Executive neurocognition, memory systems, and borderline personality disorder

Clinical Psychology Review 26 (2006) 346–375

Executive neurocognition, memory systems,

and borderline personality disorder

Eric A. Fertucka,T, Mark F. Lenzenwegerc, John F. Clarkind,

Simone Hoermanne, Barbara Stanleya,b

aNew York State Psychiatric Institute, Columbia University, College of Physicians and Surgeons, United StatesbJohn Jay College, City University of New York, United StatescState University of New York at Binghamton, United StatesdWeill Medical College of Cornell University, United States

eColumbia University Medical Center, United States

Received 13 April 2004; accepted 9 May 2005

Abstract

Borderline Personality Disorder (BPD) is a common, disabling, and burdensome psychiatric condition. It is

characterized by turbulent fluctuations of negative emotions and moods, unstable and conflictual interpersonal

relationships, an incoherent and often contradictory sense of self, and impulsive, potentially lethal self-injurious

behaviors. The neurobehavioral facets of BPD have not been extensively studied. However, clinical theoreticians

and researchers have proposed that the symptoms and behaviors of BPD are, in part, associated with disruptions

in basic neurocognitive processes. This review summarizes and evaluates research that has investigated the

relationship between executive neurocognition, memory systems, and BPD. Three historical phases of research

are delineated and reviewed, and the methodological and conceptual challenges this body of investigation

highlights are discussed. Laboratory-based assessment of executive neurocognition and memory systems is

integral to an interdisciplinary approach to research in BPD. Such an approach holds promise in elucidating the

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E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375 347

neurobehavioral facets, development, diagnostic boundaries, prevention, and optimal interventions for this

debilitating and enigmatic disorder.

D 2005 Elsevier Ltd. All rights reserved.

Keywords: Borderline personality; Memory systems; Memory; Cognition; Executive function; Neurocognition; Neuropsy-

chology; Neuroscience

Borderline personality disorder (BPD; Diagnostic and Statistical Manual, 4th Edition; DSM-IV;

American Psychiatric Association, 1994) is characterized by turbulent, anxious, angry, and depressive

emotional states, unstable interpersonal relationships, an incoherent and often contradictory self-concept,

and impulsive and often dangerous behaviors such as self-injury and drug abuse. Following the

pioneering clinical descriptions of borderline personality (Grinker, Werble, & Drye, 1968; Kernberg,

1967), empirical research of BPD has progressed over the last 20 years. Based on recent population

prevalence estimates (0.3–0.7%), between six-hundred thousand and 1.4 million adults in the United

States meet diagnostic criteria for BPD (Lenzenweger, Loranger, Korfine, & Neff, 1997; Samuels et al.,

2002; Torgersen, Kringlen, & Cramer, 2001). The suicide rate for BPD individuals is about 10% (Paris,

2002; Stone, 1993), comparable to the other psychiatric disorders such as schizophrenia and major

depression. In addition, 69% to 75% of individuals with BPD engage in self-injurious behaviors (Clarkin,

Widiger, Frances, Hurt, & Gilmore, 1983; Cowdry, Pickar, & Davies, 1985), and the frequency of self-

injurious behaviors is more than in any other psychiatric diagnosis (Stanley, Winchel, Molcho, Simeon, &

Stanley, 1992). Individuals with BPD exhibit high drop out rates and variable improvement in

psychotherapy (Clarkin, 1996), and respond only partially to psychopharmacological therapies (Soloff,

2000). Additionally, this diagnostic group utilizes health care services more frequently than any other

psychiatric group (Bender et al., 2001). Despite this troubling clinical picture, BPD has not received

research attention and widespread clinical focus commensurate with the suffering and mortality it causes.

There is considerable reason to suspect that there are disruptions in basic executive neurocognition

and memory processes in BPD. Central to the symptoms of BPD is unstable and dysregulated inhibitory

control over behavior, emotion, and cognition. The acquisition of executive neurocognition is

inextricably linked to emotion and personality development, and inhibitory capacity influences the

acquisition of prosocial behaviors, affect regulation, and problem solving abilities (Derryberry & Reed,

1994; Posner & Rothbart, 2000). These capacities are commonly impaired in BPD. From a clinical

perspective, neurocognitive function predicts response to intervention in other clinical groups (e.g.,

Smith, Hull, Romanelli, Fertuck, & Weiss, 1999). Should BPD individuals, or subgroups of them,

evidence a characteristic constellation of inhibitory and memory characteristics, treatment could be

tailored to complement them, leading to improved treatment planning and interventions. From a

scientific vantage point, BPD is a diagnostic entity that can be used to elaborate the understanding of

basic cognitive and affective processes. The study of emotion, mood, temperament, affect regulation,

and their relationship with personality, cognition, and psychopathology are at the center of rapid,

exciting developments in cognitive (Gazzaniga, 2000) and affective science (Davidson, Scherer, &

Goldsmith, 2003).

Previous reviews have emphasized the clinical implications of neurocognitive functioning in BPD and

other personality disorders (see Gorton, Swirsky-Sacchetti, Sobel, Samuel, & Gordon, 1999; O’Leary &

Cowdry, 1994). This review, by contrast, focuses on research that has attempted to systematically

E.A. Fertuck et al. / Clinical Psychology Review 26 (2006) 346–375348

characterize executive neurocognition and memory systems in BPD. First, we define the types and

subtypes of executive neurocognition and memory of relevance to BPD. A historical review of three

phases of research in executive neurocognition, memory, and BPD follows. Finally, then we discuss the

literature in this area as it relates to the neurobiology and neuroscience, development, and clinical

understanding BPD.

1. Memory systems and cognitive inhibition: domains and methodologies

1.1. Memory systems

Memory can be organized into five distinct systems (see Schacter, Wagner, & Buckner, 2000 for

review): working memory, semantic memory, episodic memory, the perceptual representational system,

and procedural memory. Studies of BPD to date have almost exclusively focused on working memory,

semantic memory, and, to a lesser extent, episodic memory in BPD.

Working memory involves the conscious storage and manipulation of mental representations. It

involves a tripartite set of functions, a central executive system, and the phonological loop and visuo-

spatial subsystems. Brain imaging studies have implicated the activation of the left inferior prefrontal,

dorsolateral prefrontal, supplementary motor, premotor, posterior–parietal, and cerebellar cortices in

verbal working memory. In comparison, the posterior, inferior prefrontal, premotor and dorsolateral

prefrontal cortices have been observed in spatial working memory. The central executive system

consistently involves the dorsolateral prefrontal cortex, in particular for more complex tasks (Baddeley,

1998; Schacter et al., 2000).

Episodic, or, autobiographical memory is the recollection of periods from personal history that

involve the encoding of the specifics of time, context, and place. The encoding of such memories

involves the left inferior prefrontal cortex and the anterior medial temporal lobe, including the

hippocampus. Retrieval of episodic memories involves both the right anterior prefrontal cortex and the

medial parietal cortex (Schacter et al., 2000).

Finally, procedural memory involves storage of behavioral, motoric, affective, and cognitive skills

and habits. Even with damage to medial temporal lobe structures, the acquisition of procedural skills is

not affected, indicating the functional dissimilarity between procedural and other forms of memory. As

procedural tasks that are just being learned become automatized over time, there is a transition from the

use of prefrontal and premotor activation to more non-deliberative neural pathways (Schacter et al.,

2000).

1.2. Executive neurocognition

Executive neurocognition involves the delay or termination of a cognitive or motor response in order

to achieve a less immediate goal or reward. Executive neurocognitive controls are relevant to

psychopathology research, as impairments in such functions are implicated in inattention, impulsivity,

and affective dysregulation.

Executive neurocognition can be divided into several subtypes (see Nigg, 2000; Posner &

Rothbart, 2000; Rothbart, Ahadi, & Evans, 2000). Nigg (2000) has proposed a useful taxonomy of

the major types of executive neurocognition. (A) Interference control involves the conscious,


deliberative control of one’s attention and motoric behaviors. The neural system that subserves this

function is the connection between the dorsolateral and orbitofrontal cortices and subcortical

structures, such as the anterior cingulate. The most well-known neurocognitive test of this function

is the Stroop Task (Stroop, 1935). In the Stroop task it takes an individual longer to name the ink

color of a color word printed in a differing color (e.g., naming the color blue when the word bredQis printed in blue ink) than a neutral stimulus (e.g., bxxxxQ) printed in the same ink color.1 (B)

Cognitive inhibition is the ability to suppress information from working memory. There are both

effortful and implicit types of this capacity. The effortful type is illustrated in the bdirected forgettingQtask. This paradigm presents subjects with a series of words. After each word is presented, subjects

are instructed to either forget (F) or remember (R) the word, and then subjects are asked to recall as

many of the words that they can, regardless of what they were instructed to do initially. The implicit

version of cognitive inhibition is exemplified in the bnegative primingQ tasks (Tipper, 1985). For thistask, first, a person must respond to a stimulus (e.g., name the blue object and ignore the yellow

object). In the subsequent bprobeQ trial, the stimulus to be named is the same as the one that was

ignored in the previous trial. For instance, if the person suppressed a (blue) chair to name a (yellow)

car, they now are asked to name a (blue) chair. It takes more time for individuals to identify an

object after they have been asked to ignore it in a prior trial than when it was not presented in an

earlier trial. (C) Behavioral inhibition involves the inhibition of a cognitive expectation and/or

motoric behavior in order to follow a different behavioral directive, expectation, or cognitive rule.

