posner, 2005).
In this framework of temperament and its
neurocognitive basis, BPD is then hypothesized
as an adult outcome of a combination of strong
negative affectivity and impaired effortful con-
trol. This combination of temperamental ex-
tremes is proposed to provide the basis for
interpersonal dysfunction, one of the central
difficulties in BPD (Posner et al., 2003).
Negative affectivity is hypothesized to be related
to subcortical limbic hyperactivity, whereas im-
paired effortful control is hypothesized to be
because of impaired ACC and dorsolateral PFC
function. Although there is an important role
for emotion in this model, Posner, Rothbart,
and colleagues (2003) indicate that it is advanta-
geous to consider the comprehensive neurocog-
nitive functions of these neurobiological sys-
tems, because general deficits may exist in
these systems whose impact extends beyond
the clinical content areas of difficulty for a given
disorder. This perspective suggests that measures
of cold cognition have potential utility in the
assessment of how these systems relate to clini-
cal phenomena that are nonetheless imbued
with emotion, such as disturbances of personal-
ity and attachment. This two-part model is quite
similar to other models of BPD, both neurobio-
logical (Corrigan, Davidson, & Heard, 2000),
and clinical, including an influential formula-
tion of BPD, which posits a basis for social/
emotional dysregulation in the combination of
a temperamental predisposition to emotional
vulnerability with an environmentally modu-
lated emotional dyscontrol (Shearin & Linehan,
1994).
Neurocognitive and Neuroimaging
Studies in BPD
Empirical studies of neurocognition support
these hypothesized dysfunctions in BPD pa-
tients. Early investigations of neurocognition
in BPD found consistent evidence for deficits
in working memory and delayed recall (each
with both verbal and nonverbal material) and
cognitive control measures (such as the Stroop),
with mean effect sizes across these studies
at .0.60 (see Fertuck, Lenzenweger, Clarkin,
Hoermann, & Stanley, 2006, for review).
More recent studies have confirmed and ex-
tended these findings. BPD patients have been
found to exhibit deficits in cognitive control
tasks such as the Emotional Stroop (Arntz,
Appels, & Sieswerda, 2000) and the Attention
Network Task (Posner et al., 2002). BPD pa-
tients also exhibit deficits on simulated gambling
tasks (Bazanis et al., 2002; Dowson et al., 2004)
and passive avoidance tasks (Hochhausen, Lo-
renz, & Newman, 2002), which are both based
in the function of an OFCamygdala circuit.
BPD patients also show deficits in planning
and problem-solving tasks such as the Wisconsin
Card Sort Test (Lenzenweger, Clarkin, Fertuck,
& Kernberg, 2004) and the Tower of London
(Bazanis et al., 2002), as well as on tasks of
working memory (Stevens, Burkhardt, Hunt-
zinger, Schwartz, &Unckel, 2004) and other execu-
tive functions (Dinn et al., 2004; van Reekum
et al., 1996). Consistent evidence has also been
found for verbal recall and recognition deficits
among BPD patients (Dinn et al., 2004; Kurtz
& Morey, 1999; Monarch, Saykin, & Flashman,
2004), including on a task requiring conscious
control over the contents of memory (the di-
rected forgetting paradigm; Korfine & Hooley,
2000). Not all studies of BPD patients have
found deficits on executive function or delayed
recall tasks, however (Kunert, Druecke, Sass,
& Herpertz, 2003; Sprock, Rader, Kendall, &
Yoder, 2000).
Neuroimaging studies of BPD patients de-
monstrate consistent alterations in structure
and/or activity of the brain regions that support
these neurocognitive functions (reviewed in
Schmahl & Bremner, 2006). In the PFC,
volume loss and lower resting metabolism has
been found in the ACC (de la Fuente et al.,
1997; Hazlett et al., 2005; Tebartz van Elst
et al., 2003) and OFC (Lange et al., 2005; So-
loff et al., 2003; Tebartz van Elst et al., 2003)
and decreased N-acetylaspartate, a measure of
neuronal integrity, in dorsolateral PFC (Tebartz
van Elst et al., 2001). Measures of local seroto-
nergic function also show deficits in the ACC
(Frankle et al., 2005; Leyton et al., 2001; New
et al., 2002, 2004; Oquendo et al., 2005; Siever
et al., 1999) and OFC (Soloff, Meltzer, Greer,
Constantine, & Kelly, 2000) of BPD patients.
Volume loss and lower resting metabolism
has also been found in both hippocampus and
amygdala, which are often measured as one
contiguous complex (Brambilla et al., 2004;
Driessen et al., 2000; Juengling et al., 2003;
Rusch et al., 2003; Schmahl, Vermetten, Eli-
zinga, & Bremner, 2003; Tebartz van Elst
et al., 2003). In addition, hypometabolism in
the lateral temporal lobe has been correlated
with memory deficits in BPD patients (Lange,
Kracht, Herholz, Sachsse, & Irle, 2005). Func-
tional magnetic resonance imaging studies have
shown amygdala hyperresponsivity to social
and emotional stimuli in BPD patients (Done-
gan et al., 2003; Herpertz et al., 2001). BPD pa-
tients also exhibit an exaggerated ACC deacti-
vation in response to both recall of traumatic
memories and abandonment scripts (Schmahl,
Elzinga, et al., 2003; Schmahl, Vermetten, El-
zinga, & Bremner, 2004). Taken together, these
neuroimaging studies provide a clear indication
of pathology in subcortical limbic and midline
PFC structures, particularly the hippocampus/
amygdala, and ACC/OFC, respectively. These
are not only key brain structures implicated in
attachment phenomena in the models outlined
above, but they also form the putative basis
for the functional deficits in both learning and
recall, and cognitive control, respectively, that
are consistently observed in BPD patients.
Although neurocognitive impairment has been
hypothesized to be a moderator in the develop-
ment of BPD, and an influence on the attach-
ment disturbance of BPD patients (Judd, 2005),
no studies to date have examined the relationship
of neurocognitive dysfunction to attachment in
this disorder.
Childhood Maltreatment Is Associated
With Adult Attachment Disturbances
One issue that is fundamental to any proposed
neurobiological model of adult BPD attach-
ment disturbance is the role of early maltreat-
ment in both the clinical phenomena and its
neurobiological substrate. Adults with BPD
endorse a wide range of early experiences of
abuse, neglect, and other adverse events such
as witnessing domestic violence (reviewed in
Zanarini, 2000). It is not yet clear how early
in development these experiences may occur
for BPD patients, because these studies rely
on retrospective recall by the patients (either
in interview or self-report formats). Neverthe-
less, the association between maltreatment
and adult outcomes such as suicidal and other
impulsive behaviors (Brodsky & Stanley,
2001), and diagnoses of mood, anxiety,
impulse control, and personality disorders are
well recognized (Cohen, Brown, & Smailes,
2001; Kendler et al., 2000). In addition, how-
ever, maltreatment appears to be also related
to a range of outcomes that are more interper-
sonal in nature. For instance, among BPD pa-
tients, childhood sexual abuse is related to adult
victimization (Zanarini et al., 1999) and intoler-
ance of being alone (Silk, Lee, Hill, & Lohr,
1995) and childhood abuse and neglect are re-
lated to higher scores on the interpersonal rela-
tionships section of the Diagnostic Interview
for BorderlinesRevised (Zanarini et al.,
2002). Among heterogeneous clinical or com-
munity samples of adults, childhood abuse
has been related to symptoms of interpersonal
sensitivity (Bryer, Nelson, Miller, & Krol,
1987), hostility (Bryer et al., 1987; Roy,
2001), antisocial behavior (Burgess, Hartman,
& McCormack, 1987), victimization by rape
(Nelson et al., 2002), and sexual, marital and
parenting dysfunctions (Nelson et al., 2002;
Rodgers et al., 2004; Rumstein-McKean &
Hunsley, 2001; Ruscio, 2001), including abuse
of the adults own children (Widom, 1989).
These behaviors may reflect the effects of
maltreatment on adult attachment (Alexander,
1992), as empirical studies have shown that
early adversity is related to insecure attachment
measured later in life. Studies of maltreated
infants have consistently found elevated rates
of insecure attachment (reviewed in Morton
& Browne, 1998), although it is presently
unknown whether this attachment insecurity
persists into adulthood. Childhood exposure to
physical or sexual abuse, or alternatively to se-
vere neglect, are each related to both anxious
and avoidant adult attachment (Mickelson
et al., 1997). Insecure attachment may mediate
the relationship of childhood maltreatment
with adult relationship difficulties (McCarthy &
Taylor, 1999) and psychopathology (Muller &
Lemieux, 2000); however, insecure adult ro-
mantic attachment may itself be more strongly
related to childhoodparent attachment than to
childhood abuse (Styron & Janoff-Bulman,
1997). In addition, a community study of adult
incest victims, employing the Shaver adult
attachment model, found increased rates of fear-
ful and preoccupied attachment, which were
associated with elevations on the Borderline
Scale of the Millon Clinical Multiaxial Inven-
tory (Alexander et al., 1998). This suggests
that childhood sexual abuse is associated with
insecure adult attachment characterized by
negative affect and in some cases withdrawal.
