Van Dijk.2750-Proefschrift 10 - COnnecting REpositories · 2018-07-07 · 507383-L-bw-van Dijk ª...

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507383-L-bw-van Dijk507383-L-bw-van Dijk507383-L-bw-van Dijk507383-L-bw-van Dijk

Fiona van Dijk



ISBN

978-94-6284-086-7

Cover illustration

Alexander Hertog

Design/lay-out

Promotie In Zicht, Arnhem

Print

Ipskamp Printing, Enschede

© Fiona van Dijk, 2017

All rights reserved. No part of this thesis may be reproduced or printed in any form or by any means,

electronically, mechanically, including photocopy, recording or any information storage and retrieval

system without written permission of the author.



Proefschrift

ter verkrijging van de graad van doctor

aan de Radboud Universiteit Nijmegen

op gezag van de rector magnificus prof. dr. J.H.J.M. van Krieken,

volgens besluit van het college van decanen

in het openbaar te verdedigen op vrijdag 3 maart 2017

om 16.30 uur precies

door

Fiona Eva van Dijk

Geboren op 2 december 1973

te Hardenberg



Promotoren

Prof. dr. J.K. Buitelaar

Prof. dr. R.J. Verkes

Copromotoren

Dr. J.C. Glennon

Dr. C.C. Kan

Manuscriptcommissie

Prof. dr. J.B. Prins

Prof. dr. P.P.G. Hodiamont

Dr. J.J.S. Kooij (PsyQ, Den Haag)



Contents

Chapter 1 General introduction 7

Chapter 2 ADHD, personality and its disorders 19

Chapter 3 Lifespan attention deficit/hyperactivity disorder and

borderline personality disorder symptoms in female patients:

a latent class approach

49

Chapter 4 Symptomatic overlap between attention-deficit/hyperactivity

disorder and borderline personality disorder in women:

the role of temperament and character traits

71

Chapter 5 Do cognitive measures of response inhibition differentiate

between attention deficit/hyperactivity disorder and

borderline personality disorder?

89

Chapter 6 Five Factor Model personality traits relate to adult attention-

deficit/hyperactivity disorder but not to their distinct

neurocognitive profiles

109

Chapter 7 Summary and General Discussion 131

Nederlandse samenvatting

List of publications

Dankwoord

Curriculum Vitae

Donders Graduate School for Cognitive Neuroscience

155

159

161

165

167



General introduction

1



9

GENERAL INTRODUCTION

1

General introduction

This thesis originates from clinically driven questions about the relationship

between adult attention-deficit/hyperactivity disorder (ADHD) and borderline

personality disorder (BPD) symptoms. It intends to contribute to the understanding

of the origin of the overlap and differences in both disorders on the level of

classification, personality traits, and neurocognition. The general introduction is

a synopsis of what is currently known about adult ADHD and BPD in general and

more specifically about their clinical overlap, temperament traits, and neuro-

cognitive features. After that, I will describe the overall aim and outline of this

thesis.

Adult attention-deficit hyperactivity disorder ADHD is defined as a childhood-onset neurodevelopmental disorder in the American

Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders

(5th edition; DSM-5) and is characterized by the presence of developmentally

inappropriate and impairing levels of inattention, hyperactivity, and impulsivity

(APA 2013). ADHD was perceived as a childhood-onset disorder with limited effect

on adult psychopathology. However the symptoms and impairments that define

ADHD often affect the adult population, for an overview of key conceptual issues

in adult ADHD see (Asherson, Buitelaar et al. 2016). The estimated prevalence of

ADHD in adults ranges from 2-5% to 3-4% (Fayyad, De Graaf et al. 2007; Simon,

Czobor et al. 2009). Worldwide, up to 50% of children with ADHD continue to meet

diagnostic criteria for ADHD as adults (Lara, Fayyad et al. 2009) with some

European studies suggesting persistence rates of ADHD even up to 80% (van

Lieshout, Luman et al. 2016). Although there is the possibility that ADHD might

emerge after childhood (Moffitt, Houts et al. 2015), for most adult patients with

ADHD there is a clear history of ADHD from childhood. A male: female adult ratio

of 3-4:1 is recorded in epidemiological samples (Biederman, Kwon et al. 2005) but

in clinical practice the rate of persistent ADHD does not significantly differ across

genders (Cortese, Faraone et al. 2016). Factors influencing course and outcome of

ADHD include general cognitive ability, severity of ADHD, causal factors (genes

and environment), brain maturation and development, and the presence of

co-occurring mental health and neurodevelopmental disorders (Faraone, Asherson

et al. 2015).

Despite the high prevalence of adult ADHD and known links to psychosocial,

functional, and mental health problems, high rates of undiagnosed or untreated

ADHD have been found (Huntley, Maltezos et al. 2012; Young, Moss et al. 2015).

Therefore, improving understanding of the clinical presentation of ADHD in

adulthood is of great importance.



10

CHAPTER 1

Symptoms of ADHD cluster together in two major dimensions: inattention

and hyperactivity-impulsivity. They reflect continuous traits rather than a categorical

disorder which also means that the symptoms do not reflect a change from the

premorbid state (as is also the case in personality disorders). The definition of a

clinically significant disorder is therefore based on the presence of clinically

significant impairment of functioning (APA 2013). The core symptoms of ADHD

tend to decline with age, although inattentive features persist over the longer

term across the lifespan (Faraone, Biederman et al. 2006). In clinical practice a full

understanding of the broader issues in ADHD is needed to improve diagnostic

outcome. ADHD is also linked to executive function impairments, sleep problems,

emotional dysregulation, mental restlessness, in addition to functional impairments

such as traffic accidents and occupational underachievement (Van Veen, Kooij et al.

2010; Adler, Dirks et al. 2013; Skirrow and Asherson 2013; Surman, Biederman

et al. 2013; Mowlem, Skirrow et al. 2016). High levels of concurrent comorbidity

with other neurodevelopmental disorders such as autism spectrum disorder,

learning and motor disorders, intellectual disability, and tic disorders exist in

those with ADHD (Jensen and Steinhausen 2015). In addition ADHD also co-occurs

with substance use disorders, anxiety, depression, personality disorders, and conduct

problems (Jensen and Steinhausen 2015; Matthies and Philipsen, 2016; Smith and

Samuel, 2016). Understanding the similarities and differences between adult

ADHD and common co-occurring mental disorders is important in order to

prevent under-diagnosis of ADHD. The pervasive nature of emotional instability

in adult mental health means that all individuals with a non-episodic form

of emotional instability should be screened for ADHD, including those with

personality disorders (Asherson, Buitelaar et al. 2016).

Borderline personality disorder Borderline personality disorder is characterized by a pervasive pattern of instability

in emotional regulation, interpersonal relationships and self-image, along with

marked impulsivity. It is associated with suicide, high rates of comorbid mental

disorders, and substantial costs to society (Leichsenring, Leibing et al. 2011).

Despite continued controversy regarding the diagnosis of BPD prior to adulthood

there is a growing body of research showing that youth BPD is a valid construct,

supporting the clinical recognition of the disorder in youth (Winsper, Lereya et al.

2016). Etiological factors leading to BPD remain only partially elucidated, though

it is recognized that genetic, neurobiological and psychosocial factors all contribute

to the development of the disorder (Crowell, Beauchaine et al. 2009). BPD affects up

to 3% of the general population (Lenzenweger 2008). In primary care, the prevalence

of BPD ranges from 4 to 6% (Moran, Jenkins et al. 2000; Gross, Olfson et al. 2002).

In epidemiological samples the prevalence is roughly equal male to female, whereas



11


1

in clinical services there is a clear preponderance of women, who are more likely

to seek treatment (Torgersen, Kringlen et al. 2001; Zimmerman, Chelminski et al.

2008).

Despite evidence of the reliability and validity of the diagnosis and the

treatability of the condition, many people with BPD remain undiagnosed in

clinical practice, placing them at risk for ineffective or possibly harmful treatment

(Chanen 2015; Tyrer, Reed et al. 2015). One cause of diagnostic confusion is the

high rate of comorbid disorders. BPD is a heterogeneous condition and its symptoms

overlap considerably with depressive, schizophrenic, impulsive, dissociative and

identity disorders. This overlap is also linked to comorbidity and in clinical

practice it may therefore be difficult to determine if the presenting symptoms are

those of borderline personality disorder or a related comorbid condition.

Adult ADHD and BPD: Clinical overlap In clinical practice, ADHD and BPD can sometimes be difficult to distinguish.

Several symptoms such as impulsivity, emotional/affective instability, risk taking

behavior, difficulty in controlling anger and impaired stress tolerance are found

in ADHD as well as in BPD patients. Among these features, impulsivity has been

identified as one of the most common traits occurring within this overlap (Dowson,

Bazanis et al. 2004; Davids and Gastpar 2005). Deficits in affect regulation are a

key feature of BPD but are also recognized as an associated feature of ADHD

(Skirrow and Asherson 2013). The same applies to disturbed interpersonal

relationships; a symptom often experienced by BPD patients, but adults with

ADHD may also show interpersonal problems as a consequence of their ADHD

symptoms (Philipsen 2006). Indistinguishable comorbidity rates have been found

for substance abuse, anxiety and eating disorders and high levels of cyclothymia

(Eich, Gamma et al. 2014). Additionally, both disorders show a chronic trait like

course, and although historically BPD was seen as a disorder presenting mostly in

late adolescence and early adulthood, we now know that symptoms can already

present in childhood (Winsper, Lereya et al. 2016). Moreover, ADHD and BPD often

co-occur (Biederman 2004), with rates of BPD among adult ADHD ranging from

19% to 37% (Miller, Flory et al. 2008). Despite the evidence of overlap and

co-occurrence, the nature of the relation between both disorders remains not

fully understood. A further challenge in this field of research are the gender

differences in the prevalence of these disorders; equivalent prevalence of adult

ADHD in males and females and a higher prevalence of BPD among female versus

male patients in clinical settings (Skodol and Bender 2003). Gender may therefore

be an important factor to consider in understanding the relationship between

ADHD and BPD.



12

CHAPTER 1

Adult ADHD and BPD: temperament and personality traits Dimensional models of personality may be helpful in addressing problems of

excessive co-occurrence, heterogeneity among persons with the same diagnosis,

and artefactual or epiphenomenal diagnostic distinctions (Widiger and Simonsen

2005). While ADHD is viewed in categorical terms in the DSM-IV and DSM-5, there

is support for a dimensional view of it (Marcus and Barry 2011; Coghill and

Sonuga-Barke 2012). Similar to personality dimensions, ADHD is stable across time

and highly heritable (Biederman 2005). Indeed, ADHD and BPD share a number of

temperament/personality traits and a “typical ADHD temperament” seem to

correspond to an explosive/borderline type of personality (Anckarsater, Stahlberg

et al. 2006). Insight into the associations between temperament/personality traits

and ADHD and co-occurring BPD may help delineate possible developmental

pathways and explain comorbid disorder development. Predictive data concerning

the development of BPD comes from prospective studies and showed that a

diagnosis of ADHD in childhood was predictive of later BPD symptoms (Burke and

Stepp 2012; Stepp, Burke et al. 2012), but little is known about the process(es)

underlying this path (Storebø and Simonsen 2013). Action-oriented temperament/

personality traits like impulsivity, novelty seeking and conduct problem could

mediate the relation between childhood ADHD symptoms and adult BPD features

(Carlotta, Borroni et al. 2013).

Adult ADHD and BPD: Cognitive functioning ADHD has been associated with neurocognitive deficits in multiple cognitive

domains. The main domains of neuropsychological dysfunction in ADHD are:

memory, inhibitory control, delay aversion, decision making, timing, and response

variability. The levels of deficiency in each of these domains differ more or less

independently within patients with ADHD, and there is considerable overlap

between neuropsychological performance in patients with ADHD and normal

controls (Coghill, Seth et al. 2014). Although at a behavioral level executive

dysfunctions are strongly related to ADHD, it is much debated whether it reflects

primary causal processes in ADHD. There is substantial heterogeneity in cognitive

functioning, and there is no straightforward association between cognitive

performance and the trajectory of clinical symptoms (van Lieshout, Luman et al.

2013; Coghill, Hayward et al. 2014; Coghill, Seth et al. 2014; Mostert, Hoogman

et al. 2015; Mostert, Onnink et al. 2015).

Neuropsychological deficits have also been identified as a robust feature of

BPD. Since impulsivity is a core feature in PD, it is not surprising that poor

inhibitory functioning has been a consistent finding in BPD (Nigg, Silk et al. 2005).

However, compared to healthy controls significant impairment was found across

the full range of traditional neuropsychological tests. The most consistent deficits



13


1

were found in the domains of attention, cognitive flexibility, learning and memory,

planning, processing speed, and visuospatial abilities (Ruocco 2005). Meta analyses

of BPD samples with higher percentage of comorbidity (i.e. personality disorder,

major depression, eating disorders and substance abuse disorders) showed worse

neuropsychological functioning than patients with less percentage of such

comorbid disorders (Unoka and Richman 2016). A recent study examined the

comorbid presentation of ADHD and BPD and suggested more informant, but not

self-reported, symptoms of impulsivity and lower intellectual and attentional

functioning compared to a group with only ADHD (O’Malley, McHugh et al. 2016).

Co-occurring disorders thus seem to affect the cognitive performance of BPD

patients. To clarify the influence of ADHD and BPD on each other and improve

their phenotypic characterization, it is important to establish whether and how

ADHD and BPD are related on a neurocognitive level.

Aims and outline of the thesis The aim of the current thesis was to critically appraise the association between

Adult ADHD and BPD. This was assessed by investigating the overlap and differences

between adult ADHD and BPD on the level of symptoms, temperament (and

character) traits, and neurocognitive performance. In chapter 2 we presented a

literature review on ADHD, personality disorders, and personality traits. This

work resulted in a book chapter for ADHD in Adults: Characterization, Diagnosis

and Treatment (van Dijk and Anckarsater 2011). In chapter 3, Latent Class Analyses

were undertaken to identify mutually exclusive classes of female ADHD and BPD

subjects with homogeneous symptom profiles (van Dijk, Lappenschaar et al. 2011).

This first study provided a basis for its sequel (chapter 4). In chapter 4, we build on

the knowledge that ADHD and BPD seem to share a number of temperament and

character traits. In this study we account for the comorbid presence of BPD in

ADHD and vice versa. We examined the role of temperament and character traits

in the differentiation of classes of patients with similar ADHD and BPD symptom

profiles and possible pathways between early temperament and future ADHD and/

or BPD were evaluated in a female population (van Dijk, Lappenschaar et al. 2012).

In chapter 5 we studied whether cognitive measures of response inhibition derived

from a Continuous Performance Task are able to differentiate between adult

ADHD, BPD and healthy controls (van Dijk, Schellekens et al. 2014). Response

inhibition was chosen as a cognitive construct to study given the significant

impairment in this domain reported in ADHD and BPD. Finally, in chapter 6 we

investigated interactions between adult ADHD, cognitive profiles, and personality

traits in comparison to healthy controls. (Van Dijk, Mostert et al. 2016). In chapter 7

all studies presented in this thesis are integrated and a critical discussion along

with suggestions for future directions presented.



14

CHAPTER 1

References

Adler, L. A., B. Dirks, et al. (2013). “Self-Reported quality of life in adults with attention-deficit/hyperactivity

disorder and executive function impairment treated with lisdexamfetamine dimesylate: a randomized,

double-blind, multicenter, placebo-controlled, parallel-group study.” BMC Psychiatry 13: 253.

Anckarsater, H., O. Stahlberg, et al. (2006). “The impact of ADHD and autism spectrum disorders on

temperament, character, and personality development.” Am J Psychiatry 163(7): 1239-1244.

APA (2013). Diagnostic and Statistical Manualof Mental Disorders - DSM 5. Washington, DC, American

Psychiatric Publishing.

Asherson, P., J. Buitelaar, et al. (2016). “Adult attention-deficit hyperactivity disorder: key conceptual issues.”

The Lancet.

Biederman, J. (2004). “Impact of comorbidity in adults with attention-deficit/hyperactivity disorder.” J Clin

Psychiatry 65 Suppl 3: 3-7.

Biederman, J. (2005). “Attention-deficit/hyperactivity disorder: a selective overview.” Biol Psychiatry 57(11):

1215-1220.

Biederman, J., A. Kwon, et al. (2005). “Absence of gender effects on attention deficit hyperactivity disorder:

findings in nonreferred subjects.” Am J Psychiatry 162(6): 1083-1089.

Burke, J. D. and S. D. Stepp (2012). “Adolescent disruptive behavior and borderline personality disorder

symptoms in young adult men.” J Abnorm Child Psychol 40(1): 35-44.

Carlotta, D., S. Borroni, et al. (2013). “On the relationship between retrospective childhood ADHD symptoms

and adult BPD features: the mediating role of action-oriented personality traits.” Compr Psychiatry

54(7): 943-952.

Chanen, A. M. (2015). “Borderline Personality Disorder in Young People: Are We There Yet?” J Clin Psychol

71(8): 778-791.

Coghill, D. and E. J. Sonuga-Barke (2012). “Annual research review: categories versus dimensions in the

classification and conceptualisation of child and adolescent mental disorders--implications of recent

empirical study.” J Child Psychol Psychiatry 53(5): 469-489.

Coghill, D. R., D. Hayward, et al. (2014). “A longitudinal examination of neuropsychological and clinical

functioning in boys with attention deficit hyperactivity disorder (ADHD): improvements in executive

functioning do not explain clinical improvement.” Psychol Med 44(5): 1087-1099.

Coghill, D. R., S. Seth, et al. (2014). “A comprehensive assessment of memory, delay aversion, timing,

inhibition, decision making and variability in attention deficit hyperactivity disorder: advancing

beyond the three-pathway models.” Psychol Med 44(9): 1989-2001.

Cortese, S., S. V. Faraone, et al. (2016). “Gender differences in adult attention-deficit/hyperactivity disorder:

results from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC).” J Clin

Psychiatry 77(4): e421-428.

Crowell, S. E., T. P. Beauchaine, et al. (2009). “A biosocial developmental model of borderline personality:

Elaborating and extending Linehan’s theory.” Psychol Bull 135(3): 495-510.

Davids, E. and M. Gastpar (2005). “Attention deficit hyperactivity disorder and borderline personality

disorder.” Prog Neuropsychopharmacol Biol Psychiatry 29(6): 865-877.

Dowson, J., E. Bazanis, et al. (2004). “Impulsivity in patients with borderline personality disorder.” Compr

Psychiatry 45(1): 29-36.

Eich D., Gamma A. et al. (2014). Temperamental differences between bipolar disorder, borderline personality

disorder, and attention deficit/hyperactivity disorder: some implications for their diagnostic validity.

J Affect Disord. 169:101-104.

Faraone, S. V., P. Asherson, et al. (2015). “Attention-deficit/hyperactivity disorder.” Nat Rev Dis Primers 1: 15020.

Faraone, S. V., J. Biederman, et al. (2006). “The age-dependent decline of attention deficit hyperactivity

disorder: a meta-analysis of follow-up studies.” Psychol Med 36(2): 159-165.

Fayyad, J., R. De Graaf, et al. (2007). “Cross-national prevalence and correlates of adult attention-deficit

hyperactivity disorder.” Br J Psychiatry 190: 402-409.

Gross, R., M. Olfson, et al. (2002). “Borderline personality disorder in primary care.” Arch Intern Med 162(1):

53-60.



15


1

Huntley, Z., S. Maltezos, et al. (2012). “Rates of undiagnosed attention deficit hyperactivity disorder in

London drug and alcohol detoxification units.” BMC Psychiatry 12: 223.

Jensen, C. M. and H. C. Steinhausen (2015). “Comorbid mental disorders in children and adolescents with

attention-deficit/hyperactivity disorder in a large nationwide study.” Atten Defic Hyperact Disord 7(1):

27-38.

Lara, C., J. Fayyad, et al. (2009). “Childhood predictors of adult attention-deficit/hyperactivity disorder:

results from the World Health Organization World Mental Health Survey Initiative.” Biol Psychiatry

65(1): 46-54.

Leichsenring, F., E. Leibing, et al. (2011). “Borderline personality disorder.” Lancet 377(9759): 74-84.

Lenzenweger, M. F. (2008). “Epidemiology of personality disorders.” Psychiatr Clin North Am 31(3): 395-403, vi.

Marcus, D. K. and T. D. Barry (2011). “Does attention-deficit/hyperactivity disorder have a dimensional

latent structure? A taxometric analysis.” J Abnorm Psychol 120(2): 427-442.

Matthies S. and Philipsen A. (2016). Comorbidity of Personality Disorders and Adult Attention Deficit

Hyperactivity Disorder (ADHD)--Review of Recent Findings. Curr Psychiatry Rep. 18(4):33.

Miller, C. J., J. D. Flory, et al. (2008). “Childhood attention-deficit/hyperactivity disorder and the emergence

of personality disorders in adolescence: a prospective follow-up study.” J Clin Psychiatry 69(9):

1477-1484.

Moffitt, T. E., R. Houts, et al. (2015). “Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder?

Evidence From a Four-Decade Longitudinal Cohort Study.” Am J Psychiatry 172(10): 967-977.

Moran, P., R. Jenkins, et al. (2000). “The prevalence of personality disorder among UK primary care

attenders.” Acta Psychiatr Scand 102(1): 52-57.

Mostert, J. C., M. Hoogman, et al. (2015). “Similar Subgroups Based on Cognitive Performance Parse

Heterogeneity in Adults With ADHD and Healthy Controls.” J Atten Disord.

Mostert, J. C., A. M. Onnink, et al. (2015). “Cognitive heterogeneity in adult attention deficit/hyperactivity

disorder: A systematic analysis of neuropsychological measurements.” Eur Neuropsychopharmacol.

Mowlem, F. D., C. Skirrow, et al. (2016). “Validation of the Mind Excessively Wandering Scale and the

Relationship of Mind Wandering to Impairment in Adult ADHD.” J Atten Disord.

Nigg, J. T., K. R. Silk, et al. (2005). “Disinhibition and borderline personality disorder.” Dev Psychopathol

17(4): 1129-1149.

O’Malley G.K., McHugh L. et al. (2016). Characterizing adult attention-deficit/hyperactivity-disorder and

comorbid borderline personality disorder: ADHD symptoms, psychopathology, cognitive functioning

and psychosocial factors. Eur Psychiatry. 31:29-36.

Philipsen, A. (2006). “Differential diagnosis and comorbidity of attention-deficit/hyperactivity disorder

(ADHD) and borderline personality disorder (BPD) in adults.” Eur Arch Psychiatry Clin Neurosci 256

Suppl 1: i42-46.

Ruocco, A. C. (2005). “The neuropsychology of borderline personality disorder: a meta-analysis and review.”

Psychiatry Res 137(3): 191-202.

Simon, V., P. Czobor, et al. (2009). “Prevalence and correlates of adult attention-deficit hyperactivity

disorder: meta-analysis.” Br J Psychiatry 194(3): 204-211.

Smith T.E. and Samuel D.B.(2016). A Multi-Method Examination of the Links Between ADHD and Personality

Disorder. J Pers Disord. 4:1-23.

Skirrow, C. and P. Asherson (2013). “Emotional lability, comorbidity and impairment in adults with attention-

deficit hyperactivity disorder.” J Affect Disord 147(1-3): 80-86.

Skodol, A. E. and D. S. Bender (2003). “Why are women diagnosed borderline more than men?” Psychiatr Q

74(4): 349-360.

Stepp, S. D., J. D. Burke, et al. (2012). “Trajectories of attention deficit hyperactivity disorder and oppositional

defiant disorder symptoms as precursors of borderline personality disorder symptoms in adolescent

girls.” J Abnorm Child Psychol 40(1): 7-20.

Storebø O.J. and Simonsen E. (2013). Is ADHD an early stage in the development of borderline personality

disorder? Nord J Psychiatry. 64:1-7.

Surman, C. B., J. Biederman, et al. (2013). “Understanding deficient emotional self-regulation in adults with

attention deficit hyperactivity disorder: a controlled study.” Atten Defic Hyperact Disord 5(3): 273-281.



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CHAPTER 1

Torgersen, S., E. Kringlen, et al. (2001). “The prevalence of personality disorders in a community sample.”

Arch Gen Psychiatry 58(6): 590-596.

Tyrer, P., G. M. Reed, et al. (2015). “Classification, assessment, prevalence, and effect of personality disorder.”

Lancet 385(9969): 717-726.

Unoka, Z. and M. J. Richman (2016). “Neuropsychological deficits in BPD patients and the moderator effects

of co-occurring mental disorders: A meta-analysis.” Clin Psychol Rev 44: 1-12.

van Dijk, F., M. Lappenschaar, et al. (2011). “Lifespan attention deficit/hyperactivity disorder and borderline

personality disorder symptoms in female patients: a latent class approach.” Psychiatry Res 190(2-3):

327-334.

Van Dijk, F., J. Mostert, et al. (2016). “Five Factor Model personality traits relate to Adult Attention-Deficit/

Hyperactivity Disorder but not to their distinct neurocognitive profiles.” Under review..

van Dijk, F., A. Schellekens, et al. (2014). “Do cognitive measures of response inhibition differentiate

between attention deficit/hyperactivity disorder and borderline personality disorder?” Psychiatry

Res 215(3): 733-739.

van Dijk, F. E. and H. Anckarsater (2011). ADHD, personality, and its disorders. ADHD in Adults: Character-

ization, Diagnosis and Treatment. J. Buitelaar, C. C. Kan and P. Asherson. Cambridge, Cambridge

University Press.

van Dijk, F. E., M. Lappenschaar, et al. (2012). “Symptomatic overlap between attention-deficit/hyperactivity

disorder and borderline personality disorder in women: the role of temperament and character

traits.” Compr Psychiatry 53(1): 39-47.

van Lieshout, M., M. Luman, et al. (2013). “Does neurocognitive functioning predict future or persistence of

ADHD? A systematic review.” Clin Psychol Rev 33(4): 539-560.

van Lieshout, M., M. Luman, et al. (2016). “Neurocognitive Predictors of ADHD Outcome: a 6-Year Follow-up

Study.” J Abnorm Child Psychol.

Van Veen, M. M., J. J. Kooij, et al. (2010). “Delayed circadian rhythm in adults with attention-deficit/

hyperactivity disorder and chronic sleep-onset insomnia.” Biol Psychiatry 67(11): 1091-1096.

Widiger, T. A. and E. Simonsen (2005). “Alternative dimensional models of personality disorder: finding a

common ground.” J Pers Disord 19(2): 110-130.

Winsper, C., S. T. Lereya, et al. (2016). “The aetiological and psychopathological validity of borderline

personality disorder in youth: A systematic review and meta-analysis.” Clin Psychol Rev 44: 13-24.

Young, S., D. Moss, et al. (2015). “A meta-analysis of the prevalence of attention deficit hyperactivity disorder

in incarcerated populations.” Psychol Med 45(2): 247-258.

Zimmerman, M., I. Chelminski, et al. (2008). “The frequency of personality disorders in psychiatric

patients.” Psychiatr Clin North Am 31(3): 405-420, vi.



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Published as:

Van Dijk, FE & Anckarsäter, H. (2011). ADHD, personality, and its disorders.

In J.K. Buitelaar, C.C.Kan & P. Asherson (Eds.), ADHD in Adults: Characterization, Diagnosis,

and Treatment (pp174-190). New York, Cambridge University Press.

ADHD, personality and its disorders

2



21

ADHD, PERSONALITY AND ITS DISORDERS

2

Introduction

From clinical, neurocognitive, and neurobiological perspectives (Faraone, 2005),

ADHD is regarded as a meaningful diagnosis today, in childhood as well as in

adulthood. However, the adult symptom profile and ADHD’s complex pattern of

overlap with other mental health problem constellations have yet to be detailed

and clarified (McGough & Barkley, 2004; Nigg, Blaskey, et al., 2002). So far, relatively

little attention has been paid to the relationship of ADHD to maladaptive

personality traits and personality disorders in adults (Lewinsohn et al., 1997;Nigg,

John, et al., 2002), most probably because of the theoretical hiatus between the

fields of child neuropsychiatry and adult personality and its disorders. Yet the

coexistence of ADHD and personality disorders certainly does matter, not only for

longitudinal prediction but especially for a deeper understanding of adult problem

arrays, for better phenotype characterization in neurobiological research, and for

the development of new treatment strategies.

ADHD is the term chosen for the fourth edition of the Diagnostic and

Statistical Manual of Mental Disorders (American Psychiatric Association, 1994),

whereas the two earlier editions – DSM-III (American Psychiatric Association,

1980) and DSM-III-R (American Psychiatric Association, 1987) – contained related

diagnostic definitions focusing on the inattentive facet of the syndrome disorder.

In DSM-IV, ADHD is diagnosed on the basis of problems with attention (inattentive

subtype), action and impulse control (hyperactive subtype), or both (combined

subtype).The current version of the International Classification of Diseases (ICD-10;

WHO, 1990) includes a definition based on hyperactivity – hyperkinetic disorder

– in which inattention is seen as a frequently complicating, coexisting problem

rather than as an aspect of the syndrome. As this textbook sets out from the ADHD

concept, we consistently use the term “hyperactivity,” which thus covers also the

description of hyperkinesia.