Behavioral inhibition involves, but is not limited to, premotor areas their reciprocal connection to

lateral and orbitofrontal areas of the prefrontal cortex. An example of behavioral inhibition is the Go–

No-Go Task (Casey et al., 1997). This task requires a subject to bgoQ (e.g., press a button) when a

frequent stimulus (e.g., the letter bXQ) appears but to withhold a button response (bno-goQ) when an

infrequent stimulus (e.g., the letter bYQ) appears.

Motivational-affective inhibition is defined as the deliberative interruption of a propensity or

behavior due to a motivational–emotional state. A laboratory paradigm for affective inhibition is the

Emotional Stroop Test. In this version of a traditional Stroop task, reaction times are longer for

naming the ink color of emotion-related words or other psychopathologically relevant content

(Williams, Mathews, & MacLeod, 1996). An example of motivational inhibition is the Passive

Avoidance Task (Newman & Kosson, 1986), in which participants are instructed to use trial-and-error

to learn if responding to stimuli will result in monetary reward or loss. Passive avoidance errors refer

to the number of times that a participant responds to losing stimuli (commission errors). Misses refer

to the number of times that a participant failed to respond to a rewarding, or, winning stimuli

(omission errors).

2. Historical phases of cognitive inhibition and memory research on BPD

In the next section, we review and summarize the findings from three historical phases of research of

cognitive inhibition and memory in the borderline personality.

1Due to space limitations we cannot summarize in detail the instructions and psychometric properties of all the referenced neurocognitive

measures. An excellent resource for this information is Spreen & Strauss (1998).

Table 1

Phase II studies of executive neurocognition and memory in BPD compared to control groups

Burgess (1990) Burgess (1991) O’Leary et al. (1991) Swirsky-Sacchetti et al.

(1993)

Carpenter et al. (1993)

Gender (% female) 33% Not reported 81% 100% 100%

Diagnosis DSM-III-R DSM-III-R DSM-III-R DSM-III-R DSM-III-R

Interview Unstructured interview 2 independent evaluations,

unstructured

SCID II+DIB-R

N6+ impulsive

aggressive behavior

SCID II+DIB-R N6 Interview

Co-occurring Axis I

conditions excluded

No BPD group no concurrent

Axis I

- Substance

dependence in 2 years

- bacuteQ Axis Iincluding MDD

Yes, not specified

- Current Affective d/o - Substance

dependence in 2 years

Medical/Neurological/

Head trauma excluded

Not reported Not reported Cardiovascular, renal,

hepatic, or seizure

disorder

HIV, neurological/medical

d/o known to affect cog-

nition, head trauma, brain

injury

N/A

Matched normal

control

Yes No (compared BPD to ma-

jor depression and schizo-

phrenia)

Yes Yes N/A

Group age differences Not reported Not reported No No Not reported

Psychiatric control No Yes Schizophrenia,

and MDD

No No No

Medication status Off N1 week Not reported Off N2 weeks 8 subjects on meds Med free; unknown

length

Medication class Not reported Not reported Not reported 2 on 2 classes; 2 on 3

classes

Not reported

Setting Outpatient acute Outpatient acute Outpatient nonacute Outpatient nonacute Inpatient nonacute

Sample size 18 BPD, 14 Control 27 BPD, 20

Schizophrenia, 17 MDD

16 BPD, 16 Control 10 BPD, 10 Control 17 BPD, 17 Control

Control for Depression/

Affect/Other

No No Co-occurring MDD

(N =7) did not affect

results

Not reported

Working Memory Yes No Yes Yes Yes

- Serial 7s; - 3 Step Commands - WAIS Digit Symbol - WMS-R Visual

Memory

- WMS-R Visual

Reproduction- Digit Span

No

- Immediate Repetition - WMS-R Associate

Learning

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Delayed Memory Yes Yes Yes Yes Yes

- Delayed Memory

Screen

- Delayed Memory; - Rey-Osterrieth - Rey-Osterrieth - Rey-Osterrieth

- (Embedded Figures) No No

- (Corsi Blocks)

- WMS-R Logical

Memory

- WMS-R

Logical Memory

Psycho-motor Skill Yes No Yes Yes Not Assessed

- Rhythm

reproduction test

- Rhythm Reproduction - (WAIS Digit Symbol) - Luria Motor Skills

- Luria Motor No - Finger Tapping Test

Behavioral Inhibition /

Inhibitory Control/

Cognitive Inhibition

Yes Yes Yes Yes

- Perseverative

Screening Test

- Omission Errors subtests - WAIS Picture

Arrangement

- Trails A and B

No No No No

- Similarities - WCST - WCST - WCST

- Serial 7 - Trails A and B - (CPT)

- Proverb Interpretation

Interference Control Not assessed Not Assessed Yes Yes No

- Embedded Figures

Test

- Stroop - CPT

- Road Map

- Corsi Blocks

Affective Inhibition Not assessed Not Assessed Not Assessed Not Assessed Not Assessed

IQ Not assessed Not assessed Yes Yes Yes

- WAIS Performance

IQ

- WAIS Verbal,

Performance, and

Full Scale IQ

- On three WAIS subtests

administered Digit Symbol,

Block Design lower in

BPD, but not Vocabulary

(continued on next page)

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Judd and Ruff

(1993)

Van Reekum et al.

(1996)

Cornelius et al.

(1989)

Driessen et al.

(2000)

Sprock et al. (2000)

Part I

Sprock et al. (2000)

Part II

Gender (% female) 80% N/A 66% 100% 100% 100%

Diagnosis DSM-III Not reported DIB DSM-IV DSM-III-R DSM-III-R

Interview Interview+DIBN6 DIB N6 DIB N6 SCID-II SCID-II SCID-II

Co-occurring Axis I

conditions excluded

- Affective disorder,

substance abuse,

psychotic disorder

- Primary substance

abuse, Peabody

Picture Vocabulary

b80

Substance

dependence,

psychotic d/o, and

bipolar d/o

Anorexia,

schizophrenina,

schizoaffective, MDD

w/psychotic Sxs,

Substance abuse,

psychotic disorder;

Depressed group no

other axis I or II d/os

Substance abuse,

psychotic disorder;

Depressed group no

other axis I or II d/os

Medical/Neurological/

Head trauma excluded

History of

neurological d/o or

head trauma excluded

- Organicity, physical

disorders of known

psychiatric

significance

Seizure d/o, bphysicaldisorder with know

psychaitric

consequenceQ, mental

retardation

Infectious disease,

endocrine d/o

neurological d/o,

head trauma, mental

retardation

Neurological, sensory,

and motor d/os

Neurological, sensory,

and motor d/os

Matched normal

control

Yes (archival control

matched on gender,

age, and education)

No No (test norms) Yes Yes Yes

Group age differences No Not reported No No Yes, BPD group older No

Psychiatric control No Yes No No Yes, current MDD or

Dysthymia

Yes current MDD or

Dysthymia

Medication status Off N2 weeks Not reported Off N1 week Off N1 week Not reported Not reported

Medication class Not reported Not reported Not reported Not reported Not reported Not reported

Setting Outpatient nonacute Inpatient nonacute Inpatient acute 18 inpatients, 3

outpatients

Outpatient Outpatient

Sample size 25 BPD, 25 Control 24 BPD, 11 TBI 24 BPD 21 BPD, 21 Control 18 BPD, 17

Depressed, 16 Control

18 BPD, 18

Depressed, 18 Control

Control for Depression/

Affect/Other

No Not reported No Yes Controlled for Age

and WAIS Block

Design

Controlled for

education

and estimated IQ

Working Memory No No No No No No

- Controlled Oral

Word Association

- Digit Span - WAIS Digit Span - WAIS Digit Symbol

Test

- Rey-Osterreith Copy - Rey-Osterreith Copy

- R Digit Span - WMS-Digit Span - WMS Visual Memory,

Associate Learning

- Story Recall Immediate

- WMS-Digital Span

- WAIS-R Digit Symbol

Table 1 (continued)

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Delayed Memory Yes Yes No No No No

- Rey-Osterrieth - Rey-Osterrieth - Crosses

- Star Drawing

- Rey Osterreith

- WMS Logical

Memory

- Rey-Osterreith - Story Recall

—Delayed on Neutral

Words

- Luria Selective

Reminding Test

(Total score for copy,

immediate, and 5-min.