Childhood Maltreatment Is Associated
With Neurobiological and Cognitive
Dysfunction
A range of neurobiological changes have been
identified in association with early maltreat-
ment and adversity, which may influence the
long-term consequences of maltreatment for
adult relational dysfunction. Prolonged mater-
nal separation among infant rats leads to persis-
tent cortisol elevations, with deleterious effects
(including increased cell death) in the hippo-
campus, medial PFC (including ACC and
OFC homologs) and other limbic regions that
mediate attachment phenomena (Sanchez,
Ladd, & Plotsky, 2001). Neuroimaging studies
of children and adolescents with posttraumatic
stress disorder (PTSD) related to childhood
abuse have found lower intracranial volumes,
which are correlated positively with age of
abuse onset and negatively with abuse duration
and PTSD symptoms (DeBellis et al., 1999).
These patients also exhibit measures of neu-
ronal disruption in the ACC (DeBellis, Kesha-
van, Spencer, & Hall, 2000). Decreased hippo-
campal volume has also been found in adults
with PTSD related to childhood abuse (Brem-
ner et al., 1997; Stein, Koverola, Hanna,
Torchia, & McCarty, 1997), although not in
all studies (reviewed in Teicher et al., 2003).
Nevertheless, relative decreases in hippocam-
pal blood flow have been found during a verbal
recall task (Bremner et al., 1999), and altered
OFC and ACC blood flow changes (Bremner
et al., 2003; Shin et al., 1999) are found when
adults with childhood sexual abuse related
PTSD are prompted to recall the abuse. Altered
activity in the ACCand amygdala has also been
found among child abuse related PTSD patients
in a fear-conditioning paradigm (Bremner,
2003).
Impairment of cognitive performance has
also been found in children exposed to maltreat-
ment. These studies have generally used mea-
sures of global cognitive function, including
various intelligence measures, which reveal
consistent IQ decrement among abused chil-
dren compared to demographically matched
nonabused children (reviewed in Cahill, Kami-
ner, & Johnson, 1999). This includes a study of
413 adults in their 20s who were subject to
court-substantiated abuse and neglect 20 years
prior, all before age 11 (Perez & Spatz Widom,
1994). This study found the abused adults as
a group to score 1 SD in intelligence (on the
Quick Test) below a well-matched control
group, and 2 SD below published norms. Expo-
sure to violence in childhood has also been
associated with lower IQ (Delaney-Black et al.,
2002). Although neurocognitive and neuro-
imaging studies of adults with BPD have fre-
quently included patients with abuse histories,
the effects of these experiences on cognitive
and neurobiological function have not been
directly addressed within the study samples.
Among those BPDneurocognition studies cited
above where intelligence tests were adminis-
tered, four found significantly lower intelli-
gence in their patient groups compared to con-
trols (Driessen et al., 2000; Monarch et al.,
2004; OLeary, Brouwers, Gardner, & Cowdry,
1991; Swirsky-Sacchetti et al., 1993), four
found small, nonsignificant IQ deficits among
the patient group (Bazanis et al., 2002; Dowson
et al., 2004; Kunert, Dreucke, Sass, &Herpertz,
2003; Stevens et al., 2004), and one found no
IQ difference among the patient group
(Sprock et al., 2000). These studies all appear
to have utilized convenience samples, and
widely differing intelligence measures, typi-
cally subtests selected from a given intelligence
battery. In addition, intelligence does not ap-
pear to have been tested as an a priori hypoth-
esis in these studies. As a result, the presence
and role of intelligence deficit in BPD remains
to be adequately addressed (see Discussion
section).
The domain specificity of cognitive deficits
found in the studies of abused individuals in the
community remains to be characterized. How-
ever, a recent study of children does begin to
address the role of maltreatment and specific
neurocognitive functions as risk factors for
BPD. This study found, among 185 maltreated
and 175 nonmaltreated children, that those
with high scores on a measure of BPD
phenomenological precursors exhibited selec-
tive impairments in cognitive control on the
Attention Network Task (ANT; Rogosch &
Cicchetti, 2005). This finding is very consistent
with the results of the Posner et al. (2003) BPD
study, which used the same cognitive control
task. In addition, however, Rogosch and Cic-
chetti found that maltreatment and cognitive
control impairment were not related to each
other, and that each (but not the interaction of
the two) independently predicted the level of
BPD precursors. This suggests that cognitive
control deficits, and exposure to maltreatment,
may exist as independent risk factors for BPD
in adulthood. In an analogous manner, we
presently test the contributions of cognitive
control and abuse history to adult attachment
disturbance among adults with BPD (see
below).
Hypotheses in the Present Study
In summary, theoretical models and empirical
studies of attachment (in animal models and hu-
mans), temperament, and BPD pathophysiol-
ogy, all suggest a distinction between reactivity
and control, instantiated in cognitive functions
of medial temporal lobe limbic areas and mid-
line PFC areas, respectively. This suggests
that disturbances along each adult attachment
dimension among BPD patients may have
distinct neurocognitive correlates. Established
neurocognitive dysfunction in BPD includes
verbal and nonverbal memory, and cognitive
control functions, which are likely related to
the findings of pathology in BPD patients in
the medial temporal lobe and midline PFC
areas, respectively. Childhood maltreatment is
associated with similar changes in brain and
cognitive functions in other populations, and
adult attachment disturbance as well. As a
result, maltreatment may be related to adult
neurocognitive dysfunction in BPD, but may
also contribute independently to the adult
attachment disturbances seen in this disorder.
Thus, we tested the following hypotheses:
1. The BPD group will be impaired on tests of
short-term recall, and executive functions
that are concerned with cognitive control
and decision making.
2. Among the BPD group, short-term recall
performance is associated with attachment
anxiety, whereas executive dysfunction in
the cognitive control and decision-making
domains is associated with attachment
avoidance.
3. Among the BPD group, childhood maltreat-
ment severity is associated with both short-
term recall and executive dysfunction.
4. Neurocognitive performance and childhood
maltreatment history each make an indepen-
dent contribution to the degree of adult at-
tachment disturbance.
5. Because of limbic dysregulation in BPD and
the role of emotion-regulation in attach-
ment-related behavior, the cognitive deficits
hypothesized in Hypothesis 1 are exacer-
bated by emotionally salient stimuli.
Methods and Materials
Subjects
Forty-three individuals with BPD between 18
and 60 years old were recruited from the com-
munity, including individuals both in and out
of outpatient mental health treatment (Table 1).
Recruitment strategies included both direct
contact with clinical providers in the commu-
nity, advertisements placed in public places
and on-line, and word of mouth. Exclusion cri-
teria included comorbid diagnoses of schizo-
phrenia, schizoaffective, or bipolar spectrum
disorders, or current diagnoses of major depres-
sive disorder, PTSD, or substance dependence;
and history of neurological disease. Although
PTSD is a common comorbid condition in
BPD, we excluded these individuals as PTSD
patients exhibit deficits in various neurocogni-
tive functions, including verbal recall and ex-
ecutive functions (such as Stroop performance;
Golier & Yehuda, 2002), which would there-
fore confound the results of the present study.
All BPD subjects were clinically stable; none
were hospitalized in the month prior to study,
and none had psychotic or dissociative symp-
toms at the time of study. The mean (+SD)
Global Assessment of Function was 57 (+9).
Seventy-five percent were on psychiatric
medications at study (Table 1). BPD subjects
underwent psychiatric diagnostic evaluation
with the Structured Clinical Interview for
Axis II (SCID-II) using DSM-IV criteria, after
completing the SCID-II screening questionnaire
(First, Gibbon, Spitzer, Williams, & Benjamin,
1997). Axis I disorders were evaluated with the
SCID-I (First, Spitzer, Gibbon, Williams, &
Benjamin, 1995). The diagnostic interviews
of 21 (53%) BPD subjects were randomly cho-
sen for videotaping, which was reviewed by a
second SCID-trained diagnostician (doctoral-
level clinical psychologist). Interrater agree-
ment for BPD criteria was high (k .81). Co-
morbid Axis I diagnoses included panic disor-
der (n 2), dysthymic disorder (n 6),
bulimia (n 2), gender identity disorder (n 1),
amphetamine abuse (n 1), and cannabis
abuse (n 1). Comorbid Axis II diagnoses in-
cluded paranoid (n 10), schizoid (n 3),
schizotypal (n 4), antisocial (n 5), histrionic
(n 3), narcissistic (n 5), avoidant (n 19),
dependent (n 8), and obsessivecompulsive
(n 6).