According to DSM-IV, the essential feature of a personality disorder is “an

enduring pattern of inner experience and behavior that deviates markedly from

what is expected in the individual’s culture.” This definition contains several

problems. Inner experiences are difficult to operationalize into diagnostic criteria,

whereas diagnosing personality disorders on the basis of behavioral patterns may

short-circuit attempts to “explain” behaviors by personality traits. At the same

time, systematic definitions of behaviors are the most readily available features

and will remain central among diagnostic criteria as long as interrater agreement

is a priority. In this situation, it is important to recognize behaviorally defined

disorders for what they are – relatively stable phenotypes for the study of cognitive,

biological, and/or social covariates.



22

CHAPTER 2

Although Axis II of DSM-IV is theoretically available to record personality

disorders at all ages (with the exception of antisocial personality disorder), these

disorders are rarely diagnosed before young adulthood (i.e. at an age when a more

stable personality organization is being developed). Conversely, disorders classified

as “usually first diagnosed in infancy, childhood, or adolescence” are not often

assessed in adults. There is, however, every reason to assume that personality traits

or such differences in reaction patterns (temperaments) that form the basis on

which adult traits develop are discernible at a very early stage of child development

(Caspi et al., 2003). By tradition, temperaments and personality are defined on the

basis of the variance in the whole population, whereas psychiatric diagnoses, such

as ADHD or personality disorders, focus on small groups of persons with disabling

or distressful symptoms; these different perspectives have made it difficult to

understand that different designations may refer to similar underlying phenomena.

The growing awareness of “childhood” disorders, such as ADHD, among adults,

of temperament differences already in infancy, and of manifestations of some

Axis II disorders at least by adolescence (Lewinsohn et al., 1997) certainly calls

for cross-disciplinary reexamination of data and definitions.

ADHD and personality disorders

Antisocial personality disorderA number of diagnostic definitions have been proposed to capture specific personality

traits among persistently aggressive, destructive and dishonest persons, children

as well as adults. These definitions have mainly relied on behavioral criteria, such

as those in the DSM system, which defines ASPD as a pervasive and stable pattern

of aggressive and/or covert antisocial behaviors with onset before the age of 15,

corresponding to the diagnostic criteria for conduct disorder (CD). As an

“intermediary” diagnosis between ADHD and CD, the DSM system has included

oppositional-defiant disorder (ODD) to describe severely oppositional attitudes

and provocative behaviors. The combination of early-onset disruptive behaviors

with deficient emotional reactions to others and to the consequences of one’s

own behavior, as well as with dishonest and dominance- seeking interpersonal

strategies, has been described as “psychopathy,” first in the European psychiatric

tradition of personality disorders and then in North America, based on Cleckley’s

1951 book, The Mask of Sanity. This proposed syndrome has not been included in the

ICD or DSM classifications, even if the ICD-10 dissocial personality disorder includes

more criteria reflecting interpersonal and emotional aspects than the more

behavior-based DSM-IV definition of ASPD. However, this proposed syndrome has

had considerable impact on research on personality in association with criminal



23


2

behaviors, especially violence, not least because of its operationalization in the

PsychopathyChecklist (PCLR; Hare, 1980).

Factor analyses of the items in this checklist demonstrated a three-factor

structure comprising “destructive and impulsive behavioral patterns” (factor 3),

“blunted emotional integration of morally charged cognitions” (factor 2), and “a

glib, dominance-seeking and dishonest interpersonal style” (factor 1; Cooke &

Michie, 2001); Hare later proposed that the behavioral factor be split in two,

distinguishing impulsive behaviors from outright norm-breaking. By comparing

this factor structure to ADHD and other childhood-onset neuropsychiatric

problems, we hope to add clarity to the nosology of these factors. The behavioral,

third factor of the PCL-R and DSM-IV diagnostic criteria for ASPD and childhood

disruptive behavior disorders, especially CD and ODD but also ADHD, all contain

items that reflect impulsive, aggressive, or self-promoting behaviors with negative

consequences that are not sufficiently evaluated before action takes place. However,

the different diagnoses are based on criteria describing such behaviors in relation

to heterogeneous settings or situations that occur at different stages of development,

so that hyperactivity can be noted in an infant, whereas norm-breaking demands

at least a basic understanding of what norms are meant to be. Inattention is defined

by behaviors in task-related situations that require painstaking control, ODD by

interpersonal norm-breaking, and CD by infractions of social norms for behavior

during childhood, getting farther and farther into the realm of criminal acts as

the perpetrator gets older.

There is no lack of longitudinal, prospective studies assessing the long-term

development of ADHD or related definitions. Longitudinal studies that have used

clinical diagnostic definitions are briefly reviewed in Table 16.1. Because they

require diagnostics, the studies presented are mostly based on clinic referrals.

In addition, several population-based studies have followed representative cohorts

and are informative about longitudinal development and associations between

symptom assessments at various stages and outcomes; for example, studies from

San Francisco (Babinski et al., 1999), Pittsburgh (Loeber et al., 1998), Dunedin

(Moffitt & Caspi, 2001), Sweden (Klinteberg et al., 1993) and London (Farrington,

2000). We reference these population-based studies in the following sections when

appropriate, but let us start by summarizing the main findings from the clinical

studies; we then examine a number of methodological problems that need to be

considered when interpreting and using the results.

Comparisons of children identified as hyperactive to controls clearly and

consistently show increased risks for CD, ASPD, and criminality later in life (Table

16.2). It may even be concluded with reasonable confidence that a majority of clin-

ic-referred children with hyperactive ADHD (i.e. combined or hyperactive subtype),

at least during some phase, exhibit oppositional-defiant attitudes and behaviors,



24

CHAPTER 2

that at least one-third develop an early-onset CD, and that at least one-fifth go on

to develop adult ASPD, according to a recent meta-analysis based on all longitudinal,

prospective studies providing prevalence figures among index cases and controls

(Hofvander et al., 2009). Another salient finding was that only small subgroups of

those initially identified with hyperactivity or ADHD still met criteria for these

diagnoses at follow-up. Longitudinal studies invariably have to deal with attrition,

but the majority of the studies discussed here have high follow-up rates, and even

in the single study with the highest attrition, the one from Montreal, indirect

information from parents and official records supported that those retained in the

study were representative of the whole initial group, at least regarding criminal

histories (Weiss et al., 1985).

To avoid leaving the longitudinal literature with an oversimplified view of the

findings, we must examine some methodological problems in these studies. Let us

start with the manner of recruitment and the inclusion criteria for both index

subjects and controls. The longitudinal studies’ samples are either clinic referred

or population based. Clinic-referred children may not be representative of the

hyperactive children in the general population. This is difficult to establish as the

reports often omit more specific information on how and by whom the subjects

were referred. Criteria for study inclusion have included “minimal brain

dysfunction (MBD),” “hyperkinesia,” “hyperactivity/ impulsivity,” or ADHD, often

casually understood as ADHD in its broadest sense. Having found no study where

attention-deficit disorder without hyperactivity (ADD or ADHD inattentive type)

has been specifically investigated in relation to ASPD or associated features, we

conclude that inattention is not confirmed as a risk factor in this context.

Population based studies generally provide more detailed information on the

background population and ways of selection, but use broader definitions to

describe traits rather than conditions and often have arbitrary cutoffs within the

assumed normal distribution of problems (such as the lowest or highest quartile or

ratings below or above two standard deviations from the mean) to yield proxies for

diagnoses.

As hyperactivity is a common phenomenon among children, group comparisons

between index subjects and controls thought to form a representative sample from

the general population (including hyperactives) will differ from those using

controls selected to be “hypernormal” (i.e. without signs of this or that), and thus

they are no longer “normal” in a statistical sense. Controls recruited among

children referred for other mental health problems will naturally differ from

controls recruited among friends or from school registers. We also know that

subjects with hyperactivity or ADHD more often than not have other concomitant

behavioral or mental problems. It is therefore crucial to know whether such

problems precluded inclusion in the first place and whether the included children



25


2

were seen as representative of all hyperactive children or only of subgroups with

or without some specific combination of problem areas. For example, in the study

of outcome in the form of conduct problems, criminality, or diagnoses including

such behaviors, the extent to which index children had these or similar problems

already at inclusion and which definitions were used at follow-up are essential

information.

Longitudinal studies also challenge our capacity to keep the effects of time on

the studied phenomena constantly in mind. For the developmental problems of

interest to us, the degree of overlap between behavior types and thereby between

disorders depends on the age at which the cross-section is done. Unfortunately, the

majority of studies used broad age ranges already at inclusion, often recruiting

small children as well as prepubertal or pubertal adolescents. Operational criteria

for categorical diagnoses often mix current symptoms with lifetime problem

histories, which may obscure both developmental features and the role of

subsyndromal problems. Our targeted conditions are also most likely to represent

problems that follow a waxing and waning course and thereby may oscillate over

and under any diagnostic cut-off (Biederman et al., 2001; Lahey et al., 2002). These

methodological problems have to be considered when reassessing whether ADHD

in the absence of early-onset conduct deviance is really a risk factor for adult

antisocial behaviors (Lilienfeld &Waldman, 1990).

The Montreal study, which did not exclude children with conduct problems

at inclusion, demonstrated that all subjects who eventually developed ASPD had

an early onset of conduct problems as noted at the initial screening or at the

first follow-up (Herrero, Hechtman, & Weiss, 1994). In the Wisconsin study, adult

“predatory-overt” criminality was predicted by teenaged CD only (Barkley et al.,

2004). In the Developmental Trends Study, in which boys referred to outpatient

clinics had annual assessments, ADHD in the absence of conduct problems at

inclusion did not predict the later onset of CD (Loeber et al., 1995). In the Los

Angeles study, the absence of childhood conduct problems indicated a very low

risk for later CD and criminality, as illustrated by 16 children with hyperactivity

but no conduct problems who committed only minor adolescent offenses in two

cases and no adult offenses at follow-up (Satterfield & Schell, 1997). The Pittsburgh

study showed that ”callous unemotional behaviors,” depression, and onset of

marijuana use between 13 and 17 years of age predicted antisocial personality

development, whereas ODD and ADHD in the absence of conduct problems showed

no such association (Loeber et al., 2002). In the London based study, 8- and 9-year-old

boys were classified according to the presence or absence of hyperactivity

impulsivity and conduct problems. Follow-up results indicated that both factors

were independently predictive for adolescent convictions (age 10–16), whereas for

adult convictions (age 17–25), conduct problems alone remained a significant



26

CHAPTER 2

predictor (Farrington, 2000). A cluster analysis of teacher assessments of 13-

year-old boys in Sweden followed until ages 18–23 documented an increased risk

for criminality in the aggression-hyperactivity-inattention cluster, but not in the

hyperactivity-inattention cluster (Bergman & Magnusson, 1986). In several of the

studies, it was noted that the presence of even one single behavioral problem in

childhood (e.g. fighting, stealing, or lying) was an important risk factor for

subsequent antisocial development (e.g. Montreal, Los Angeles).The risk of

antisocial development was also higher in subjects with persistent hyperactivity

than in those who had remitted during the follow-up period. Children who did not

display any behavioral risk factors generally fared well (Herrero et al., 1994).

However, some studies have reported conflicting findings and claim that there

is a direct relationship between ADHD and ASPD, even in the absence of early-onset

CD. The New York City longitudinal study tried to establish study groups of

children with hyperactivity but no conduct problems at inclusion. Again, the

increased risk of adolescent CD and antisocial personality development was

significantly associated with previously noted, even low-grade, conduct problems,

just as in the Montreal study; however, in the New York study increased risk was

seen also among children who had reportedly shown no conduct problems at

inclusion. Hyperactivity in itself, even in the absence of early conduct problems,

was therefore claimed to constitute a risk factor for the later development of

antisocial behaviors and/or ASPD (Mannuzza et al., 2004). This claim is problematic

as conduct problems were not systematically assessed at inclusion, especially not

in the first New York study group. Included boys were reported not to have

aggressive behaviors as the “primary reason for referral” (Mannuzza et al., 1993) or

“clinically significant presenting problems involving aggression or other antisocial

behaviors” (Mannuzza et al., 1998). A report from the San Francisco study also

portrayed hyperactivity-impulsivity as an independent predictor of adult criminality,

which actually was the case only for some categories of less severe crimes among

males only. Crimes against people were again only predicted by conduct problems

(Babinski et al., 1999).

Many longitudinal studies have also included children of considerably varying

ages at the “baseline” assessments. In the New York City study discussed earlier,

children were included from the age of 6, and in the San Francisco study from the

age of 5, which means that no matter how carefully conduct problems were

assessed at inclusion, it would be possible for subgroups of children to develop an

early-onset CD after inclusion in the study, but before the age of 10 (which is the

DSM definition for early-onset CD) or at least the onset of puberty, and then go on

to have adult problems. The Pittsburgh study also included first, fourth, and fifth

graders, which may have influenced the authors’ perspective on overlap between

hyperactivity-impulsivity and conduct problems. The Boston study demonstrated



27


2

that, in children with ADHD, CD almost always developed before the age of 12

(Biederman et al., 1996), and it has been reported that the mean age at onset of CD

may be early in childhood (Kim-Cohen et al., 2005); however, we actually know

little about the development of CD in relation to prepuberty. The best hypothesis

therefore remains that ADHD is a precursor to early-onset conduct problems and

aggression and then, and only then, constitutes a major risk factor for adulthood

severe criminality and ASPD.

As for the nosological status of ODD, Loeber and co-workers (2002) proposed

that ODD symptoms act as an independent risk factor in addition to ADHD and CD

or as an intermediary state between those conditions. In most of the reviewed

studies (e.g. New York City, Developmental Trends, and Boston), however, ODD did

not predict CD development in a statistical sense, probably as it is so common

among children with ADHD at some stage. ADHD-based ODD and CD instead seem

to represent two sequential developmental complications of hyperactivity and

may, of course, result from interacting or additional risk factors in the form of

genetic factors associated with aggression or environmental factors related to

criminality. This does not make them “independent” disorders. In the Boston and

New York studies, virtually all children with ADHD who developed CD had already

developed ODD, and early-onset CD almost always develops out of a condition

marked by hyperactivity or the like (Lahey & Loeber, 1997).

Support for this notion also comes from twin studies that demonstrate

common genetic mechanisms underlying hyperactivity and oppositional/conduct

problems (Nadder et al., 2002; Silberg et al., 1996). A recent twin study examined

possible explanatory models for the overlap between ADHD and CD and found that

a model with “three different disorders” could be rejected, as both common genetic

and environmental effects for ADHD and CD could be identified (Rhee et al., 2008).

We have now arrived at the question of prediction. Is there any reliable way to

assess traits or features that give a valid prediction of later antisocial outcome

among children? Despite the number of studies presented, no predictive model

has yet been established, and in view of the figures presented, it seems reasonable

to assume that the increased risks are so unspecific that predictions will over

include children to such a degree that they become of little practical value. No

other feature is as predictive as early-onset antisocial behaviors (“nothing predicts

behavior as behavior”), and this effect precludes additions of predictive value from

other factors in statistical models, even if it could be interesting to study more

detailed characteristics of childhood behavior, such as age at onset or severity.

Underlying this continuity of aggression and antisocial behaviors, genetic effects

explain between 65% and 70% of the inter-individual variance in aggression (Burt,

2009; Frisell et al., 2010), and some of these effects are common with ADHD (Rhee

et al., 2008).



28

CHAPTER 2

Another salient feature that seems to be associated with poor outcomes of

ADHD is its persistence or that of some of its symptoms, such as restlessness, into

adulthood. In both the Montreal and New York studies, the risk of antisocial

behaviors was associated with the persistence of ADHD or of ADHD-related

symptoms. This, however, is not of much use for prediction. Lynam’s (1996)

suggestion that the combination of ADHD and CD identifies a group of “fledgling

psychopaths” may be consistent with the literature to the extent that this

combination represents the most risk laden subgroup, but as we have seen, at least

one-third of all children with ADHD also develop CD, and a considerable

proportion, between one-third and one-half in the cited studies, of these children

will not go on to be antisocial or criminal in adulthood. Note that the definitions

of “criminality” are quite loose and seldom include severe violent crimes. Figures

on the group level may also be elusive, as when 160 of 174 non theft crimes in the

Montreal study were perpetrated by four subjects (Hechtman &Weiss, 1986). Of

course, it would have been of societal good to be able to identify these 4 among the

initial 104 kids, but research at its current level is very far from being able to do so.

ADHD and the early-onset progression into ODD and CD ending up in ASPD

thus explain the third, behavioral factor of the proposed psychopathy construct.

The second factor of psychopathy describes deficient handling of stimuli and

words related to concepts such as “guilt,” “responsibility,” “love,” and “fear”

without appropriate accompanying emotional resonance, indicating both that the

person has a reduced or aberrant understanding of their meaning and will not

have the same access to emotions to guide behavioral reactions as others. This was

already referred to as “semantic blindness” by Cleckley (1951), who thought that it

was a core deficit in the condition he described. It is reflected by the operational

criteria for ASPD and has been demonstrated in many psychophysiological

research models (Hofvander et al., 2009). This emotional deficit facet of psychopathy

or ASPD was also associated both with ADHD and childhood autistic traits in a

retrospective study of adult offenders (Soderstromet al., 2005) and may be the

result of autistic-like traits interacting with disruptive behavior problems on the

ADHD-ODD-CD spectrum.

Finally on treatment, there is a striking contrast between our relatively

detailed knowledge about the longitudinal outcome of hyperactivity and the

means available for treatment aimed at preventing or changing a destructive

development. The established treatment for ADHD, psychostimulants, does not

have documented efficacy for treating either ODD or CD and nearly all the

longitudinal studies have included children who have actually been treated with

stimulants (Table 16.1). More recently, atypical neuroleptics have been used to treat

disruptiveness, but they are so far not recommended for general use because of

their considerable side effects and the lack of evidence for efficacy from controlled



29


2

trials. Other therapeutic measures for ADHD or CD, such as cognitive-behavior

therapy, group therapies, and psychoeducative measures or training, are equally

untested in the longitudinal developmental frame discussed in this chapter.

Borderline personality disorder BPD is a complex and seriously disabling mental disorder. It is estimated to occur

in about 1% or 2% of the general population (Torgersen, Kringlen, & Cramer, 2001),

and it is the most common personality disorder in psychiatric clinical settings.

Studies commonly suggest a three-factor structure consisting of a pervasive pattern

of disturbed relations to other persons, affective or emotional dysregulation, and

behavioral dyscontrol or impulsivity (Sanislow, Grilo, & McGlashan, 2000).These

factors are thought to express core dimensions of borderline psychopathology,

which may reflect underlying abnormal neurobiological processes involving

genetic and developmental susceptibility. The three factors are conspicuously

analogous to the factor solution proposed for psychopathy, again capturing the

triad of interpersonal attitudes, emotional processing, and behavior dyscontrol.

Even if this structure may merely represent one common to personality disorders,

there is an obvious overlap for at least the impulsivity of the third factor, and it is

also evident from a clinical point of view that patients with ADHD, ASPD and BPD

share symptoms of impulsivity. Of course, a common trait such as this one may

cause artifactual coexistence and obscure the aspects that really are specific for

the conditions.

Over the past years, a few studies have addressed a possible relationship

between ADHD and BPD. In contrast to the high-quality prospective follow-up

studies that have assessed the association between ADHD and ASPD, studies on

ADHD and BPD have generally relied on clinical cross-sectional designs. BPD is

mainly diagnosed in women and seems to have a presumed gender ratio that is the

reverse of that for ASPD (American Psychiatric Association, 1994). In addition, as

familial associations between ASPD and BPD are well demonstrated (Goldman,

D’angelo, & DeMaso, 1993), a closer investigation of the relationship between

ADHD and BPD seems well justified. In contrast to the previous section, here we

review the literature chronologically. Again we have to take into account several

methodological problems when interpreting the results. Ways of recruitment and

inclusion of subjects and controls, small sample sizes, and the definitional vagaries

that were already discussed have to be kept in mind.

Research on ADHD symptomatology and BPD started in the early 1980s.

Andrulonis and co-workers identified three distinct subtypes of BPD in a group of

106 hospitalized adult borderline patients: those with no history of organicity;

those with a history of trauma, encephalitis, or epilepsy; and those with a history

of attention deficits or learning disabilities. They reported a considerable overlap



30

CHAPTER 2

Table 1 The main reviewed prospective longitudinal studies on the association between childhood hyperactivity (using clinical diagnostic categories at inclusion) and antisocial personality disorder

Study, Main Reference

Approximate years of inclusion Cases Controls Treatment Follow-up

Clinic-referred study groups

MontrealWeiss et al., 1985Hechtman & Weiss, 1986

1962-1965 104 (95 boys and 9 girls) long-term hyperactive children (aged 6-12)

45 matched ‘hypernormal’a

school-mate controls

4 received psychostimulants, and 20 a conventional high-dose neuroleptic

59% were followed up after 15 years at 21-33 years of age, by blind and non-blind clinical assessments, court records, and for those lost to follow-up by parental contacts, contacts over the phone etc.

New YorkGroup 1Gittelman et al., 1985Mannuzza et al., 1993Group 2Mannuzza et al., 1991Mannuzza et al., 1998Group 1 & 2Mannuzza et al., 2004

1970-1977 115 (Group 1) and 111 (Group 2) hyperactive boys (aged 6-12)

178 matched hypernormal non-psychiatric outpatient controls

All subjects had “medication and/or behavior therapy”

About 90% were followed after a mean interval of 16.1 and 17 years at mean ages 26, 24.1 och 23.5, by blind structured assessments and, for the first group, by official files.

BostonBiederman et al., 1992 (basic), 1996 (follow-up)

1992 basic1996 follow-up

140 referred or recruited boys with ADHD (aged 6-17)

120 unmatched control boys from out-patient services or recruited by advertisements

89% had a life-time history of treatment with psychostimulants, 44% during the follow-up period

91% were followed-up after 4 years by blind/semiblind new assessments

Los AngelesSatterfield et al., 1982

1970-1972 110 hyperactive boys between (aged 6-12)

75 matched payed public school controls, 13 non-ADHD brothers of cases

“most” or “all” subjects had CS medication 81% were followed up until age 25 through official records

WisconsinBarkley et al., 2004Fischer, 2002

1979-1980 158 consecutive hyperactive children (144 boys, 14 girls, aged 4-12)

81 matched non-hyperactive controls recruited among the subjects’ friends

22% vs 0% had treatment with stimulants during the high-school years

≥90% were followed up after a mean interval of 13.8 years at between 19-25 y o a through structured interviews and official records.

Developmental Trends StudyLoeber et al., 1987

1987 177 out-patient boys at three clinics, (aged 7-12), 75% of whom referred for disruptive behaviours

No controls Medication in an unknown proportionb but required to discontinue two days prior to assessments

About 90% remained in the study and were followed by blind structured assessments yearly until ages 18-19.

Population-based study

Rasmussen & Gillberg, 2000 1977 61 7-years old children (47 boys, 14 girls) with ADD with or without DCD (about 90%), most of whom met DSM-IV criteria for AD/HD, or with DCD (about 10%)

51 population-based controls (27 boys, 24 girls) matched for SES and age

No one had medication with psychostimulants 90% were followed up with blind structured assessments and official files at 22 years of age.

Note: Several well-known longitudinal studies are referred in the text but not included in the table as

they did not use clinical diagnostics at baseline (e.g. the Dunedin and Philadelphia studies). For a more

comprehensive table including these studies and meta-analyses of results please see Hofvander et al.,

2009.



31


2

Table 1 The main reviewed prospective longitudinal studies on the association between childhood hyperactivity (using clinical diagnostic categories at inclusion) and antisocial personality disorder

Study, Main Reference

Approximate years of inclusion Cases Controls Treatment Follow-up

Clinic-referred study groups

MontrealWeiss et al., 1985Hechtman & Weiss, 1986

1962-1965 104 (95 boys and 9 girls) long-term hyperactive children (aged 6-12)

45 matched ‘hypernormal’a

school-mate controls

4 received psychostimulants, and 20 a conventional high-dose neuroleptic

59% were followed up after 15 years at 21-33 years of age, by blind and non-blind clinical assessments, court records, and for those lost to follow-up by parental contacts, contacts over the phone etc.

New YorkGroup 1Gittelman et al., 1985Mannuzza et al., 1993Group 2Mannuzza et al., 1991Mannuzza et al., 1998Group 1 & 2Mannuzza et al., 2004

1970-1977 115 (Group 1) and 111 (Group 2) hyperactive boys (aged 6-12)

178 matched hypernormal non-psychiatric outpatient controls

All subjects had “medication and/or behavior therapy”

About 90% were followed after a mean interval of 16.1 and 17 years at mean ages 26, 24.1 och 23.5, by blind structured assessments and, for the first group, by official files.

BostonBiederman et al., 1992 (basic), 1996 (follow-up)

1992 basic1996 follow-up

140 referred or recruited boys with ADHD (aged 6-17)

120 unmatched control boys from out-patient services or recruited by advertisements

89% had a life-time history of treatment with psychostimulants, 44% during the follow-up period

91% were followed-up after 4 years by blind/semiblind new assessments

Los AngelesSatterfield et al., 1982

1970-1972 110 hyperactive boys between (aged 6-12)

75 matched payed public school controls, 13 non-ADHD brothers of cases

“most” or “all” subjects had CS medication 81% were followed up until age 25 through official records

WisconsinBarkley et al., 2004Fischer, 2002

1979-1980 158 consecutive hyperactive children (144 boys, 14 girls, aged 4-12)

81 matched non-hyperactive controls recruited among the subjects’ friends

22% vs 0% had treatment with stimulants during the high-school years

≥90% were followed up after a mean interval of 13.8 years at between 19-25 y o a through structured interviews and official records.

Developmental Trends StudyLoeber et al., 1987

1987 177 out-patient boys at three clinics, (aged 7-12), 75% of whom referred for disruptive behaviours

No controls Medication in an unknown proportionb but required to discontinue two days prior to assessments

About 90% remained in the study and were followed by blind structured assessments yearly until ages 18-19.

Population-based study

Rasmussen & Gillberg, 2000 1977 61 7-years old children (47 boys, 14 girls) with ADD with or without DCD (about 90%), most of whom met DSM-IV criteria for AD/HD, or with DCD (about 10%)

51 population-based controls (27 boys, 24 girls) matched for SES and age

No one had medication with psychostimulants 90% were followed up with blind structured assessments and official files at 22 years of age.

a Hypernormal meaning that controls have been selected on a number of criteria, such as not being

hyperactive, and are therefore not representative for the general population. b When stated that no information is provided, this is based on the main references as cited. Some of

these studies are published in a large number of papers and chapters and even if we have scrutinized

this literature to the best of our ability, some sources of information may have been missed.



32

CHAPTER 2

(about 25%) between the latter two subtypes and minimal brain dysfunction (a

term that was abandoned in 1980 when ADD was introduced in the DSM, with a

considerable conceptual overlap between MBD and ADD). The patients with

minimal brain dysfunction consisted mainly of males with early developmental

difficulties. They were characterized by aggressive and hyperactive behavior,

academic difficulties during childhood, and antisocial acting out with drug/

alcohol abuse during adolescence (Andrulonis et al., 1981, 1982). These studies

showed that a significant subgroup of borderline patients have a “spectrum”

disorder on an organic brain dysfunction continuum, which includes symptoms

that have later been referred to the ADHD domain.