recall)

- WMS Logical

Memory

- WMS-R Logical

Memory

Psycho-motor Skill Yes Not assessed No No No Not Assessed

- (WAIS-R Block

Design)

- Grooved Pegboard - (Digit Symbol Test) - Porteus Mazes

No - Finger Tapping Test

- Grooved Pegboard

- Finger Tapping Test

Behavioral Inhibition / Yes Yes Not Assessed No No Not Assessed

Inhibitory Control

Cognitive Inhibition

- Ruff figural fluency - Trails A and B (time

to complete)

- (Block Design) - Porteus Mazes

No No - Trailmaking B

- Trails A and B

(errors)

- WCST (number of

correct sorts)

Interface Control No Not assessed Not Assessed No Yes Not Assessed

- Stroop - Embedded Figures - Stroop (Neutral

Words), (Depressed

also impaired on

this task)

Affective Inhibition Not Assessed Not assessed Not Assessed Not Assessed No No

- Emotional Stroop - Word Recall

emotional vs. neutral

- Story Recall:

positive, negative,

and neutral; immediate

and delayed

IQ No Not assessed Not Assessed No Yes No

WAIS-R - WAIS-R

Information, Similarities,

Picture completion, and

Block Design subtests

- WAIS-R Vocabulary

and Block Design; BPD

better than Depressed

Group on Block Design

- WAIS-R Vocabulary

and Block Design

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2.1. Phase I: phenomenological description of the BPD construct

We have characterized Phase I, before the DSM-III definition of BPD, as one of the phenomenological

descriptions. The broad class of bborderlandQ disturbances began to be described in the late 19th Century(Stone, 1986). Later, Kernberg (1967, 1976, 1996), based on the approaches of descriptive psychiatry

and psychoanalytic theory, proposed a pioneering and still influential definition of borderline personality

organization (BPO), a forerunner of the current BPD nomenclature. During Phase I, standard

psychological testing assessed cognition and perception in BPO, most often utilizing the Wechsler Adult

Intelligence Scales (WAIS; Wechsler, 1955) and the Rorschach Inkbot Test. Using these measures,

borderline subjects were reported to exhibit relatively intact intellectual performance on the WAIS, but

disturbed or deviant Rorschach responses (Rapaport, Gill, & Schafer, 1968). Subsequent reviews of this

early Rorschach research (Gartner, Hurt, & Gartner, 1989; Widiger, 1982) have questioned whether the

subjects in these studies would be considered BPD by DSM standards, and the methodology and data

analysis.

Gunderson and Singer (1975) reviewed the literature on the diagnostic indicators of BPD, and this

effort ultimately led to the DSM-III (American Psychiatric Association, 1980) criteria for BPD. This

review brought an organizational focus to previously disparate observations of BPD, and helped inspire

an interest in a more behavioral and reliable approach for classifying borderline personality, and

increased the reliability of the BPD diagnosis. Phase I of research in BPD concluded with the emergence

of a consensus that a BPD was a disorder that had some syndromal qualities worthy of further clinical

attention, both in terms of description and assessment. However, assessment methodologies for the

diagnosis of BPD were in their infancy and there was no laboratory science of BPD.

2.2. Phase II: studies that utilized comprehensive neuropsychological batteries to compare BPD to other

psychiatric and control groups

With the advent of the DSM-III (American Psychiatric Association, 1980) and the Axis II system with

its explicit batheoreticalQ criteria, a categorical approach that often used behavioral criteria was initiated

in the psychiatric classification of the disorder. This period corresponded to a shift in psychiatry to an

empirical research perspective that emphasized reliability, validity, and psychometric efficiency

(Cronbach & Meehl, 1955; Meehl & Rosen, 1955). As a result of this focus there was increased

standardization and reliability of psychiatric diagnosis by semi-structured interviews (e.g., IPDE;

International Personality Disorder Examination; Loranger, 1999) and self-report instruments (e.g.,

Millon Clinical Multiaxial Inventory-III; Millon, Davis, & Millon, 1997). Concurrently, during the

1980s, the neuropsychological test batteries evolved to assess a wide range of functions in a more

principled manner and were increasingly applied to psychiatric populations.

Ten publications and conference presentations were identified from this phase of research. Criteria for

inclusion here included an assessment of BPD as defined by either the DSM or the International

Classification of Diseases (ICD) diagnostic systems, comparison with a non-clinical control group and/

or a psychiatric comparison group, and publication or presentation in a peer-reviewed scientific

publication or meeting. PsycINFO and Medline databases and references from previous review chapters

were used to identify studies. Table 1 summarizes the 10 (with one study, Sprock, Rader, Kendall, &

Yoder, 2000, reporting two studies in the same paper) peer-reviewed publications and conference

presentations from Phase II.


2.2.1. Methodological comparison between significant difference (SD) and no significant difference

(NSD) studies in phase II

There were several studies in Phase II which documented inhibitory and/or memory deficits the

BPD group relative to control groups (Burgess, 1990, 1991; Carpenter, Gold, & Fenton, 1993; Judd &

Ruff, 1993; O’Leary, Brouwers, Gardner, & Cowdry, 1991; Swirsky-Sacchetti et al., 1993; Van

Reekum et al., 1996) which we label the Significant Difference (SD) studies. There were also several

studies that did not find statistically significant deficits in BPD groups compared to control groups

(Cornelius et al., 1989; Driessen et al., 2000) which we label Non-Significant Difference Studies

(NSD). Overall, the SD and NSD studies used comparable methodologies with reasonably well

characterized patient groups. However, the NSD studies appear to have more carefully addressed

confounding factors such as neurological and medical history, Axis I co-occurrence, and IQ

differences. Additionally, the NSD studies appear to have utilized a higher percentage of female

participants compared to the significant studies. These observations suggests that predominantly

female BPD samples with fewer co-occurring conditions are less likely to demonstrate neurocognitive

impairments relative to comparison groups. However, in clinical settings BPD cases without co-

occurring conditions are rare, raising question about the representativeness of these BPD samples.

Additionally, three of the four studies in the SD group that assessed IQ found relative deficits in the

BPD group when compared to the control group. By contrast, only one of three studies that assessed

IQ in the NSD group exhibited this problem, and, in this study, IQ was used as a covariate in an

attempt to control for its effect on neurocognitive performance (Sprock et al., 2001, Study I). We,

consequently, speculate that group IQ differences may account for some of the apparent findings

comparing the BPD and control groups in the significant group of studies.

Recognizing the limitation of focusing primarily on null hypothesis significance testing (Rosenthal,

Rosnow, & Rubin, 2000), we also evaluated the effect sizes of the Phase II studies. Five of the ten

studies reported means and standard deviations for both a BPD and comparison group. Based on these

data, Table 2 summarizes effect sizes (Cohen’s d; Rosenthal et al., 2000) that were calculated on

executive neurocognition and memory domains, contrasting the BPD with the comparison groups

(clinical or normal control). We conducted a preliminary meta-analysis of Cohen’s d effect sizes within

each memory and cognitive domains. For each study, a mean domain effect size was calculated (some

studies had several instruments in one domain, others had none). These study domain means were then

averaged, yielding a mean domain effect size across all studies (see the last row of Table 2). These

preliminary mean effect sizes indicate that BPD groups perform more poorly across executive

neurocognition and memory domains compared to contrast groups. The largest effect size is in the area

of delayed nonverbal memory, which is in the blargeQ range by conventional effect size standards. Other

domain effect sizes are at least in the bmediumQ range. This preliminary meta-analysis indicates that

memory and cognitive inhibitory weaknesses are commonly detected in BPD, but a distinct

configuration of deficits does not emerge.

In summary, while memory and executive neurocognitive impairments appear common in at least

subgroups of BPD subjects, the inconsistent findings from Phase II do not clearly implicate any particular

executive neurocognitive or memory system impairment in BPD. Further caution is warranted considering

that individuals with other clinical syndromes can exhibit comparable impairments in executive

neurocognition and memory functions—including subtypes of geriatric depression (e.g., Kiosses,

Klimstra, Murphy, & Alexopoulos, 2001) and schizophrenia spectrum disorders (e.g., Lenzenweger,

Cornblatt, & Putnick, 1991; Park, Holzman, & Lenzenweger, 1995; Trestman et al., 1995).