Table 1. Demographic and clinical
characteristics of subjects
BPD Group
(Mean+SD)
Control Group
(Mean+SD)
No. of subjects 43 26
Gender (% female) 88 89
Age (years) 35+13 34+9
Education (years) 14+3* 16+2
Parental education
(years) 15+3 15+2
Ethnicity (%)
European
American 77 77
African
American 7 8
Latino American 5 4
Asian American 9 12
Native
American 2 0
Age at symptom
onset 12+6 NA
Global functioning
(GAF) 56+9 NA
On medications at
study 77% NA
Note: BPD, borderline personality disorder group; SD,
standard deviation; GAF, Global Assessment of Function
Scale (DSM-IVAxis IV).
*Significant group difference by t test ( p , .05).
Control subjects were also recruited fromthe
community. They were similar to the BPD
group in age, parental education, and employ-
ment (Table 1). Prospective control subjects
were screened for personality disorders using
the SCID-II screening questionnaire, and for
Axis I disorders using a modified version of
the SCID-I Nonpatient version. These Axis I
diagnoses included schizophrenia, schizoaffec-
tive disorder, bipolar affective disorder Type I
and II, cyclothymia, major depressive disorder,
dysthymic disorder, PTSD, panic disorder, gen-
eralized anxiety disorder, substance-related dis-
orders, and intermittent explosive disorder.
Exclusion criteria included any past or present
psychiatric diagnosis or treatment, or neuro-
logical disease. No control subject met more
than one DSM-IV criterion for BPD, or neared
the screening threshold for any other personal-
ity disorders. After complete description of
the study to the subjects, written informed
consent was obtained. All subjects were paid
for participation at a rate of approximately
$12/hr.
Self-report measures
Experiences in close relationships (ECR). This
36-item self-report questionnaire (Brennan
et al., 1998) assesses patterns of social attach-
ment in adult relationships. The 18 items on
each subscale were selected from those with
the highest loadings on one of two factors that
represent the latent dimensions underlying var-
iation in self-reported social attachment. Items
are rated on a 7-point Likert scale from agree
strongly to disagree strongly, and examples
on each respective dimension include I worry
about being abandoned and Just when my
partner starts to get close to me I find myself
pulling away. Scores are generated for each
of the two underlying dimensions: attach-
mentanxiety and attachmentavoidance. Di-
mensional scores can also be converted to at-
tachment categories (represented by quadrants
of two-dimensional space) for comparison
to typological attachment schemes. However,
the ECRcreators recommend analysis of dimen-
sional scores, which provide greater power and
precision in the measurement of attachment
(Brennan et al., 1998). The internal consistency
reliability for each dimension is excellent in the
present sample (Cronbach a .93 and .94, re-
spectively). The ECR also appears adequate
(and superior to other self-report adult attach-
ment instruments) on psychometric measures
derived from item response theory (Fraley,
Waller, & Brennan, 2000). Three subjects did
not complete the ECR: one who reported no his-
tory of romantic relationships, and two who did
not complete the study. A recent study of 99
adults with BPD using the ECR found most to
be described by preoccupied or fearful attach-
ment types, corresponding to high attachment
anxiety (in both) and low versus high attach-
mentavoidance, respectively (Levy, 2005).
Among a sample of inpatients with major
depression, ECR attachmentavoidance was
modestly positively related to depression scores,
and negatively to both marital satisfaction and
recalled opposite-gender parental care (using
the Parental Bonding Instrument; Difilippo &
Overholser, 2002). In a nonclinical sample of
students, both ECR dimensional scores were
related to alexithymia scores (Picardi, Toni, &
Caroppo, 2005).
Childhood Trauma Questionnaire (CTQ). This
28-item retrospective self-report (Bernstein &
Fink, 1998) assesses patterns of maltreatment
in childhood and adolescence. It contains five
scales: emotional abuse, sexual abuse, physical
abuse, emotional neglect, and physical neglect.
Total abuse and total neglect are reported as
summary scores. Cronbach a values ranges
from .66 for physical neglect to .92 for sexual
abuse; the 4-month testretest reliability ranges
from .70 to .86 (Bernstein & Fink, 1998). The
CTQ is also strongly associated with therapist
and interviewer ratings of abuse and neglect
(Bernstein & Fink, 1998).
Recall measures
Verbal Learning Test. We developed a test of
verbal recall containing emotionally neutral
and emotionally charged words. This test is de-
rived from the Hopkins Verbal Learning Test
(HVLT; Benedict, Schretten, Groninger, &
Brandt, 1998). The original HVLT has been
found to be a very sensitive index of mild
HIV-related cognitive impairment (Carey
et al., 2004; Woods, Scott, et al., 2005). It can
discriminate verbal recall ability between the
following groups: Alzheimer disease patients
and either Parkinson disease (Grace et al.,
2005) or depressed patients (Strang, Donnelly,
Grohman, & Kleiner, 2002), mild cognitive
impairment patients from both healthy controls
and Alzheimer disease patients (De Jager, Ho-
gervorst, Combrinck, & Budge, 2003), meth-
amphetamine-dependent adults (Woods, Rip-
peth et al., 2005), and mild traumatic brain
injury patients (Bruce & Echemendia, 2003)
from healthy controls. It has also been used
to discriminate subgroups of outpatients with
schizophrenia by symptom subtype (Mahurin,
Velligan, & Miller, 1998), and predicts their
vocational outcome (Abi-Saab, Fiszdon, Bry-
son, & Bell, 2005). It is not sensitive to depres-
sion, among outpatients with epilepsy (Letz
et al., 2003). We modified the HVLT by includ-
ing an equal number of hot negative-valence
words (e.g., murder, pus) and cold emotion-
ally neutral words (e.g., table, car), each within
three semantic categories, both to evaluate the
effect of emotional item content and to reduce
the normative ceiling effect on overall perfor-
mance. Hot words had significantly more emo-
tional content than cold words ( p , .0005) by
normative ratings (John, 1988); they were not
different in average length or frequency in the
lexicon by two published norms (Kucera &
Francis, 1967; Thorndike & Lorge, 1944). All
stimuli were digitally recorded.
Family pictures. This test from the Wechsler
Memory ScaleThird Edition presents pic-
tures of families in social interaction. Subjects
view cards depicting complex narrative scenes
of family units, each for 10 s, and are asked to
describe who is in each picture, where they
are located spatially, and what they are doing,
both immediately and after a delay of 20 min
(Wechsler, 1997). This test of episodic recall
is heavily dependent on associative feature
binding, and likely dependent primarily on
medial temporal lobe (especially hippocampal)
function (discussed in detail in Gold, Poet,
Wilke, & Buchanan, 2004). It discriminates
schizophrenia patients from healthy controls
(Gold et al., 2004), as well as right from left
temporal lobectomy patients (Doss, Chelune,
& Neugle, 2004), supporting its right hemi-
sphere lateralizing value.
Sentence repetition. This test of immediate ver-
bal memory for emotionally neutral sentences
(Spreen & Strauss, 1998) was administered in
sequence with an emotionally charged version
constructed for this study. The emotionally
charged version contained items of negative va-
lence (e.g., When cars crash head on, the win-
dows quickly shatter). This new version main-
tained the structure of the older version, with
increments of syllable length across sentences,
which were all declarative in nature. The two
versions of this test were digitally recorded
and presented in counterbalanced order across
subjects. Individual sentences were played
one at a time in fixed order (of increasing
length) for all subjects, who repeated the sen-
tence exactly as they heard it, immediately
thereafter (as they were previously instructed).
The older version discriminates the following
groups from healthy, matched controls:
adults with aphasia, Alzheimer disease, left-
hemisphere lesions, and children with dyslexia
(Spreen & Strauss, 1998). It also discriminates
left versus right temporal lobe epilepsy patients
(Hermann, Seidenberg, Haltiner, & Wyler,
1992). Among patients with schizophrenia, it
discriminates those with auditory hallucina-
tions from those without (Hoffman, Rapaport,
Mazure, & Quinlan, 1999), as well as undiffer-
entiated from paranoid schizophrenia subtypes
(Seltzer, Conrad, & Cassens, 1997); and defi-
cits on this test remain stable (relative to other
neurocognitive deficits) across a wide age range
(Harvey et al., 1995).