Table 2 Adult or follow-up outcomes of children initially identified with hyperactivity or related diagnoses vs. controls

StudyPersistence of AD/HD

Conduct Disorder

Antisocial personality disorder (cases vs. controls)

Criminality (various measures) Incarceration

Montreal 36% vs 2% had “at least one moderately or severely disabling symptom”

“about 10% … antisocial disturbed”

23% vs 2.4% Court appearances 18% vs 5%Any offence 68% vs 59%Non-theft convictions: 5% vs 0% (just 4% among those lost to follow-up)

None mentioned

New YorkGroup 1Group 2Group 1&2

8% vs 1% (group 1)4% vs 0% (group 2)

27-32% vs 8% 18% vs 2%(group 1)12% vs 3%(group 2)

Arrested 39% vs 20%, convicted 28% vs 11% aggressive crimes 6% vs 2% (group 1)No criminal record follow-up reported(group 2)

5% vs 0% (group 1)2% vs 0% (group 2)

Boston 58% vs 6% “full or subthreshold” ADHD, more common when combined with ODD/CD

23% vs.3% Not within range of follow-up

Not within range of follow-up Not within range of follow-up

Los Angeles Not assessed Not Assessed Not assessed Juvenile arrests: 46% vs 11%Felony arrests: 21% vs 1%Recidivism: 9% vs 0%

Institutionalized as adolescents 25% vs 1%Incarcerated as adults 12% vs 0%

Wisconsin 5% vs 0% 31% vs 11% developed CD at some stage

21% vs 4% Arrested ≥ 2 times 40% vs 12% None mentioned

Gothenburg Severe hyperacitivity/impulsivity 15% vs 2%Severe inattention 44% vs 7%Combination of both 9% vs 0%

6% vs 7% 18% vs 2% Any criminal conviction 19% vs 0% None mentioned



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2

At least a decade later, looking for antecedents of personality disorders in

childhood, Rey and coworkers examined continuities between Axis I disorders in

adolescents and personality disorders in young adults. They found that the

adolescents with disruptive disorders were more likely at follow-up to have a

personality disorder on the dramatic/impulsive cluster, which includes both BPD

and ASPD, than those with emotional disorders. All disruptive disorders were

associated with a wide range of personality psychopathology in adulthood. Specific

associations were found between CD and ASPD and between ADHD (with

hyperactivity) and BPD. The authors suggested that disruptive disorders in

childhood might be re-conceptualized as disorders of personality rather than as

Table 2 Adult or follow-up outcomes of children initially identified with hyperactivity or related diagnoses vs. controls

StudyPersistence of AD/HD

Conduct Disorder

Antisocial personality disorder (cases vs. controls)

Criminality (various measures) Incarceration

Montreal 36% vs 2% had “at least one moderately or severely disabling symptom”

“about 10% … antisocial disturbed”

23% vs 2.4% Court appearances 18% vs 5%Any offence 68% vs 59%Non-theft convictions: 5% vs 0% (just 4% among those lost to follow-up)

None mentioned

New YorkGroup 1Group 2Group 1&2

8% vs 1% (group 1)4% vs 0% (group 2)

27-32% vs 8% 18% vs 2%(group 1)12% vs 3%(group 2)

Arrested 39% vs 20%, convicted 28% vs 11% aggressive crimes 6% vs 2% (group 1)No criminal record follow-up reported(group 2)

5% vs 0% (group 1)2% vs 0% (group 2)

Boston 58% vs 6% “full or subthreshold” ADHD, more common when combined with ODD/CD

23% vs.3% Not within range of follow-up

Not within range of follow-up Not within range of follow-up

Los Angeles Not assessed Not Assessed Not assessed Juvenile arrests: 46% vs 11%Felony arrests: 21% vs 1%Recidivism: 9% vs 0%

Institutionalized as adolescents 25% vs 1%Incarcerated as adults 12% vs 0%

Wisconsin 5% vs 0% 31% vs 11% developed CD at some stage

21% vs 4% Arrested ≥ 2 times 40% vs 12% None mentioned

Gothenburg Severe hyperacitivity/impulsivity 15% vs 2%Severe inattention 44% vs 7%Combination of both 9% vs 0%

6% vs 7% 18% vs 2% Any criminal conviction 19% vs 0% None mentioned



34

CHAPTER 2

Axis I diagnoses (Rey et al., 1995).Thus the studies of both Andrulonis and Rey

attempted to put BPD into a developmental context and suggested a significant

relationship between ADHD features and BPD.

Fossati and co-workers tried to overcome some limitations of these pioneer

studies by evaluating the presence of specific associations between retrospectively

assessed childhood ADHD symptoms and adult BPD in a controlled design. They

administered the Wender Utah Rating Scale (WURS), a self-report instrument, to

42 consecutive BPD subjects and four control groups: admitted subjects (1) with

any cluster B personality disorder diagnosis, (2) with any cluster A or cluster C

personality disorder diagnosis, (3) with no personality disorder diagnosis, and (4)

nonclinical volunteers. This study showed a significant relationship between the

presence and severity of childhood ADHD symptoms and adult BPD. No less than

60% of the BPD subjects had probably met criteria for ADHD in childhood, even

after controlling for ASPD (Fossati et al., 2002). Such figures have to be interpreted

as suggesting the etiological heterogeneity of both disorders, and it remains

unclear which characteristics are specifically related, possibly expressing the

same underlying susceptibility, and which are not.

The specificity of clinical ADHD characteristics in adults with BPD has also

been investigated using the self-report Attention Deficit Scale for Adults (ADSA).

The statements in the ADSA relate to a wider range of characteristics than those

found in the DSM-IV, including mood lability, temper, disorganization, and

impulsivity. Dowson and co-workers showed that seven of the nine scales of the

ADSA discriminated between ADHD and BPD, despite the overlap of clinical

features involved in the two syndromes. The seven scales showing significant

intergroup differences involved attention, organization, and persistence. Impaired

task and goal persistence were the main discriminators between those with ADHD

and those with BPD, with the ADHD group being the more impaired. Nonsignificant

differences were found for two scales that were related to impatience, examples of

aggression, taking undue risks, and failure to take the likely results of actions into

account (Dowson et al., 2004). These findings seem to be in line with earlier results,

but they also provide some indication that symptoms referring to the inattention

domain of ADHD are to be specially considered in the relationship between ADHD

and BPD. A limitation of this study may be that ADHD was not excluded from the

BPD group nor was BPD excluded from the ADHD group.

In contrast to these studies, Kooij and co-authors used semi-structured clinical

interviews in the assessment procedure in their study on the relationship between

ADHD and coexisting BPD and ASPD. Their results showed that, among 53 referred

ADHD patients, 11% presented with a subthreshold diagnosis and only 4% with a

full BPD diagnosis. The most frequent symptom overlap was found for affective

instability and inappropriate anger, symptoms that have been identified as



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ADHD-associated features (Kooij et al., unpublished data). The authors explained

the difference between the prevalence of subthreshold and full diagnostic

occurrence of BPD by the use of a clinical interview to establish the ADHD

diagnosis, a more restrictive scoring system than relying on self-report scores only.

Data from ongoing research on the relationship between adult ADHD (i.e.

meeting ADHD criteria in childhood as well as in adulthood, also using semi

structured clinical interviews) and BPD in 103 clinically referred female adults

showed that 33% of a group of 63 patients with BPD also have ADHD and that 15%

of 40 adult ADHD female patients also meet criteria for BPD (Van Dijk et al.,

unpublished data). Trying to further clarify the relationship between ADHD and

BPD, the investigators used latent class analyses (LCA; McCutcheon, 1987) of the

ADHD and BPD symptoms. LCAis a statistical technique that generates hypotheses

and may thus supplement standard diagnostic categories. Four mutually exclusive

classes of patients were identified: one with only ADHD symptoms; one with BPD

symptoms and ADHD symptoms of hyperactivity; one with BPD symptoms and

ADHD symptoms of inattention, hyperactivity, and impulsivity; and one with BPD

symptoms and ADHD symptoms of inattention and hyperactivity. The hyperactive

symptoms were relatively high across all classes, indicating that this is an

unspecific symptom domain with poor differentiating value between ADHD and

BPD. A transition model, associating the adult classes with retrospective childhood

ADHD symptomatology, showed, in addition to the expected associations between

adult and childhood ADHD symptomatology, a remarkable probability that an

outcome characterized by both ADHD and BPD symptoms in adulthood might be

associated with a childhood without any significant ADHD symptomatology (i.e.

subclinical hyperactivity), whereas an adult outcome with predominantly BPD

symptoms could be traced back to combined ADHD symptoms in childhood. These

data would fit a model in which the ADHD subtypes are not viewed as discrete

categories that are permanent over time; they are also in line with the previously

discussed findings of heterotypic diagnoses at adult follow-up in the longitudinal

studies (Table 16.2) or in the Dunedin study, in which a follow-up at age 26 found

formerly disruptive children across all adult diagnostic categories without the

expected specificity (Kim-Cohen et al., 2003).

Although identifying a subgroup of patients with both ADHD and BPD may

lead to an alternative, more beneficial treatment, research on the consequences of

coexisting ADHD and borderline personality disorder is limited. Two case reports

have shown possible subjective and neurocognitive benefits from a psychostimu-

lant (methylphenidate) in two patients with BPD and ADHD (Hooberman & Stern,

1984; Van Reekum & Links, 1994). Schulz and co-workers used amphetamine to

investigate the hypothesis that patients with BPD are prone to psychosis following

ingestion of a dopamine agonist, but found that patients with a borderline



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CHAPTER 2

diagnosis without comorbidity instead improved in their general clinical condition

(Schulz et al., 1988). Considering the lack of research in this area, studies of phar-

macotherapeutical alleviation of ADHD symptoms in patients presenting with

personality disorders are urgently needed.

Dimensional personality traits

As we have seen, in the DSM system, personality disorders are recorded on a

separate axis and, in accordance with the ICD system, are defined categorically.

Both principles are controversial and disputed by most experts because empirical

data lend no support for a delineation of personality disorders from other mental

disorders or for a categorical structure of personality traits (Livesley, 2001). To

overcome the limitations of the currently used diagnostic categories, Widiger has

proposed that dimensional models of personality may be helpful in addressing

problems of excessive co-occurrence, heterogeneity among persons with the same

diagnosis, and artifactual or epiphenomenal diagnostic distinctions (Widiger, 2005).

Categorical and dimensional perspectives on personality disorders may also be

seen as complementary, and each offers valuable insights (Pickles & Angold, 2003).

A variety of alternative dimensional models have been proposed to replace the

categorical DSM-IV personality disorders in future versions of the manual (for an

overview see Widiger & Simonsen, 2005).However, there is still considerable debate

about which dimensional system is most valid and useful (Verheul, 2005). In spite

of the apparent discrepancies among the competing models for describing

personality structure, they have remarkable convergence on a set of three to five

basic personality dimensions. The five-factor model (FFM; Widiger & Costa, 1994)

and the Temperament and Character Inventory (TCI; Cloninger, Swrakic, &

Przybeck, 1993) are organized explicitly with respect to five and seven higher

order factors, respectively, with each broad domain further differentiated into

more specific facets or subscales. These two models are the ones used most

frequently in studies on dimensional models in relation to ADHD in adults. In this

section we review the studies regarding empirical associations between ADHD

and several personality traits.

Cloninger’s modelCloninger’s biopsychosocial theory of personality is based on the assumption that

personality involves four temperament dimensions and three character

dimensions. The dimensions of temperament measure individual differences in

basic emotional drives and are Harm Avoidance (i.e. pessimistic and anxious versus

optimistic and risk-taking), Novelty Seeking (i.e. impulsive and irritable versus



37


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rigid and stoical), Reward Dependence (i.e. sociable and warm versus aloof and

cold), and Persistence (i.e. persevering and ambitious versus easily discouraged and

lazy). The character dimensions measure individual differences in higher cognitive

processes that define a person’s style of mental self-government: the character

traits are described as Self-Directedness (i.e. responsible and resourceful versus

blaming and inept), Cooperativeness (i.e. helpful and principled versus hostile and

opportunistic), and Self-Transcendence (i.e. intuitive and insightful versus concrete

and conventional; Cloninger, 1987; Cloninger et al., 1993). A self-rating instrument,

the Temperament and Character Inventory (TCI; Cloninger et al., 1993), has been

developed to measure the model’s seven personality dimensions. Presence of a

personality disorder is indicated by presence of character immaturity (especially

by low Self- Directedness and/or Cooperativeness), whereas the type of disorder is

decided by the temperament configuration (Cloninger, 2000; Svrakic et al., 1993).

A few studies have investigated the TCI profiles in subjects with ADHD. Downey

and colleagues (1997) used the Tri Personality Questionnaire, a precursor to the

TCI, and found that ADHD subjects scored significantly higher than normal

subjects on the temperament scales of Novelty Seeking and Harm Avoidance.

A more recent study (Lynn et al., 2005) tested the hypothesis that Novelty Seeking

and ADHD are associated and that their association is due, in part, toDNA

variability at the DRD4 gene.When interpreting their results, it is important to

keep in mind that the subjects in the study were parents of ADHD affected sib

pairs. Not all of them had current ADHD or a lifetime history of ADHD, and it is

possible that the results cannot be generalized to other adults with ADHD. The

results partly confirmed the findings of Downey and co-workers, identifying a

strong role for Novelty Seeking as a predictive factor for ADHD diagnostic status.

However, this association was not accounted for by the presence of a risk allele at

DRD4. Consequently, it remains impossible to clarify whether Novelty Seeking

increases the risk for ADHD or whether the presence of ADHD influences the

development of a Novelty Seeking temperament or whether the two are merely

different conceptualizations of a common phenomenon. The authors also reported

the divergent finding that the temperament scale of Self-Transcendence was

actually associated more strongly with ADHD than was Harm Avoidance. Further,

they identified a significant role for the character dimension Cooperativeness,

consistent with the notion that ADHD symptoms in childhood may hamper the

maturation of character.

Another clinical study used the TCI to describe personality development and

disorders in relation to ADHD symptomatology and autism spectrum disorders

(ASD) among 240 subjects with neuropsychiatric disorders (of whom147 had

ADHD; Anckarsater et al., 2006).The assumption was that childhood-onset neuro-

psychiatric disorders would be reflected as “difficult temperaments,” deficits in



38

CHAPTER 2

character maturation, and personality disorders. The self-rated personality traits

in the sample differed dramatically from those reported by subjects in the general

population. Extremely low scores for Self-Directedness and Cooperativeness were

recorded among all subjects with neuropsychiatric disorders, again consistent

with the notion that these early problems form obstacles to character maturity. In

addition, ADHD was specifically associated with high Novelty Seeking and high

Harm Avoidance.

As these studies did not assess personality structure in subgroups of subjects

with ADHD but without personality disorders, it is difficult to pin specific personality

profiles to ADHD in itself. The cited ongoing study by Van Dijk and co-workers

using latent class analyses (McCutcheon, 1987) on the relationship between female

adult ADHD and BPD examined TCI profiles for the four latent classes of ADHD and

BPD symptoms. In this study, High Novelty Seeking was found in all classes except

for the class with symptoms of BPD and only the hyperactivity aspect of ADHD.

The highest Novelty Seeking temperament scores were found in that class of

patients with both symptoms of BPD and symptoms in all areas of ADHD. High

Harm Avoidance, low Cooperativeness, and low Self- Directedness were specifically

related to classes containing BPD symptoms.

An outspoken Novelty Seeking temperament suggests a vulnerability for the

development of ADHD and co-occurring BPD. Contrary to patients with combined

ADHD and BPD symptoms, patients with ADHD symptoms alone show normal

character development.

The Five-Factor ModelThe “Big Five” represents the hierarchical organization of five major dimensions of

normal adult personality and provides the most widely accepted description of

higher order personality traits. The five-factor model (FFM) includes the dimensions

of Neuroticism, Extraversion, Openness to Experience, Conscientiousness, and

Agreeableness. Each of these domains is composed of six subfactors called facets

(Costa & McCrae, 1992). As in the case with Cloninger’s temperament and character

dimensions, only a few studies have investigated associations between the Big Five

personality dimensions and ADHD.

Braaten and Rosen (1997) found that elevated self-reported DSM-III-R ADHD

symptoms in undergraduates correlated with high Extraversion and high Neuroticism.

The limitation here was the use of college students and assessment based on self-

reports only. Nigg and co-authors (Nigg, John, et al., 2002) subsequently obtained

larger and more diverse samples for the investigation of personality traits and ADHD

symptoms. They used three ADHD self-report instruments, trying to overcome the

limitation that the findings would be attributable to one particular approach of

assessing ADHD, as well as the NEO Five Factor Inventory (NEO FFI). They found



39


2

that ADHD symptoms were consistently related to low Conscientiousness, low

Agreeableness, and high Neuroticism. However, these correlations did not fully

explain the variation in ADHD symptoms. The data showed that attention problems

were related primarily to low Conscientiousness and high Neuroticism, and hyper-

activity-impulsivity was related to low Agreeableness. This study found no reliable

association with ADHD for Extraversion or Openness (Nigg, John, et al., 2002).

Another study addressing the relationship of ADHD symptoms with the FFM

came from Canada (Parker, Majeski, & Collin, 2004). This study used the Conners’

Adult ADHD Rating Scale (CAARS) and the NEO-FFI in a sample comprised of

psychology students. They used DSM-IV cut-off scores to categorize three groups:

the inattentive ADHD type, the hyperactive-impulsive ADHD type, and non-ADHD

controls. Contrary to the study of Nigg and co-workers, but in line with the work of

Braaten and Rosen, the Canada study found consistent associations between high

Extraversion and the hyperactive-impulsive ADHD symptoms, whereas inattentive

symptoms were not related to this personality dimension. High neuroticism was

instead found to be a significant predictor of both inattention and hyperactivity -

impulsivity symptomatology, and again, just as in the study by Nigg and co-workers,

the most powerful predictor for inattention scores was low Conscientiousness, and for

hyperactivity-impulsivity it was low Agreeableness. Both personality dimensions

were also significant predictors for the other symptom group and for total ADHD

scores.

Even considering that these studies relied on self-reported ADHD symptom

ratings, their findings nevertheless suggest substantial associations between ADHD

symptoms and four of the Big Five personality dimensions: high Neuroticism, high

Extraversion, low Conscientiousness, and low Agreeableness. However, Openness

appeared not to be related to ADHD symptomatology. The overall results from

research using the FFM overall seemless consistent and less specific than the TCI

results that associated ADHD with high Novelty Seeking and, when there was also

a personality disorder, with character immaturity.

Neurocognitive and brain domains

Its clinical presentation has suggested that ADHD is a neuropsychological disorder,

and attention and executive functions have become the focus of most theories

concerning its neuropsychological basis (Seidman et al., 2004). Both ASPD and BPD

also contain domains of emotional aberrations. Deficits in theory of mind – the

cognitive end result of both social understanding and emotional understanding

– have been shown across these categorical definitions (Sodian, Hulsken, &

Thoermer, 2003). However, the differentiation of ADHD and associated disorders



40

CHAPTER 2

on the neuropsychological level has proved much more difficult than first expected

(Nigg, 2000), and many a simplified model has failed to conform to empirical data

when put to the test. The executive and motivation systems of the brain may well

be involved in ADHD just as in various personality traits (Nigg, Butler, et al., 2002).

Executive functions have also been found to be less specific on the neuropsycho-

logical level than first assumed and seem to develop in close connection with

empathy and emotional processing (Pacherie, 1997; Perner, 1998), possibly because

self-restraint also boosts comprehension of others and emotional reactivity and

processing are necessary elements of self-restraint. Empathy is a highly complex

function based on nonlinear interactions among theory of mind, emotional

mirroring, executive functions, and situational determinants (Anckars¨ater &

Cloninger, 2007). It is therefore obvious that prior designations of specific brain

systems thought to be involved in either social functioning (especially the limbic

circuitry) or executive functions (especially the prefrontal cortex) have to be

reinterpreted in a wide “social brain,” encompassing interactions among widely

disparate systems.

Analogously, most attention in the psychiatric context has been given to the

systems using monoamines as neurotransmitters, and there is indeed every reason

to assume that monoamines are of central importance: almost all major psycho-

pharmaceuticals have been shown to exert their effects through modulations of

these systems. The complex phenotypes we have approached in this chapter,

however, probably relate to many other transmitter systems; for example,

modifications of dopamine activity may only be hoped to modify some very specific

parts of the problem constellations. In contrast, it is obvious that the pharmacolog-

ical angle in longitudinal research is weak and that drug response may form a key

to disentangling complex phenotypes. Preliminary evidence has also implied a

shared genetic origin for executive functions and personality disorders or

associated features (Coolidge, Thede, & Jang, 2004).

The early “effortful control” (regulation) system in young children is thought

to involve the same neural system as the executive processes related to ADHD,

combined type. A critical role of this system in the developing personality is

reflected in research showing that effortful control is positively related to the

development of conscience and negatively to the expression of aggression

(Kochanska, Murray, & Coy, 1997; Rothbart & Ahadi, 1994).The definition of

temperament as individual differences in constitutionally based (emotional,

motor, and attentional) reactivity and self-regulation (“effortful control”)may

allowus to consider both the initial state of individual differences and the early

development of emotional and attentional systems (Rothbart, 2004). Multiple

pathways in early development related to distinct kinds of temperamental or

cognitive vulnerability might form the basis for phenotypical definitions,



41


2

dimensional or categorical depending on the research models they are applied in,

but clearly defined in relation to specific contexts, developmental stages, and

challenges such as stimuli or tasks.

Ultimately, the pathways between early temperament and future personality

(and possible psychopathology) are likely to be complex and nonlinear, because

children’s development unfolds on the basis of partially genetic constitutional

factors through the context of social relationships, cognition, and experience.

Both continuity and change must eventually be understood in such contexts

(Rothbart, 2004), and it will be necessary for future research to account for all

these aspects to arrive at a better understanding of the role of early neurodevelop-

mental variants in shaping adult personality.

Summary and conclusion

In this chapter we have dealt with complex concepts and issues concerning the

relation of ADHD to personality disorders and traits. We make no pretense at

completeness, but we hope to have contributed to the discussion aiming at a better

understanding of ADHD in relation to personality.

Based on this literature review, we would like to propose the following distinctions

as providing a plain account of the risk for ASPD and criminality carried by ADHD.

Early-onset disruptive behavior disorder (corresponding to the combination of

ADHD, ODD, and CD, or hyperkinetic conduct disorder) carries a sharply increased

risk for later ASPD and aggressive criminality. The adult personality disorder consists

of destructive behavior patterns generally accompanied by deficient or aberrant

emotional processing of thought and reactions. This concept contains most of the

variation in what has been called “psychopathy,” which because of its moral

connotations is an unsuitable term in clinical practice. The disorder is associated

with an increased risk both for ”hands-on” criminal acts and the remaining

unique factor of psychopathy (referred to as the first factor of the PCL-R); that is,

the wicked way of seeking dominance over others through manipulation and

deceit. It remains an open question whether such undesired behavioral consequences

should be dealt with as mental disorders. Thorough clinical diagnoses of the

problem constellation in a developmental perspective are always warranted, not

least as a large proportion of children with early-onset disruptive behaviors also

have attention and learning problems, other forms of social interaction and

communication problems that sometimes correspond to the autism spectrum

definitions, and a wide range of psychiatric coexisting problems. The clinical

assessment forms the basis for possible treatment strategies. In the absence of

early-onset conduct problems, ADHD per se, inattentive or combined type, has not



42

CHAPTER 2

been linked to an increased risk for an adult antisocial development, and late-onset

(adolescent) conduct problems do not share the same developmental basis or

associations to other problem types as the early-onset form nor its grave prognosis.

With regard to associations between ADHD and BPD, systematic data are

meager. Overall, the reviewed studies mainly show symptom overlap between

ADHD and BPD in the disruptive hyperactivity-impulsivity domain, whereas

inattention characteristics are likely to differentiate among the problem types.

More, as well as more diverse, research is needed to better understand the

relation ship between ADHD and BPD, to clearly unravel their shared characteristics,

to propose possible pathways leading to a BPD outcome, and to improve the

understanding of possible truly unique aspects of the categories.

Then, we discussed ADHD in relation to personality traits, as defined by the

Big Five and Cloninger’s temperament and character model. ADHD as a clinical

disorder seems to express an extreme end of extroversion or novelty seeking, with

possible hampered character development or decreased conscientiousness. Harm

avoidance may interact in creating the risk for BPD among subjects with ADHD.

However, because few studies included subgroups with ADHD in which adult

personality disorders had been controlled for, it is difficult to draw specific

conclusions on the delineations and overlap among ADHD, personality disorders,

and personality traits.

Finally, we pointed out the critical role of early regulation and reactivity

systems in the development of temperamental or cognitive vulnerability. In

closing this chapter, we again want to stress the importance of the integration of

theories on psychopathology, temperament, and cognition, which represents a

promising future line of research.

AcknowledgmentsAgneta Brimse and Monika Montell are gratefully acknowledged for their expert

secretarial assistance. The study of longitudinal studies was carried out in close

collaboration with Bj¨orn Hofvander and Daniel Ossowski.



43


2

References

American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders. 3rd ed.

Washington DC: American Psychiatric Association.

American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders. 3rd ed. rev.


American Psychiatric Association. (1994). Diagnostic and Statistical manual of mental disorders. 4th ed.


Anckars¨ater H, Cloninger CR. (2007).The genetics of empathy. In: Farrow T, Woodruff P, eds. Empathy in

Mental Illness and Health. New York: Cambridge University Press: 261–88.

Anckars¨ater H, Stahlberg O, Larson T, Hakansson C, Jutblad SB, Niklasson L, et al. (2006).The impact of

ADHD and autism spectrum disorders on temperament, character, and personality development. Am

J Psychiatry 163:1239–44.

Andrulonis PA, Glueck BC, Stroebel CF, Vogel NG. (1982). Borderline personality subcategories. J Nerv Ment

Dis 170:670–9.

Andrulonis PA, Glueck BC, Stroebel CF, Vogel NG, Shapiro AL, Aldridge DM. (1981). Organic brain dysfunction

and the borderline syndrome. Psychiatr Clin North Am 4:47–66.

Babinski LM, Hartsough CS, Lambert NM. (1999). Childhood conduct problems, hyperactivity-impulsivity,

and inattention as predictors of adult criminal activity. J Child Psychol Psychiatry 40:347–55.

Barkley RA, FischerM, Smallish L, Fletcher K. (2004). Young adult follow-up of hyperactive children:

antisocial activities and drug use. J Child Psychol Psychiatry 45:195–211.

Bergman LR, Magnusson D. (1986). Type A behavior: a longitudinal study from childhood to adulthood 20.

Psychosom Med 48:134–42.

Biederman J, Faraone SV, Keenan K, Benjamin J, Krifcher B, Moore C, et al. (1992). Further evidence for family-

genetic risk factors in attention deficit hyperactivity disorder. Patterns of comorbidity in probands

and relatives psychiatrically and pediatrically referred samples. Arch Gen Psychiatry 49: 728–38.

Biederman J, Faraone SV, Milberger S, Jetton JG, Chen L, Mick E, et al. (1996). Is childhood oppositional

defiant disorder a precursor to adolescent conduct disorder? Findings from a four-year follow-up

study of children with ADHD. J AmAcad Child Adolesc Psychiatry 35:1193–1204.

Biederman J, Mick E, Faraone SV, BurbackM. (2001). Patterns of remission and symptom decline in conduct

disorder: a four-year prospective study of an ADHD sample. J Am Acad Child Adolesc Psychiatry 40: 290–8.

Burt SA. (2009). Are there meaningful etiological differences within antisocial behavior? Results of a

meta-analysis. Clin Psychol Rev 29(2): 163–78.

Caspi A, Harrington H, Milne B, Amell JW, Theodore RF, Moffitt TE. (2003). Children’s behavioral styles at

age 3 are linked to their adult personality traits at age 26. J Pers 71:495–513.

Cleckley HM. (1951).The mask of sanity. Postgrad. Med 9:193–7.

Cloninger CR. (1987). A systematic method for clinical description and classification of personality variants.

A proposal. Arch Gen Psychiatry 44:573–88.

Cloninger CR. (2000). A practical way to diagnosis personality disorder: a proposal. J Pers Disord 14:99–108.

Cloninger CR, Svrakic DM, Przybeck TR. (1993). A psychobiological model of temperament and character.

Arch Gen Psychiatry 50:975–90.

Cooke DJ, Michie C. (2001). Refining the construct of psychopathy: towards a hierarchical model. Psychol

Assess 13:171–88.

Coolidge FL, Thede LL, Jang KL. (2004). Are personality disorders psychological manifestations of executive

function deficits? Bivariate heritability evidence from a twin study. Behav Genet 34:75–84.

Costa PT, Jr, McCrae RR. (1992). The Revised NEO Personality Inventory (NEO-PI-R) and NEO Five-Factor Inventory

(NEO-FFI) Professional Manual. Odessa, FL: Psychological Assessment Resources.

Downey KK, Stelson FW, Pomerleau OF, Giordani B. (1997). Adult attention deficit hyperactivity disorder:

psychological test profiles in a clinical population. J Nerv Ment Dis 185:32–8.

Dowson JH, McLean A, Bazanis E, Toone B, Young S, Robbins TW, et al. (2004).The specificity of clinical

characteristics in adults with attention-deficit/ hyperactivity disorder: a comparison with patients

with borderline personality disorder. Eur Psychiatry 19:72–8.



44

CHAPTER 2

Faraone SV. (2005).The scientific foundation for understanding attention-deficit/hyperactivity disorder as a

valid psychiatric disorder. Eur Child Adolesc Psychiatry 14:1–10.

Farrington DP. (2000). Psychosocial predictors of adult antisocial personality and adult convictions. Behav

Sci Law 18:605–22.

FischerM, Barkley RA, Smallish L, Fletcher K. (2002). Young adult follow-up of hyperactive children:

self-reported psychiatric disorders, comorbidity, and the role of childhood conduct problems and

teen CD. J Abnorm Child Psychol 30:463–75.

Fossati A, Novella L, Donati D, DoniniM, Maffei C. (2002). History of childhood attention deficit/

hyperactivity disorder symptoms and borderline personality disorder: a controlled study. Compr

Psychiatry 43:369–77.

Frisell T, Lichtenstein P, L angstr¨om N. (2010). Violent crime runs in families: a total population study of

12.5 million individuals. Psychol Med 25:1–9.

Gittelman R, Mannuzza S, Shenker R, Bonagura N. (1985) Hyperactive boys almost grown up. Arch Gen


Goldman SJ, D’Angelo EJ, DeMaso DR. (1993). Psychopathology in the families of children and adolescents

with borderline personality disorder. Am J Psychiatry 150:1832–5.