Table 2

Effects size (ES; Cohen’s d) of BPD compared to control groups in executive neurocognition and memory systems in phase II studies

Study; Sample Working Memory-

Verbal

ES Working Memory-

Non-verbal

ES Delayed Memory-

Verbal

ES Delayed Memory-

Non-verbal

ES Behavioral-Cognitive

Inhibition

ES Interference

Control

ES

Burgess, 1991;

27 BPD; 20 MDD

Digit Span 0.58 Rhythm

Reproduction

0.46 Delayed Memory 1.44 Perseveration errors 0.57 Serial Sevens

subtraction

0.58

Immediate Repetition -1.25 Irrelevant addition

errors

-0.35

Three-Step Commands 0.14 Omission errors 0.88

Inversion errors 0.68

O’Leary et al., 1991; Digit Span 0.09 Digit Symbol 1.27 WMS 1.45 Rey O 0.98 WCST 0.92 Embedded Figures 1.06

16 BPD; 16 Control WMS 0.77 Seashore Test 0.24 - Delayed Logical

Memory

- Delayed Recall - Categ. achieved 0.29 - Score 0.93

- Logical Memory 0.43 - Rhythm 0.55 - Persev. Errors 0.55 - No. of failures

- Digits Forward 0.63 - Tonal memory 1.12 - Nonpers. Errors 0.45

- Digits Backward Rey O. - Trials to first cat. 0.30

- Recall - Unique responses 0.06

- Failure to maintain

set

Swirsky-Sacchetti WMS 2.0 WMS 1.14 WMS 0.10 WMS 0.88 Trails B 0.37 Stroop Color-Word 0.52

et al. (1993);

10 BPD; 10 Control

- Logical Memory - Figural Memory 0.37 - Delayed Logical

Memory

- Delayed Figural

Memory

WCST 0.00 - Word 0.54

Rey - No. categories 0.53 - Color 0.71

- Recall - No. Errors - Color-Word 0.37

Verbal Learning -0.12

- Emotional Interference

- Neutral Interference

Judd and Ruff (1993);

25 BPD; 25 Control

Selective reminding

test

0.65 Rey O. 1.07a Selective reminding

test

0.13 Stroop Test 0.15

- Sum recall 0.14 - Immediate Recall 0.09 - Delayed recall - Time 0.32

Digits Span Seashore Rhythm 0.93 - Error

Digit Symbol 1.19

Ruff Figural Fluency

Driessen et al., 2000;

21 BPD; 21 Control

WMS Immediate 0.95 Digit Symbol 0.87 Rey O. 0.28 WMS Delay 0.80 Embedded Figures

Rey-Immediate

Recall

0.27 - Delayed - Time/figure 1.02

- No. Errors 0.83

- No. Repeats 0.58

Cohen’s d Domain

Mean for all Studies

0.73 0.68 0.68 0.89 0.39 0.61

Cohen’s d utilized for effect size calculation, using a pooled standard deviation from BPD and comparison groups.aThere was a probable error in the decimal place of the standard deviation reported in this study. The effect size here is based on a presumed correction, but should be considered speculative.

E.A.Fertu

cket

al./Clin

icalPsych

ologyReview

26(2006)346–375

356


2.3. Phase III: recent studies of executive neurocognition and memory systems in BPD

During the period from 1999 to the present, studies investigated executive neurocognition and

memory systems to BPD in a more differentiated and ecologically valid manner than the Phase II studies.

Another characteristic of Phase III is a move away from conventional neuropsychological assessment.

This is most apparent in the use of instruments that assess the influence of motivation, emotional state,

affective valence, and episodic memories in BPD and comparison groups.2

2.4. Executive neurocognition

2.4.1. Cognitive interference control

Posner et al. (2002) report that BPD subjects (without current mood disorder; n=39), compared to

healthy control participants (n=30), are specifically deficient in a neural network associated with the

voluntary inhibition of thoughts and behaviors. These researchers utilized the Attention Network Task

(ANT; Fan, McCandliss, Sommer, Raz, & Posner, 2002) laboratory test, which assesses three

independent attentional functions. The first is alerting, the capacity to sustain an alert cognitive state.

The second is orienting, which involves focused identification and selection of sensory stimuli. The third

is conflict which is the capacity to voluntarily decide among competing responses based upon a principle

or goal, using a visual flanker task. The anterior cingulate is a brain region which is essential to cognitive

interference controls as measured by a conflict task (Botwinick, Braver, Barch, Carter, & Cohen, 2001)

such as in the ANT. The BPD participants in the Posner et al. (2002) study were specifically impaired

relative to control participants in the conflict task as assessed by the ANT. Further, a group of individuals

who exhibited temperamental features similar to BPD (n=22), yet did not meet criteria for BPD,

performed better than the BPD group on the conflict index of the ANT. However, the temperamentally

matched group was not significantly different from the other two groups on this conflict task.

2.4.2. Cognitive inhibition/encoding

There have been three studies of cognitive inhibition and encoding in BPD. Cloitre, Cancienne,

Brodsky, Dulit, and Perry (1996) studied a DSM-III-R diagnosed BPD sample of 48, comparing those

who had and had not reported experience of childhood sexual abuse (24 each), to a healthy control group

of 24 subjects. The study utilized the experimental bdirected forgetting paradigm,Q which has been

described previously. In this study, words were presented with positive, neutral, and negative emotional

valences. The BPD group with a history of abuse had better recall of neutral words they were asked to

remember relative to the non-abused BPD group and the control group. Additionally, across the total

sample, the number of Remember-Neutral words recalled was positively correlated with self-reported

dissociative experiences. The authors argue that, among traumatized BPD subjects, the ability to shift

attention from distressing memories of abuse to more neutral, dissociated sensory experiences allows for

the maintenance of positive memories of caretakers and the avoidance/suppression of negative memories.

While this is one plausible interpretation of the findings, it would be strengthened if the traumatized BPD

group also had remembered fewer negative words they were asked to remember. Further, since the finding

2Two recent studies of executive neurocognition in BPD are not reviewed here due to the methodological drawbacks of lack of semi-

structured diagnostic assessment of BPD (Dinn et al., 2004) and the use of unconventional cut off scores to make the BPD diagnosis (Kunert,

Druecke, Sass, & Herpertz, 2003, see p. 500).


was only apparent in the traumatized BPD sample, it is unclear if this is a marker of BPD or of a history of

childhood trauma independent of diagnostic status.

Korfine and Hooley (2000) compared 22 day hospital and 23 community ascertained DSM-IV BPD

subjects (diagnosis was established using the IPDE; Loranger, 1999) to 20 healthy control subjects, also

utilizing the directed forgetting paradigm. This directed forgetting procedure utilized valenced words

that were positive, borderline salient (e.g., abandon, reject, and cruel), negative, and neutral. The BPD

subjects were found to be more likely to remember borderline salient words they were told to forget than

normal subjects. These findings suggested enhanced encoding of BPD salient stimuli and, perhaps, a

disinhibition in forgetting borderline salient words. This is the first study to show an affective cognitive

inhibition bias in BPD. The findings from this study are consistent with the Emotional Stroop findings in

BPD (Arntz, Appels, & Sieswerda, 2000) summarized below.

2.4.3. Behavioral inhibition

Consistent with these findings, BPD subjects (without current mood disorder; n=24) exhibit relative

deficits in cognitive planning and set-shifting functions on the Wisconsin Card Sort Test (WCST;

Heaton, 1981) compared to healthy control subjects (n=68; Lenzenweger, Clarkin, Fertuck, &

Kernberg, 2004). These BPD subjects evidenced no significant differences with control participants on

other measures of spatial working memory and sustained attention. This study also found that BPD

individuals exhibit significantly higher levels of negative affect, lower levels of positive affect, and

lower levels of non-affective constraint (an index of behavioral inhibition) as assessed by the self-report

Multidimensional Personality Questionnaire (MPQ; Tellegen, 1982) as compared to population norms.

Additionally, non-affective constraint on the MPQ was negatively associated with performance on the

WCST indexes in this BPD sample.

Two reports (Lenzenweger et al., 2004; Posner et al., 2002) drew from the same BPD patient pool.

Twenty-two BPD subjects from this pool completed both the ANT and WCST protocols. In this BPD

sample, the number of BPD criteria met was associated with more impaired attentional performance on

the ANT (Fertuck, Lenzenweger, & Clarkin, 2005). These associations were independent of the effects

of age and medication status (approximately half the BPD subjects in these studies were on medication).

2.4.4. Motivational cognitive inhibition

Four studies have investigated motivational cognitive inhibition in BPD utilizing an experimental

design. In the first study, (Dougherty, Bjork, Huckabee, Moeller, & Swann, 1999), 14 hospitalized

female BPD subjects were compared to age, race, and education level matched control participants on

several aggression and impulsivity measures. One lab task utilized was the Impulsivity Task (IT; Cherek

& Dougherty, 1997) which offers participants a choice between immediate vs. delayed monetary

rewards, where the delayed rewards are larger. During the task, the larger reward is progressively

delayed. On the IT task, the BPD subjects responded to avoid longer delays for reward than the controls,

but were otherwise similar to the controls.