Executive function measures
Stroop Test. A computer-administered version
was used to measure both classic and emotional
Stroop effects. Subjects were asked to name the
color of ink used to print the following five
blocks of stimuli (20 items each): color naming
(colored Xs), cold words, hot words, color
word congruent, and colorword incongruent.
Both the order of blocks and the order of items
within each block were randomized. The hot
and cold words had the same average letter
length and frequency in the lexicon (Kucera &
Francis, 1967). Hot words contained signifi-
cantly more emotional content than cold words
( p ,.0005) by normative ratings (John, 1988).
Classic Stroop Interference was computed as
the ratio of mean response times (RTs) in cor-
rect trials of two conditions: colorword incon-
gruent/color naming. Likewise, Emotional
Stroop Interference was computed as the ratio
of mean RTs in correct trials of two conditions:
hot word/cold word. Subjects were instructed
to name the color of the word despite what
the subject saw on screen, and to go as fast
as you can without making mistakes. Each
subject demonstrated an accurate recognition
of each color before the test began. Twenty-
four practice items (from color-naming and
cold word categories) were presented, leading
into the experimental trials (40 per block) with-
out interruption. The literature on the classic
Stroop is immense (over 400 published papers
as of 1991; MacLeod, 1991), including studies
of psychiatric populations such those with
schizophrenia (reviewed in Henik & Salo,
2004). Among mood and anxiety disorder
patients, it discriminates manic from depressed
and remitted bipolar I patients (Dixon, Krava-
riti, Frith, Murray, & McGuire, 2004), bipolar
from unipolar depressed patients (Borkowska &
Rybakowski, 2001), psychotic from nonpsy-
chotic major depression patients (Schatzberg
et al., 2000), and obsessivecompulsive disor-
der patients from healthy controls (Penades,
Catalan, Andres, Salamero, & Gasto, 2005).
The emotional Stroop has also been used
among psychiatry patients, particularly those
with mood and anxiety disorders, who show
consistent differences in interference effects
compared to control groups; it is interesting
that those with PTSD appear to exhibit the
greatest interference effects (reviewed in Wil-
liams, Mathews, & MacLeod, 1993). Both the
classic and emotional Stroop have shown dif-
ferences between BPD patients and controls
(see introductory section; reviewed in Fertuck
et al., 2006).
Hayling Sentence Completion Test. The Hay-
ling Test (Burgess & Shallice, 1997) is consid-
ered to be a test of response selection (Elliot,
Dolan, & Frith, 2000) and response inhibition,
an aspect of cognitive control (Burgess &
Shallice, 1996). This test is sensitive to PFC in-
jury (Burgess & Shallice, 1996), and in func-
tional brain imaging paradigms activates OFC
(Collette et al., 2001; Elliot et al., 2000), ACC
(Nathaniel-James, Fletcher, & Frith, 1997),
and dorsolateral PFC(Nathaniel-James &Frith,
2002). Digitally recorded incomplete sentences
were presented in random order for the subject
to complete with a single word. In Section 1,
subjects were instructed to complete the sen-
tence immediately by saying any single word
that made sense, as fast as possible without
repeating any words. In Section 2, incomplete
sentences were presented but the subject was
instructed to provide a word that does not fit,
that is completely unrelated to the sentence in
any way, again as fast as possible without
repeating words. For this study, we modified
Section 2 items to include 16 emotionally hot
sentence stems (e.g., The baby cried and upset
her ___) and 16 emotionally neutral (cold)
sentence stems (e.g., It took a while for the
paint to ___). These were drawn fromsentence
completion norms (Bloom & Fischler, 1980) or
created by the first author. Section 2 responses
were rated for their semantic relation to the sen-
tence stems according to established criteria
(Burgess & Shallice, 1996). Directly and indi-
rectly related responses were scored as errors.
As in the Stroop, Hayling interference effects
were computed as the ratio of RTs in correct
trials: Section 2/Section 1, and hot items/cold
items. Impairment of cognitive control on the
Hayling is associated with both auditory
hallucinations (Waters, Badcock, Maybery, &
Michie, 2003) and social dysfunction in schizo-
phrenia (Chan, Chen, Cheung, &Cheung, 2004),
and is found together with attenuated midline
PFC activation in alcohol-dependent subjects
(Noel et al., 2002). Performance on this test
also discriminates manic, depressed, and remitted
bipolar patients fromeach other and fromhealthy
controls (Dixon et al., 2004), and children with
attention deficit disorder with hyperactivity
from those with oppositional defiant disorder
or conduct disorder (Clark, Prior, & Kinsella,
2000).
Gamblers Test. This computer-administered
test simulates a card game, and assesses the
ability to evaluate the consequences of choices
and revise ones choices to optimize rewards
(Bechara, Damasio, Damasio, & Anderson,
1994). On screen are four decks of cards with
a similar appearance. Subjects are instructed
to choose from any deck they please, and per-
mitted to change deck choices at any time, in
order to win as much money as possible. Sub-
jects are given $2000 in play money at the out-
set, and each card choice reveals either a gain or
loss of money, or both. The test terminates after
100 choices. Unbeknownst to the subject, these
decks vary by frequency and amount of gains
and losses associated with choices from them:
in two (bad) decks gains are more frequent
but losses are larger, leading to net loss over
time; in the other two (good) decks, gains
are smaller in individual trials but net gains
are larger over time. Subjects are considered
to be sensitive to future consequences if their
tendency to choose is guided by the large
losses, away from the bad decks over time;
subjects insensitive to future consequences per-
sist in choosing from bad decks despite the
adverse consequences. This test is sensitive to
OFC injury (Bechara et al., 1994) and amyg-
dala disease (Bechara et al., 1999), and has
been utilized to demonstrate decision-making
impairment in clinical populations related to
BPD, such as substance abusers (Bechara,
Dolan, & Hindes, 2002; Grant, Contoreggi, &
London, 2000; Petry, Bickel, & Arnett, 1998),
antisocial alcoholism (Mazas, Finn, & Stein-
metz, 2000) and intermittent explosive disorder
(Best, Williams, & Coccaro, 2002), and non-
clinical subjects with high psychopathy ratings
(Van Honk, Hermans, Putman, Montagne, &
Schutter, 2002).
Intelligence measures
The Wechsler Abbreviated Scale of Intelli-
gence (WASI; Wechsler, 1999) comprises vo-
cabulary, similarities, block design, and matrix
reasoning subtests. The test provides estimates
of verbal (VIQ), performance (PIQ), and full-
scale IQs (FSIQ), which are highly correlated
with these indices on the full Wechsler Adult
Intelligence ScaleThird Edition (Wechsler,
1999). In this study, we used the WASI as a sup-
plementary measure, to allow comparison of
performance on the above tests to more general
cognitive abilities.
Results
General statistical analytic strategy
We first computed Z scores for all cognitive mea-
sures, based on their means and standard devia-
tions inthe CONgroup (subaverage performance
defined as a negative z score). Composite recall
and executive indices were obtained from mean
z scores of the three recall and three executive
measures, respectively. We also computed hot
and cold indices from mean z scores of the four
hot and four cold conditions (in Verbal Learning,
Sentence Repetition, Stroop, and Hayling Tests).
We then conducted a set of preliminary infer-
ential tests as follows. Preliminary tests of
significance consisted of (a) a mixed-model
analysis of variance to evaluate the effects of
hot versus cold condition and (b) canonical
correlations to evaluate the relationship of cog-
nitive scores to attachment and maltreatment
indices for the BPD group. All correlations
between cognition and either attachment or mal-
treatment are computed for the BPDgroup only.
We identified significant effects from the
preliminary analyses, and then continued to
four main inferential tests of hypotheses indi-
cated in the introductory section: (a) compari-
son of BPD versus CON cognitive scores, as
univariate analyses on neurocognitive indices
and individual neurocognitive measures; (b)
bivariate correlation of cognitive performance
with attachment in the BPD group, including
a direct statistical comparison (Cohen &Cohen,
1983) of the correlations (Pearson r coeffi-
cients) of attachmentanxiety with recall versus
executive function, and in a parallel compari-
son, attachmentavoidance with executive
function versus recall; (c) bivariate correlation
of cognitive performance with maltreatment in
the BPD group; and (d) a regression analysis
to determine the respective contribution of neu-
rocognitive performance and maltreatment (and
their interaction) to attachment scores, also in
the BPDgroup. We also evaluated partial corre-
lations in a post hoc manner, controlling sepa-
rately for medication status (i.e., presence vs.
absence of concurrent psychotropic medication
treatment), illness severity (GAF scores), and
the presence or absence of comorbid Axis II
Cluster C diagnoses on DSM-IV in the BPD
group. We report group comparisons on cog-
nitive measures, as well as correlations with
attachment and maltreatment, all with and
without controlling for intelligence, to allow the
reader to compare the corresponding effects.