Hare RD. (1980). A research scale for the assessment of psychopathy in criminal populations. Pers Individ Diff

1:111–19.

Hechtman L,Weiss, G. (1986). Controlled prospective fifteen year follow-up of hyperactives as adults:

non-medical drug and alcohol use and anti-social behavior. Can J Psychiatry 31(6):557–67.

Herrero ME, Hechtman L, Weiss G. (1994). Antisocial disorders in hyperactive subjects from childhood to

adulthood: predictive factors and characterization of subgroups. Am J Orthopsychiatry 64:510–21.

Hofvander B, Ossowski B, Lundstr¨om S, Anckars ater H. (2009). Continuity of aggressive antisocial behavior

from childhood to adulthood: the question of phenotype definition. Int J Law Psychiatry 32(4): 224–34.

Hooberman D, Stern TA. (1984). Treatment of attention deficit and borderline personality disorders with

psychostimulants: case report. J Clin Psychiatry 45:441–2.

Kim-Cohen J, Arseneault L, Caspi A, PoloThom asM, Taylor A, Moffitt TE. (2005). Validity of DSM-IV Conduct

Disorder in 41/2-5-year-old children: a longitudinal epidemiological study. Am J Psychiatry 162:1108–17.

Kim-Cohen J, Caspi A, Moffitt TE, Harrington H, Milne BJ, Poulton R. (2003). Prior juvenile diagnoses in

adults with mental disorder: developmental follow-back of a prospective-longitudinal cohort. Arch

Gen Psychiatry 60:709–17.

Klinteberg B, Andersson T, Magnusson D, Stattin H. (1993). Hyperactive behavior in childhood as related to

subsequent alcohol problems and violent offending: a longitudinal study of male subjects. Pers Individ

Diff 15:381–8.

Kochanska G, Murray K, Coy KC. (1997). Inhibitory control as a contributor to conscience in childhood: from

toddler to early school age. Child Dev 68:263–77.

Lahey BB, Loeber R. (1997). ADHD and antisocial behavior. In: Stoff DM, Breiling J, Maser JD, eds. Handbook

of Antisocial Behavior. NewYork: Wiley& Sons: 243–54.

Lahey BB, Loeber R, Burke J, Rathouz PJ, McBurnett K. (2002).Waxing and waning in concert: dynamic

comorbidity of conduct disorder with other disruptive and emotional problems over 7 years among

clinic-referred boys. J Abnorm Psychol 111:556–67.

Lewinsohn PM, Rohde P, Seeley JR, Klein DN. (1997). Axis II psychopathology as a function of Axis I disorders

in childhood and adolescence. J AmAcad Child Adolesc Psychiatry 36:1752–9.

Lilienfeld S, Waldman ID. (1990).The relation between childhood attention-deficit hyperactivity disorder

and adult antisocial behavior re-examined: the problem of heterogeneity. Clin Psychol 10:699–725.

LivesleyWJ. (2001). Commentary on reconceptualizing personality disorder categories using trait

dimensions. J Pers 69:277–86.

Loeber R, Burke JD, Lahey BB. (2002).What are adolescent antecedents to antisocial personality disorder?

Crim Behav Ment Health 12:24–36.

Loeber R, Farrington DP, Stouthamer-LoeberM, Moffitt TE, Caspi A. (1998).The development of male

offending: key findings from the first decade of the Pittsburgh youth study. Stud Crime Prevent, 141–71



45


2

Loeber R, Green SM, Keenan K, Lahey BB. (1995).Which boys will fare worse? Early predictors of the onset of

conduct disorder in a six-year longitudinal study. J Am Acad Child Adolesc Psychiatry 34:499–509.

Loeber R, Green SM, Lahey BB, Frick PJ, McBurnett K. (2000). Findings on disruptive behavior disorders from

the first decade of the developmental trends study. Clin Child Fam Psychol Rev 3:37–60.

Lynam DR. (1996). Early identification of chronic offenders: who is the fledgling pyschopathy? Psychol Bull

120(2):209–34.

Lynn DE, Lubke G, Yang M, McCracken JT, McGough JJ, Ishii J, et al. (2005). Temperament and character

profiles and the dopamine D4 receptor gene in ADHD. Am J Psychiatry 162:906–13.

Mannuzza S, Klein RG, Abikoff H, Moulton JL, III. (2004). Significance of childhood conduct problems to

later development of conduct disorder among children with ADHD: a prospective follow-up study.

J AbnormChild Psychol 32:565–73.

Mannuzza S, Klein RG, Bessler A, Malloy P, LaPudalaM. (1993). Adult outcome of hyperactive boys.

Educational achievement, occupational rank, and psychiatric status. Arch Gen Psychiatry 50:565–76.

Mannuzza S, Klein RG, Bessler A, Malloy P, LaPudalaM. (1998). Adult psychiatric status of hyperactive boys

grown up. Am J Psychiatry 155:493–8.

Mannuzza S, Klein RG, Bonagura N, Malloy P, Giampino TL, Addalli KA. (1991). Hyperactive boys almost

grown up. V. Replication of psychiatric status. Arch Gen Psychiatry 48:77–83.

McCutcheon AL. (1987). Latent Class Analyses. Newbury Park, CA: Sage.

McGough JJ, Barkley RA. (2004). Diagnostic controversies in adult attention deficit hyperactivity disorder.

Am J Psychiatry 161:1948–56.

Moffitt TE, Caspi A. (2001). Childhood predictors differentiate life-course persistent and adolescence

limited antisocial pathways among males and females. Dev Psychopathol 13:355–75.

Moffitt TE, Caspi A, Harrington H, Milne BJ. (2002). Males on the life-course-persistent and adolescence-

limited antisocial pathways: follow-up at age 26 years 12. Dev Psychopathol 14:179–207.

Nadder TS, Rutter M, Silberg JL, Maes HH, Eaves LJ. (2002). Genetic effects on the variation and covariation

of attention deficit-hyperactivity disorder (ADHD) and oppositional-defiant disorder/conduct disorder

(Odd/CD) symptomatologies across informant and occasion of measurement. Psychol Med 32:39–53.

Nigg JT. (2000). On inhibition/disinhibition in developmental psychopathology: views from cognitive and

personality psychology and a working inhibition taxonomy. Psychol Bull 126:220–46.

Nigg JT, Blaskey LG, Huang-Pollock CL, RappleyMD. (2002). Neuropsychological executive functions and

DSM-IV ADHD subtypes. J AmAcad Child Adolesc Psychiatry 4:59–66.

Nigg JT, Butler KM, Huang-Pollock CL, Henderson JM. (2002). Inhibitory processes inadults with persistent

childhood onset ADHD. J ConsultClin Psychol 70:153–7.

Nigg JT, John OP, Blaskey LG, Huang-Pollock CL, Willcutt EG, Hinshaw SP, et al.(2002). Big five dimensions

and ADHD symptoms: links between personality traitsand clinical symptoms. J Pers Soc Psychol 83:451–69.

Pacherie E. (1997). On being the product of one’s failed actions. In: Russel J, ed. ExecutiveDifficulties in Autism.

Oxford: Oxford University Press: 215–55.

Parker JDA, Majeski SA, Collin VT. (2004). ADHD symptoms and personality: relationshipswith the

five-factor model. Pers Individ Diff 36:977–87.

Perner J. (1998) The meta-intentional nature of executive functions and theory of mind. In:Carruthers P,

Boucher J, eds. Language andThought: Interdisciplinary Themes.Cambridge: Cambridge University Press:

270–83.

Pickles A, Angold A. (2003). Natural categories or fundamental dimensions: on carvingnature at the joints

and the rearticulation of psychopathology 3. Dev Psychopathol15:529–51.

Rassmussen P, Gillberg C. (2000). Natural outcome of ADHD with developmentalcoordination disorder at

age 22 years: A controlled, longitudinal, community-basedstudy. J Am Acad Child Adolescent Psychiatry

39(11):1424–31.

Rey JM, Morris-Yates A, SinghM, Andrews G, Stewart GW. (1995). Continuities betweenpsychiatric disorders

in adolescents and personality disorders in young adults. Am JPsychiatry 152:895–900.

Rhee SH,Willcutt EG, Hartman CA, Pennington BF, DeFries JC. (2008) Test of alternativehypotheses

explaining the comorbidity between Attention-Deficit/ HyperactivityDisorder and Conduct Disorder.

J AbnormChild Psychol 36:29–40.



46

CHAPTER 2

Robbins, LN, Rutter M. (1990). Straight and Devious Pathways from Childhood toAdulthood. Cambridge: Cambridge

University Press.

Rothbart MK. (2004). Commentary: differentiated measures of temperament and multiplepathways to

childhood disorders. J Clin Child Adolesc Psychol 33:82–7.

Rothbart MK, Ahadi SA. (1994). Temperament and the development of personality. JAbnorm Psychol

103:55–66.

Sanislow CA, Grilo CM, McGlashan TH. (2000). Factor analysis of the DSM-III-R borderlinepersonality

disorder criteria in psychiatric inpatients. Am J Psychiatry 157:1629–33.

Satterfield JH, Hoppe CM, Schell, AM. (1982). A prospective study of delinquency in 110adolescent boys with

Attention Deficit Disorder and 88 normal adolescent boys. Am JPsychiatry 139:795–8.

Satterfield JH, Schell A. (1997). A prospective study of hyperactive boys with conductproblems and normal

boys: adolescent and adult criminality. J AmAcad Child AdolescPsychiatry 36:1726–35.

Schulz SC, Cornelius J, Schulz PM, Soloff PH. (1988).The amphetamine challenge test inpatients with

borderline disorder. Am J Psychiatry 145:809–14.

Seidman LJ, Doyle A, Fried R, Valera E, Crum K, Matthews L. (2004).Neuropsychological function in adults

with attention-deficit/hyperactivity disorder.Psychiatr Clin North Am 27:261–82.

Silberg J, Rutter M, Meyer J, Maes H, Hewitt J, Simonoff E, et al. (1996). Genetic andenvironmental influences

on the covariation between hyperactivity and conductdisturbance in juvenile twins. J Child Psychol


Soderstrom H, Nilsson T, Sjodin AK, Carlstedt A, Forsman A. (2005).The childhood-onset neuropsychiatric

background to adulthood psychopathic traits and personalitydisorders. Compr Psychiatry 46:111–16.

Svrakic DM, Whitehead C, Przybeck TR, Cloninger CR. (1993). Differential diagnosis ofpersonality disorders

by the seven-factor model of temperament and character. ArchGen Psychiatry 50:991–9.

Torgersen S, Kringlen E, Cramer V. (2001).The prevalence of personality disorders in acommunity sample.

Arch Gen Psychiatry 58:590–6.

Van Reekum R, Links PS. (1994). N of 1 study: methylphenidate in a patient with borderlinepersonality

disorder and attention deficit hyperactivity disorder. Can J Psychiatry39:186–7.

Verheul R. (2005). Clinical utility of dimensional models for personality pathology. J PersDisord 19: 283–302.

Weiss G, Hechtman L, Milroy T, Perlman T. (1985). Psychiatric status of hyperactives asadults: a controlled

prospective 15-year follow-up of 63 hyperactive children. JAmAcad Child Psychiatry 24: 211–20.

Widiger TA, Costa PT, Jr. (1994). Personality and personality disorders. J Abnorm Psychol103:78–91.

Widiger TA, Simonsen E. (2005). Alternative dimensional models of personality disorder:finding a common

ground. J Pers Disord 19:110–30.

World Health Organization (WHO). (1990). ICD-10 – International Statistical Classificationof Diseases and Related

Health Problems. Geneva: WHO.



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Published as:

Van Dijk FE, Lappenschaar GAM, Verkes RJ, Kan CC & Buitelaar JK. (2011).

Life span attention deficit /hyperactivity disorder and borderline

personality disorder symptoms in female patients: a latent class approach.

Psychiatry research, 190 (2): 327-335.

Lifespan attention deficit/hyperactivity disorder and borderline personality

disorder symptoms in female patients: a latent class approach

3



50

CHAPTER 3

Abstract

Attention-deficit/hyperactivity disorder (ADHD) and borderline personality

disorder (BPD) are frequently comorbid. To contribute to a better understanding

of the associations regularly found between ADHD and BPD, on the one hand, and

the developmental pathways for these disorders, on the other hand, latent class

analyses (LCA) were undertaken to identify classes differing in profiles of childhood

symptoms of ADHD and adult symptoms of ADHD and BPD. Diagnostic interviews

with 103 female outpatients meeting the criteria for ADHD and/or BPD were used

to assess current DSM-IV symptoms; childhood symptoms of ADHD were assessed

in parent interviews. The latent classes were examined in relation to the DSM-IV

conceptualizations of ADHD and BPD. And relations between childhood and adult

classes were examined to hypothesize about developmental trajectories. LCA revealed

an optimal solution with four distinct symptom profiles: only ADHD symptoms;

BPD symptoms and only ADHD symptoms of hyperactivity; BPD symptoms and

ADHD symptoms of inattention and hyperactivity; BPD symptoms and ADHD

symptoms of inattention, hyperactivity and impulsivity. All patients with BPD

had some ADHD symptoms in both adulthood and childhood. Hyperactivity was

least discriminative of adult classes. Adult hyperactivity was not always preceded

by childhood hyperactivity; some cases of comorbid ADHD and BPD symptoms

were not preceded by significant childhood ADHD symptoms; and some cases of

predominantly BPD symptoms could be traced back to combined symptoms of

ADHD in childhood. The results underline the importance of taking ADHD

diagnoses into account with BPD. ADHD classification subtypes may not be

permanent over time, and different developmental pathways to adult ADHD and

BPD should therefore be investigated.



51

LIFESPAN ADHD AND BPD SYMPTOMS IN WOMEN

3

Introduction

Attention deficit/hyperactivity disorder (ADHD), characterized by a persistent

pattern of inattentive and hyperactive-impulsive behavior and commonly known

as a developmental disorder starting in childhood, has been accepted as a valid and

reliable diagnosis in adulthood from both clinical and neurobiological perspectives

(Faraone, 2005). Up to 78% of adult patients with ADHD present with other DSM-IV

disorders (Biederman et al., 1993; Wilens et al., 2002; Kessler et al., 2006) while

relatively little attention has been paid to the associations of ADHD with adult

personality disorders. This is because disorders “usually first diagnosed in infancy,

childhood, or adolescence” — such as ADHD — are often not assessed in adulthood.

And conversely, Axis II of the DSM-IV can in principle be applied to determine the

presence of personality disorders — with the exception of the antisocial personality

disorder — at an early age, but this is typically not done until late adolescence.

There are nevertheless good reasons to assume that the personality traits or

individual differences in reaction patterns (i.e., temperament) that form the basis

for the development of adult traits are discernible during early child development

(Caspi et al., 2003).

Growing awareness of (1) the incidence of “childhood” disorders such as ADHD

in adulthood, (2) the presence of temperament differences already in infancy, and

(3) the manifestation of at least some Axis II personality disorders in adolescence

(Lewinsohn et al., 1997) thus calls for a cross-disciplinary re-examination of data

and definitions. In the present study, we therefore examined the relations between

adult ADHD and borderline personality disorder (BPD), which is the most common

personality disorder in clinical psychiatric settings. BPD is a complex and seriously

disabling mental disorder with an estimated incidence of 1% to 2% in the general

population (Torgersen et al., 2001). Almost 75% of the patients receiving therapy

for BPD is female (APA, 2000). A three-factor explanatory structure consisting of a

pervasive pattern of disturbed relations to other persons, affective or emotional

dysregulation, and behavioral impulsivity is commonly assumed (Sanislow et al.,

2000).

Viewed from a clinical perspective, patients with ADHD and BPD clearly share

symptoms of impulsivity. The expression of symptoms can vary, but a common

underlying trait such as impulsivity can create co-existence and/or obscure condi-

tion-specific symptoms. Specification of the relations between ADHD and BPD can

thus help refine diagnostic and therapeutic decision-making procedures but also

facilitate identification of childhood precursors to BPD. While the developmental

trajectories leading to BPD in adulthood are unclear, impulsivity appears to be one

of the earliest traits to emerge for those later diagnosed with BPD (Crowell et al.,

2009). We thus adopt a developmental model of psychopathology in which it is



52

CHAPTER 3

assumed that all psychiatric disorders are of a developmental nature and that the

manifestation of a particular disorder may change with the developmental stage

of the individual (Pennington, 2002).

Previous studies have indeed documented associations between symptoms of

ADHD in either childhood or adulthood and BPD (Davids & Gaspar, 2005; La Barbera

et al., 2009). In the early eighties, for example, it was shown that a significant

subgroup of with BPD had symptoms that were later referred to in the domain of

ADHD (Andrulonis et al., 1981; Andrulonis et al., 1982). A decade later, it was shown

that adolescents with disruptive disorders are more likely to have a personality

disorder from the dramatic/impulsive cluster, which includes BPD, at follow-up

when compared to adolescents with any emotional disorders. Specific associations

of ADHD with hyperactivity and BPD were also reported (Rey et al., 1995). More

recently, the results of a longitudinal study have again shown individuals

diagnosed with childhood ADHD to have an increased risk of personality disorders,

specifically the DSM-IV cluster B type of personality disorders in late adolescence

(Miller et al., 2008).

Research evaluating the presence of specific associations between retrospectively

assessed childhood ADHD symptoms and adult BPD in a controlled design has

revealed a significant relationship between the presence and severity of childhood

ADHD symptoms and adult BPD. At least 60% of the BPD subjects probably met the

criteria for ADHD in childhood (Fossati et al., 2002). In addition, research

investigating the prevalence of adult ADHD of the combined type in patients with

BPD showed a prevalence of 16.1% (Philipsen et al., 2008). Yet another very recent

study found 38.1% of BPD patients to be diagnosed with comorbid adult ADHD

(Ferrer et al., 2010). Such data can be taken to indicate the etiological heterogeneity

of both ADHD and BPD but does not indicate which characteristics are specifically

related and express the same underlying susceptibility or not.

In adults with BPD, the specificity of clinical ADHD characteristics has been

investigated and it has been shown that “impatience,” “aggressive behavior,”

“taking undue risks,” and “failure to take the likely results of actions into account”

are overlapping clinical features. Significant inter-group differences occurred for

“attention,” “organization,” and “persistence,” however (Dowson et al., 2004).

Furthermore, ADHD in male adults has been found to be associated with BPD

symptoms of impulsive aggression (Dowson & Blackwell, 2010). While these results

are in line with prior results, there is nevertheless still some indication that

symptoms referring to the inattention domain of ADHD should be considered in

the relationship between ADHD and BPD. ADHD subtype differences have not

been evaluated in prior studies of the associations between ADHD and BPD.

Moreover, in studies including patients with ADHD, adult personality disorders

have not been carefully controlled for.



53


3

To contribute to a better understanding of the associations previously found

between ADHD and BPD, on the one hand, and the developmental pathways for

these disorders, on the other hand, analyses were undertaken to identify mutually

exclusive classes of subjects with homogeneous symptom profiles. Latent class

analyses (LCA) is a statistical technique used for exploratory and hypothesis-gener-

ating purposes (McCutcheon, 1987). Exploration of symptomatology using this

approach has the major advantage of not losing valuable information (i.e. in the

DSM-IV classification those who score just below the diagnostic threshold are

regarded as non-cases). To the best of our knowledge, there are currently no studies

performing LCA on ADHD and BPD symptoms.

The specific aims of the present research were as follows. To (1) classify female

patients with different profiles of childhood ADHD, adult ADHD, and symptoms

of BPD; (2) examine the latent classes in relation to the DSM-IV conceptualizations

of ADHD and BPD; and (3) explore the relations between the childhood and adult

classifications to identify possible developmental trajectories. This study also

provides the basis for its sequel, which examines the roles of temperament and

character in the differentiation of the classes of patients with similar ADHD / BPD

symptom profiles and the pathways from early temperament to future ADHD and/

or BPD (Van Dijk et al., 2011).

Methods

Participants and assessmentFemale patients were recruited from referrals to the outpatient ADHD program

or the outpatient BPD program of the Department of Psychiatry at the Radboud

University Nijmegen Medical Centre in the Netherlands. To be included in the

study, the patients thus had to meet the DSM-IV criteria for ADHD or BPD.

Patients were excluded in cases of clinically significant chronic medical conditions,

mental retardation, organic brain disorders or schizophrenia. Patients with other

comorbid psychiatric disorders were not excluded to ensure that the study sample

was as representative as possible of the population in clinical practice.

The patients underwent comprehensive clinical assessment, which included

psychiatric evaluation and both structured and semi-structured diagnostic interviews

conducted by trained psychologists or psychiatric trainees supervised by a senior

psychiatrist. The assessment was part of research projects approved by the local

Medical Ethical Committee. All patients signed an informed consent form prior to

participation.



54

CHAPTER 3

The presence of current and childhood ADHD symptoms was assessed using a

Semi-Structured Interview for adult ADHD (Kooij, 2002). The authors have used

this semi-structured interview in previous studies of adult ADHD, and it has been

shown to be both reliable and valid (Kooij et al., 2001; Kooij et al., 2005; Kooij et al.,

2007). Collateral information on the occurrence and developmental history of

childhood symptoms was obtained from the parents or, when unavailable, an

older sibling. To gain further information on the exact DSM-IV criteria for current

and childhood ADHD, we used the Dutch translation of four ADHD DSM-IV Rating

Scales (i.e., patient, spouse, parent and investigator versions) (DuPaul et al., 1998).

To be fully diagnosed as having adult ADHD, the following criteria had to be met:

(1) the patient had to meet 6 of the 9 DSM-IV criteria for inattention and/or

hyperactivity/impulsivity in childhood and at least 5 of the 9 criteria in adulthood,

(2) a chronic course of symptoms of ADHD from childhood to adulthood had to be

the case, and (3) a moderate to severe level of impairment had to be attributed to

the symptoms of ADHD. A cut-off point of 5 out of the 9 criteria was set for the

adult diagnosis of ADHD as this is in keeping with the research literature and

epidemiological data using the same DSM-IV ADHD Rating Scales (Murphy &

Barkley, 1996; Biederman et al., 2000; Kooij et al., 2005).

The Structured Clinical Interview for DSM-IV Axis II Personality Disorders

(SCID-II) was used to determine the BPD classifications. (Weertman et al., 2000).

A classification was given only if no axis I disorder could account for the complaints

or dysfunctions. Other axis-I comorbidity was examined using the Structured

Clinical Interview for DSM-IV axis I (SCID-I) (Groenestijn et al., 1999).

The Global Assessment of Functioning Scale (GAF) from the DSM-IV was used

to assess the global social and professional functioning of the patient. In addition,

information on the social-economic status of the patient (i.e., living on income

from work or welfare) and the highest level of education completed by the patient

was collected.

Out of a total of 78 patients from the BPD program, 3 dropped out without

notification; 11 did not qualify as having BPD according to the DSM-IV; and 1 was

diagnosed with schizophrenia. Out of a total of 45 patients from the ADHD

program, 4 dropped out without notification and 1 said she could not complete the

assessment because it was too aggravating. The final sample thus consisted of 84%

of the original sample or a total of 103 female patients in the end: 40 from the

ADHD program and 63 from the BPD program. Of the ADHD patients, 6 (15%) were

diagnosed with a co-occurrent BPD. Of the BPD patients, 21 (33%) were diagnosed

with co-occurrent ADHD (i.e., ADHD in both childhood and adulthood). This

yielded a total of 27 patients with both ADHD and BPD. We were unable to attain

informant accounts of childhood symptoms of ADHD from 13 patients who all met

the criteria for BPD. Of these, 5 met the criteria for ADHD in adulthood but the



55


3

diagnosis could not be confirmed due to missing childhood data; the other 8 cases

did not meet the criteria for ADHD in adulthood, which led to the rejection of the

diagnosis of ADHD. This left a total of 37 patients with only BPD.

Statistical analysesLatent class analysis (LCA) (McCutcheon, 1987) was used to find the smallest

number of groups of individuals (i.e., classes) with similar patterns of symptoms

that could explain the associations observed among a set of variables. LCA describes

the probabilities of a set of observed categorical variables across groups of

individuals when the group membership of the individuals is unknown. Instead of

using predefined criteria for the presence or absence of a disorder, LCA uses ratings

of subjects on several symptoms. Calculations were made with Mplus version 4.1

(Muthén & Muthén, 2006). Mplus provides a number of decision parameters (22) of

which the Bayesian Information Criterium (BIC) and the Lo-Mendell-Rubin (LMR)

likelihood ratio tests are used in the exploratory phase of the analysis. The data are

analyzed with an increasing number of classes until there is no improvement in

any of the decision criteria (i.e., lower BIC values and more significant p-values

for the LMR indicate improvement over the previous model with one less class).

A small number of candidate models is thus identified for further analysis.

These models are investigated with the bootstrap likelihood ratio test (BLRT) to

determine the most likely number of classes. All analyses are run with a number

of different starting values to minimize the influence of local extremes. Given a

small sample size, the average number of individuals within a class should be

equal to at least the number of variables used in the model and the BLRT should be

superior to the LMR and BIC (Nylund et al., 2007).

The analyses were conducted in steps. To start with, the childhood and adult

symptoms were modeled separately to identify the different classes of patients (i.e.,

symptom profiles) for these different periods of life. For the childhood model, 18

ADHD variables were used, which meant that solutions containing more than 5

classes should be rejected for our sample size of 103. For the adult model, 18 ADHD

+ 9 BPD variables were used, which meant that solutions containing more than 4

classes should be rejected. Using SPSS version 14, the patient’s class membership

was then compared to the patient’s original group membership (i.e., DSM-IV

classification of ADHD only, BPD only or ADHD plus BPD). Regression in Mplus of

the adult classes on the childhood classes was finally undertaken to determine the

latent transition probabilities between adulthood and childhood.



56

CHAPTER 3

Results

Adult classes of ADHD and BPD symptomsWe analyzed two through five latent classes of adult symptoms of ADHD and BPD.

The BIC values and corresponding number of free parameters were 3430 (53), 3233

(81), 3237 (109), and 3301 (137), respectively. The LMR values and corresponding

p-values were 1203 (< 0.001), 184 (0.220), 117 (0.167), and 75 (0.211), respectively. The

BIC suggested solutions with three or four classes as good candidates, whereas the

LMR values did not provide useful decision criteria. Given that the evaluation with

the BLRT values and corresponding p-values of 186 (< 0.001) and 118 (< 0.001)

showed the solution with four classes of symptoms to be significantly better than

the solutions with three or two classes, the solution with four classes was adopted.

Another reason to adopt the solution with four classes of symptoms was hypothesis

generation. The solution with three classes greatly overlapped the existing DSM-IV

classifications: one class reflected only ADHD symptomatology; one class reflected

symptoms of both ADHD and BPD; and one class reflected mainly symptoms of

BPD with some ADHD symptomatology. Working with these classes would not

have provided more specific or new information while it was nevertheless clear

that BPD symptoms did not appear alone (I.e., without ADHD symptomatology).

It was therefore decided to analyze the solution with four classes further. To be

more specific, we adopted the four profiles of adult symptoms of ADHD and BPD as

indicated in Figure 1.

In keeping with recent evidence that shows a three-factor structure for ADHD

(i.e., attention problems, hyperactivity problems, and impulsivity problems) to

better fit the adult symptom profile than the two-factor DSM-IV structure of

attention problems and hyperactivity/impulsivity problems (Span et al., 2002;

Barkley et al., 2007), the DSM-IV domain of hyperactivity/impulsivity was divided

into separate symptom clusters. In the end in our study, thus, Class 1 (29/103, 28%)

showed high probabilities for symptoms of inattention and hyperactivity,

intermediate probabilities for symptoms of impulsivity, and low probabilities for

BPD symptoms. Class 2 (20/103, 19%) showed low probabilities for symptoms of

inattention and impulsivity, intermediate probabilities for symptoms of hyper-

activity, and high probabilities for BPD symptoms. Class 3 (32/103, 31%) showed

high probabilities for both ADHD and BPD symptoms. Class 4 (22/103, 21%) showed

high probabilities for most but not all symptoms of inattention (i.e., scored low on

“fails to pay attention” and “difficulty listening”), showed intermediate to high

probabilities for symptoms of hyperactivity, high probabilities for BPD symptoms,

and low probabilities for symptoms of impulsivity.



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3

One class thus had symptoms of the combined type of ADHD, without

symptoms of BPD. The other three classes had high symptoms of BPD combined

with different symptoms of ADHD to different degrees. One class had symptoms of

the combined type of ADHD together with symptoms of BPD. Another had

symptoms of hyperactivity and inattention together with symptoms of BPD. And

the last class had only symptoms of hyperactivity together with symptoms of BPD.

Symptoms in the ADHD domain of hyperactivity showed the least variation across

the four classes and did not discriminate between the different classes, which is in

contrast to the symptoms of inattention and impulsivity (see Table 1). The data

thus show symptoms of ADHD to behave less consistently than symptoms of BPD

for this clinical population and symptoms of hyperactivity to have little value for

the discrimination of ADHD from BPD. Symptoms of BPD were also not found to

occur without at least some ADHD symptomatology; a completely comorbid

diagnosis of ADHD may not be the case but symptoms of ADHD in one or more

domains and to a greater or lesser extent were found to consistently co-occur with

symptoms of BPD.