Using another laboratory paradigm, the passive avoidance task (described previously), Hochhausen,

Lorenz, and Newman (2002) compared incarcerated females with (n=39) and without BPD (n=127) on

this passive avoidance task. They found that the BPD group exhibited significantly more errors in

responding to the non-winning numbers that the controls. Further, there was a trend towards the BPD

group also failing to respond to winning numbers. Accordingly, the BPD group also reported more

impulsive behaviors. The errors in responding to non-winning numbers in this BPD sample are similar to


deficits identified in psychopathy on the passive avoidance task. However, the fact that BPD individuals

also exhibited fewer responses to reward (errors of omission) in this study is not typically found with in

psychopathic groups. The authors conclude that BPD subjects may be impulsive predominantly in their

disinhibition in avoiding punishments. This finding may explain why the Dougherty et al. (1999) study

did not find that the IT task was related to impulsivity in BPD. The IT task does not assess the inhibition

of responding to non-reinforced (as opposed to reinforcing) stimuli.

In the context of a serotonin synthesis study in BPD, participants were assessed using a computerized

go/no-go task of behavioral inhibition (Leyton et al., 2001). Eleven healthy control participants (6

women and 5 men) were compared to 13 medication-free BPD subjects (8 women and 5 men). The BPD

group was not currently depressed. The go/no-go task requires one to learn, based on rewards and

punishment, when to respond and not to respond to a stimulus. Punishment–reward commission errors

represent an error in inhibiting a response that will be punished, based on prior learning. The BPD group

committed significantly more punishment–reward commission errors than the control group. Serotonin

synthesis was associated with these same go/no-go errors, specifically in the medial frontal gyrus,

anterior cingulate gyrus, temporal gyrus, and striatum.

Executive and motivational cognitive inhibitions were compared in 42 BPD (without current

depression) and 42 healthy control participants (Bazanis et al., 2002). Motivational inhibition was

assessed with a decision making task which asked participants to make bbetsQ on choosing whether a

token is hidden in one of two boxes. In the ascending phase of the task bets become progressively larger.

A descending phase involves the bets becoming progressively smaller. The instrument assesses

deliberation time, the proportion of responses on which the participant bet the most likely outcome, the

amount the participant bet, and the extent to which participants bet risky vs. less risky amounts of money.

Participants in this study were also administered a Tower of London planning task, and a visual

recognition memory task. The BPD subjects took significantly longer to decide upon the bets, they chose

the most likely outcome significantly less often than the control group participants, and they responded

more often to the early bets than the later. The BPD subjects also did more poorly on the Tower of London

task than the control subjects. There were no differences in visual recognition memory between the two

groups. These results are consistent with the three prior studies of motivational cognitive inhibition in

BPD, and the Tower of London findings reinforce non-motivational deficits in behavioral inhibition.

2.4.5. Affective-cognitive inhibition

Finally, using the Emotional Stroop Test paradigm, Arntz et al. (2000) tested the hypothesis that 15

BPD individuals would exhibit more difficulty in processing negative emotion words than neutral words

compared to 15 healthy controls and to 12 participants with Cluster C personality disorders. They used

four classes of negative words, three of which were BPD salient: negative views of others, negative

views of self, sexual abuse-related words, and general negative words. Words were presented both

supraliminally (at an interval that can be registered in consciousness) and subliminally (at an interval

shorter than can be consciously registered). They found that both the personality disordered groups

exhibited significantly more difficulty processing the supraliminally, but not subliminally, presented

emotion words. The study suggests that emotional valence impairs the interference control subtype of

executive neurocognitive processing in BPD and Cluster C personality disorder individuals compared to

controls. The study did not find differences between the personality disordered groups on this task,

which may indicate either a lack of statistical power, or that performance on this version of the

Emotional Stroop is associated with personality disorder more broadly defined.


2.5. Memory systems

Experimental investigations of memory systems and BPD are few in number. The studies that have

been conducted have focused on autobiographical–episodic and semantic memory and encoding in BPD

subjects.

2.5.1. Autobiographical–episodic memory

Heard, Startup, Swales, Williams, and Jones (1999) compared 23 BPD subjects to 23 matched

controls (18 females and 5 males were in each group) on episodic–autobiographical memory. To

measure autobiographical memory the investigators utilized the Autobiographical Memory Test (AMT;

Williams & Broadbent, 1986). In the AMT, subjects are asked to recall episodic–autobiographical events

related to the cue words. A bspecificQ memory happened on a particular day, and a bgeneralQ memory

happened repeatedly or over extended periods of time. These investigators predicted that BPD

individuals with dissociative symptoms would exhibit less retrieval of specific autobiographical

memories, or, conversely, more general autobiographical memories. The BPD group demonstrated

significantly more bgeneralQ episodic–autobiographical memories on the AMT and also exhibited higher

levels of trait anger, depression, and anxiety, and dissociative experiences than the control group. In

addition, bgeneralQ memories were correlated with dissociative experiences. In assessing cue valence,

BPD subjects produced more general memories to negative cues than the control group. This pattern of

findings is consistent with responses by subjects with PTSD and Acute Stress Disorder (ASD; e.g.,

McNally, Lasko, Macklin, & Pitman, 1995). A weakness of the study is that there was no assessment of

history of traumatic experiences.

In a follow-up study, Startup, Heard, Swales, and Jones (2001) assessed BPD subjects with a history

of parasuicide (18 females and 5 males) using the Autobiographical Memory Test (AMT; see above).

Contrary to their hypotheses, these investigators found that bspecificQ recall of episodic memories, higher

levels of anxiety and depression (but not anger), each independently contributed to the prediction of

increased number of suicide and parasuicidal behaviors. If self-injury is triggered by specific, concrete,

and detailed recall of negative, traumatic episodes, these authors argue that more bgeneralQ recall ofmemories may be part of an affect regulatory strategy that prevents self-injury.

While the above studies suggest that BPD individuals produce over-general autobiographical

memories with negative memory cues, another study suggests that BPD participants do not exhibit over-

general autobiographical memories using only neutral cue words (Arntz, Meeren, & Wessel, 2002). This

pattern of findings further reinforces the importance of considering affective valence in the memory

processing of BPD, as negatively valenced memories appear to have a more influential effect on the

form of autobiographical memories than neutral memories. Similar to the Cloitre et al. (1996) study, the

autobiographical memory studies suggest a link between BPD and the impaired encoding and retrieval

of negatively valenced episodic memories, possibly leading to the clinical manifestation of dissociation.

These studies also establish the utility of an experimental approach using laboratory memory tasks as

indicators of risk factors and to investigate patterns of memory consolidation and dissociation in clinical

and non-clinical subjects.

2.5.2. Memory and neurocognitive deficits in bpd with current major depression

Whether co-occurring major depression (MDD) exists is crucial in investigating memory and

neurocognition in BPD, as MDD is the most common co-occurring disorder in BPD (cf.


Zimmermann & Mattia, 1999). MDD is characterized by deficits in episodic and semantic

(declarative) memory, verbal fluency, and attentional performance relative to healthy control groups

(see Zakzanis, Leach, & Kaplan, 1998 for review). Two studies have focused on comparing current

MDD to current MDD with co-occurring BPD on memory and neurocognitive domains. In the first

study, memory functions with positive, negative, ambivalent, and neutral words were compared in

three groups: 40 subjects with symptoms of major depressive disorder (MDD; 20 subjects with a

comorbid diagnosis of BPD and 20 subjects without BPD), and 20 control participants (Kurtz &

Morey, 1999). The two patient groups exhibited comparable severity of depressed mood, general

level of distress, and co-occurring psychiatric conditions. Forty-eight words (12 in each valence

category) were presented to the participants on a computer. This was followed by a free recall 5 min

after the presentation, and a recognition recall (including 48 distracter words) 50 min after the

presentation. The investigators identified more impairment in recall and recognition memory among

the BPD with MDD group compared to the control group. There was also greater impairment in

recognition memory in the MDD with BPD group compared to MDD subjects without BPD.

Controls and BPD subjects showed a positive word selectivity in recall, while MDD subjects showed

nonsignificant selectivity differences.

In the second study (Fertuck et al., 2005, submitted for publication), 55 subjects with MDD (33 of

these subjects did not meet criteria for any DSM-IV Axis II Personality Disorder [PD], and 22 met

criteria for BPD) were administered a comprehensive neuropsychological battery that assessed 7

domains of performance: attention, working memory, general intellectual functioning, memory,

executive cognitive control, psychomotor skill, and motor skill. Additionally, the mood state was

assessed. MDD with BPD subjects reported higher levels of state anger, anxiety–tension, and higher

levels of overall negative affect than individuals with MDD without PD. While neuropsychological

performance appeared similar in these two groups in standard group comparisons, when levels of anxiety

were controlled, BPD-MDD subjects exhibited superior general intellectual performance, psychomotor

speed, and attention. The impact of anxiety on neuropsychological performance in BPD further

reinforces the need for future experimental studies of the effects of mood on cognitive function in BPD.

Such research is required to determine whether mood dysregulation, rather than core depressive

symptoms, underlies cognition impairments in BPD.

2.6. Integrative summary of the three phases

During Phase I the phenomenology of BPD was described and the stage was set for more systematic

studies of executive neurocognition, memory, and BPD. Phase II compared well-characterized BPD

groups to controls on comprehensively assessed, non-affective neuropsychological performance.