This data is presented to inform the issue of in-
telligence deficit in BPD, as we believe this to
remain an important but largely unaddressed is-
sue in the literature to date (see introductory and
Discussion sections). For all tests, the criterion
of statistical significance was p , .05, two
tailed (except as indicated). However, to permit
consideration of possible Type II errors, we also
report any trends that approach significance
( p , .10).
Results of Preliminary Analyses
Effects of emotion content on cognitive
performance
In the total sample, there was a significant main
effect of emotion condition, F (1, 59) 6.78, p
.01. This was accounted for by significantly
greater recall of hot items than cold items on the
Verbal Learning Test, F (1, 64) 11.03, p
.001, and Sentence Repetition Test, F (1, 63)
104.8, p , .0005, as well as significantly
greater interference from hot items than cold
items on the Emotional Stroop, F (1, 64)
6.60, p .01. On the Hayling Test, hot and
cold items showed a nonsignificant trend in the
same direction, F (1, 60) 3.00, p .09. These
results confirm that the manipulation of hot ver-
sus cold emotional content generally produced
the intended experimental effect on these tasks.
There was no significant interaction of
Group (BPD, CON) Condition (hot, cold) in
the overall test, F (1, 59) 1.86, p .2, nor
in separate univariate tests on each cognitive
task (all p values ..4). In addition, differences
in hot versus cold performance were uncorre-
lated with the attachment and maltreatment
measures (all p . .11). This indicates that add-
ing emotional content to the cognitive tasks had
comparable effects in the BPD and CON
groups, and that these effects were unrelated
to attachment scores or maltreatment history.
Consequently, no further analyses of hot versus
cold items will be presented. The hot index and
cold index were very highly correlated with one
another (r .94, p , .001). Thus, for the re-
mainder of this study, we used the mean of
hot and cold scores on the Verbal Learning,
Sentence Repetition, and Hayling Tests, and
we analyzed classic Stroop (not Emotional
Stroop) interference effects.
Canonical correlation between cognitive
performance and both attachment scores and
childhood maltreatment in the BPD group
In a preliminary test of significance, lower
scores on the Recall Index and Executive Index
were correlated with attachmentanxiety and
attachmentavoidance (canonical R 2.53,
p .006), and in a separate analysis, with abuse
and neglect (canonical R 2.57, p .01).
Main Inferential Test Results
Hypothesis 1: Cognitive performance is
impaired among the BPD group
The composite recall and executive indices
were significantly correlated with one another
in BPD (r .43, p .008) and less so in
CON (r .34, p .11), which means that these
indices measure distinct, but not completely in-
dependent, cognitive domains. Table 2 sum-
marizes differences between BPD and CON
subjects on cognitive measures. On the Recall
Index, BPD performed worse than the CON
group by nearly 1 SD, F (1, 62) 8.03, p
.006. This was mainly accounted for by signif-
icantly poorer recall on the Verbal Learning
Test, F (1, 62) 7.75, p .007. Sentence repe-
tition showed a trend in the same direction, but
did not attain statistical significance ( p .08).
Performance on family pictures was not signif-
icantly different between groups ( p .14). On
further analysis of the Verbal Learning Test,
BPD also performed significantly worse than
CON on the delayed recognition trial, F (1,
64) 6.70, p .01. This suggests that the
BPD groups poorer recall was not simply be-
cause of inefficient information retrieval, but
reflected reduced learning and retention of
new information.
Similarly, on the Executive Index, BPD per-
formed worse than the CON group by nearly 1
SD, F (1, 60) 7.03, p .01. This was mainly
accounted for by significantly worse perfor-
mance on the Gambler Test, F (1, 64) 4.58,
p .04. The Stroop and Hayling interference
effects were greater for the BPD group, but
these did not attain significance ( p .11 and
0.18, respectively). Figure 1 illustrates each
groups performance across epochs on the
Gambler Test. There was no significant Group
Epoch interaction on this test, F (4, 63) .56, p
.5. These results indicate that BPD subjects
made fewer advantageous deck choices across
trials than CON subjects, but that the shape of
the learning curve was similar in the two groups.
Figure 1. Gamblers Test performance. Performance over time by two subject groups (mean +standard
deviation). Each epoch comprises a block of 20 sequential card choices. The Y axis is the number of strate-
gically advantageous choices minus disadvantageous choices (see Methods section). The difference
between BPD and control subjects was significant, as was subjects overall improvement over time;
there was no significant GroupEpoch interaction (see Results section for details).
Table 2. Cognitive performance of borderline group compared to control group
Neurocognitive
Measures
BPD Z Score
(Mean+SD)
Significance
( p)
Recall Index 20.9+1.4 .006
Verbal Learning Test
Learning trials (13) 20.8+1.2 .006
Delayed recall 20.7+1.3 .036
Recognition 21.1+2.0 .012
Sentence repetition 20.5+1.2 .080
Family pictures
Immediate recall 20.4+1.0 .145
Delayed recall 20.4+1.0 .150
Executive Index 20.9+1.5 .010
Gamblers Test (15) 20.6+1.3 .036
Stroop Test (interference) 20.5+1.5 .110
Hayling Test (interference) 20.4+1.3 .182
General intelligence 20.9+1.4 .007
BPD IQs CON IQs
Full-scale IQ 105+15 115+11 .007
Verbal IQ 106+16 115+11 .032
Performance IQ 103+14 112+13 .008
Note: The above z scores are computed fromthe mean and standard deviation of the control group, with negative
z scores indicating below-average performance. In addition, IQ scores from the Wechsler Abbreviated Scale of
Intelligence are shown. Statistical significance levels are by analysis of variance (see Results for details).
FSIQ was 10 points lower in the BPD group
than in the CON group, F (1, 64) 7.86, p
.007. This difference is approximately two-
thirds of 1 SD among the general population
(i.e., from published norms), and was apparent
in both VIQ, F (1, 64) 4.84, p .03, and PIQ,
F (1, 64) 7.50, p .008. FSIQ was correlated
with the recall index (r .61, p , .0005) and
with the executive index (r .46, p .004).
Because of the group differences in intelli-
gence, we reassessed the above group compari-
sons on all cognitive measures by covarying
for VIQ (for tests that used verbal content),
except for family pictures and the Gamblers
Test, where we covaried for PIQ. In this analysis,
statistically significant group impairment in the
BPD group persisted for the recall index, F (1,
61) 4.14, p .046, and Verbal Learning
Test, F (1, 62) 4.10, p .047, with a trend to-
ward impairment in the BPD group observed on
the executive function index, F (1, 58) 3.75,
p .058. The significant BPDgroup impairment
on the Gamblers Test was abolished upon co-
varying for PIQ ( p .2), and no other statisti-
cally significant group differences were found.
related to attachment disturbance in BPD
Table 3 lists bivariate Pearson correlations be-
tween the cognitive and attachment measures
in the BPD group. Attachmentanxiety was as-
sociated with lower scores on the recall index (r
2.43, p .005). This was mainly accounted
for by significant correlations of attachment
anxiety with verbal learning and family pictures
recall. In a direct comparison, attachmentanx-
iety was negatively correlated to a significantly
greater degree with recall than with executive
function (t 21.784, df 37, p , .025 one
tailed). Conversely, attachmentavoidance was
associated with lower scores on the executive
index (r 2.49, p .002). This was mainly
accounted for by significant correlations of
attachmentavoidance with interference effects
on the Stroop and Hayling Tests (r .33 and r
.35, respectively, p , .04). In a direct com-
parison, attachmentavoidance was negatively
correlated to a significantly greater degree
with executive function than with recall (t
21.655, df 37, p , .05 one tailed). Attach-
ment scores on both dimensions showed non-
significant tendencies to be correlated with
lower sentence repetition scores, and attach-
mentanxiety with Gamblers Test performance
( p , .10). Controlling for medication, illness
severity (GAF), or comorbid Cluster C diagno-
ses had negligible effect on these correlations
(all partial r values were within .07 of the
zero-order correlations). Similarly, controlling
for IQ (as in the between-group comparisons
above) had modest to minimal effect on these
Table 3. Relationship of neurocognition to adult attachment and childhood
maltreatment in borderline personality disorder group
Neurocognitive Measures
Attachment Maltreatment
Anxiety Avoidance Abuse Neglect
Recall Index 2.43** 2.29* 2.31* 2.14
Verbal learning (13) 2.35* 2.21 2.28* .01
Family pictures 2.35* 2.17 2.21 .02
Sentence repetition 2.29* 2.27* 2.21 2.32**
Executive Index 2.18 2.49*** 2.48*** 2.09
Gamblers Test 2.30* 2.22 2.35** .07
Stroop interference .03 .33** .37** .23
Hayling interference .07 .35** .21 2.03
General intelligence (FSIQ) 2.27* 2.38** 2.12 .14
Verbal IQ 2.28* 2.31** 2.12 .15
Performance IQ 2.20 2.36** 2.22 .10
Note: FSIQ, full-scale IQ; Pearson correlation coefficients.