Figure 1 Latent class probabilities for adult symptoms of ADHD and BPD in female patients with a diagnosis of ADHD, BPD, or both

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ers

Dif

ficu

lty

awai

tin

g tu

rn

Inte

rru

pts

or

intr

ud

es

Avo

ids

aban

don

men

t

Un

stab

le a

nd

in

ten

se i

nte

rper

son

al r

elat

ion

ship

s

Ind

enti

ty d

istu

rban

ces

Pote

nti

ally

sel

f d

amag

ing

imp

uls

ivit

y

Self

mu

tila

tin

g or

su

icia

l be

hav

ior

Aff

ecti

ve i

nst

abil

ity

Ch

ron

ic f

eeli

ngs

of

emp

tin

ess

Dif

ficu

lty

con

trol

lin

g an

ger

Stre

ss-r

elat

ed p

aran

oia

or d

isso

ciat

ion

Perc

enta

ge

Class 1 (n=29) Class 2 (n=20) Class 3 (n=32) Class 4 (n=22)



58

CHAPTER 3

Childhood classes of ADHD symptomsWe analyzed two through five latent classes of childhood ADHD symptoms. The

BIC values and corresponding number of free parameters were 1860 (37), 1826 (56),

1851 (75), and 1903 (94), respectively. The LMR values and corresponding p-values

were 412 (0.002), 118 (0.005), 60 (0.129), and 33 (0.833), respectively. The BIC

suggested a three-class solution as the best model. Given that the LMR indicated

that this solution was significantly better than a two-class solution, which was

also supported by the BLRT value and corresponding p-value of 119 (0.000), the

solution with three classes was analyzed further.

Figure 2 shows the symptom profiles for the retrospective childhood measurement

of ADHD symptoms. Class 1(47/90, 52%) shows high probabilities for both inattention

Figure 2 Latent class probabilities for childhood history of symptoms of ADHD in adult female patients with a diagnosis of ADHD, BPD, or both

0

10

20

30

40

50

60

70

80

90

100

110

120

Fail

s to

pay

att

enti

on t

o d

etai

ls

Dif

ficu

lty

sust

ain

ing

Dif

ficu

lty

care

full

y li

sten

ing

Dif

ficu

lty

foll

owin

g th

rou

gh o

f fi

nis

hin

g w

ork

Dif

ficu

lty

orga

niz

ing

task

s

Avo

ids

sust

ain

ing

men

tal

effo

rt

Lose

s th

ings

Easi

ly d

istr

acte

d

Forg

etfu

lnes

s

Fid

gest

wit

h h

and

s an

d f

eet

Oft

en l

eave

s se

at

Res

tles

snes

s m

otor

or

men

tal

acti

vity

Dif

ficu

lty

enga

gin

g in

lei

sure

Dri

ven

by

a m

otor

Talk

s ex

cess

ivel

y

Blu

rts

out

answ

ers

Dif

ficu

lty

awai

tin

g tu

rn

Inte

rru

pts

or

intr

ud

es

Perc

enta

ge

Class 1 (n=47) Class 2 (n=23) Class 3 (n=20)



59


3

and hyperactivity/impulsivity symptoms in childhood; class 2 (23/90, 26%) shows

high probabilities for inattention and low probabilities for hyperactivity/impulsivity

symptoms in childhood and class 3 (20/90, 22%) shows almost no probabilities

for inattention symptoms and low probabilities for hyperactivity/impulsivity

symptoms in childhood. These results are consistent with DSM-IV field trials

among children, which confirm the validity of the DSM-IV combined ADHD

disorder and the Predominantly Inattentive ADHD disorder. Less support is

provided by the present data for the Predominantly Hyperactive-Impulsive type of

ADHD, which is included in the DSM-IV but occurs in almost only 4- to 6- year olds

(Lahey et al., 1994).

Adult Class membership compared to DSM-IV diagnosesThe relations between the adult class memberships and DSM-IV diagnoses for the

patients in our study are summarized in Figure 3. Almost all of the patients with

only a DSM-IV diagnosis of ADHD showed up in adult class 1 with high probabilities

for ADHD symptoms and low probabilities for BPD symptoms. The patients with

only a DSM-IV diagnosis of BPD were about equally distributed across classes 2, 3,

and 4 with high probabilities for BPD symptoms in all cases. Note that over

two-thirds of these patients with a diagnosis of only BPD were assigned to classes

3 and 4, which have high probabilities for ADHD symptoms. Most of the patients

with both a DSM-IV diagnosis of ADHD and BPD were assigned to classes 3 and 4

with high probabilities for all symptoms. At the level of symptoms, thus, symptoms

of ADHD were found to be less specific to the latent classes than symptoms of BPD

(see Figure 1); at the level of DSM-IV diagnoses, however, ADHD related more

specifically to the latent classes than BPD (see Figure 3).

Characteristics of the adult latent classes and DSM-IV Diagnostic groups The descriptive data for the DSM-IV diagnostic groups and the adult classes are

presented in Table 1. A more differentiated picture was found for the adult latent

classes than for the DSM-IV diagnostic groups. With regard to educational level, a

significant difference was found to occur between class 1 containing ADHD

symptoms and no BPD symptoms versus class 4 containing mostly symptoms of

inattention and symptoms of BPD. The patients in class 4 were less educated than

the patients in class 1. The patients in class 4 also had lower socio-economic levels

than the patients in the other three classes. The GAF score was highest for those

patients with only symptoms of ADHD (class 1).

Further inspection of the symptom profiles showed the patients with a DSM-IV

diagnosis of ADHD and the patients with a DSM-IV ADHD and comorbid BPD

diagnosis to not differ on the amount of hyperactivity and impulsivity symptoms.



60

CHAPTER 3

The latent classes again showed a more differentiated picture (Table 1). Class 3 had

significantly more symptoms of hyperactivity and impulsivity than the other

three classes.

Latent transition probabilities between adult and childhood classes

In Figure 4, the latent transition probabilities between the adult and childhood

latent classes are presented together with the number of subjects. About 50% of the

patients in adult class 1— with high levels of inattention, intermediate levels of

hyperactivity and impulsivity, and very low levels of BPD symptoms — had a

childhood history of class 1 combined ADHD; the other 50% had a childhood

history of class 2 only inattention ADHD. Adult class 2 — with high levels of BPD

symptoms — had either a childhood history of class 1 combined ADHD or class 3

with low levels of ADHD symptoms. Most of the patients in adult class 3 — with

high probabilities for all ADHD and BPD symptoms — had a childhood history of

class 1 combined ADHD. Finally, adult class 4 — with BPD, inattention and hyper -

activity symptoms — showed an equal distribution across the three latent childhood

classes and thereby a diffuse pattern of transition from childhood to adulthood.

Figure 3 Adult latent class membership broken down by DSM-IV classifications

Class 1: combined ADHD symptoms. Class 2: BPD symptoms + hyperactivity. Class 3: BPD symptoms +

combined ADHD symptoms. Class 4: BPD symptoms + hyperactivity + inattention symptoms.

0

5

10

15

20

25

30

Class 1 Class 2 Class 3 Class 4

Nu

mb

er o

f p

atie

nts

DSM-IV ADHD

DSM-IV BPD

DSM-IV ADHD + BPD



61


3

Figure 4 Number of patients and latent transition probabilities in percentages for adult classes and childhood classes of female patients with attention deficit/hyperactivity disorder, borderline personality disorder, or both

Adult class 1: combined ADHD symptoms. Adult class 2: BPD symptoms + hyperactivity . Adult class 3:

BPD symptoms + combined ADHD symptoms. Adult class 4: BPD symptoms + hyperactivity + inattention

symptoms. Childhood class 1: combined ADHD symptoms. Childhood class 2: inattention symptoms.

Childhood class 3: mild hyperactivity + impulsive symptoms.

15 (52%)

14 (48%)

7 (47%)

8 (53%)

21 (66%)

7 (22%)

4 (28%)

5 (36%)

5 (36%)

4 (12%)

Adult class 1

Adult class 2

Adult class 3

Adult class 4

Child class 1

Child class 2

Child class 3



62

CHAPTER 3

Tab

le 1

Ch

arac

teri

stic

s of

fem

ale

pat

ien

ts c

lass

ified

acc

ord

ing

to D

SM-I

V a

nd

Lat

ent

Cla

ss A

nal

ysis

Ch

arac

teri

stic

DSM

-IV

LCA

AD

HD

(N

=34)

BPD

(N=3

7)C

om

bin

ed(N

=27)

1(N

=29)

2(N

=20)

3(N

=32)

4(N

=22)

N%

N%

N%

N%

N%

N%

N%

Edu

cati

on (<

BSc

)21

b,*,

c,*

6233

8923

8519

g,*

6617

8524

7521

96

Wel

fare

8 b,

**,c

,*24

2978

1556

7 e,

**,g

,**

2414

g,*

7015

g,**

4721

96

Mea

nSD

Mea

nSD

Mea

nSD

Mea

nSD

Mea

nSD

Mea

nSD

Mea

nSD

Age

(yea

rs)

35 b*

*,*

1231

732

935

1232

732

933

9

GA

F sc

ore

65 b,

**,c

,**

855

1059

765

e,**

,f,*

*,g,

**7

5611

599

559

IA7.

7 b,

**,c

,**

1.3

3.0

c,**

2.4

6.3

2.1

7.7

e,**

,f,*

*,g,

**1.

41.

3 f,

**,g

,**

1.4

6.4

2.1

5.4

1.7

H3.

3 b,

*1.

32.

6 c,

**1.

33.

60.

93.

0 e,

**,f

,**

1.2

2.1

f,**

1.0

4.1

g,**

0.7

2.5

1.1

I2.

2 b,

**1.

50.

8 c,

**1.

22.

41.

61.

9 e,

**,f

,**,

g,**

1.4

0.6

f,**

0.8

3.1 g

,**

1.1

0.2

0.4

Tota

l IA

+H/I

13.2

b,**

2.9

6.4

c,**

4.0

12.3

3.1

12.6

e,**

,g,*

*2.

74.

0 f,

**,g

,**

2.7

13.6

g,**

2.7

8.1

2.3

BPD

*1.

0 b,

**,c

**1.

26.

51.

46.

01.

00.

8 e,

**,f

,**,

g,**

1.1

6.5

1.3

5.6

1.7

6.3

1.5

0In

dep

end

ent

sam

ple

T-t

est

for

mu

ltip

le c

omp

aris

on o

f age

, GA

F, I

A, H

, I, t

otal

IA

+ H

/I a

nd

BPD

ou

tcom

e b

etw

een

DSM

-IV

su

btyp

es a

nd

bet

wee

n L

CA

cla

sses

; Fis

her

’s

exac

t te

st f

or m

ult

iple

com

par

ison

of

edu

cati

on a

nd

wel

fare

ou

tcom

e b

etw

een

DSM

-IV

su

btyp

es a

nd

bet

wee

n L

CA

cla

sses

. Abb

revi

atio

ns:

AD

HD

= a

tten

tion

-defi

cit/

hyp

erac

tivi

ty d

isor

der

; BPD

= b

ord

erli

ne

per

son

alit

y d

isor

der

; com

bin

ed =

bot

h A

DH

D a

nd

BPD

; GA

F =

Glo

bal

Ass

essm

ent o

f Fu

nct

ion

ing;

IA

= in

atte

nti

on s

ymp

tom

s;

H =

hyp

erac

tivi

ty s

ymp

tom

s; I

= i

mp

uls

ivit

y sy

mp

tom

s; B

PD*

= BP

D s

ympt

oms.

a Vs.

DSM

-IV

AD

HD

sub

type

s. b

Vs.

DSM

-IV

BPD

su

btyp

es. c V

s. D

SM-I

V c

ombi

ned

su

btyp

es.

d V

s. L

CA

cla

ss 1

. e V

s. L

CA

cla

ss 2

. f V

s. L

CA

cla

ss 3

. g V

s. L

CA

cla

ss 4

. * p

_0.0

5. *

* p≤

0.01

.



63


3

Discussion

For both adult and childhood symptoms, latent classes representing qualitatively

different profiles were identified rather than simply differences in the clinical

severity of the symptoms as commonly found in latent class analyses of ADHD

symptoms with or without added comorbidities (Acosta et al., 2008).

The solution with four latent classes tells us more about the construct of BPD

than the construct of ADHD. Patients with a primary diagnosis of ADHD and no

BPD were all allocated to latent class 1 with indeed no symptoms of BPD. In

contrast, patients with a diagnosis of BPD were distributed across the three other

classes and all had some ADHD symptomatology. This heterogeneous picture is in

line with the results of other studies of BPD and its diagnostic comorbidity

(Zimmerman & Mattia, 1999; Shea et al., 2004) but also provides new insights

regarding the coexistence of ADHD and BPD. In clinical practice, ADHD may

frequently be missed in patients with a diagnosis of BPD and thus lead to

insufficient and possibly inadequate treatment.

ADHD symptoms of hyperactivity were found to be high for all of the latent

classes of patients, which indicate that hyperactivity has a poor diagnostic value

for the differentiation of ADHD and BPD. Hyperactivity appears to be characteristic

of not only most ADHD patients but also many patients with BPD. This may be due

to the indistinct, unspecific, and broad formulation of the DSM-IV criteria for

hyperactivity (e.g. “restless motor or mental activity” and “difficulty in engaging

leisure”), which boils down to the measurement of overall restlessness — possibly

confounded by stress or anxiety. Earlier results suggest that individuals with BPD

also exhibit inhibitory dysfunction (Swirsky-Sacchetti et al, 1993; Bazanis et al

2002; Possner et al, 2002; Nigg, 2005). To date, however, only one comparative study

has shown symptoms of BPD to still correlate with response inhibition after

control for comorbidity with ADHD (Nigg, 2005). In another comparative study, it

was concluded that, in contrast to ADHD, BPD is not characterized by a specific

attentional deficit (Lampe et al, 2007). In the present study, however, we found a

class of patients with BPD and also inattention problems. Further research is thus

needed to clarify the coexistence of attention and inhibition problems with BPD.

The three childhood classes of ADHD symptoms corresponded well with

known clinical findings and reflected the combined inattentive and hyperactive

impulsive type of ADHD, the strictly inattentive type, and the hyperactive

impulsive type (Lahey et al., 1994). Assuming that the four adult classes provided

information beyond our knowledge of the DSM-IV classifications, it is surprising

that the four classes all showed relatively high probabilities for symptoms of

hyperactivity. This suggests that the existence of adult hyperactivity does not

automatically imply the existence of childhood hyperactivity, which raises



64

CHAPTER 3

questions about the validity of the hyperactivity construct and the stability of the

construct of ADHD over time.

There were three adult classes that had high probabilities for symptoms of

ADHD but contained patients with only very few symptoms of hyperactivity and

impulsivity in childhood. In other words, having almost no symptoms of ADHD in

childhood does not automatically imply a low probability of such symptoms in

adulthood. An explanation for this may lie in the age of onset adopted for ADHD

in the present study, namely 12 years. There are recent indications that late onset

adult ADHD is valid and that the age of onset recommended by the DSM-IV, namely

7 years, might be too stringent. (Faraone et al., 2006a; Faraone et al., 2006b).

Furthermore, an adult class of patients with almost only BPD symptoms but a

history of combined ADHD symptoms was identified in the present study, which

suggests that ADHD can remit later in life (Faraone et al., 2006a).

Examination of the latent transition possibilities suggests several developmental

pathways. One possible pathway leads from combined inattention and hyperactive/

impulsive symptoms or mainly inattention symptoms in childhood to an adult

profile containing only symptoms of ADHD and not BPD. Another possible pathway

leads from a childhood profile with at least low levels of hyperactive/impulsive

symptoms but no inattention problems to an adult profile with symptoms of BPD.

Hyperactive/impulsive symptoms could thus play a mediating role in the

development of BPD along this pathway. The actual causal relations between

ADHD and BPD are still unclear, however. We should also bear in mind that (1) LCA

is mainly used for exploratory and hypothesis-generating purposes and (2) a

retrospective design, which is susceptible to recall bias, was used. To diminish the

possible effects of poor memory, we triangulated the self-report information with

regard to current and past symptomatology using other data sources (i.e., parents,

older siblings, spouses) before making a diagnosis. The present results are

nevertheless in line with the results of many longitudinal prospective studies of

the criteria for ADHD and related definitions.

There are some other possible limitations on the present study. The study

group consisted of patients at an academic medical centre and may therefore be

sensitive to referral bias. The results certainly cannot be generalized to nonreferred

samples. Furthermore, the number of subjects within the individual classes met

the minimal criteria but the sample size was still small for LCA and the sample

only included females. Given that it is mostly women who receive therapy for BPD

while the sex ratio for adult patients with ADHD is more equally divided, the

results of this study are probably more representative for the population with BPD.

The question of whether the results hold for males thus remains to be answered.

The results must be replicated and extended to larger independent samples.

Nonetheless, the use of a well-described and diagnosed sample showed — in



65


3

keeping with the results of other studies (Lahey et al., 2005) — that the DSM-IV

subtypes of ADHD cannot be viewed as discrete, nominal categories that are

relatively permanent over time.

In closing, we would like to mention some clinical implications of the present

results and directions for future research. A first implication is that in cases of a

diagnosis of BPD, ADHD should also always be considered. This is because BPD has

been found to frequently occur with symptoms of ADHD; over one third of patients

diagnosed with BPD also receive a co-occurring ADHD diagnosis. It is plausible

that unrecognized ADHD can worsen the course of BPD and treatment outcome.

Conversely, the detection of BPD in cases of ADHD can also be of importance for

the selection and outcome of treatment. A second implication is that ADHD should

not be differentiated from BPD on the basis of symptoms of hyperactivity.

Hyperactivity has little discriminative value for these disorders. The present

results thus challenge us to further unravel the relations between ADHD and BPD,

identify their unique and shared characteristics, and illuminate the possible

pathways to adult ADHD — either with or without comorbid BPD. The latent classes

identified in this research should be validated with the addition of external

variables. The next step in our research is therefore to analyze the associations of

a number of factors to the combination of ADHD and BPD: temperament and

character features (Van Dijk et al., 2011), neurocognitive measures, and genetic

data. In light of the present results, our main hypothesis for the future will be that

impulsivity continues to be a shared feature of ADHD and BPD and to possibly play

a mediating role in the development of adult BPD not only at the level of symptoms

but also at the level of personality traits and neurocognitive outcome. The

specificity of inattention symptoms in adult ADHD and BPD remains to be seen,

however.

AcknowledgementsRose Collard, Marjan Knippenberg, and Marleen Bastiaanse, are gratefully

acknowledged for their expert research assistance. Pieter van den Broek is

gratefully acknowledged for his close collaboration on the data collection.



66

CHAPTER 3

References

Acosta, M.T., Castellanos, F.X., Bolton, K.L., Balog, J.Z., Eagen, P, Nee L.,2008. Latent class subtyping of atten-

tion-deficit/hyperactivity disorder and comorbid conditions. Journal of the American Academy of

Child and Adolescent Psychiatry 47, 797-807.

American Psychiatric Association, 1994. Diagnostic and Statistical Manual of Mental Disorders, fourth ed.

APA, Washington, D.C.

Andrulonis, P.A., Glueck, B.C., Stroebel, C.F., Vogel, N.G., Shapiro, A.L., Aldridge, D.M., 1981. Organic brain

dysfunction and the borderline syndrome. Psychiatric Clinics of North America 4, 47-66.

Andrulonis P.A., Glueck B.C., Stroebel C.F., Vogel N.G., 1982. Borderline personality subcategories. Journal

of Nervous and Mental Disease 170, 670-9.

Barkley, R.A., Murphy, K.R., Fischer, M., 2007. The Science of ADHD in Adults: Clinic- Referred Adults and

children Grown Up. Guilford, New York.

Bazanis, E., Rogers, R. D., Dowson, J. H., Taylor, P., Meux, C., Staley, C., Nevinson- Andrews, D., Taylor, C.,

Robbins, T. W., Sahakian, B. J., 2002. Neurocognitive deficits in decision-making and planning of

patients with DSM-III-R borderline personality disorder. Psychological Medicine 32, 1395–1405.

Biederman, J., Faraone, S.V., Spencer, T., Wilens, T., Norman, D., Lapey, K.A., 1993. Patterns of psychiatric

comorbidity, cognition and psychosocial functioning in adults with Attention Deficit Hyperactivity

Disorder. American Journal of Psychiatry 150, 1792-8.

Biederman, J., Mick, E., Faraone, S.V., 2000. Age-dependent decline of symptoms of attention deficit

hyperactivity disorder: impact of remission definition and symptom type. American Journal of

Psychiatry 157, 816-8.

Caspi A, Harrington H, Milne B, Amell JW, Theodore RF, Moffitt TE., 2003. Children’s behavioral styles at

age 3 are linked to their adult personality traits at age 26. Journal of Personality 71, 495–513.

Crowell, S.E., Beauchaine, T.P., Linehan, M.M., 2009. A biosocial development model of borderline

personality: Elaborating and extending Linehan’s theory. Psychological Bulletin 135,495-510.

Davids, E., Gaspar M., 2005. Attention deficit hyperactivity disorder and borderline personality disorder.

Progress in Neuro-Psychopharmacology and Biological Psychiatry 29, 865-977.

Dowson, J.H., McLean, A., Bazanis, E., Toone, B., Young, S., Robbins, T.W., 2004. The specificity of clinical

characteristics in adults with attention-deficit/hyperactivity disorder: a comparison with patients

with borderline personality disorder. European Psychiatry 19, 72-8.

DuPaul, G.J., Power TJ, Anastopoulos, A.D., Reid, R., 1998. ADHD Rating Scale-IV. Checklists, Norms and

Clinical Interpretation. The Guilford press, New York.

Faraone, S.V., 2005. The scientific foundation for understanding attention- deficit/hyperactivity disorder as

a valid psychiatric disorder. European Child & Adolescent Psychiatry 14, 1-10.

Faraone, S.V., Biederman, J., Spencer, T., Mick, E., Murray, K., Petty, C., 2006a. Diagnosing adult attention

deficit hyperactivity disorder: are late onset and subthreshold diagnoses valid? American Journal of


Faraone, S.V., Biederman, J., Doyle, A., Murray, K., Petty, C., Adamson, J.J., 2006b. Neuropsychological studies

of late onset and subthreshold diagnoses of adult attention-deficit/hyperactivity disorder. Biological

Psychiatry 15,1081-7.

Ferrer, M., Andion, O., Matali, J., Valero, S., Navarro, J.A., Ramos-Quiroga, J.A., Torrubia, R., Casas, M., 2010.

Comorbid attention-deficit/hyperactivity disorder in borderline patients defines an impulsive

subtype of borderline personality disorder. Journal of Personality Disorders 24, 812-822.

Fossati, A., Novella, L., Donati, D., Donini, M., Maffei, C., 2002. History of childhood attention deficit/

hyperactivity disorder symptoms and borderline personality disorder: a controlled study. Comprehensive


Groenestijn, M.A.C., Akkerhuis, G.W., Kupka, R.W., Schneider, N., Nolen, W.A., 1999. Structured Clinical

Interview for DSM-IV Axis I Disorders. Swets & Zeitlinger BV, Lisse, The Netherlands.

Kessler, R.C., Adler, L., Barkley, R., Biederman, J., Conners, C.K., Demler, O., 2006. The prevalence and

correlates of adult ADHD in the United States: results from the National Comorbidity Survey

Replication. American Journal of Psychiatry 163, 716- 23.



67


3

Kooij, J.J., Aeckerlin, L.P., Buitelaar, J.K., 2001. Functioning, comorbidity and treatment of 141 adults with

attention deficit hyperactivity disorder (ADHD) at a psychiatric outpatient department. Nederlands

Tijdschrift voor Geneeskunde 145, 1498-501.

Kooij, J.J.S., 2002. ADHD bij volwassenen. Inleiding in diagnostiek en behandeling [ADHD in adults.

Introduction in diagnostics and treatment]. Swets & Zeitlinger, Lisse.

Kooij, J.J., Buitelaar, J.K., van den Oord, E.J., Furer, J.W., Rijnders, C.A., Hodiamont, P.P., 2005. Internal and

external validity of attention-deficit hyperactivity disorder in a population-based sample of adults.

Psychological Medicine 35, 817-27.

Kooij, J.S., Boonstra, A.M., Vermeulen, S.H., Heister, A.G., Burger, H., Buitelaar, J.K., 2007. Response to meth-

ylphenidate in adults with ADHD is associated with a polymorphism

in SLC6A3 (DAT1). American Journal of Medical Genetics

Part B: Neuropsychiatric Genetics 147B, 201–208.

La Barbera, D., Sideli, L., Mistretta, C., Sartorio, C., Grillo, G., 2009. Attention deficit/hyperactivity disorder

and borderline personality disorder: Differential diagnosis and comorbidity from childhood to

adulthood. Italian Journal of Psychopathology 15, 250-268.

Lahey, B.B., Applegate, B., McBurnett, K., Biederman, J., Greenhill, L., Hynd, G.W., 1994. DSM-IV field trials

for attention deficit hyperactivity disorder in children and adolescents. American Journal of


Lahey, B.B., Pelham, W.E., Loney, J., Lee, S.S., Willcutt, E., 2005. Instability of the DSM-IV Subtypes of ADHD

from preschool through elementary school. Archives of General Psychiatry 62, 896-902.

Lampe, K., Konrad K., Kroener, S., Fast, K., Kunert, H.J., Herpertz, S.C., 2007. Neuropsychological and

behavioural disinhibition in adult ADHD compared to borderline personality disorder. Psychological

Medicine 37, 1717-1729.

Lewinsohn PM, Rohde P, Seeley JR, Klein DN., 1997. Axis II psychopathology as a function of Axis I disorders

in childhood and adolescence. Journal of the American Academy of Child & Adolescent Psychiatry 36,

1752–9.

McCutcheon, A.L., 1987. Latent Class Analysis. Sage, Newbury Park, CA.

Miller, C.J., Flory, J.D., Miller, S.R., Harty, S.C., Newcorn, J.H., Halperin, J.M., 2008. Childhood attention-defi-

cit/hyperactivity disorder and the emergence of personality disorders in adolescence: A prospective

follow-up study. Journal of Clinical Psychiatry 69, 1477-1484.

Murphy, K., Barkley, R.A., 1996. Prevalence of DSM-IV symptoms of ADHD in adult licensed drivers:

Implications for clinical diagnosis. Journal of Attention Disorders 1, 147-61.

Muthén, L,K., Muthén, B.O., 2006. Mplus user’s guide. Statistical analysis with latent variables (4th ed.;

version 4.1). Muthén & Muthén, Los Angeles.

Nigg, J.T., Silk, K.R., Stavro G., Miller, T., 2005. Disinhibition and borderline personality disorder.

Developmental Psychopathology 17, 1129-1149.

Nylund, K,L., Asparouhov, T., Muthén, B., 2007. Deciding on the number of classes in latent class analysis

and growth mixture modeling: a Monte Carlo simulation study. Structural Equation Modeling: A

Multidisciplinary Journal 14, 535-69.

Pennington, B.F. ,2002. The development of psychopathology: Nature and nurture. New York: Guilford

Press.

Philipsen, A., Limberger, M.F., Lieb, K., Feige, B., Kleindienst, N., Ebner-Priemer, U., 2008. Attention-deficit

hyperactivity disorder as a potentially aggravating factor in borderline personality disorder. British

Journal of Psychiatry 192, 118-23.

Posner, M. I., Rothbart, M. K., Vizueta, N., Levy, K. N., Evans, D. E., Thomas, K. M., Clarkin, J. F., 2002.

Attentional mechanisms of borderline personality disorder. Proceedings of the National Academy of

Sciences of the United States of America 99, 16366–16370.

Rey, J.M., Morris-Yates, A., Singh, M., Andrews, G., Stewart, G.W., 1995. Continuities between psychiatric

disorders in adolescents and personality disorders in young adults. American Journal of Psychiatry

152, 895-900.

Sanislow CA, Grilo CM, McGlashan TH., 2000. Factor analysis of the DSM-III-R borderline personality

disorder criteria in psychiatric inpatients. American Journal of Psychiatry 157, 1629–33.



68

CHAPTER 3

Span, S.A., Earleywine, M., Strybel, T.Z., 2002. Confirming the factor structure of attention deficit

hyperactivity disorder symptoms in adult, nonclinical samples. Journal of Psychopathology and

Behavioral Assessment 24, 129-36.

Shea, M.T., Stout, R.L., Yen, S., Pagano, M.E., Skodol, A.E., Morey, L.C., 2004. Associations in the course of

personality disorders and Axis I disorders over time. Journal of Abnormal Psychology 113, 499-508.

Swirsky-Sacchetti, T., Gorton, G., Samuel, S., Sobel, R., Genetta-Wadley, A., Burleigh, B.,1993. Neuropsycho-

logical function in borderline personality disorder. Journal of Clinical Psychology 49, 385–396.

Torgersen S, Kringlen E, Cramer V., 2001.The prevalence of personality disorders in a community sample.