Compared to controls, BPD subjects studied in this Phase did not demonstrate a consistent constellation

of deficits in executive neurocognition or memory. A preliminary meta-analysis suggests that BPD

groups are more compromised than controls in all measured executive neurocognition and memory

domains, with effect sizes in the medium to large range. A lack of specificity and sensitivity of findings

from the Phase II research highlights the importance of studying the impact of affective stimuli and

arousal, risk factors, and co-occurring conditions associated with BPD, which has begun in the current

Phase III. While the Phase III studies provide interesting leads and results regarding the impact of affect

on cognition and memory in BPD, none of the studies have been replicated, and should be considered

preliminary.


Summary of Phase III findings:

1. Preliminary reports consistently point to impaired executive neurocognition in BPD, independent of

affective influences (Bazanis et al., 2002; Lenzenweger et al., 2004; Posner et al., 2002). In these

studies of non-depressed BPD subjects, other basic cognitive processes (working memory, attention,

etc.) remain relatively intact under affectively neutral conditions. Further, the extent of BPD

pathology appears associated with greater impairment in attentional and cognitive interference control

performance (Fertuck et al., 2005).

2. There is enhanced encoding and impaired cognitive inhibition of negatively valenced emotional

stimuli in BPD relative to healthy control subjects (Korfine & Hooley, 2000).

3. Motivational (Bazanis et al., 2002; Dougherty et al., 1999; Hochhausen et al., 2002; Leyton et al.,

2001) and affective (Arntz et al., 2000) cognitive inhibition are compromised in BPD compared to

control participants. Moreover, poorer performance in motivational cognitive inhibitory performance

is associated with behavioral indices of impulsivity in BPD (Hochhausen et al., 2002).

4. Negatively valenced episodic memories in BPD appear less specific than in control participants

(Heard et al., 1999). Additionally, greater specificity in the recall of episodic memories contributes to

the prediction of increased number of suicide and parasuicidal behaviors in BPD (Startup et al., 2001).

5. BPD subjects in an episode of MDD appear similar in neurocognitive performance to uncomplicated

MDD, yet are also more affectively aroused than MDD. Elevated anxiety, when controlled for in

BPD, highlights that BPD subjects perform better than uncomplicated MDD in psychomotor,

attentional, and general intellectual performance (Fertuck et al., 2005, submitted for publication).

3. General discussion

Several questions emerge from the existing studies. (1) How does the literature on executive

neurocognition and memory contribute to the understanding of BPD from developmental and

neurobiological perspectives? (2) What are the implications of these findings for modeling BPD and

refining the taxonomy of BPD in relation to neighboring disorders? (3) What is the clinical relevance of

these findings? (4) Can clinical perspectives of BPD help guide future research in this area?

3.1. Neurobiological and neuroscience approaches

Current theories of BPD emphasize emotional dysregulation (cf., Linehan, 1993; Westen, 1994;

Westen, Muderrisoglu, Fowler, Shedler, & Koren, 1997) and are not as explicit about the potential for

mutually interacting impairments in executive neurocognition and memory disruption. Depue and

Lenzenweger (2001, 2005) have proposed that BPD and other personality disorders arise out of an

interaction between multiple neurobehavioral systems. They posit that BPD is an emergent phenotype

reflective of a highly reactive negative affectivity system, high levels of social fear, low levels of positive

affect, and low levels of non-affective constraint. This model emphasizes the interaction between these

processes as crucial to understanding the phenomenology of BPD. Central to the study of executive

neurocognition, a non-affective constraint system has been conceptualized from a neurobiological

perspective as the central nervous system’s primary modulator or regulator of motor behavior, positive

and negative affect systems, and cognition (Depue & Lenzenweger, 2001, 2005). The existence of a non-


affective constraint system is supported by research in both personality theory (e.g., Tellegen & Waller,

in press) and neurobiological theory (Depue & Lenzenweger, 2001, 2005), with an emphasis on the

influence of serotonin (Depue & Collins, 1999).

Another highly relevant circuit is stress responsiveness of the hypothalamic pituitary adrenal (HPA)

axis. Individuals with a long history of excessive social stress, such as would occur in childhood trauma,

are vulnerable to HPA hyperreactivity (Putnam & Trickett, 1997). With such hyperreactivity, there is an

overly rapid transition from inhibition and planning to reflexive, fight-or-flight action. The neural

mechanism related to this is related to a switch from prefrontal, inhibitory to posterior-limbic, affective

processing (Mayes, 2000). Executive neurocognitive capacities may be seriously compromised at

relatively low levels of emotional arousal in BPD, manifested in a premature shift to fight-or-flight

emotional states in response to threateningly perceived stimuli.

In partial support of this conceptualization, BPD individuals with a history of childhood trauma,

compared to both BPD individuals without a history of childhood trauma and healthy controls, have

demonstrated higher adrenocorticotrophic hormone (ACTH) and cortisol response to a combined

dexamethasone/corticotropin releasing hormone (DEX/CRH) test (Rinne et al., 2002). Chronic HPA

reactivity also influences episodic (particularly spatial) and semantic (often called declarative) memory

encoding, possibly due to dendritic cell atrophy in the hippocampus (McEwen, 1999). This would seem

in accord with our finding that, compared to controls, BPD participants exhibited the largest deficits in

delayed nonverbal memory performance, with an effect size in the large range. Compellingly, there is

corroborating evidence for hippocampal cell atrophy in BPD individuals who have been traumatized in

that three volumetric brain imaging studies have found smaller hippocampal volumes in BPD subjects

compared to control subjects (Driessen et al., 2000; Schmahl, Vermetten, Elzinga, & Bremner, 2003; van

Elst et al., 2003). These studies, however, do not address the question of whether reduced hippocampal

volume is in itself a pre-existing vulnerability (cf. Gilbertson et al., 2002) or, a consequence of adverse

experience. Another possibility is that such hippocampal atrophy is primarily due to chronic depressive

symptoms.

Finally, biological, neuroendocrine, and imaging studies provide evidence for the involvement of

serotonergic activity in impulsive aggression (Coccaro et al., 1989; Gurvits, Koenigsberg, & Siever,

2000; Siever & Trestman, 1993) in working memory, and inhibitory processes (Depue, 1995; Depue &

Lenzenweger, 2001, 2005). Consequently, compelling areas for research are in the interface of relevant

neurobehavioral systems, such as the serotonergic system, the HPA circuit, non-affective constraint,

negative affectivity, and impulsive-aggression in BPD and related disorders.

3.2. Neuroimaging

The functional neuroimaging of cognitive and memory processes can elucidate their neural substrates.

There are reports of high reactivity of the amygdala in processing social-affective stimuli in BPD using

functional magnetic resonance imaging (fMRI; Donegan et al., 2003). With respect to emotional

reactivity and impulsivity, a preliminary fMRI study of BPD subjects compared to healthy controls

suggests a disrupted interaction between the arousal of negative affect (the amygdala) and the affect

regulating capacities of inhibitory systems (dorsolateral and orbitofrontal cortex) using a emotionally

valenced variation of a go/no-go cognitive and task (Silbersweig et al., 2002). Amygdala reactivity to

emotional stimuli may discriminate BPD from antisocial individuals, who fail to show physiological

activation to sad faces and lack empathy for the distress of others (Blair, Jones, Clark, & Smith, 1997).


The instruments reviewed in the domains of executive neurocognition and memory systems in BPD can

provide challenge paradigms for imaging studies. Conversely, imaging findings may inform the types of

cognitive and memory processes to study in more differentiation, such as the spatial and

autobiographical encoding that is facilitated by the hippocampus.

3.3. Developmental influences on executive neurocognition and memory in BPD

3.3.1. Genetics

The development and acquisition of higher order cognitive functions such as working memory,

attentional systems, and aspects of cognitive inhibition appear to be powerfully influenced by genetics

(e.g., Goldsmith, Lemery, Buss, & Campos, 1999; Gottesman, 1997). Further, there is evidence of strong

familial association of impulsivity and affective instability in BPD (Silverman, Pinkham, Horvath, &

Coccaro, 1991). It is plausible that genetically influenced deficits in inhibitory processes may contribute

to heritable differences in impulsivity and affective instability in BPD and related disorders. Another

potential outcome of a focus on neurocognition and memory processing in BPD is the identification of

endophenotypes (Gottesman & Gould, 2003; Gottesman & Shields, 1972) for BPD that can inform

genetic and risk factor studies of the development of BPD. An endophenotype is a reliable and valid

marker of liability for a form of psychopathology that is not visible to the unaided, naked eye (i.e., it

requires instrumentation or an advanced technology for detection). This concept has long been

influential in research on schizophrenia and schizotypy (Lenzenweger, 1999; Lenzenweger et al., 1991)

and has recently been adopted by those with an interest in BPD (e.g., Siever, Torgersen, Gunderson,

Livesley, & Kendler, 2002).