*p , .10. **p , .05. ***p , .01. Two-tailed significance.
correlations: all partial r values remained within
.10 of significant zero-order correlations.
related to childhood maltreatment in BPD
Table 3 lists bivariate Pearson correlations be-
tween the cognitive and maltreatment measures
in the BPD group. Abuse was significantly
correlated with the Executive Function Index
(r 2.48, p .003), including with Gamblers
Test (r 2.35, p .03) and Stroop impair-
ment (r .37, p .02). Abuse showed a
trend-level correlation with poorer recall (r
2.31, p .06) and verbal learning (r
2.28, p .09). Neglect was correlated only
with lower sentence repetition (r 2.32, p
.05). Intelligence measures were not correlated
with abuse or neglect. Controlling for IQ (as
in the between-group comparisons above) had
minimal downward effect on these correlations:
all partial r values were within .02 of the zero-
order correlations. In contrast, partial correla-
tions of neglect with three cognitive measures,
controlling for IQ, caused the partial r values
to be raised over their corresponding zero-order
r values: with the recall index, r changed
from 2.14 to 2.27 (new p .10); with sen-
tence repetition correlation, r changed
from 2.32 to 2.44 (new p .006), and with
the Stroop, r changed from .23 to .28 (new
p .09). Controlling for medication, illness se-
verity (GAF), or comorbid Cluster C diagnoses
had negligible effect on the zero-order correla-
tions of maltreatment with neurocognitive per-
formance (all partial r values remained within
.07 of the zero-order correlations).
Hypothesis 4: Neurocognitive dysfunction
and maltreatment make independent
contributions to adult attachment
disturbance in BPD
In regression analysis, attachmentanxiety was
significantly predicted by recall index scores (b
20.89, p ,.0005) and abuse (b 0.64, p ,
.0005), as well as the interaction between the
two (b 0.71, p .014; with R
2
for the model
.44).
In a separate analysis, attachmentavoidance
was significantly predicted by Executive Func-
tion Index scores (b 20.43, p .001) and
abuse (b 0.25, p .05; with R
2
for the model
.36). The interaction between executive func-
tion and abuse was not associated with signifi-
cant variance in attachmentavoidance scores.
Discussion
Attachmentanxiety and impaired recall
Studies addressing attachment-related phenom-
ena and models of temperament (both in nor-
mal development and in BPD) have identified
variation in these phenomena because of the
factor of reactivity. This factor appears to have
a basis in subcortical limbic function, particu-
larly the medial temporal lobe structures, the
amygdala, and hippocampus. Given the consis-
tent findings in BPD of impaired (verbal and
nonverbal) recall, a cognitive function that is
primarily dependent on the medial temporal
lobe (Squire, Stark, & Clark, 2004), and which
shows altered structure and function in BPD,
we hypothesized that a measure of reactivity
in attachment settings would be related to recall
impairment. Consistent with this hypothesis,
attachmentanxiety scores were specifically
related to short-term recall deficits. These rela-
tionships were unaccounted for by intelligence
deficits, nor by clinical factors such as medica-
tion status, illness severity, or comorbid Cluster
Cpersonality disorders. This association is con-
sistent with the finding by Gillath et al. (2005)
that attachmentanxiety is associated with ele-
vated activity in the hippocampus while healthy
subjects think of negatively valenced relation-
ship outcomes. This association could reflect
a few possible underlying scenarios: that im-
paired recall (reflecting underlying medial tem-
poral lobe dysfunction) results in attachment-
related reactivity; that this reactivity, driven by
other causes, leads to impaired recall (e.g.,
Kim & Diamond, 2002); or that both the reac-
tivity and the recall impairment are related by
a common unidentified mechanism. The con-
sistent evidence for altered medial temporal
lobe structure and function in brain imaging
studies of BPD (Brambilla et al., 2004; Done-
gan et al., 2003; Driessen et al., 2000; Herpertz
et al., 2001; Juengling et al., 2003; Rusch
et al., 2003; Schmahl, Vermetten, et al., 2003;
Tebartz van Elst et al., 2003) suggests that recall
deficits and medial temporal lobe dysfunction in
BPD are not merely downstream effects of dis-
turbances in other brain regions. It is certainly
possible that other brain areas that mediate re-
sponses to environmental stimuli (such as visual
association cortices, other subcortical limbic
areas, or brainstem monoamine nuclei) may
also be dysfunctional in BPD, with either paral-
lel effects on attachment reactivity and recall, or
on reactivity which then in turn affects recall ad-
versely. Unfortunately, these other areas have
not yet been examined for structural or func-
tional integrity in BPD patients. Of interest,
we found that attachmentanxiety was also
related to impairment on the Gamblers Test.
This test is sensitive to neurological disease
affecting both the OFC (Bechara et al., 1994)
and the amygdala (Bechara et al., 1999), and
in addition, impairment on this task is found
among several populations characterized by in-
terpersonal dysfunction (see task description in
Methods). This finding, then, is consistent with
the notion that impairment in neurocognitive
function with a basis in OFCamygdala cir-
cuitry is another important feature of interper-
sonal dysfunction. Ultimately, the relationship
of attachment reactivity to more direct measures
of neural function will be necessary to deter-
mine the neural basis for the relationships
observed in the present study.
Attachmentavoidance and executive
dysfunction
As hypothesized, elevated attachmentavoid-
ance in BPD was specifically associated with
executive dysfunction on tasks of cognitive
control. Although the deficit of the BPD group
was reduced to a trend level of significance
( p .058) upon covarying for intelligence,
the significant correlation (among the BPD
group) between attachmentavoidance and the
executive index persisted. This suggests that
this association is not merely an artifact of sub-
ject selection that is biased by intelligence (see
below for fuller discussion of the issue of intel-
ligence and maltreatment in BPD). These ex-
ecutive functions have a basis in the function
of the midline PFC, including ACC and OFC,
which are areas implicated in models of attach-
ment outlined in the introductory section. In
these models (e.g., MacLean, 1985; Schore,
1994, 2001), ACC and OFC serve as the apex
of control systems that integrate social and emo-
tional information, with resulting descending
regulation of subcortical limbic activity and as-
sociated hormonal and physiological output. In
addition, the ACC and OFC organize complex
behavioral sequences that represent expressions
of attachment behavior, such as the separation
distress call and other proximity-seeking be-
haviors that are common across mammalian
species (Hofer, 1996; MacLean, 1985). Cog-
nitive control is a cognitive function that has
been implicated not only in attachment models,
but also in models of temperament that have
direct implications for the pathophysiology of
BPD (Posner et al., 2003). In these latter mod-
els, cognitive control ability forms the neuro-
cognitive basis for the effortful control factor
that is related to social development in children.
There is consistent evidence that cognitive con-
trol is impaired among adults with BPD
(reviewed in the introductory section), and this
deficit can be observed among children in asso-
ciation with BPD phenomenological precursors
(Rogosch & Cicchetti, 2005).
We propose that BPD patients use the emo-
tional and behavioral strategies of attachment
avoidance in part as a compensatory strategy
for deficient executive regulation of negative
affect states that arise in attachment settings.
In this scenario, the impaired ability of the
BPD patients cognitive control processes to
both internally mitigate negative affect, and
to adaptively engage interpersonal processes to
aid in this affect regulation (through expression
of normal attachment system activation), leads
to overt, cyclic interpersonal distancing strate-
gies to compensate in relational settings. How-
ever, other interpretations of this relationship
are possible. For example, attachmentavoid-
ance may be a direct manifestation of executive
dysfunction, to the extent that cognitive control
is necessary to maintain engagement with an
attachment object (in this case, a romantic
partner).
Although the present study does not allowus
to distinguish between these alternate interpre-
tations, we note the role of emotion regulation
in normative social attachment (Mikulincer
et al., 2003), and the active nature of attach-
mentavoidance as reflected in the manifest
content of the attachment measure (ECR). In
addition, hallmark features of BPD include
emotion dysregulation (Linehan, 1993) and os-
cillating social attachment (Melges & Swartz,
1989). Taken together, these observations sug-
gest that attachmentavoidance is an interper-
sonal strategy employed by BPD patients in a
cyclic manner to bring about emotion regula-
tion that cannot be achieved in a more adaptive
(executive) manner. This scenario does not di-
minish the role of experiential factors (e.g.,
maltreatment), which could hypothetically ex-
ert effects on adult attachment either related to
executive dysfunction or by some other uniden-
tified mechanism. Indeed, the results of the re-
gression analyses suggest that maltreatment
and neurocognitive dysfunction exert both in-
dependent and interacting effects on attachment
disturbance (discussed below).