Archives of General Psychiatry 58, 590–6.

Van Dijk, F.E., Lappenschaar, M., Kan, C.C., Verkes, R.J., Buitelaar, J.K., 2011. Symptomatic overlap between

attention-deficit/hyperactivity disorder and borderline disorder in women: the role of temperament

and character traits. Comprehensive Psychiatry, DOI: 10.1016/j.comppsych.2011.02.007

Weertman, A., Arntz, A., Kerkhofs, M.L.M., 2000. Structured Clinical Interview for DSM-IV Axis II

Personality Disorders. Swets & Zeitlinger BV, Lisse, the Netherlands.

Wilens, T.E., Biederman, J., Spencer, T.J., 2002. Attention deficit/hyperactivity disorder across the lifespan.

Annual Review of Medicine 53, 113-31.

Zimmerman, M., Mattia, J.I., 1999. Axis I diagnostic comorbidity and borderline personality disorder.

Comprehensive Psychiatry 40, 245-52.



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3



Published as:

Van Dijk FE, Lappenschaar GAM, Verkes RJ, Kan CC & Buitelaar JK. (2012)

Symptomatic overlap between attention deficit/hyperactivity disorder

and borderline personality disorder: The role of temperament and character traits.

Comprehensive psychiatry, 53(1): 39-48.

Symptomatic overlap between attention-deficit/hyperactivity disorder

and borderline personality disorder in women: the role of temperament

and character traits

4



72

CHAPTER 4

Abstract

Objective: There is substantial symptomatic overlap between Attention-Deficit/

Hyperactivity Disorder (ADHD) and borderline personality disorder (BPD) in adults,

but the nature of the relationship between these disorders needs further

clarification. The role of temperament and character traits in the differentiation

of classes of patients with similar ADHD and BPD symptom profiles was examined

and possible pathways between early temperament and future ADHD and/or BPD

were hypothesized.

Method: Structured diagnostic interviews were conducted in 103 female patients

to assess current DSM-IV symptoms of ADHD and BPD, and parent interviews were

used to assess ADHD symptoms in childhood. Classes of subjects with homogeneous

symptom profiles were identified using latent class analysis (LCA). Temperament

and character traits were assessed using Cloninger’s Temperament and Character

Inventory; scores were then compared across the latent classes.

Results: LCA revealed four mutually exclusive classes of patients: one with only

ADHD symptoms; one with BPD symptoms and ADHD symptoms of hyperactivity;

one with BPD symptoms and ADHD symptoms of inattention, hyperactivity, and

impulsivity; and one with BPD symptoms and ADHD symptoms of inattention and

hyperactivity. High Novelty Seeking was found in all classes except for the class

with symptoms of BPD and only the hyperactivity aspect of ADHD. The highest

Novelty Seeking temperament scores were found in that class of patients with

both symptoms of BPD and symptoms in all areas of ADHD. High Harm Avoidance,

low Cooperativeness, and low Self-Directedness were specifically related to classes

containing BPD symptoms.

Conclusions: Classes of ADHD and BPD symptoms are associated with specific

temperament and character configurations. Novelty Seeking was associated with

the inattention symptoms of ADHD. An outspoken Novelty Seeking temperament

suggests a vulnerability for the development of ADHD and co-occurring BPD.

Contrary to patients with combined ADHD and BPD symptoms, patients with only

symptoms of ADHD showed normal character development and thus an absence of

a personality disorder. Assessment of temperament and character traits can

improve our understanding of the complex relationship between ADHD and BPD.



73

TEMPERAMENT AND CHARACTER IN FEMALE ADHD AND BPD

4

Introduction

Research has shown significant co-occurrence of DSM-IV defined attention-deficit/

hyperactivity disorder (ADHD) and borderline personality disorder (BPD) in adults

[1-6]. In our previous latent class analyses (LCA) [7], groups of women with differing

profiles of childhood symptoms of ADHD, adult symptoms of ADHD, and adult

symptoms of BPD showed BPD to be accompanied by adult symptoms of ADHD but

the hyperactivity symptoms of ADHD to be least discriminative. Adult hyperactivity

was not always preceded by childhood hyperactivity; some cases of comorbid

ADHD and BPD symptoms were not preceded by significant childhood ADHD

symptoms; and some cases of predominantly BPD symptoms could be traced back

to combined symptoms of ADHD in childhood [8]. These results prompted us to

further our work on the relationships between ADHD and BPD but from a more

developmental perspective.

To gain greater insight into the different possible pathways leading to ADHD

with or without BPD, the roles of temperament and personality traits in the

co-occurrence of ADHD and BPD were examined. Associations with temperament

and personality may provide clues to the structure and outcome of ADHD and

thereby etiological theories [9 -12]. ADHD is characterized by three domains of

behavioral problems (i.e., inattention, hyperactivity, and impulsivity) and, for this

reason, ADHD particularly lends itself to an examination of the roles of temperament

and personality in its occurrence. Although the inattention, hyperactivity and

impulsivity symptom domains cluster together to constitute ADHD as a syndrome,

the different domains of symptoms may nevertheless have partially distinct

etiological determinants. The pathways for the different domains of symptoms for

ADHD may, moreover, overlap with the BPD problems that frequently accompany

ADHD. Temperament and personality may thus shape the course of ADHD and

help clarify the nature of the relations between adult ADHD and BPD.

Temperament and character dimensionsIn the present research, we draw upon Cloninger’s theory of personality because it

addresses the genetic and neurobiological bases of personality in interaction with

the environment and learning [13]. In this theory, it is assumed that personality

can be typified in terms of four temperament dimensions and three character

dimensions.

The temperament dimensions of personality manifest themselves early in life,

are assumed to be independently heritable, reflect individual differences in basic

emotional drives, and are defined in terms of differing responses to novelty, harm,

reward, and tasks requiring persistence [14]. The temperament dimensions of

personality include Novelty Seeking (i.e., impulsive and irritable versus rigid and



74

CHAPTER 4

stoical), Harm Avoidance (i.e., pessimistic and anxious versus optimistic and

risk-taking), Reward Dependence (i.e., sociable and warm versus aloof and cold),

and Persistence (i.e., persevering and ambitious versus easily discouraged and

indolent).

The character dimensions of personality are hypothesized to mature in adulthood

via conceptual or insight-based learning and to reflect individual differences in

those higher cognitive processes that define a person’s style of mental self-government.

The character dimensions of personality include Self-Directedness (i.e., responsible

and resourceful versus blaming and inept), Cooperativeness (i.e., helpful and

principled versus hostile and opportunistic), and Self-Transcendence (i.e., intuitive

and insightful versus concrete and conventional) [15,16].

The seven dimensions of personality are measured using the Temperament

and Character Inventory (TCI), which is a self-rating instrument [16]. Each of the

seven temperament and character traits is multifaceted, consisting of several facets

or lower order components. Twenty five facets altogether (12 facets of temperament

and 13 facets of character) make up the TCI. From a clinical perspective, the

presence of a personality disorder is indicated by character immaturity (i.e., low

Self-Directedness and/or Cooperativeness scores); the type of personality disorder

is indicated by the configuration of temperament scores [17,18]. Studies have shown

the character dimensions of Self-Directedness and Cooperativeness to discriminate

between patients with or without a diagnosed personality disorder and different

patterns of temperament scores to correlate significantly with different personality

disorders [14,19,20].

Previous research on temperament and character in ADHD and BPD Previous studies report significant correlations between BPD and high Novelty

Seeking and Harm Avoidance, on the one hand, and low Self-Directedness and low

Cooperativeness, on the other hand [19-21]. One study extended this research to

take gender and comorbidity into account [22]. Women with BPD showed high

levels of Harm Avoidance but not Novelty Seeking with very low levels of Self

Directedness.

Few studies have investigated the TCI profiles of adults with ADHD, but the

available results show a similar set of associations as for BPD. Adult ADHD subjects

score significantly higher than normal subjects on the temperament dimensions

of Novelty Seeking and Harm Avoidance [23-25]. Also compared to the general

population, much lower scores on the character dimensions of Self-Directedness

and Cooperativeness are reported. It is therefore suggested that these findings are

consistent with the notion that early problems form obstacles for later character

maturation and may predict a high rate of clinically significant personality

disorder. The study by Anckarsater et al is of particular interest within this context



75


4

[25] as they measured TCI traits and symptoms of personality disorder in a group

of outpatients with ADHD. ADHD was associated with low scores for Self-Directedness

and Cooperativeness but high scores for Harm Avoidance and Novelty Seeking; the

group of outpatients with ADHD also had high rates of BPD (37%). In light of the

fact that the personality disorders were described in this study using both the TCI

and the Structured Clinical Interview for DSM-IV Personality Disorders, the authors

conclude that the results confirm the assumption that neuropsychiatric disorders

with a childhood onset reflect a difficult underlying temperament, deficits in

character maturation, and personality disorders. They also conclude that a “typical

ADHD temperament” corresponds to an explosive/borderline type of personality

with high Novelty Seeking and Harm Avoidance in combination with low Reward

Dependence.

These results thus appear to show ADHD and BPD to share a number of

temperament and character traits. In these earlier studies, however, neither the

comorbid presence of ADHD in the BPD samples nor the comorbid presence of BPD

in the ADHD samples were controlled for.

Aims of the present studyAmong the aims of the present study was examination of the role of temperament

and character traits in the differentiation of groups of ADHD and BPD patients

with differing degrees of ADHD and BPD symptoms. In order to do this, latent

classes of individuals with similar symptom profiles were used rather than DSM-IV

subgroups. The advantage of using latent classes as opposed to actual DSM-IV

subgroups is that the latent classes are phenomenologically homogeneous groups

(i.e., groups composed of individuals with clearly similar symptom profiles);

subgroups formed on the basis of the DSM-IV, in contrast, tend to be less

homogeneous as an ADHD classification without a BPD classification, for example,

does not imply a total absence of BPD symptoms.

Given that the different temperament dimensions of personality are supposed

to reflect individual differences in basic emotional drives, clear differences in the

TCI profiles of the latent classes of individuals were expected to be found. Given

that BPD is characterized by a greater instability of emotion regulation than

ADHD, the latent classes with mainly BPD symptomatology were expected to show

comparatively high levels of Harm Avoidance (first hypothesis). Given that ADHD

and BPD are both characterized by impulsive behavior, high Novelty Seeking

scores were expected to be found for all of the latent classes of ADHD and BPD with

those classes with both BPD and ADHD symptomatology showing the highest

scores (second hypothesis). In keeping with Cloninger’s assumption that low

character scores are indicative of personality disorders and that ADHD is not a

personality disorder, lower Self-Directedness and Cooperativeness scores were



76

CHAPTER 4

expected to be found for the latent classes of individuals with BPD symptomatology

than for the latent classes of individuals with only ADHD symptomatology (third

hypothesis).

Method

Subjects and assessmentParticipants were consecutively recruited female patients referred to the ou t-

patient ADHD program or outpatient BPD program at the Department of Psychiatry,

Radboud University Nijmegen Medical Centre, The Netherlands. The patients were

recruited during a period of approximately 3 years and had to meet the DSM-IV

criteria for ADHD or BPD to be included in the study. Patients with clinically

significant chronic medical conditions, mental retardation, organic brain disorders,

or schizophrenia were excluded from the study. Patients with other comorbid

psychiatric disorders were not excluded in order to make the sample as

representative of the actual clinical population as possible. Diagnostic assessment

was part of the standard clinical diagnostic procedures and the part related to the

present ADHD research projects was approved by the local Medical Ethical

Committee. All patients signed an informed consent form prior to participation.

Out of a total of 45 patients recruited from the ADHD program, 5 were

excluded: 4 dropped out without notification and 1 considered the procedure too

stressful. Out of a total of 78 patients recruited from the BPD program, 15 were

excluded: 3 dropped out without notification, 11 did not meet the DSM-IV criteria

for BPD, and 1 was diagnosed with schizophrenia. The final sample thus included

103 patients (or 84% of the recruited patients): 40 from the ADHD treatment

program and 63 from the BPD treatment program. Six (or 15%) of the ADHD

patients had a comorbid diagnosis of BPD, leaving 34 patients in this group with

ADHD alone (mean age = 35, SD = 12). Of the 63 BPD patients, 21 (or 33%) had a

comorbid diagnosis of ADHD (i.e., ADHD in childhood and adulthood), which left

42 patients in this group with what appeared to be BPD alone. We were unable to

attain informant accounts of childhood symptoms of ADHD for 13 of the 42

patients meeting the criteria for BPD. Of these 13, 5 met the criteria for ADHD in

adulthood; the other 8 cases did not meet the criteria for ADHD in adulthood,

which meant rejection of a possible diagnosis of ADHD. This left a total of 37

patients with a diagnosis of BPD alone (mean age = 31, SD=7). A total of 27 patients

had a clear diagnosis of both ADHD and BPD (mean age = 32, SD = 9).

Patients underwent comprehensive clinical assessment. This included psychiatric

evaluation and both structured and semi-structured diagnostic interviews, which

were conducted by trained psychologists or psychiatric trainees under the



77


4

supervision of a senior psychiatrist. The interviewers were blind to all prior

clinical diagnoses.

The presence of ADHD symptoms in childhood and adulthood (i.e., current)

was assessed using a Semi-Structured Interview for ADHD [26]. This interview has

been used in previous studies of adult ADHD [27-29] and shown to be both reliable

and valid. Confirmation of the developmental history and childhood occurrence

of ADHD symptoms was obtained from the parents or, when unavailable, an older

sibling of the patient. In addition, the Dutch versions of the ADHD-DSM-IV Rating

Scales [30] were completed by patient, spouse, parent, and investigator to gather

information on the exact DSM-IV criteria for ADHD in childhood and adulthood.

The following was required to be the case for assignment of a full diagnosis of

adult ADHD: (1) at least 6 of the 9 DSM-IV criteria for inattention and/or

hyperactivity/impulsivity had to be met for diagnosis of childhood ADHD and at

least 5 of the 9 criteria for diagnosis of adult ADHD; (2) a chronic course of persistent

ADHD symptoms from childhood to adulthood had to be reported; and (3) a

moderate to severe level of impairment that can be attributed to the symptoms of

ADHD had to be experienced. The cut-off point of 5 out of the 9 criteria for diagnosis

of adult ADHD is based upon the literature and epidemiological data using the

same DSM-IV ADHD Rating Scale [28,31,32].


(SCID-II) was used to determine the presence of BPD [33]. A BPD diagnosis was only

given when no Axis I syndrome (i.e., clinical disorder) could account for the

patient’s complaints or dysfunctioning. Axis-I comorbidity was assessed using the

Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I) [33].

The Dutch version of Cloninger’s Temperament and Character Inventory (TCI)

was used to measure the temperament and character dimensions of personality.

The TCI has been shown to have good psychometric qualities on the basis of 1034

healthy individuals from the general population [35,36].

Statistical analysesIn previous work [8], latent class analysis (LCA) [7] was used to identify mutually

exclusive classes of ADHD and BPD patients with homogeneous symptom profiles.

Using Mplus version 4.1 [37], BPD symptoms in addition to childhood and adulthood

symptoms of ADHD were used to create symptom profiles for these periods. In the

present work, the scores of the patients on the TCI scales and subscales were

compared across the four latent classes of patients with adult diagnoses of ADHD

or BPD and homogeneous symptom profiles. The raw TCI subscale scores were

converted into gender corrected T-values using the Dutch/Flemish population

norms [36]. Given that part of the data was not normally distributed — as indicated

by Detrended Normal Q-Q plots and the Shapiro-Wilks test — the non-parametric



78

CHAPTER 4

Mann-Whitney U rank sum test for independent samples was adopted. The T-values

for the temperament and character dimensions of personality were compared to

an expected population mean of 50 (SD=10). All tests were two-tailed and the

p-value was set at .05. These calculations were done using SPSS (version 16.0).

Results

In Figure 1, an overview of the occurrence of adult ADHD and BPD symptoms for

the latent classes of patients is presented. Class 1(29/103 = 28%) shows ADHD

symptoms but no symptoms of BPD. The other three latent classes show BPD

symptoms in addition to symptoms of ADHD. Class 2 (20/103 = 19%) shows high

levels of BPD symptoms and moderate to high levels for the hyperactivity symptoms

of ADHD. Class 3 (32/103 = 31%) shows high levels of BPD symptoms and high levels

of symptoms for the inattention, hyperactivity, and impulsivity aspects of ADHD

(i.e., all aspects). Class 4 (22/103 = 21%) shows high levels of BPD symptoms and high

Figure 1 Latent class probabilities of adulthood ADHD and BPD symptoms in 103 female patients with ADHD, BPD, or both

0

10

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80

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Class 1 (n=29) Class 2 (n=20) Class 3 (n=32) Class 4 (n=22)



79


4

levels for the inattention and hyperactivity aspects of ADHD. In Figure 2, the TCI

profiles for the four latent classes of patients are presented. The scores are

T-corrected means with 50 thus representing the expected population mean.

When the corrected TCI temperament scores for the latent classes of patients were

compared to the expected norm and across the different classes (Table 1), Novelty

Seeking showed significantly higher scores for classes 1, 3, and 4 relative to the

norm population. Only class 2, which was composed of patients with symptoms of

BPD and only symptoms of ADHD hyperactivity, produced average Novelty Seeking

scores when compared to the norm. Comparison of the latent classes of patients

showed Novelty Seeking in class 3, which involved high levels of both BPD and

ADHD symptoms in all areas, to be highest and significantly different from

Novelty Seeking in the other latent classes. The subscales of Novelty Seeking show

Figure 2 Temperament and Character Inventory profile in female adult classes of ADHD and BPD symptoms

Scores are given as T-corrected means. NS indicates Novelty Seeking; HA, Harm Avoidance; RD, Reward

Dependence; P, persistence; SD, Self-directedness; CO, Cooperativeness; ST, Self-Transcendence. Class 1:

ADHD inattention, hyperactivity, and impulsivity symptoms; class 2: BPD symptoms + ADHD hyperactivity

symptoms; class 3: BPD symptoms + ADHD inattention, hyperactivity, and impulsivity symptoms; class 4:

BPD symptoms + ADHD inattention and hyperactivity symptoms.

75

70

65

60

55

50

45

40

35

30

25NS HA RD P SD CO ST

T-sc

ore

Temperament & Character scales

Class 1 : 28,2%

Class 2 : 19,4%

Class 3 : 31,1%

Class 4 : 21,4%



80

CHAPTER 4

Tab

le 1

T-c

orre

cted

mea

ns

(an

d S

D) f

or t

emp

eram

ent

and

ch

arac

ter

dim

ensi

ons

of p

erso

nal

ity

in l

aten

t cl

asse

s of

10

3 fe

mal

e p

atie

nts

wit

h A

DH

D, B

PD, o

r b

oth

Cla

ss 1

(n

= 2

9)C

lass

2

(n =

20)

Cla

ss 3

(n

= 3

2)C

lass

4

(n =

22)

1 vs

21

vs 3

1 vs

42

vs 3

2 vs

43

vs 4

Mea

n (S

D)

Mea

n (S

D)

Mea

n (S

D)

Mea

n (S

D)

P

Nov

elty

See

kin

g60

(9.5

)a 5

5.7

(10.

9)

66.7

(7.5

)a59

.7 (1

1)a

NS

.005

NS

<.00

1N

S.0

18

Exp

lora

tory

exc

itab

ilit

y55

.3 (1

0.7)

48.3

(11.

4)51

.9 (9

.6)

47.8

(7.7

).0

39N

S.0

05N

SN

SN

S

Imp

uls

iven

ess

57.4

(10.

7)a

53.0

(11.

2)65

.3 (6

.0) a

59.1

(8.3

) aN

S.0

04N

S<.

001

NS

.005

Extr

avag

ance

57.0

(8.6

) a54

.2 (9

.5)

59.7

(9.9

) a59

.8 (9

.6) a

NS

NS

NS

.017

.030

NS

Dis

ord

erli

nes

s55

.4 (8

.5)b

60.3

(8.6

) a66

.1 (9

.6) a

58.1

(12.

4) a

NS

<.00

1N

S.0

29N

S.0

14

Har

m A

void

ance

54.4

(10.

9)59

.2 (1

1.9)

b61

.9 (9

.1) a

64.7

(5.1

) aN

S.0

09.0

01N

SN

SN

S

An

tici

pat

ory

wor

ry54

.6 (1

1.6)

57.6

(10.

3) b

63.1

(9.3

) a63

.1 (7

.5) a

NS

.003

.009

NS

NS

NS

Fear

of

un

cert

ain

ty49

.9 (1

2.2)

53.2

(12.

9)50

.2 (1

1)52

.7 (8

.6)

NS

NS

NS

NS

NS

NS

Shyn

ess

50.5

(7.3

)56

.3 (8

.1) b

55.6

(7.5

) a56

.9 (6

.3) a

.012

.011

.002

NS

NS

NS

Fati

gabi

lity

an

d a

sth

enia

57.4

(12.

5) b

59.2

(11.

8) b

64.7

(9.1

) a69

.3 (6

.3) a

NS

.022

<.00

1N

S.0

03.0

39

Rew

ard

Dep

end

ence

52.3

(9.8

)44

.6 (9

.4)

44.2

(10.

8) b

47.4

(8.8

).0

1.0

04.0

47N

SN

SN

S

Sen

tim

enta

lity

49.2

(9.5

)45

.0 (8

.6)

45.1

(10.

6)50

.4 (7

.8)

NS

NS

NS

NS

NS

NS

Att

ach

men

t53

.2 (9

.6)

46.2

(12.

9)47

.9 (1

0.7)

45.9

(10.

5)N

SN

S.0

29N

SN

SN

S

Dep

end

ence

53.2

(9.5

)49

.2 (9

.2)

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ss 1

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nat

ten

tion

, h

yper

acti

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, an

d i

mp

uls

ivit

y sy

mp

tom

s; c

lass

2:

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sym

pto

ms

+ A

DH

D h

yper

acti

vity

sym

pto

ms;

cla

ss 3

: B

PD s

ymp

tom

s +

AD

HD

inat

ten

tion

, hyp

erac

tivi

ty, a

nd

im

pu

lsiv

ity

sym

pto

ms;

cla

ss 4

: BPD

sym

pto

ms

+ A

DH

D i

nat

ten

tion

an

d h

yper

acti

vity

sym

pto

ms.

Man

n-W

hit

ney

U r

ank

sum

tes

t fo

r

ind

epen

den

t sa

mp

les

was

ad

opte

d f

or c

omp

aris

on o

f te

mp

eram

ent

and

ch

arac

ter

scal

es b

etw

een

late

nt

clas

ses.

α w

as s

et a

t .0

5.a D

iffe

ren

ce w

ith

nor

m g

rou

p (T

-cor

rect

ed m

ean

± S

D, 5

0 ±

10) i

s si

gnifi

can

t at

th

e .0

01 le

vel (

2-t

aile

d).

b Dif

fere

nce

wit

h n

orm

gro

up

(T-c

orre

cted

mea

n ±

SD

, 50

± 10

) is

sign

ifica

nt

at t

he

.01

leve

l (2

-tai

led)

.



81


4

Tab

le 1

T-c

orre

cted

mea

ns

(an

d S

D) f

or t

emp

eram

ent

and

ch

arac

ter

dim

ensi

ons

of p

erso

nal

ity

in l

aten

t cl

asse

s of

10

3 fe

mal

e p

atie

nts

wit

h A

DH

D, B

PD, o

r b

oth

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ss 1

(n

= 2

9)C

lass

2

(n =

20)

Cla

ss 3

(n

= 3

2)C

lass

4

(n =

22)

1 vs

21

vs 3

1 vs

42

vs 3

2 vs

43

vs 4

Mea

n (S

D)

Mea

n (S

D)

Mea

n (S

D)

Mea

n (S

D)

P

Nov

elty

See

kin

g60

(9.5

)a 5

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(10.

9)

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1)a

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S.0

18

Exp

lora

tory

exc

itab

ilit

y55

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4)51

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).0

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SN

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S

Imp

uls

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ess

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001

NS

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Extr

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60.3

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14

Har

m A

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An

tici

pat

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ry54

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63.1

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NS

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Fear

of

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cert

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ty49

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53.2

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NS

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50.5

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55.6

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.011

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gabi

lity

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d a

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57.4

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64.7

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39

Rew

ard

Dep

end

ence

52.3

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Sen

tim

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lity

49.2

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6)50

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NS

NS

NS

NS

NS

Att

ach

men

t53

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46.2

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9)47

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45.9

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5)N

SN

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SN

SN

S

Dep

end

ence

53.2

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44.9

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S

Pers

iste

nce

51.9

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51.3

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49.9

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S

Self

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44 (1

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b33

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a28

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Res

pon

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48.4

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Purp

osef

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43.7

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NS

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44.8

(9.3

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a32

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a35

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001

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NS

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gru

ent

seco

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nat

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46.8

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al a

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pfu

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54.2

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rted

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s53

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Self

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46.4

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53.6

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S

Tran

sper

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al id

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fica

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45.2

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SN

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ss 1

: A

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D i

nat

ten

tion

, h

yper

acti

vity

, an

d i

mp

uls

ivit

y sy

mp

tom

s; c

lass

2:

BPD

sym

pto

ms

+ A

DH

D h

yper

acti

vity

sym

pto

ms;

cla

ss 3

: B

PD s

ymp

tom

s +

AD

HD

inat

ten

tion

, hyp

erac

tivi

ty, a

nd

im

pu

lsiv

ity

sym

pto

ms;

cla

ss 4

: BPD

sym

pto

ms

+ A

DH

D i

nat

ten

tion

an

d h

yper

acti

vity

sym

pto

ms.

Man

n-W

hit

ney

U r

ank

sum

tes

t fo

r

ind

epen

den

t sa

mp

les

was

ad

opte

d f

or c

omp

aris

on o

f te

mp

eram

ent

and

ch

arac

ter

scal

es b

etw

een

late

nt

clas

ses.

α w

as s

et a

t .0

5.a D

iffe

ren

ce w

ith

nor

m g

rou

p (T

-cor

rect

ed m

ean

± S

D, 5

0 ±

10) i

s si

gnifi

can

t at

th

e .0

01 le

vel (

2-t

aile

d).

b Dif

fere

nce

wit

h n

orm

gro

up

(T-c

orre

cted

mea

n ±

SD

, 50

± 10

) is

sign

ifica

nt

at t

he

.01

leve

l (2

-tai

led)

.



82

CHAPTER 4

this difference to be mainly due to the high scores on Impulsivity and Disorderliness

for class 3. In line with the total Novelty Seeking score on which class 2 scored

average compared to the norm, class 2 also scored average on Impulsivity and

Extravagance but above average on Disorderliness.

Significantly higher scores relative to the norm population were also found

for Harm Avoidance for classes 2, 3, and 4; class 1, which involved only symptoms

of ADHD hyperactivity, was an exception. Comparison of the latent classes of

patients showed Harm Avoidance to be highest in the latent classes with high

levels of BPD symptoms together with high levels of symptoms in all areas of

ADHD (class 3) and together with high levels of ADHD symptoms in the areas of

Inattention and Hyperactivity (class 4). The subscales of Harm Avoidance showed a

similar pattern: classes 2, 3 and 4 showed scores significantly above the normal

range with classes 3 and 4 also in particular with respect to class 1.

For the Reward Dependence aspect of temperament, a significantly lower score

than normal was found for class 3. Comparison of the latent classes showed Reward

Dependence to be significantly lower in classes 2, 3 and 4, which have the most

symptoms of ADHD in conjunction with BPD, than in class 1 with only symptoms

of ADHD. The RD subscales showed scores equal to the norm for all classes

Comparison of the classes revealed differences between classes 1 and 3 and classes

1 and 4 on the Attachment and Dependence subscales; class 1 scored significantly

higher on these subscales. All four of the latent classes showed normal scores for

the Persistence aspect of temperament.

With regard to the character dimensions of personality, significantly lower

Self-Directedness scores relative to the norm were found in all of the latent classes.

Comparison of the latent classes themselves showed the scores in class 1 with only

symptoms of ADHD to be significantly higher than the scores in the other three

classes, which all involve symptoms of both BPD and ADHD. The same pattern was

found for all 5 subscales of Self Directedness.

For Cooperativeness, significantly higher scores were found relative to the

norm for all of the latent classes with the exception of class 1 (i.e., the class with

only symptoms of ADHD). Comparison of the latent classes themselves showed

classes 2, 3, and 4 to not differ significantly from each other but to have significantly

higher Cooperativeness scores than class 1. The Cooperativeness subscales show a

similar pattern with the class 1 scores in the normal range and the scores for the

other classes below the normal range. The scores for the Self-Transcendence aspect

of character were average for all of the latent classes.

Overall, the present results show a high Novelty Seeking temperament in all

of the latent classes with the exception of that class with mostly BPD symptoms

(i.e., class 2). The highest Novelty Seeking temperament scores were found in that

class of patients with both symptoms of BPD and symptoms in all areas of ADHD



83


4

(i.e., class 3). The class of patients with only ADHD symptoms (i.e., class 1) scored

normal on Harm Avoidance while the other three classes of patients with BPD

symptoms in addition to symptoms of ADHD scored significantly higher than

normal on Harm Avoidance. With regard to the character dimensions of personality,

scores that were particularly lower than normal were found for Self-Directedness

and Cooperativeness in those classes of patients with BPD symptoms.