3.3.2. Temperament

Posner, Rothbart, and colleagues (Posner & Rothbart, 2000; Rothbart et al., 2000), within a

framework of temperament theory, describe effortful control as involving any deliberative inhibition of a

dominant task to perform a subdominant task. The effortful control aspect of temperament complements

more established aspects such as emotional reactivity and sensitivity. Effortful control allows for restraint

in the face of immediate, emotionally arousing rewards or punishments to obtain a longer-term goal.

This approach shares many similarities to the model proposed by Depue and Lenzenweger (2001). While

there are similarities between effortful control and non-affective constraint, they are not synonymous.

Effortful control is a deliberative process whereas the constraint concept relates to a neurobiological

system that affects and is impacted by other systems.

The temperament perspective has yielded compelling findings with infants and young children that

have direct implications for understanding BPD as developing from transactional influences between

genes, temperament, biological maturation, and social experience. Kochanska (1997) has demonstrated

that children’s capacity to understand the emotional state of others and their capacity for prosocial

interactions arise out of temperaments involving high levels of effortful control. By contrast, a

temperament high in negative affective intensity and reactivity and low in voluntary control over

behavior would appear to pave the way for impaired social interactions with peers and adults.

Accordingly, this may also be a temperamental disposition paving the way for the expression of BPD

(Fertuck et al., 2005; Posner et al., 2002; Lenzenweger et al., 2004). However, additional genetic and

environmental factors are likely involved (Clarkin & Posner, 2005). In a retrospective study of 18-year-

old young adults, structural modeling of the developmental predictors of adult BPD found that the


temperamental dimensions of disinhibition (or, low effortful control) and increased levels of negative

affectivity operate in concert with childhood abuse, parental disinhibitory disorder, and parental mood

disorder to predict the expression of adult BPD (Trull, 2001).

3.3.3. Adverse early experience

The association between childhood adversity (trauma and neglect) and the adult BPD diagnosis is

strongly established, with up to 9 of 10 BPD subjects reporting having endured abuse or neglect

(Zanarini et al., 1997).3 There is now other evidence that impairments in executive function, when they

exist in the context of such traumatic and adverse childhood experience, further predispose children to

BPD features. Zelkowitz, Paris, Guzder, and Feldman (2001) demonstrated that deficits in executive

function (on a childhood version of the WCST) and the experience of psychological trauma or neglect

made significant and independent contributions to predicting an increased level of borderline pathology

in these children.

3.3.4. Attachment organization

The security of adult attachment organization is frequently disrupted in BPD (see Agrawal, Gunderson,

Holmes, & Lyons-Ruth, 2004 for review). In convergence with temperament researchers, contemporary

attachment researchers have proposed that the quality of early attachment organization can impact the

development of cognitive capacities such as effortful control (Fonagy, 2003). Further, they argue the

impact of trauma and disrupted attachment security initiates a developmental pathway leading to adult

BPD, particularly its interpersonal dimensions. Interestingly, a gene that is implicated in dopaminergic

processes, the DRD4, is associated with both anterior cingulate activation during performance on the

ANT in adults (Fan, Fossella, Sommer, Wu, & Posner, 2003) and disorganized attachment patterns in 12-

month-old infants (Lakatos et al., 2000). These findings point to potential gene–environment interactions

that impact on both cognitive and attachment organization relevant to BPD.

3.4. Implications for taxonomies of BPD and neighboring disorders

3.4.1. Co-occurring disorders

From the vantage point of the taxonomy of BPD, the high co-occurrence with other disorders,

heterogeneity, and absence of theoretically and psychometrically sound diagnostic thresholds suggests

that the current DSM nosology is not carving out borderline phenomena bat the jointsQ (Meehl, 1992). As

a way to account for co-occurring disorders, and to identify whether there is specificity of inhibition

impairment to diagnostic groups, Nigg (2000) and Korfine and Hooley (2000) recommend that more

than one type of inhibitory and memory process be studied concurrently across several disorders.

There are several frequently co-occurring disorders of particular relevance to BPD in the context of

cognition and memory, which could serve as optimal psychiatric comparison groups in future studies.

Antisocial personality and psychopathy are associated with executive cognitive control deficits, similar

to some of the findings we have reviewed in BPD (cf. Dolan & Park, 2002). Anxiety disorders and

3A limitation of research on childhood abuse and neglect and BPD is a reliance on patient reports. Individuals with BPD (and others) may

exaggerate or minimize experiences of abuse and neglect for various reasons such as memory distortions, reluctance to be open with the

interviewer, amnesia, etc. Prospective, longitudinal studies of high-risk populations, starting in childhood, could best address this issue. Such an

approach would ideally rely on additional forms of evidence of abuse and neglect (e.g., medical records, police reports, and records from child

protective services). Such a study has not been conducted, to our knowledge.


depressive disorders are associated with affective cognitive and memory biases perhaps in some

similar and some contrasting ways compared to BPD (cf. Williams et al., 1996). Bipolar disorders are

characterized by mood instability and many have argued that BPD is a variant of the bipolar spectrum

disorders (cf. Deltito et al., 2001). One of the distinctions between the emotional dysregulation in

BPD vs. bipolar spectrum disorders may be the degree to which such dysregulations are sensitive to

socio-emotional and other environmental stimuli. Accordingly, experimental manipulation of such

stimuli when comparing BPD and bipolar subjects’ inhibitory and memory processing could begin to

address this distinction systematically. Affective memory biases, such as those found in BPD (Korfine

& Hooley, 2000) have been extensively documented in depressed individuals (see Mineka & Nugent,

1995 for review). Similar results have been obtained in individuals with Post Traumatic Stress

Disorder (PTSD). PTSD often co-occurs with BPD, and individuals with BPD have higher rates of

childhood and adult trauma and neglect than non-BPD individuals (Zanarini et al., 1997). For a fuller

consideration of the crucial area of diagnostic co-occurrence in BPD, and the role of neurobehavioral

studies in this area, we refer the reader to recent discussions of this issue (Lyons, Tyrer, Gunderson, &

Tohen, 1997).

3.5. Interface of neurocognition with clinical research, theory, and treatment of BPD

To the clinician who engages in the complex, often turbulent and challenging treatment of BPD,

executive neurocognition and memory systems may seem strikingly irrelevant to day-to-day therapeutic

challenges in this patient population. The pressing issues in the clinical engagement with individuals

with BPD include diagnostic confusion, suicidality and para-suicidality, complicated impasses,

enactments of interpersonal difficulties in the therapeutic relationship, and frequent interruptions and

drop-out from treatment. The following sections elaborate beginning connections that may forge

stronger links between the research cognition and memory and clinical practice with BPD.

3.5.1. Assessment

Increased understanding of the neurobehavioral facets of BPD should translate into more refined

diagnostic subtyping and, consequently, more targeted prevention and treatment initiatives for BPD. It

is reasonable to speculate that differing patterns of inhibitory and memory processes will respond

divergently to differing treatment approaches. In particular, the study of potential convergences

between phenomenological and neurocognitive domains would be a powerful paradigm for subtyping

BPD, with implications for differential treatment planning. Initial work in this area is promising. Using

a self-report adult temperament questionnaire developed by Rothbart, Posner and colleagues, BPD

subjects have been clustered into three subtypes based on the dimension of effortful control

(Hoermann, Clarkin, Levy, & Hull, 2005). The BPD cluster characterized by the lowest effortful

control exhibited the highest symptoms of depression, hostility, anxiety, and psychoticism, the most

social alienation, and the most difficulty with identity and reality testing. The converse was found for

the high effortful control sub-group, and the middle cluster was intermediate on most of these

dimensions.

With regard to the most life-threatening aspect of BPD, cognitive inhibition may to be a strong

predictor suicidality and parasuicidality. Keilp et al. (2001) compared three groups of subjects with

DSM-IV major depressive disorder (those without a history of suicide attempts, those with low lethality

suicide attempts, and those with high lethality suicide attempts), to non-patient control participants on


measures of attention, memory, and cognitive inhibition. They found that depressed subjects with prior

highly lethal suicide attempts had significantly greater deficits on cognitive inhibition compared to the

non-suicide depressed and normal subjects. By contrast, all depression subgroups were significantly

lower than the controls on measures of attention and memory. This finding seems consistent with a less

well-designed study (Burgess, 1991), which found that, within a BPD group, self-injurious behavior was

associated with neurocognitive impairment, but not with depression levels. These findings suggest that

deficits in executive neurocognition may be used to identify the highest risk BPD subjects, and intervene

accordingly to prevent suicidality and parasuicidality.