The relationship of childhood maltreatment
to neurocognitive dysfunction and to adult
attachment disturbance
We found significant relationships of childhood
abuse history with both neurocognitive dys-
function on one hand, and adult attachment dis-
turbance on the other hand. Animal models
indicate deleterious effects of early adversity
on both hippocampal and ACC structure and
function, which persist into adulthood (Sanchez
et al., 2001). Empirical studies of children and
adults with abuse histories have similarly
shown evidence of altered structure and func-
tion of subcortical limbic areas and the midline
PFC. The hippocampus and ACC in particular
have been strongly implicated here as well. Al-
though these brain areas are also disturbed in
BPD, the effects of childhood maltreatment
on either neuroanatomy or associated cognitive
functions has not yet been directly addressed
for BPD patients.
In our sample, we found that a history of
child abuse was related to impaired verbal re-
call. It is interesting that the nonverbal measure
of short-term memory (family pictures), which
is generally dependent more on right hippo-
campal function (Doss et al., 2004), did not
show a significant group difference and was
not associated with maltreatment. This may re-
flect lateralized effects of abuse, because chil-
dren and adults with histories of abuse show
more consistent deficits in left hippocampal
structure and function (Bremner, 2003; Stein
et al., 1997). It also remains possible that preex-
isting hippocampal atrophy or dysfunction is a
risk factor for later vulnerability to adversity,
weakening the individuals capacity to buffer
the effects of maltreatment. A definitive answer
to this problem will need to await long-term
longitudinal or twin studies of neuroimaging
and neurocognition in maltreated or at-risk
individuals.
We also found that abuse was related to
executive dysfunction. This included perfor-
mance on a measure of cognitive control
(Stroop interference) and a measure of decision
making (the Gamblers Test). Although this re-
lationship has also been unexamined to date for
BPD patients, a recent study found that ACC-
based cognitive control dysfunction is related
to the degree of BPD phenomenological pre-
cursors in a sample of children (Rogosch &
Cicchetti, 2005). Of interest, performance on
that task (the ANT, which involves response
conflict just as the Stroop and Hayling tests
do, with a similar basis in ACC function) was
not worse for the maltreated group compared
to a matched nonmaltreated group. Despite
some similarities between that study and the
present one, in the study design and research
problems addressed, other significant differ-
ences are evident, which may account for the
divergent findings. In contrast to that study,
we analyzed maltreatment as a continuous mea-
sure, with the rationale that it would be difficult
to dichotomize a sample that is likely to endorse
great heterogeneity in the type and severity of
childhood maltreatment experiences. Our sta-
tistical approach may have conferred greater
sensitivity to detect significant associations be-
tween maltreatment and cognitive control mea-
sures. Conversely, the Rogosch and Cicchetti
study evaluated maltreatment more thoroughly,
in a more objective manner by structured review
of each childs federal Department of Human
Services records, and of course, in a time frame
much closer to the reported events, in contrast
to the present study of adults who provided
retrospective self-reports of maltreatment.
Furthermore, that study involved a nonclinical
sample; in comparison, the present study may
be more susceptible to biases in selection and
measurement, yet of course remains more
directly relevant to the issue of maltreatment
effects in BPD. It may be that child abuse is
related to cognitive control deficits only among
those who progress to a full DSM diagnosis of
BPD in adulthood. Just as for the relationship
of abuse to memory dysfunction, this scenario
could reflect either the effect of abuse on cog-
nitive control (which may emerge only later in
development) or cognitive control dysfunction
as a preexisting risk factor for vulnerability to
the effects of abuse.
In any event, we found that attachment
avoidance was predicted by abuse and execu-
tive dysfunction independently, without inter-
acting effects. This finding is very consistent
to the findings of the Rogosch and Cicchetti
study, where the level of BPD precursors was
also related to both maltreatment and cognitive
control dysfunction in an independent manner.
The present results suggest that clinical hetero-
geneity in the expression of attachmentavoid-
ance may reflect varying mixtures of cognitive
control deficit and maltreatment exposure. For
example, the distinction in the Shaver adult at-
tachment model between preoccupied and fear-
ful attachment types is a function of variation
along the attachmentavoidance scale, where
the preoccupied type is low (approach oriented)
and the fearful high (withdrawal oriented; both
types being high on attachmentanxiety).
Among BPD patients, this distinction may rest
on varying mixtures of cognitive control deficit
and abuse severity. To obviate the fallacy of
Cartesian dualism, some form of physical
(i.e., biological) substrate should be implicated
in the mediation of experiential effects on future
behavior, such as how childhood maltreatment
translates into adult relational dysfunction.
The present evidence suggests that there exists
an unidentified cognitive/biological factor
(other than cognitive control dysfunction) that
mediates the effect of maltreatment on adult
attachmentavoidance.
Of interest, we also found that both recall
impairment and abuse were related to attach-
mentanxiety, in an independent and interact-
ing manner. This suggests that variation across
BPDpatients in relational reactivity may also be
a function of both underlying neurocognitive
(medial temporal lobe based) and experiential
factors. This would have consequences for the
distinction between fearful and dismissing
avoidant types (both high on attachmentavoid-
ance). In contrast to attachmentavoidance,
where neurocognition and experience appear
to exert parallel (and probably additive) effects,
relational reactivity may also exhibit sensitivity
to these two factors in interaction. The discov-
ery of biologicalenvironmental interactions is
one of the most exciting current topics in the
study of adult mental illness (Moffitt, Caspi,
& Rutter, 2005), and likely to be found widely
across adult psychiatric disorders. BPD should
serve as a primary target for this type of study,
given the established role of both genetic and
environmental factors in its emergence (re-
viewed in Skodol et al., 2002).
In contrast to the correlations of abuse with
neurocognitive dysfunction, severity of neglect
was generally unrelated to neurocognitive per-
formance, with the exception of short-term sen-
tence recall. The role of early neglect in BPD
remains obscure. Although a high proportion
of adults with BPD endorse various experi-
ences of childhood neglect (Zanarini, 2000),
this experience has been unaddressed in studies
of pathophysiology in BPD. This may be be-
cause of the challenge of properly conceptualiz-
ing and measuring this type of experience
(reflected in the relatively lower internal
reliability for neglect on the CTQ). The reliable
measurement of early neglect may be limited in
part by relatively greater difficulty for patients
to encode and then recall experiences of neglect
decades later, in comparison to experiences of
abuse. This is another research area in great
need of further development, particularly given
that neglect may be much more prevalent than
abuse in the community (Allin, Wathen, &
Macmillan, 2005).
Intelligence in BPD
In the present BPD sample, the mean IQ was
significantly lower than in the healthy control
group, and may be partly responsible for
the association of attachmentavoidance with
executive dysfunction. The latter finding may
not be surprising, given the generally strong
loading of executive functions on Spearmans
G, which also shows a strong PFC dependence
(Kane & Engle, 2002). Nevertheless, inexplic-
ably the role of lower IQ has to date been unad-
dressed in BPD. This is despite the prevalence
of childhood maltreatment in BPD (Zanarini,
2000), and the strong evidence that child abuse
and neglect result in adult intelligence deficits of
at least 1 SDon average (reviewed in Cahill et al.,
1999). This is comparable to the mean IQ decre-
ment observed in our BPD subjects, relative to
demographically matched healthy control sub-
jects.
Although IQ was not associated with self-
reported childhood maltreatment, the group
difference in intelligence appears to be illness
related because parental education and socio-
economic status were not different between
groups. It is possible that the CTQ may not cap-
ture the type of maltreatment that has signifi-
cant effects on intelligence (because of occur-
rence at a very early age, for instance), or that
there is no simple linear relationship between
maltreatment and subsequent intelligence defi-
cit. It is also possible that relatively lower IQ
may be a risk factor for BPD, as it is for
PTSD (Brewin, Andrews, & Valentine, 2000)
and schizophrenia (David, Malmberg, Brandt,
Allebeck, & Lewis, 1997). Furthermore, re-
duced general intelligence may predispose
BPD patients to lower performance in other
cognitive domains, as implied above. In any
event, it appears likely that intelligence deficits
may be a meaningful measure of cognitive dys-
function in BPD, and investigations that match
subject groups on IQ may be vulnerable to the
matching fallacy emphasized in studies of
schizophrenia (Meehl, 1970).