Discussion

In the present research, the TCI results for previously identified latent classes of

patients with similar ADHD and BPD symptom profiles were examined to identify

shared and unique personality characteristics. This was done to also gain greater

insight into the possible pathways from early temperament, in particular, to

future ADHD and/or BPD outcome. Specifically, we expected high scores on Novelty

Seeking for all classes of patients and perhaps even higher scores for those patients

with symptoms of both ADHD and BPD (i.e., classes 2, 3, and 4). We also expected

particularly high Harm Avoidance and low Cooperativeness for the class of patients

with mostly BPD symptomatology (i.e., class 2).

With the exception of the class of patients with mostly symptoms of BPD and

only ADHD symptoms of hyperactivity (i.e., class 2 patients), all of the patients

scored significantly above average on Novelty Seeking. Contrary to most previous

studies that associate a high Novelty Seeking temperament with BPD, it can

therefore be suggested that an above-average Novelty Seeking temperament is

most strongly linked to ADHD and less strongly linked to BPD. When the scores on

the subscales of Novelty Seeking were analyzed, we also found the patients in class

2 to show average scores on Impulsivity and Extravagance but above average scores

on Disorderliness, which indicates quick temperedness.

The highest Novelty Seeking scores were found for the class of patients with

symptoms of BPD and symptoms in all areas of ADHD (i.e., class 3 patients). These

patients not only scored highest compared to the expected population mean but

also compared to the other latent classes of patients. The question, thus, is why the

patients with the least ADHD symptoms (i.e., class 2) show only average scores for

Novelty Seeking (i.e., Impulsivity) while the highest Novelty Seeking scores are

found for those patients with the most symptoms of ADHD in combination with

symptoms of BPD (i.e., class 3). Regarding the first part of this question, we would

like to point out that the class 2 of patients was characterized by an absence of

problems in the ADHD area of inattention while inattention scores (i.e., this aspect

of ADHD) and Novelty Seeking scores (i.e., this aspect of temperament) were found

to be related for the other classes of patients. A temperament tendency towards



84

CHAPTER 4

impulsivity in response to novel stimuli (i.e., high Novelty Seeking) may thus be

strongly influenced by inattention problems. Regarding the second part of the

question, it is conceivable that a temperament predisposition for very high Novelty

Seeking can lead to the development of BPD in addition to ADHD. Having an

outspoken Novelty Seeking temperament and thus a predisposition to actively

respond to novel stimuli may well foster risky behavior on the part of the

individual, and this may — in turn — alter the course of the individual’s personality

development and thereby lead to the development of BPD at times. That is, insight

into the Novelty Seeking dimension of personality can shed light upon the relation

between ADHD and BPD as comorbid disorders.

As expected, we found the patients with BPD symptoms (i.e., those in classes

2,3, and 4) to score significantly higher than normal on Harm Avoidance with no

differences between these classes whereas those patients with only symptoms of

ADHD scored within the normal range. This finding appears to contradict previous

work in which ADHD was found to be associated with high Harm Avoidance [23-25]

but, as already mentioned, previous research may have been biased because there

was no control for comorbid personality disorders like BPD. We suspect that high

Harm Avoidance may be specifically linked to BPD, as demonstrated in previous

studies, but not to ADHD. And the present data suggests that ADHD patients

without symptoms of BPD are indeed less predisposed to be nervous, tense, and

insecure than ADHD patients with symptoms of BPD. That is, the present findings

are perfectly in line with the characterization of BPD in terms of emotional

instability.

Finally, the patients with symptoms of ADHD but no symptoms of BPD scored

significantly higher on the character dimensions Self-Directedness and Coopera-

tiveness than the other patients and, in fact, showed normal character development.

All of the patients with symptoms of BPD, in contrast, showed Self-Directedness

and Cooperativeness scores that point in the direction of deviant character

development. These results confirm Cloninger’s assumption that low scores on the

character scales of his inventory indicate a personality disorder. They are also in

line with other evidence showing low Self-Directedness and Cooperativeness

scores to be associated with BPD [19-22]. While ADHD thus relates to temperament

and thereby personality, it should not be conceptualized as a personality disorder.

This is an important finding with clear clinical implications. Using the TCI, it is

possible to differentiate ADHD accompanied by a mature character versus ADHD

accompanied by a personality disorder. It goes without saying that such

information is important for the indication and outcome of treatment.

A limitation in the present research is that a relatively small sample of only

female subjects was used. The sample was acceptable for LCA but limited to female

ADHD and BPD populations. The research should thus be extended and replicated



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4

with larger and more varied samples. A definite strength of the present study is

nevertheless that it used a well-defined and carefully diagnosed sample; clinical

interviews with a number of parties and not just patient self-reports were also

employed.

To summarize, the female patients with similar patterns of ADHD and BPD

symptoms (i.e. the four classes) in the present study showed different temperament

and character traits. It is therefore suggested that the temperament trait of high

Novelty Seeking is linked to ADHD and, more specifically, to the inattention

domain of ADHD while the temperament trait of high Harm Avoidance and the

character traits of low Self-Directedness and low Cooperativeness appear to be

linked to BPD. An outspoken Novelty Seeking temperament may nevertheless

predispose the individual to develop a comorbid BPD although this is only part of

a more complicated picture.

Novelty Seeking — perhaps in combination with Harm Avoidance — may well

play a role in the etiology of BPD but, as for most mental disorders, no single factor

can explain the emergence and development of BPD. Multiple risk factors,

biological, psychological, and social, play a role in the etiology of mental disorders

and certainly BPD [38]. It is well-known, for example, that sexual and physical

abuse can contribute to the occurrence of borderline symptoms and that such

abuse often occurs within the context of a disturbed family environment [39,40].

However, the co-occurrence of these factors makes it difficult to distinguish the

effects of the abuse from the effects of the family environment. The personality

characteristics of parents may also contribute genetically, environmentally, and

interactively to the development of personality pathology. In future research, all

of these factors must be taken into consideration in order to better understand the

role of early differences in personality in the shaping of adult personality and the

occurrence of such psychiatric disorders as ADHD and BPD. In the present study,

the focus was on the biological factor of personality (i.e. temperament) and a valid

manner of exploring the co-occurrence of ADHD and BPD in adulthood was shown

to help us to map the heterogeneous course of these overlapping syndromes.

AcknowledgmentsRose Collard, research nurse, Marjan Knippenberg, MSc, and Marleen Bastiaanse,

MSc, are gratefully acknowledged for their expert research assistance. Pieter van

de Broek is gratefully acknowledged for his close collaboration on the data

collection.



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References

[1] Andrulonis PA, Glueck BC, Stroebel CF, Vogel NG, Shapiro AL, Aldridge DM. Organic brain dysfunction

and the borderline syndrome. Psychiatr Clin North Am 1981 Apr;4(1):47-66.

[2] Andrulonis PA, Glueck BC, Stroebel CF, Vogel NG. Borderline personality subcategories. J Nerv Ment

Dis 1982 Nov;170(11):670-9.

[3] Dowson JH, McLean A, Bazanis E, Toone B, Young S, Robbins TW, et al. The specificity of clinical char-

acteristics in adults with attention-deficit/hyperactivity disorder: a comparison with patients with

borderline personality disorder. Eur Psychiatry 2004 Apr;19(2):72-8.

[4] Fossati A, Novella L, Donati D, Donini M, Maffei C. History of childhood attention deficit/hyperactivity

disorder symptoms and borderline personality disorder: a controlled study. Compr Psychiatry 2002

Sep;43(5):369-77.

[5] Philipsen A, Limberger MF, Lieb K, Feige B, Kleindienst N, Ebner-Priemer U, et al. Attention-deficit

hyperactivity disorder as a potentially aggravating factor in borderline personality disorder. Br J

Psychiatry 2008 Feb;192(2):118-23.

[6] Rey JM, Morris-Yates A, Singh M, Andrews G, Stewart GW. Continuities between psychiatric disorders

in adolescents and personality disorders in young adults. Am J Psychiatry 1995 Jun;152(6):895-900.

[7] McCutcheon A.L. Latent Class Analysis. Newbury Park: CA: Sage; 1987.

[8] Van Dijk FE, Lappenschaar GAM, Kan CC, Van den Broek PJ, Verkes R.J., Buitelaar JK. Lifespan

attention deficit/hyperactivity disorder and borderline personality disorder symptoms in female

patients: a latent class approach. Under Review 2011.

[9] White JD. Personality, temperament, and ADHD: a review of the literature. Personality and Individual

Differences 1999;27:589-98.

[10] Martel MM, Nigg JT, von EA. How do trait dimensions map onto ADHD symptom domains? J Abnorm

Child Psychol 2009 Apr;37(3):337-48.

[11] Nigg JT. Temperament and developmental psychopathology. J Child Psychol Psychiatry 2006

Mar;47(3-4):395-422.

[12] Sonuga-Barke EJ. Causal models of attention-deficit/hyperactivity disorder: from common simple

deficits to multiple developmental pathways. Biol Psychiatry 2005 Jun 1;57(11):1231-8.

[13] Cloninger CR, Svrakic DM, Przybeck TR. A psychobiological model of temperament and character.

Arch Gen Psychiatry 1993 Dec;50(12):975-90.

[14] Cloninger CR. A systematic method for clinical description and classification of personality variants.

A proposal. Arch Gen Psychiatry 1987 Jun;44(6):573-88.

[15] Cloninger CR. A systematic method for clinical description and classification of personality variants.

A proposal. Arch Gen Psychiatry 1987 Jun;44(6):573-88.

[16] Cloninger CR, Svrakic DM, Przybeck TR. A psychobiological model of temperament and character.

Arch Gen Psychiatry 1993 Dec;50(12):975-90.

[17] Cloninger CR. A practical way to diagnosis personality disorder: a proposal. J Personal Disord

2000;14(2):99-108.

[18] Svrakic DM, Whitehead C, Przybeck TR, Cloninger CR. Differential diagnosis of personality disorders

by the seven-factor model of temperament and character. Arch Gen Psychiatry 1993 Dec;50(12):991-9.

[19] de la Rie SM, Duijsens IJ, Cloninger CR. Temperament, character, and personality disorders. J Pers

Disord 1998;12(4):362-72.

[20] Svrakic DM, Whitehead C, Przybeck TR, Cloninger CR. Differential diagnosis of personality disorders

by the seven-factor model of temperament and character. Arch Gen Psychiatry 1993 Dec;50(12):991-9.

[21] Fossati A, Donati D, Donini M, Novella L, Bagnato M, Maffei C. Temperament, character, and

attachment patterns in borderline personality disorder. J Pers Disord 2001 Oct;15(5):390-402.

[22] Barnow S, Herpertz SC, Spitzer C, Stopsack M, Preuss UW, Grabe HJ, Kessler C, Freyberger HJ.

Temperament and character in patients with borderline personality disorder taking gender and

comorbidity into account. Psychopathology 2007;40:369- 379.

[23] Downey KK, Stelson FW, Pomerleau OF, Giordani B. Adult attention deficit hyperactivity disorder:

psychological test profiles in a clinical population. J Nerv Ment Dis 1997 Jan;185(1):32-8.



87


4

[24] Lynn DE, Lubke G, Yang M, McCracken JT, McGough JJ, Ishii J, et al. Temperament and character

profiles and the dopamine D4 receptor gene in ADHD. Am J Psychiatry 2005 May;162(5):906-13.

[25] Anckarsater H, Stahlberg O, Larson T, Hakansson C, Jutblad SB, Niklasson L, et al. The impact of

ADHD and autism spectrum disorders on temperament, character, and personality development.

Am J Psychiatry 2006 Jul;163(7):1239-44.

[26] Kooij JJS. ADHD bij volwassenen. Inleiding in diagnostiek en behandeling. Lisse: Swets & Zeitlinger;

2002.

[27] Kooij JJ, Aeckerlin LP, Buitelaar JK. [Functioning, comorbidity and treatment of 141 adults with

attention deficit hyperactivity disorder (ADHD) at a psychiatric outpatient department. Ned Tijdschr

Geneeskd 2001 Aug 4;145(31):1498-501.

[28] Kooij JJ, Buitelaar JK, van den Oord EJ, Furer JW, Rijnders CA, Hodiamont PP. Internal and external

validity of attention-deficit hyperactivity disorder in a population- based sample of adults. Psychol

Med 2005 Jun;35(6):817-27.

[29] Kooij JS, Boonstra AM, Vermeulen SH, Heister AG, Burger H, Buitelaar JK, et al. Response to methyl-

phenidate in adults with ADHD is associated with a polymorphism in SLC6A3 (DAT1). Am J Med

Genet B Neuropsychiatr Genet 2007 Oct 22.

[30] DuPaul GJ, Power TJ, Anastopoulos AD, Reid R. ADHD Rating Scale-IV. Checklists, Norms and Clinical

Interpretation. New York: The Guilford press; 1998.

[31] Murphy K, Barkley RA. Prevalence of DSM-IV symptoms of ADHD in adult licensed drivers:

Implications for clinical diagnosis. Journal of Attention Disorders 1996;1(3):147-61.

[32] Biederman J, Mick E, Faraone SV. Age-dependent decline of symptoms of attention deficit hyperactivity

disorder: impact of remission definition and symptom type. Am J Psychiatry 2000 May;157(5):816-8.

[33] Weertman A, Arntz A, Kerkhofs MLM. Structured Clinical Interview for DSM-IV Axis II Personality

Disorders. Lisse, the Netherlands: Swets & Zeitlinger BV; 2000.

[34] Groenestijn MAC, Akkerhuis GW, Kupka RW, Schneider N, Nolen WA. Structured Clinical Interview

for DSM-IV Axis I Disorders. Lisse, the Netherlands: Swets & Zeitlinger BV; 1999.

[35] Cloninger CR. A practical way to diagnosis personality disorder: a proposal. J Personal Disord

2000;14(2):99-108.

[36] Duijsens IJ, Spinhoven Ph. Handleiding van de Nederlandse Temperament en Karakter Vragenlijst.

Leiderdorp: Datec; 2000.

[37] Muthén LK, Muthén BO. Mplus user’s guide. Statistical analysis with latent variables (4th ed.; version

4.1). Los Angeles: Muthén & Muthén; 2006.

[38] Paris J. Borderline personality disorder. CMAJ 2005 Jun 7;172(12):1579-83.

[39] Bandelow B, Krause J, Wedekind D, Broocks A, Hajak G, Ruther E. Early traumatic life events, parental

attitudes, family history, and birth risk factors in patients with borderline personality disorder and

healthy controls. Psychiatry Res 2005 Apr 15;134(2):169-79.

[40] Bradley R, Jenei J, Westen D. Etiology of borderline personality disorder: disentangling the

contributions of intercorrelated antecedents. J Nerv Ment Dis 2005 Jan;193(1):24-31.



Published as:

Van Dijk FE, Schellekens AFA, Van den Broek P, Kan CC, Verkes RJ & Buitelaar JK. (2014)

Do cognitive measures of response inhibition differentiate between

Attention Deficit/Hyperactivity Disorder and Borderline Personality Disorder?

Psychiatry Research, 215(3):733-9.

Do cognitive measures of response inhibition differentiate between

attention deficit/hyperactivity disorder and borderline personality disorder?

5



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Abstract

This study examined whether cognitive measures of response inhibition derived

from the AX-CPT are able to differentiate between adult attention deficit/hyper -

activity disorder (ADHD), borderline personality disorder (BPD), and healthy

controls (HC). Current DSM-IV-TR symptoms of ADHD and BPD were assessed by

structured diagnostic interviews, and parent developmental interviews were used

to assess childhood ADHD symptoms. Patients (14 ADHD, 12 BPD, 7 ADHD and BPD,

and 37 HC) performed the AXCPT. Seventy percent of AX-CPT trials were target

(AX) trials, creating a bias to respond with a target response to X probes in the

nontarget (AY, BX, BY) trials. On BX trials, context, i.e. the non-‘A’ letter, must be

used to inhibit this prepotent response tendency. On AY trials context actually

causes individuals to false alarm. The effects of ADHD and BPD on AX-CPT outcome

were tested using two-way ANOVA. BPD was associated with higher percentage of

errors across the task and more errors and slower responses on BX trials, whereas

ADHD was associated with slower responses on AY trials. The findings suggest

response inhibition problems to be present in both ADHD and BPD, and patients

with BPD to be particularly impaired due to poor context processing.



91

RESPONSE INHIBITION IN ADHD AND BPD

5

Introduction

Previous research has shown significant co-occurrence of DSMIV-TR defined

borderline personality disorder (BPD) and attention deficit hyperactivity disorder

(ADHD) in adults with the use of self-report questionnaires or structured psychiatric

interviews. Up to 60% of BPD patients met criteria for ADHD in childhood and up

to 38% of BPD patients showed a co-occurring adult ADHD diagnosis. Impulsivity

symptoms and traits are important overlapping features (Andrulonis et al., 1981,

1982; Rey et al., 1995; Fossati et al., 2002; Dowson et al., 2004a; Philipsen et al., 2008;

Ferrer et al., 2010; van Dijk et al., 2011, 2012). This behavioral overlap influences

diagnostic outcome and indications for treatment. It is therefore important to

clarify whether the shared symptoms are pointing to the same underlying

cognitive processes or whether BPD and ADHD can be differentiated at the level

of cognitive processes.

It is suggested that impulsive behavior, broadly defined as the tendency to act

prematurely without foresight, is not a unitary construct, but rather consists of

several independent dimensions involving various forms of impaired cognitive

control. Impulsivity could incorporate behavior that has not adequately sampled

sensory evidence (“reflection impulsivity”), a failure of motor or response inhibition

(“impulsive action”), a tendency to accept small immediate or likely rewards versus

large delayed or unlikely ones (“impulsive choice”) and risky behavior, in the

context of decision making (Evenden, 1999).

Reviews (Woods et al., 2002; Hervey et al., 2004; Seidman et al., 2004; Boonstra

et al., 2005; Schoechlin and Engel, 2005) and several more recent single studies

(Fischer et al., 2005; Nigg et al., 2005b; Faraone et al., 2006; Biederman et al., 2007;

Stavro et al., 2007; Boonstra et al., 2010) are clear in showing that adults with

ADHD have deficits in executive functioning in general and response inhibition

(i.e. the behavioral phenomena of “impulsive action”) in particular. In fact,

inhibitory dysfunction is regarded as underpinning one of a number of dissociable

and different pathways to ADHD (Nigg et al., 2005c; Sonuga-Barke et al., 2010).

However, it remains unclear if inhibition deficiencies are specific for ADHD,

especially with regard to BPD. Non-ADHD clinical control groups with mood and

anxiety disorders appeared to perform better on response inhibition tasks than

adults with ADHD (Barkley et al., 2001; Epstein et al., 2001; Murphy et al., 2001),

but patients with schizophrenia perform equally worse as patients with ADHD

(Ross et al., 2000).

The results of neuropsychological studies of patients with BPD are mixed but

mostly indicate that individuals with BPD also exhibit inhibitory dysfunction.

Problems with an impulsive response style with difficulty delaying, a preference

for immediate gratification, and impairments that reflect the inhibition of



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ongoing responses are frequently found in mostly female patients with BPD when

compared to healthy controls (Leyton et al., 2001; Bazanis et al., 2002; Dinn et al.,

2004; Nigg et al., 2005a; de Bruijn et al., 2006; Grootens et al., 2008b; Rentrop et al.,

2008; McCloskey et al., 2009; Volker et al., 2009; Lawrence et al., 2010).

Deficient inhibitory control in its broadest sense may thus underlie both

ADHD and BPD. However, it is currently unclear to what extent BPD is associated

with response inhibition problems independently of the frequently co-occurring

ADHD. To date, we found four studies comparing patients with ADHD and BPD

in terms of neuropsychological overlap and differences.

The first one, although not focusing on response inhibition in particular,

compared adults with ADHD, BPD and healthy controls (each group N¼19). No

significant group differences were found for spatial working memory and spatial

recognition memory, but the mean deliberation time for the decision-making task

was significantly longer in the BPD than in the other groups, and with a significant

difference between the BPD and ADHD group. The authors concluded that subjects

with ADHD and BPD may have dissociable patterns of neuropsychological

impairments (Dowson et al., 2004b).

Another study did focus on response inhibition in particular and measured

stop signal reaction times in 105 adults with ADHD (of whom 20% with co-occurring

BPD) and 90 controls (Nigg et al., 2005a). The results provided evidence that problems in

response inhibition are specific to BPD symptoms even when symptoms of other

personality disorders, lifetime depression, anxiety, and posttraumatic symptoms

are controlled for. However, this effect could still be due to the overlap of BPD and

ADHD symptoms. When ADHD symptoms were entered as a predictor, response

inhibition ceased to be significantly associated with BPD symptoms, probably due

to the high correlation of ADHD and BPD in the sample. The authors emphasize

the importance of clarifying whether BPD per se is related to problems of response

inhibition.

A third study compared four groups of participants (22 ADHD, 21 BPD, 20

ADHD with BPD and 20 Healthy Controls) on various inhibitory functions. ADHD

patients performed significantly worse on tasks that measure the ability to

interrupt an already ongoing response, but showed no significant deficits in the

capacity to suppress prepotent responses as tested with the error rate of a go/no go

test. In all inhibitory tasks, ADHD subjects showed generally longer RTs than

controls. Patients with ADHD and BPD did not differ significantly from those with

pure ADHD on any cognitive task and the BPD group achieved better results than

the ADHD group in most tasks. The authors conclude that impaired inhibition is a

core feature in adults with ADHD, but not in adults with BPD, and that ADHD and

BPD have no common attention or inhibitory deficits (Lampe et al., 2007).



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5

The most recent study explored the role of stress in different components of

impulsivity, including response inhibition, in four groups of participants (15 BPD,

15 BPD with ADHD, 15 ADHD and 15 healthy controls) (Krause-Utz et al., 2013). The

results showed impaired response inhibition as measured with the Immediate and

Delayed Memory Task (IMT/DMT) in patients with both BPD and ADHD, but not in

those with BPD but without ADHD.

In summary, these studies seem to contradict the probable shared response

inhibition problems between ADHD and BPD as well as the previous findings of

inhibitory dysfunction in BPD. Given these inconsistencies might be explained in

part by heterogeneity in the inclusion and exclusion criteria, the issue of response

inhibition in BPD and ADHD needs further investigation.

Continuous performance tasks (CPT’s) are among the most used tasks to assess

impulsive action. CPT’s are based on the paradigm that a global prepotency of

response is created that must occasionally be overridden by voluntary control

(Rosvold and Delgado, 1956). Research on this paradigm has been relatively

voluminous, in both the experimental and the clinical literature (Riccio and

Reynolds, 2001; Riccio et al., 2002). Several studies have associated ADHD with

impaired CPT performance but comparison with clinical samples is scarce (Woods

et al., 2002; Hervey et al., 2004). We found four studies reporting specifically on

CPT performance in BPD of which the results are ambiguous. One study showed

slightly but not significantly more errors in female BPD patients compared to

healthy controls but not to individuals with depression (Volker et al., 2009). Yet two

other studies found significantly more errors and more inattentiveness on the CPT

indices in patients with BPD compared with non-psychiatric controls (Rubio et al.,

2007; Ruocco et al., 2012). The most recent study investigated response inhibition

and working memory together with elementary cognitive processes in BPD

and healthy controls (Hagenhoff et al., 2013). As in other tasks, they found no

impairments of response inhibition in the AX-CPT results. Moreover they found

faster responses along with comparable accuracy, suggesting a superiority of faster

cognitive processing in BPD. Correctly, the authors mention that it has to be

investigated whether this alteration might shift into a disadvantage when task

characteristics favor impulsive responding. Also, faster motor reactions may be an

indication of response inhibition deficit (Conners, 2000).

In the present study we aim to examine whether cognitive measures of

response inhibition derived from an Expectancy AX version of the Continuous

Performance Task (AX-CPT) are able to differentiate between ADHD, BPD, and

healthy controls. An advantage of using the AX-CPT is that it takes into account

that response inhibition also depends on context processing, i.e. the representation,

maintenance and updating of context in prefrontal networks (Braver et al., 2009).

From this perspective, inhibition is the processing of task-relevant information to



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provide the top down support needed to allow secondary responses to compete

effectively with distracting information. In the AX-CPT task, contextual information,

conceptualized as any task relevant information that is internally represented, is

required to drive or inhibit responses to a target stimulus (Braver and Barch, 2002).

In the Expectancy AX-CPT, AX trials comprise a large portion (70%) of the overall

task which creates a strong expectancy and tendency toward responding with the

target button. Participants ability to inhibit this prepotent tendency is particularly

evident on the small portion (10%) of the remaining trials in which the cue letter

A is followed by a probe letter other than X (i.e. an AY trial). Errors occur if

participants respond when they are required to inhibit their response and high

error rate points to difficulties with response inhibition.

On another portion (10%) of the non-target trials, a cue letter other than A is

followed by the probe letter X (i.e. a BX trial). Note that on BX trials, the internal

representation of context should improve performance, by inhibiting an

inappropriate response bias. However, on AY trials, representation of context

should impair performance, by creating an inappropriate expectancy bias.

Thus, if context representations are intact, AY performance should be worse

than BX performance (both in errors and or RT). Conversely, if context representa-

tions are impaired, BX performance should be worse than AY performance.

Performance on AX target trials should also be poorer if context processing is

impaired, since determination of targets is dependent upon the context provided

by the cue. However, AX performance should not be as impaired as BX performance,

since on AX trials, the response bias works in subjects favor, by increasing the

tendency to make the correct target response. Finally, a third type of nontarget

trial, BY, provides a useful internal control, since in these trials the influence of

context on performance should be relatively small (given that both the cue and the

probe always map to a nontarget response) (Servan-Schreiber et al., 1996; Cohen et

al., 1999; Barch et al., 2004; Bodner et al., 2012). The expectancy variant of the AX

CPT paradigm has the potential to produce a double dissociation in performance:

individuals with a context-processing deficit would show impaired performance

on BX trials, whereas those with intact context-processing would perform worse

on AY trials (MacDonald, 2008).

We aim to examine whether cognitive measures of response inhibition derived

from an Expectancy AX version of the Continuous Performance Task (AX-CPT) are

able to differentiate between ADHD, BPD, and healthy controls. We anticipate

finding response inhibition problems in BPD independent of ADHD. Further, given

that BPD is a personality disorder encompassing deficits in social and emotional

functioning that are broader than just impulse control, we expect BPD to be

associated with problems in context processing.



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Method

SubjectsParticipants were consecutively recruited patients referred to the in- and

outpatient ADHD program or BPD program at the Department of Psychiatry of

the Radboud University Nijmegen Medical Centre, the population of the GGZ

Oost Brabant (sites Oss and Veghel) and Spatie Mental Health Centre (Apeldoorn) in

The Netherlands. The patients were recruited during a period of approximately

2 years and had to meet the DSM-IV criteria for ADHD or BPD to be included in the

study. Patients were excluded if they met DSM-IV-TR criteria for depressive disorder,

bipolar disorder, schizophrenia, schizoaffective disorder, schizophreniform disorder,

delusional disorder, other psychotic disorders, schizoid or schizotypal personality

disorder, (history of) alcohol- or substance dependence, and if they had first degree

relatives with DSM-IV axis I schizophrenia, or schizophreniform disorder. Patients

with a history of trauma capitis, visual and auditory disorders, neurological

disorders, and if they had first-degree relatives with any relevant neurological or

psychiatric disorders were also excluded. Diagnostic assessment was part of the

standard clinical diagnostic procedures.

The healthy volunteers were recruited by means of advertisements in local

newspapers. The volunteers had a negative history for psychiatric disorders and

were matched with the patient groups on sex, age and education. All subjects were

paid 10 euro per hour for their participation. The present study was conducted in

accordance with the declaration of Helsinki. Approval of this study was obtained

from the local ethics committee. All participants signed an informed consent

form prior to participation. A total of 78 subjects, aged 18 to 50, participated in the

study on the basis of informed consent and having been diagnosed according to

the DSM-IV-TR system with ADHD (N=19) or BPD (N=17), or being healthy controls

(HC) (N=42). All diagnoses were established after a systematic and comprehensive

psychiatric assessment had been performed. This included a psychiatric evaluation

and both structured and semi-structured diagnostic interviews, which were

conducted by trained psychologists or psychiatric trainees under the supervision

of a senior

psychiatrist.