3.5.2. Treatment

Cognitive and memory impairments may improve during treatment. For instance, putative

hippocampal atrophy in relation to stress levels (McEwen, 1999) may be reversed by effective

psychopharmacologic and psychotherapeutic interventions, as the hippocampus exhibits much plasticity

throughout development. A parallel concept to stress reactivity, affect regulation, may also provide a

useful framework for linking BPD treatment with lab-based assessment of cognition and memory in

BPD. Affect regulation is defined as the deliberate and automatized procedures and individual uses to

enhance positive affects, and decrease negative and aversive emotions (cf. Dozier & Kobak, 1992; Perry

& Cooper, 1989). The deliberative aspects of affect regulation most likely involve the aspects of non-

affective constraint and effortful control systems. The automatized, non-voluntary aspects of affective

coping and regulatory strategies can be conceptualized as, in part, functions of procedural memory

(Bucci, 1997; Westen, 1994) that involve the automatized ways in which mental processes of attention,

self-appraisal, abstraction, and episodic memory recall increase or decrease affective reactions to internal

and external stimuli.

As both the temperament and attachment literature suggest, the quality of social bonds may

profoundly influence the development of memory systems and cognitive processing. The study of

social cognition (Westen, 1991) and adult attachment research (Fonagy, Target, Gergely, Allen, &

Bateman, 2003) are relevant paradigms in this arena. Preliminary assessment of aspects of social

cognition in adult BPD subjects indicate that they exhibit deficits in affect tone, complexity of

person perception, capacity for interpersonal investment, commitment to values and moral principles,

and self-understanding. Such deficits have been operationalized in the psychopathology and

psychodynamic literature as the quality of object relations (see Blatt, Auerbach, & Levy, 1997;

Hupricha & Greenberg, 2003, and Westen, 1991 for reviews). The object relations literature has

demonstrated that BPD individuals are vulnerable to experiencing interpersonal relationships as more

need gratifying, dangerous, and potentially exploitive than comparison groups. This literature has

also highlighted the difficulty BPD individuals have in interpreting ambiguous and complex social

stimuli, and in establishing accurate and unbiased causal attributions of interpersonal interactions.

Similarly, Fonagy et al. (1996) have demonstrated that traumatized BPD subjects can be

differentiated from other psychiatric subjects and matched control subjects by exhibiting lower

ratings on the capacity to be aware of the mental states of themselves and others. The extent to

which these social cognitive impairments are independent of or are mutually influential with

neurocognitive processes in BPD has not been studied, yet is crucial. Extrapolating these paradigms

to the study of the impact of psychotherapy on both social cognition and neurocognition in BPD

may provide exciting insights into the interplay between these two domains of information pro-

cessing during the treatment process.


4. Limitations and caveats

The studies of executive neurocognitive and memory processes and BPD share many

measurement and methodological limitations, and investigating BPD individuals raises many unique

challenges in clinical research, which we mention briefly. (1) The polythetic nature of DSM-IV

(American Psychiatric Association, 1994) BPD diagnostic system creates the frequent occurrence

that even individuals who meet criteria for BPD have quite different clinical presentations. (2) The

absence of empirically and prognostically meaningful diagnostic thresholds represents another

taxonomic and measurement issue. Widiger, Sanderson, and Warner (1986) found that those with

five BPD criteria, the minimum needed for the diagnosis, resemble non-DSM BPD individuals more

than BPD individuals. (3) Most of the studies reviewed demonstrated some attempt to assess non-

medicated BPD individuals, or to control for the effects of medication. In doing so, the trend was to

indicate in a binary manner whether a given participant was taking medication. However, few

studies indicated the class, dosage, number and type of different concurrent medications, and/or

length of medication use. There are more studies needed with subjects not on medication. (4) There

is considerable instability in the BPD diagnosis, and longitudinal studies indicate that both borderline

features (Lenzenweger, Johnson, & Willett, 2004; Stone, 1990, 1993; Zanarini, Frankenburg,

Hennen, & Silk, 2003) and neurocognitive performance (Kramer, Hahn, & Gopher, 1999; West,

1996) decrease significantly with age. While this may appear paradoxical, we speculate that

executive neurocognition may be less crucial as affective instability in BPD diminishes during

middle adulthood. However, only longitudinal studies of executive neurocognition and affective

instability and the course of BPD can assess this theory. (5) Most of the studies do not directly

address state/trait differentiation in cognition, memory, affect, and personality variables. This limits

the ecological validity of many of the studies, particularly since BPD is characterized in part by

rapidly shifting, context-sensitive affective states and cognitive appraisals. (6) Most studies utilized

either entirely female samples or predominantly female samples. This is consistent with the 3:1 ratio

of females to males found in clinically ascertained BPD samples (Corbitt & Widiger, 1995). Data on

male BPD subjects is particularly important given there is compelling evidence that gender

differences in BPD prevalence rates are only found in clinical settings (Corbitt & Widiger, 1995;

Torgersen et al., 2001). An earlier study suggested that gender differences in neurodevelopmental

history and clinical presentation were prominent in BPD (Andrulonis, Glueck, Stroebel, & Vogel,

1982). (7) Groups in the reviewed studies were not consistently matched on IQ and education level,

and these variables may underlie apparent group difference in executive neurocognition and memory

performance.

Finally, the association between executive neurocognition and impulsivity in BPD may simply reflect

an obvious tautology between the clinically rated diagnostic feature of impulsivity and its neurocognitive

correlates. If this was the case, there would be no additive advantage in using executive neurocognitive

assessment to reify the diagnostic features of BPD. This argument would, however, dismiss advantages

of a neurocognitive approach to research in BPD and impulsivity. Impulsivity appears to be a

multidimensional construct, with attentional, motor, and nonplanning subtypes (Patton, Stanford, &

Barratt, 1995). Executive neurocognitive tasks can contribute to parsing subtypes of impulsivity in

different psychiatric disorders. Neurocognitive measurement of constructs such as impulsivity can be

used to track changes over time and to decompose the sub-facets of such constructs. Also, the in-vivo

neurobiological correlates of impulsivity (such as 5HT synthesis; cf. Leyton et al., 2001) and


relationships to normal personality traits such as non-affective constraint (cf. Lenzenweger et al., 2004)

can then be both identified with lab based cognitive assessment.

5. Conclusion

In distillation, the main findings of this review are: (1) Well-characterized groups of BPD subjects

appear to exhibit non-specific deficits in multiple domains of executive neurocognitive and memory

performance in comparison to psychiatric and non-clinical groups. On a cautionary note, complicating

factors such as co-occurring conditions, state-dependent effects, omnibus measurement, small sample

sizes, and a limited number of studies implore us to be tentative about this pattern of findings. (2) Phase

III studies, while also limited in number and unreplicated, consistently suggest that motivational

influences and negative affects have a disorganizing and disruptive influence on executive

neurocognitive and memory performance in BPD compared to comparison groups.

There are a few observations regarding overall the state of investigation in executive neurocognition,

memory, and BPD, and promising areas for future investigation. First, it appears that the more emotional

stimuli are specifically tailored to the phenomenology of BPD the greater the impact on cognitive and

memory systems (e.g., Korfine & Hooley, 2000). Second, while there are associations between task

performance on certain cognitive and memory laboratory tasks and the diagnosis of BPD, very few

researchers have taken the next step and related the task performance to actual social behavior (e.g., social

behavior in dyadic relationships, suicidality, etc.). Additionally, longitudinal designs that assess the

stability and validity of associations between neurocognition, symptomatology, affectivity, and social

behavior are called for, given the emerging longitudinal data on the instability of the diagnosis, and the

rapidly shifting, state-dependent aspects of BPD.

As a final point, it could be argued that the main findings of the review are not surprising or

illuminating, as the notion that affects have a disorganizing effect on cognition and memory in BPD is

what clinicians have been describing for decades. While this is accurate, what is promising is that

clinically relevant phenomena can be rigorously operationalized and assessed in an experimental

laboratory context. The promise of the perspective of experimental psychopathology is that the features

and symptoms of devastating clinical phenomena–even multi-faceted and heterogeneous conditions like

BPD–can be assessed and related to basic biological and psychological mechanisms and systems

(Lenzenweger & Hooley, 2003). With collaboration and cross-fertilization, this translational effort should

eventually de-mystify and de-stigmatize this enigmatic disorder. Most importantly, firmer scientific

foundation in BPD research will inform more effective, research-based interventions. As a result, there is

compelling reason for hope that the devastating suffering that BPD causes to individuals and their families

can be mitigated as the neurobehavioral facets of the disorder are increasingly understood.

Acknowledgements

Preparation of this article was supported, in part, by the Leslie Glass Foundation, the Borderline

Personality Disorder Research Foundation, and an NIH National Research Service Award (MH015144).

We would like to thank John G. Keilp, Otto F. Kernberg, Michael I. Posner, Steven Roose, the

Research Group of the Columbia University Center for Psychoanalytic Training and Research, and three


anonymous reviewers for their thoughtful comments on earlier versions of this article. Melissa Stanley

provided helpful editorial assistance on this manuscript.

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Executive neurocognition, memory systems, and borderline personality disorder

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