Study Limitations
The following limitations are evident in the pre-
sent study. First, this study did not include a
clinical comparison group with other psychiat-
ric disorders. Therefore, the specificity of these
findings to BPD remains uncertain. Studies of
community samples indicate that adult attach-
ment disturbances characterized by reactivity
or withdrawal are also related to depression vul-
nerability factors (Bifulco, Moran, Ball, & Lil-
lie, 2002), Axis I diagnoses including mood,
anxiety, and substance use disorders (Mickel-
son et al., 1997), and the full range of personal-
ity disorder symptoms (Brennan & Shaver,
1998). Reactive and/or withdrawn attachment
is also related to the full range of personality
disorder symptoms across mixed samples of
psychiatric inpatients (Fossati et al., 2003) and
personality disordered outpatients (Meyer, Pil-
konis, Proietti, Heape, & Egan, 2001). It is in-
teresting that a study of outpatients with social
anxiety disorder found these patients to exhibit
anxious reactivity in attachment relationships,
but not relational withdrawal (Eng, Heimberg,
Hart, Schneier, & Liebowitz, 2001). None of
these studies examined neurocognitive or bio-
logical factors. In the present sample, a high
rate of Cluster C personality disorder comorbid-
ity was found (particularly avoidant personality
disorder, in 43%of the BPDgroup). These rates
are quite consistent with those found in the lit-
erature, as several studies using DSM-IV report
high rates of Cluster C comorbidity among
BPD samples, including 4559% comorbidity
for avoidant personality disorder (Grilo, Miguel
Anez, & McGlashan, 2002; Grilo, Sanislow, &
McGlashan, 2002; McGlashan et al., 2000; Za-
narini et al., 2004). We did find that controlling
for Cluster C diagnoses did not alter our cog-
nitive findings, which indicates a degree of spe-
cificity in these effects among the present sam-
ple. Nevertheless, measures of reactivity and
withdrawal may be somewhat ubiquitous
among groups of psychiatric patients, and it re-
mains to be tested whether the relationships of
adult attachment disturbance to cognitive dys-
function that we found are more strongly asso-
ciated with the DSM diagnosis of BPD or alter-
natively with continuous traits that may be
found in this sample. In addition, we excluded
prospective subjects who met criteria for var-
ious comorbid psychiatric disorders (such as
PTSD and bipolar affective disorder) that are
also associated with cognitive deficits in the
measures employed here (see task descriptions
in Methods). These exclusion criteria obviated
the confounding effects of these other disorders,
yet may limit the abilityto generalize these results
to the full population of BPDpatients in the com-
munity, where these disorders are commonly
found as comorbid conditions.
Second, adult attachment was evaluated
with a self-report measure. Although this mea-
sure appears to have good construct validity and
reliability (Brennan et al., 1998), self-report
instruments in general can be susceptible to
reporting biases, and it is uncertain how self-
report attachment measures relate to attachment
as assessed with interviews or behavioral obser-
vations. Perhaps even more importantly, the re-
lationship of adult attachment to infantmother
attachment remains to be empirically ad-
dressed. In this study, we treated adult attach-
ment as an outcome measure, to examine the
neurocognitive and developmental experiential
correlates that may contribute to this important
feature of clinical dysfunction among adults
with BPD. The implications of these correlates
for early attachment processes remain unknown.
This may be addressed in the future by testing
the relationship of neurocognition and maltreat-
ment to early attachment in children at risk for
BPD.
Third, the measure of childhood adversity
was also by self-report, and retrospective. There
does appear to be good correspondence be-
tween CTQ scores and trauma ratings derived
from both research interview and research sub-
jects treating therapists (Bernstein & Fink,
1998). The concordance of responses to inter-
view and questionnaire-based instruments for
retrospective assessment of child abuse is also
observed for individuals with borderline
features (Durrett, Trull, & Silk, 2004). Never-
theless, these data are obtained in a remote, ret-
rospective manner, without corroborating evi-
dence of the nature and degree of adversity
experienced. In response to these issues, some
investigators have emphasized the advantages
of prospective design in the study of childhood
maltreatment (Widom, Raphael, & DuMont,
2004). However, others have argued that retro-
spective report of childhood maltreatment may
identify a wider sample of individuals, includ-
ing those who have suffered a greater degree
of maltreatment (unreported at the time of ex-
posure) and those who have not had the benefit
of a subsequent clinical intervention that may
modify the effects of maltreatment (Kendall-
Tackett & Becker-Blease, 2004). In addition,
an extensive earlier review of the relevant
empirical literature concluded that adults with
psychopathology probably remain generally
reliable reporters of childhood experiences
(Brewin, Andrews, & Gotlib, 1993). Neverthe-
less, approaching a gold standard for veridi-
cal assessment of childhood adversity may re-
quire the involvement of a clinical or legal
entity that can conduct a more thorough inves-
tigation of maltreatment cases.
Fourth, although multivariate tests found
significant impairment of cognition in BPD,
which included lower performance on all cog-
nitive measures, several of these univariate dif-
ferences did not attain statistical significance.
This may be because of limited statistical power
in our modest sample size. Althnough the sam-
ple size in this study is among the largest in the
existing BPD/neurocognition literature (see
Fertuck et al., 2006), subsequent investigations
may benefit by including larger samples to
better test group differences with relatively
small effect sizes.
Fifth, we altered several tests to assess the
hypothesis of differential effects of emotionally
charged stimuli in BPD subjects, and this dif-
ferential effect was not confirmed. The psycho-
metric features of these altered tests have not
been established, which might raise concerns
that they provided inadequate emotional activa-
tion to test this hypothesis. However, we ob-
tained a highly significant main effect of emo-
tional content on these tests, which confirmed
that this manipulation indeed produced the in-
tended experimental effect. This suggests that
BPD patients deficits on the present cognitive
tasks are largely independent of emotional
content.
Conclusions
Individuals with BPD exhibit deficits in short-
term recall and executive functions, which are
related to attachmentanxiety and attachment
avoidance, respectively. These associations
are consistent with two-part models of the neu-
robiology of normal attachment (in animal
models and humans), and the neurocognition
of temperament as a model for the pathophys-
iology of BPD. Individuals with BPD may
also exhibit lower general intelligence than de-
mographically matched healthy individuals. A
history of child abuse is prevalent among
BPD patients and is related to some of these
neurocognitive and interpersonal disturbances,
and appears to contribute to adult attachment
disturbance in a manner that is both indepen-
dent of and interacting with neurocognitive
dysfunction. The cognitive deficits may then
be expressions of either maltreatment and/or
preexisting factors that predispose individuals
to the effects of early stressors.
Taken together with the findings from the
study of childhood BPD precursors, the present
results suggest that early intervention may miti-
gate the effects of abuse on both neurocognitive
function and adult attachment function in adult-
hood, and possibly risk for BPD. One important
psychological factor that confers resilience to
the effects of early maltreatment is ego over-
control (Cicchetti & Rogosch, 1997; Cicchetti,
Rogosch, Lynch, &Holt, 1993), which is likely
to be associated at a neurocognitive level with
effortful control, one of the cognitive func-
tions found in the present study to relate to
adult attachment outcome. Although it remains
unknown if ego overcontrol can be improved
with clinical intervention, the evidence for cog-
nitive remediation of effortful control (Rothbart
& Posner, 2005) suggests that approaches that
target effortful control may enhance psycholog-
ical resilience to the effects of maltreatment.
This may be an implicit (and potentially ex-
plicit) feature of some cognitivebehavioral
therapies, which can be reasonably viewed
froma neurobiological perspective as involving
(in part) enhanced top-down PFC control over
subcortical limbic responsiveness, and which
presently show good evidence for efficacy in
the treatment of abused children (reviewed
in Saywitz, Mannarino, Berliner, & Cohen,
2000). In addition, however, there is evidence
that other modalities, such as attachment theory
motivated approaches or psychoeducation (de-
livered to maltreated infantmother dyads),
may ameliorate the effects of abuse on attach-
ment security (Cicchetti, 2004), and thus a wor-
thy target of future investigation would be the
possible effects of these treatment modalities
on neurocognitive functioning. For those adults
with an existing BPD diagnosis, treatment stra-
tegies that remediate existing cognitive deficits
(which could include interpersonal, cognitive,
or biological therapies) may have benefits for
the relational dysfunction that is a core feature
of BPD. Future investigations should examine
how these disturbances in adult social attach-
ment are related to altered functional neuroanat-
omy, and test Gene Environment interaction
effects to directly evaluate the role of heritable
versus environmental factors in this association.
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A neurocognitive model of borderline

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