The presence of ADHD symptoms in childhood and adulthood (i.e. current)

was assessed using a Semi-Structured Interview for ADHD (Kooij, 2002). This

interview has been used in previous studies of adult ADHD (Kooij et al., 2001, 2005)

and shown to be both reliable and valid. Confirmation of the developmental

history and childhood occurrence of ADHD symptoms was obtained from the

parents or, when unavailable, an older sibling of the patient. In addition, the Dutch

versions of the ADHD-DSM-IV Rating Scales (DuPaul et al., 1998) were completed by



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patient, spouse, parent, and investigator to gather information on the exact

DSM-IV criteria for ADHD in childhood and adulthood. The following was required

to be the case for assignment of a full diagnosis of adult ADHD: (1) at least 6 of the

9 DSM-IV criteria for inattention and/or hyperactivity/impulsivity had to be met

for diagnosis of childhood ADHD and at least 5 of the 9 criteria for diagnosis of

adult ADHD; (2) a chronic course of persistent ADHD symptoms from childhood to

adulthood had to be reported; and (3) a moderate to severe level of impairment

that can be attributed to the symptoms of ADHD had to be experienced. The cut-off

point of 5 out of the 9 criteria for diagnosis of adult ADHD is based upon the

literature and epidemiological data using the same DSM-IV ADHD Rating Scale

(Kooij et al., 2005) and in accordance with the current ADHD definition in DSM-5.


(SCID-II) was used to determine the presence of BPD (Weertman et al., 2000). A BPD

diagnosis was only given when no Axis I syndrome (i.e. clinical disorder) could

account for the patients complaints or dysfunctioning. Axis-I comorbidity was

assessed using the Structured Clinical Interview for DSM-IV Axis I Disorders

(SCIDI) (Groenestijn et al., 1999). Since we were especially interested in the differ-

entiation of the overlapping impulsivity symptoms in ADHD and BPD, we included

only those patients with impulsivity symptoms as specified in the DSM-IV for

ADHD (i.e. satisfying criteria for ADHD predominantly hyperactive/impulsive type

or ADHD combined type) and/or BPD (i.e. satisfying criterion 4 (impulsivity) of the

BPD section in the SCID-II). All patients had an estimated average or above average

intelligence based on clinical judgment and educational level. Educational level

was determined using a three level classification, (level 1: primary school or less,

level 2: secondary school, level 3: higher education or university) based on the

Dutch education system. Healthy controls were screened using the Dutch version

of the M.I.N.I. Plus structured interview (Sheehan et al., 1998) and ADHD self-report

rating scale.

Participants completed the neuropsychological testing after the instruction

not to use alcohol more than 3 units/day (one unit stands for the so called “standard

drink” in the Netherlands, which contains 12 ml or 10 g of alcohol) during the

week before the experimental measures, not to use alcohol within 24 h before

measurement, not to use cannabis or other illicit drugs within the week before

measurement, not to use any psychotropic medication, other than oxazepam,

during the 5 days before measurement, not to use oxazepam within 12 h before

measurement and not to smoke within 3 h before measurement. Patients using

methylphenidate were not allowed to use it on the day of the experiment.

Of the total sample of 78 participants, 8 participants (3 BPD and 5 HC) were

detected as obvious outliers far outside the 95% confidence interval. They made

systematically too many errors of all kind. We suspect either miscomprehension of



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the task or lack of motivation for the task. Unfortunately, we do not know the

actual cause of these outliers. We removed these cases in order to get the most

honest estimate of population parameters possible. The final sample consisted of

70 participants: 14 Patients with ADHD (mean age=41.9 years; male: female ratio 7:7),

12 patients with BPD (mean age=27.3 years; male: female ratio 0:12), 7 patients

with both ADHD and BPD (mean age=35 years; male: female ratio 3:4), and 37

healthy controls (mean age=31.1 years; male: female ratio 11:26). The small sample

size indicates that the present study should be considered as a pilot study.

AX-CPT taskAn Expectancy AX-CPT task (Fig. 1) was programmed in Delpi to run on an

WindowsXP system. Further, the program used “PerformanceCounter” with

which time differences smaller than microseconds can be measured and very

accurate inter-stimuli intervals can be produced. The measurements results of the

program are up to 1 ms precise because it synchronizes stimuli and reaction times

with the viewing screen and because the responses were measured with a special

button box that can pass on a change in the status of the buttons every millisecond.

As in typical AX-CPT tasks, participants were presented with cue probe pairs.

Single letters were consecutively shown in white on a black screen. Participants sat

in front of the response button box and were instructed to respond as quickly and

accurately as possible by giving a target response (press right button on the

button-box) after the probe ‘X’ in combination with the cue ‘A’, or a nontarget

response (press left) after any other combination of letters. Seventy percent were

target trials (Braver et al., 2001) (83 AX trials, 12 AY trials, 12 BX trials and 12 BY

trials). The letters were presented for 350 ms, with a 1200 ms interstimulus

interval. To increase task difficulty, two distracters letters were presented in red

between cue and probe. By increasing task difficulty the number of errors is

higher, and consequently the task could be shortened. This was done in order to

minimize the burden for the participants and increase their compliance to

complete the task correctly.

Following explanation of the task instructions, participants were administered

practice trials. During the practice trials all letter combinations were used.

Participants performed 10 trials. The trial session was repeated until the

participant understood the task and was able to perform the trial session with a

maximum of 1 mistake. Performance during the practice trials was closely

monitored by the examiner and if necessary additional prompting was given so to

ensure full understanding of the task before initiation of the 120 experimental

trials. Participants performed the AX-CPT for 10 min. Response time and error rate

(i.e. pressing the target button where this should have been the non-target button

or vice versa) were recorded.



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Statistical analysesFor each subject, mean reaction time (RT) and mean error rate (i.e. percentage of

pressing the target button where this should have been the non-target button or

vice versa) across all trial types were computed (Table 1). Moreover, data were

analyzed separately for the AY and BX trial types. A two way ANOVA (ADHD (two

levels)_BPD (two levels)) was used to examine the effects of disorder on these AX

CPT outcome measurements. F, p, and ηp² values are reported. Data were analyzed

using SPSS version 20. Alpha level was set at.05.

Results

Irrespective of the presence/absence of ADHD, there was a significant main effect

of BPD on overall error rate (F(1,66)=6.935, p=0.011, ηp²=0.064), BX error rate

(F(1,66)=5.288, p=0.025, ηp²=0.074), and RT on BX trials (F(1,66)=4075, p=0.048,

ηp²=0.058). There was one main effect of ADHD on RT on AY trials (F(1,66)=7485,

p=0.008, ηp²=0.102). There were no significant interaction effects found on our

main outcome measurements. However, post-hoc analyses of the AX error rate,

which was very high in the patients with BPD (Table 1), showed significant

interaction effects between ADHD and BPD (F(1,66)=4.518, p=0.037, ηp²=0.064).

Figure 1 AX-CPT task parameters and timing

A E C X A K S G

G K T X L D U T

AX AY

120 Trials: AX-70%, AY 10%, BX 10%, BY 10%.

Instruction: Your target responseis an ‘X’, but only when it follows an ‘A’. Response: press right button - target; press left button - nontarget.

Letters were presented for 350 msec with an 1200 msec interstimulus interval.

BX BY



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Discussion

Previous studies indicated behavioral overlap of impulsivity problems between

adult ADHD and BPD. Research focusing on the neurocognitive or neuropsychological

basis of this behavioral overlap is however scarce and contradictory and has not

convincingly established whether or not BPD is related to response inhibition

deficits independently of ADHD. In order to contribute to this question we

examined the effects of ADHD and BPD on AX-CPT outcome. In line with the

behavioral overlap of impulsivity symptoms, we hypothesized that both patients

groups would show impaired response inhibition. Further, we were interested in

whether performance on the specific BX and AY trial types of the AX-CPT is equally

problematic or could pinpoint to differences and a more specific interpretation of

response inhibition problems in our patient groups. In particular, we hypothesized

that BPD is associated with problems in context processing (i.e. reflected in

abnormal scores on BX trials).

The results showed that patients with BPD have the highest overall error rate

in comparison to the other groups. This difference is especially large in the AX

trials. Interestingly, statistical analysis showed that this effect interacts with

ADHD in a way that patients with both BPD and ADHD perform better than the

patients with only BPD. Patients with BPD also performed worse on the BX trials.

Table 1 AX-CPT performance of patients with ADHD, BPD, ADHD and BPD, and healthy controls

ADHD(N=14)

BPD(N=12)

ADHD+ BPD(N=7)

HC(N=37)

Overall Error-rate % (SD) 9.44 (8.66) 16.94 (13.89) 11.58 (9.81) 5.56 (6.83)

AX 9.08 (9.99) 18.91 (18.35) 9.8 (12.36) 4.74 (7.78)

AY 14.29 (14.41) 11.68 (10.51) 14.29 (11.5) 13.36 (13.3)

BX 16.78 (12.75) 20.32 (32.11) 29.77 (33.61) 7.81 (11.49)

BY 0 (0) 4.87 (12.54) 2.38 (6.3) 1.12 (2.89)

Mean RT msec (SD) 426,57 (93,15) 430.05 (132,79) 428.11 (135.36) 343.1 (56.54)

RT AX 419.19(106.67) 419.71 (141.99) 438.09 (142.82) 340.60 (49.93)

RT AY 549.91 (114.7) 447.74 (55.85) 509.32 (122.33) 455.75 (100.5)

RT BX 390.01(170.35) 512.58 (274.8) 396.95 (265.32) 302.63 (140.81)

RT BY 390.11 (133.5) 400.42 (190.74) 309.90 (134.90) 288.13 (95.12)

CPT, continuous performance task; ADHD, attention deficit/hyperactivity disorder; BPD, borderline

personality disorder; HC, healthy controls; RT, reaction time; values are given in means (S.D.).



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They made more errors and were significantly slower than the other participants.

Regarding the error rate we observed an additive effect of BPD and ADHD. Patients

with both disorders made more errors on the BX trials than patients with only

BPD. The ADHD patients showed significantly slow RTs on the AY trials, but this

did not result in a significantly worse error rate.

In sum, patients with BPD performed worse on the overall error rate, BX error

rate and BX RT. In contrast, patients with ADHD performed slow on the AY trials.

Thus, as predicted, both patient groups indeed showed deficiencies in response

inhibition, but these inhibition deficiencies seem more widespread and pervasive

in BPD than in ADHD. In fact, we found only one main effect for ADHD. Moreover,

BPD patients showed response inhibition problems independently of ADHD. The

adults with BPD were particular impaired on the AX and BX trials, whereas the

adults with ADHD seem to have needed significantly more time to perform

adequately on the AY trials.

This finding that patients with BPD performed significantly worse than

patients with ADHD on several indices is somewhat counterintuitive and not in

line with previous work that did not find convincing evidence of response

inhibition deficits in BPD. In fact, previous work reporting on AX-CPT outcome in

BPD patients showed no response inhibitions deficits at all (Hagenhoff et al., 2013).

However, contrary to this previous work, the current study used an expectancy

variant of the AX-CPT, thus favoring impulsive responding and making the task

more demanding.

Another advantage of the used expectancy variant of the AXCPT paradigm is

its potential to produce a double dissociation in performance: individuals with a

context-processing deficit would show impaired performance on BX trials, whereas

those with intact context-processing would perform worse on AY trials (MacDonald,

2008). Thus, with regard to the context-processing theory the higher error rate and

RTs on the BX trials suggest impaired context processing in our BPD patients. In

addition, the increased AX error rate can also be interpreted as a failure to

maintain the A cue until the X probe appeared (Barch et al., 2004). Poor performance

in this condition can arise from problems with maintenance and/or recall of

information from working memory, both aspects of context processing (Bodner et

al., 2012). This interpretation is quite interesting since this is in keeping with

previous work that has identified working memory deficits in BPD (Dinn et al.,

2004; Dowson et al., 2004b).

Further, that BX performance was relatively spared in our ADHD patients

suggests that here context representations were used as a mechanism to inhibit

target responding. This raises questions about the relatively intact maintenance

and/or recall of information from working memory in our ADHD patients.

Although previous studies have mostly confirmed impaired working memory



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performance in adults with ADHD (for example: (Dowson et al., 2004b; Boonstra et

al., 2005), it is unclear whether inhibitory control and working memory

impairments represent distinct deficits in ADHD or dual manifestations of a

common pathologic mechanism (i.e. an integral executive phenotype) (Castellanos

and Tannock, 2002). Our results might imply that response inhibition and working

memory are not necessarily two associated processes in adult ADHD. Two previous

studies correlated working memory and response inhibition in adult ADHD

patients with contradictory and unclear results (Clark et al., 2007; Schecklmann et

al., 2012). Future research should therefore examine the relationship between

these core deficits in larger groups of patients with ADHD.

It is also interesting to note that impaired context processing is particularly

demonstrated as a specific impairment in patients with schizophrenia, schizo-

affective disorder and schizotypal personality disorder (McClure et al., 2008),

while other psychiatric disorders like bipolar disorder and major depression have

not exhibited the same impaired context processing (Holmes et al., 2005; Brambilla

et al., 2007). This raises the question of possible shared response inhibition vulner-

abilities between BPD and schizophrenia spectrum disorders. One previous study

focused on this issue and examined whether BPD patients have inhibition deficits,

as measured with an anti-saccade eye task, similar to patients with schizophrenia.

The results suggested that inhibition deficits may be characteristic among BPD

patients with psychotic like symptoms, but do not reflect the whole group of BPD

patients (Grootens et al., 2008a). Of course, we cannot draw any conclusion from

our sample with regard to possible shared response inhibition deficits between

BPD and the schizophrenia spectrum. We lack evidence of severity and frequency

psychotic like symptoms in our BPD patients, nor do we have any evidence that

psychotic like symptoms in BPD and psychotic symptoms in schizophrenia share

the underlying cognitive mechanisms. However, we would like to argue that

because our BPD patients showed clear deficits in context processing and this is

particularly been known to be seen case in schizophrenia spectrum disorders,

psychotic like symptoms should be taken into account in future research on

response inhibition and context processing in BPD. Although the prevalence of

major psychotic disorders is low, transient psychotic like symptoms in response to

stress do occur in about 40% of BPD patients (Zanarini et al., 1990).

The current study included well diagnosed patients and matched controls,

and controlled for the presence of comorbidities and use of medication.

Interpretation of its findings must however be considered in relation to several

methodological limitations. First, the present sample size was small, indicating a

pilot study. This makes it difficult to draw general conclusions about the effects of

ADHD and BPD on cognitive control processes. For this reason, our findings cannot

be generalized to broader groups of patients. Future studies with larger sample



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sizes are needed to confirm the effect of ADHD and BPD on context processing and

response inhibition. Second, our results may not necessarily generalize to patients

with the inattentive type of ADHD who do not have high levels of impulsivity, and

BPD patients without impulsivity. Third, although the sample included men and

females, and participants of different ages, we did not have the power to analyze

gender or age effects. Nor did we control for possible effects of the different

recruitment centers, because of our small sample size.

Some considerations must also be made with regard to use of nicotine and

medication before testing. Participants were not allowed to smoke within 3 h

before measurement. This could have led to some nicotine induced attentional

improvement in both the control and patient groups (Conners et al., 1996). On the

other hand, longer periods of non-smoking prior to testing could cause tension

and anxiety which than could also interfere with the results. Patients using meth-

ylphenidate were not allowed to use it on the day of the experiment. Since the

average half-life of oral methylphenidate is reported to be 2 to 3 h (Wargin et al.,

1983; Volkow et al., 1998), the interruption of one day should be enough to prevent

the pharmacokinetics to be a confounding variable. There is however a risk of

rebound effects that could have had a negative influence on the task performance.

In conclusion, the present study suggests that response inhibition deficits are

related to BPD independently of ADHD. Moreover, contrary to patients with ADHD,

BPD patients may suffer from more widespread inhibition deficiencies and a

specific impairment in context processing. Given the limitations, future research

should attempt to replicate and expand our findings. Understanding the different

cognitive processes that lead to shared clinical symptoms of impulsivity in ADHD

and BPD could lead to more specific treatments.

AcknowledgementsThe authors are grateful to the interns who did assist in collecting data for this

study.



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References

Andrulonis, P.A., Glueck, B.C., Stroebel, C.F., Vogel, N.G., 1982. Borderline personality subcategories. The

Journal of Nervous and Mental Disease 170, 670–679.

Andrulonis, P.A., Glueck, B.C., Stroebel, C.F., Vogel, N.G., Shapiro, A.L., Aldridge, D.M., 1981. Organic brain

dysfunction and the borderline syndrome. The Psychiatric Clinics of North America 4, 47–66.

Barch, D.M., Mitropoulou, V., Harvey, P.D., New, A.S., Silverman, J.M., Siever, L.J., 2004. Context-processing

deficits in schizotypal personality disorder. Journal of Abnormal Psychology 113, 556–568.

Barkley, R.A., Murphy, K.R., Bush, T., 2001. Time perception and reproduction in young adults with

attention deficit hyperactivity disorder. Neuropsychology 15, 351–360.

Bazanis, E., Rogers, R.D., Dowson, J.H., Taylor, P., Meux, C., Staley, C., Nevinson-Andrews, D., Taylor, C.,

Robbins, T.W., Sahakian, B.J., 2002. Neurocognitive deficits in decision-making and planning of

patients with DSM-III-R borderline personality disorder. Psychological Medicine 32, 1395–1405.

Biederman, J., Petty, C.R., Fried, R., Doyle, A.E., Spencer, T., Seidman, L.J., Gross, L., Poetzl, K., Faraone, S.V.,

2007. Stability of executive function deficits into young adult years: a prospective longitudinal

follow-up study of grown up males with ADHD. Acta Psychiatrica Scandinavica 116, 129–136.

Bodner, K.E., Beversdorf, D.Q., Saklayen, S.S., Christ, S.E., 2012. Noradrenergic moderation of working

memory impairments in adults with autism spectrum disorder. Journal of the International Neuro-

psychological Society 18, 556–564.

Boonstra, A.M., Kooij, J.J., Oosterlaan, J., Sergeant, J.A., Buitelaar, J.K., 2010. To act or not to act, thats the

problem: primarily inhibition difficulties in adult ADHD. Neuropsychology 24, 209–221.

Boonstra, A.M., Oosterlaan, J., Sergeant, J.A., Buitelaar, J.K., 2005. Executive functioning in adult ADHD: a

meta-analytic review. Psychological Medicine 35, 1097–1108.

Brambilla, P., Macdonald 3rd, A.W., Sassi, R.B., Johnson, M.K., Mallinger, A.G., Carter, C.S., Soares, J.C., 2007.

Context processing performance in bipolar disorder patients. Bipolar Disorders 9, 230–237.

Braver, T.S., Barch, D.M., 2002. A theory of cognitive control, aging cognition, and neuromodulation.

Neuroscience and Biobehavioral Reviews 26, 809–817.

Braver, T.S., Barch, D.M., Gray, J.R., Molfese, D.L., Snyder, A., 2001. Anterior cingulate cortex and response

conflict: effects of frequency, inhibition and errors. Cerebral Cortex 11, 825–836.

Braver, T.S., Paxton, J.L., Locke, H.S., Barch, D.M., 2009. Flexible neural mechanisms of cognitive control

within human prefrontal cortex. Proceedings of the National Academy of Sciences of the United

States of America 106, 7351–7356.

Castellanos, F.X., Tannock, R., 2002. Neuroscience of attention-deficit/hyperactivity disorder: the search for

endophenotypes. Nature Reviews. Neuroscience 3, 617–628.

Clark, L., Blackwell, A.D., Aron, A.R., Turner, D.C., Dowson, J., Robbins, T.W., Sahakian, B.J., 2007. Association

between response inhibition and working memory in adult ADHD: a link to right frontal cortex

pathology? Biological Psychiatry 61, 1395–1401.

Cohen, J.D., Barch, D.M., Carter, C., Servan-Schreiber, D., 1999. Context-processing deficits in schizophrenia:

converging evidence from three theoretically motivated cognitive tasks. Journal of Abnormal

Psychology 108, 120–133.

Conners, C.K., 2000. Conners0 Continuous Performance Test II: Computer Program for Windows Technical

Guide and Software Manual. Multi-Health Systems, Toronto, Canada.

Conners, C.K., Levin, E.D., Sparrow, E., Hinton, S.C., Erhardt, D., Meck,W.H., Rose, J.E., March, J., 1996.

Nicotine and attention in adult attention deficit hyperactivity disorder (ADHD). Psychopharmacology

Bulletin 32, 67–73.

de Bruijn, E.R., Grootens, K.P., Verkes, R.J., Buchholz, V., Hummelen, J.W., Hulstijn, W., 2006. Neural

correlates of impulsive responding in borderline personality disorder: ERP evidence for reduced

action monitoring. Journal of Psychiatric Research 40, 428–437.

Dinn, W.M., Harris, C.L., Aycicegi, A., Greene, P.B., Kirkley, S.M., Reilly, C., 2004. Neurocognitive function in

borderline personality disorder. Progress in Neuro-Psychopharmacology & Biological Psychiatry 28,

329–341.



104

CHAPTER 5

Dowson, J.H., McLean, A., Bazanis, E., Toone, B., Young, S., Robbins, T.W., Sahakian, B., 2004a. The specificity

of clinical characteristics in adults with attentiondeficit/hyperactivity disorder: a comparison with

patients with borderline personality disorder. European Psychiatry 19, 72–78.

Dowson, J.H., McLean, A., Bazanis, E., Toone, B., Young, S., Robbins, T.W., Sahakian, B.J., 2004b. Impaired

spatial working memory in adults with attention-deficit/ hyperactivity disorder: comparisons with

performance in adults with borderline personality disorder and in control subjects. Acta Psychiatrica

Scandinavica 110, 45–54.

DuPaul, GJ, Anastopoulos, P.T., Reid R., AD, 1998. ADHD Rating Scale-IV: Checklists, Norms,and Clinical

Interpretation. The Guilford Press, New York.

Epstein, J.N., Johnson, D.E., Varia, I.M., Conners, C.K., 2001. Neuropsychological assessment of response

inhibition in adults with ADHD. Journal of Clinical and Experimental Neuropsychology 23, 362–371.

Evenden, J.L., 1999. Varieties of impulsivity. Psychopharmacology 146, 348–361.

Faraone, S.V., Biederman, J., Doyle, A., Murray, K., Petty, C., Adamson, J.J., Seidman, L., 2006. Neuropsycho-

logical studies of late onset and subthreshold diagnoses of adult attention-deficit/hyperactivity

disorder. Biological Psychiatry 60, 1081–1087.

Ferrer, M., Andion, O., Matali, J., Valero, S., Navarro, J.A., Ramos-Quiroga, J.A., Torrubia, R., Casas, M., 2010.

Comorbid attention-deficit/hyperactivity disorder in borderline patients defines an impulsive

subtype of borderline personality disorder. Journal of Personality Disorders 24, 812–822.

Fischer, M., Barkley, R.A., Smallish, L., Fletcher, K., 2005. Executive functioning in hyperactive children as

young adults: attention, inhibition, response perseveration, and the impact of comorbidity.

Developmental Neuropsychology 27, 107–133.

Fossati, A., Novella, L., Donati, D., Donini, M., Maffei, C., 2002. History of childhood attention deficit/

hyperactivity disorder symptoms and borderline personality disorder: a controlled study.

Comprehensive Psychiatry 43, 369–377.

Groenestijn, M.A.C., Akkerhuis, G.W., Kupka, R.W., Schneider, N., Nolen, W.A., 1999. Structured Clinical

Interview for DSM-IV Axis I Disorders. Swets & Zeitlinger BV, Lisse, the Netherlands.

Grootens, K.P., van Luijtelaar, G., Buitelaar, J.K., van der Laan, A., Hummelen, J.W., Verkes, R.J., 2008a.

Inhibition errors in borderline personality disorder with psychotic-like symptoms. Progress in Neu-

ro-Psychopharmacology & Biological Psychiatry 32, 267–273.

Grootens, K.P., van Luijtelaar, G., Miller, C.A., Smits, T., Hummelen, J.W., Buitelaar, J.K., Verkes, R.J., 2008b.

Increased p50 gating but intact prepulse inhibition in borderline personality disorder. The Journal of

Neuropsychiatry and Clinical Neurosciences 20, 348–356.

Hagenhoff, M., Franzen, N., Koppe, G., Baer, N., Scheibel, N., Sammer, G., Gallhofer, B., Lis, S., 2013. Executive

functions in borderline personality disorder. Psychiatry Research 210, 224–231.

Hervey, A.S., Epstein, J.N., Curry, J.F., 2004. Neuropsychology of adults with attention- deficit/hyperactivity

disorder: a meta-analytic review. Neuropsychology, 18, 485–503.

Holmes, A.J., MacDonald 3rd, A., Carter, C.S., Barch, D.M., Andrew Stenger, V., Cohen, J.D., 2005. Prefrontal

functioning during context processing in schizophrenia and major depression: an event-related fMRI

study. Schizophrenia Research 76, 199–206.

Kooij, J.J., 2002. ADHD bij Volwassenen. Inleiding in de Diagnostiek en Behandeling [ADHD in Adults.

Introduction in Diagnostics and Treatment]. Swets & Zeitlinger BV, Lisse, the Netherlands.

Kooij, J.J., Aeckerlin, L.P., Buitelaar, J.K., 2001. Functioning, comorbidity and treatment of 141 adults with

attention deficit hyperactivity disorder (ADHD) at a psychiatric outpatient department. Nederlands

Tijdscrift Voor Geneeskunde, 145, 1498–1501.

Kooij, J.J., Buitelaar, J.K., van den Oord, E.J., Furer, J.W., Rijnders, C.A., Hodiamont, P.P., 2005. Internal and

external validity of attention-deficit hyperactivity disorder in a population-based sample of adults.

Psychological Medicine 35, 817–827.

Krause-Utz, A., Sobanski, E., Alm, B., Valerius, G., Kleindienst, N., Bohus, M., Schmahl, C., 2013. Impulsivity

in relation to stress in patients with borderline personality disorder with and without co-occurring

attention-deficit/hyperactivity disorder: an exploratory study. The Journal of Nervous and Mental

Disease 201, 116–123.



105


5

Lampe, K., Konrad, K., Kroener, S., Fast, K., Kunert, H.J., Herpertz, S.C., 2007. Neuropsychological and

behavioural disinhibition in adult ADHD compared to

borderline personality disorder. Psychological Medicine 37, 1717–1729.

Lawrence, K.A., Allen, J.S., Chanen, A.M., 2010. Impulsivity in borderline personality disorder: reward-based

decision-making and its relationship to emotional distress. Journal of Personality disorders 24,

786–799.

Leyton, M., Okazawa, H., Diksic, M., Paris, J., Rosa, P., Mzengeza, S., Young, S.N., Blier, P., Benkelfat, C., 2001.

Brain Regional alpha-[11C]methyl-L-tryptophan trapping in impulsive subjects with borderline

personality disorder. The American Journal of Psychiatry 158, 775–782.

MacDonald 3rd, A.W., 2008. Building a clinically relevant cognitive task: case study of the AX paradigm.

Schizophrenia Bulletin 34, 619–628.

McCloskey, M.S., New, A.S., Siever, L.J., Goodman, M., Koenigsberg, H.W., Flory, J.D., Coccaro, E.F., 2009.

Evaluation of behavioral impulsivity and aggression tasks as endophenotypes for borderline

personality disorder. Journal of Psychiatric, Research 43, 1036–1048.

McClure, M.M., Barch, D.M., Flory, J.D., Harvey, P.D., Siever, L.J., 2008. Context processing in schizotypal

personality disorder: evidence of specificity of impairment to the schizophrenia spectrum. Journal of

Abnormal Psychology, 117, 342–354.

Murphy, K.R., Barkley, R.A., Bush, T., 2001. Executive functioning and olfactory identification in young

adults with attention deficit-hyperactivity disorder. Neuropsychology 15, 211–220.

Nigg, J.T., Silk, K.R., Stavro, G., Miller, T., 2005a. Disinhibition and borderline personality disorder.

Development and Psychopathology 17, 1129–1149.

Nigg, J.T., Stavro, G., Ettenhofer, M., Hambrick, D.Z., Miller, T., Henderson, J.M., 2005b. Executive functions

and ADHD in adults: evidence for selective effects on ADHD symptom domains. Journal of Abnormal

Psychology 114, 706–717.

Nigg, J.T., Willcutt, E.G., Doyle, A.E., Sonuga-Barke, E.J., 2005c. Causal heterogeneity in attention-deficit/

hyperactivity disorder: do we need neuropsychologically impaired subtypes? Biological Psychiatry

57, 1224–1230.

Philipsen, A., Limberger, M.F., Lieb, K., Feige, B., Kleindienst, N., Ebner-Priemer, U., Barth, J., Schmahl, C.,

Bohus, M., 2008. Attention-deficit hyperactivity disorder as a potentially aggravating factor in

borderline personality disorder. The British Journal of Psychiatry 192, 118–123.

Rentrop, M., Backenstrass, M., Jaentsch, B., Kaiser, S., Roth, A., Unger, J., Weisbrod, M., Renneberg, B., 2008.

Response inhibition in borderline personality disorder: performance in a Go/Nogo task. Psychopa-

thology 41, 50–57.

Rey, J.M., Morris-Yates, A., Singh, M., Andrews, G., Stewart, G.W., 1995. Continuities between psychiatric

disorders in adolescents and personality disorders in young adults. The American Journal of

Psychiatry 152, 895–900.

Riccio, C.A., Reynolds, C.R., 2001. Continuous performance tests are sensitive to ADHD in adults but lack

specificity. A review and critique for differential diagnosis. Annals of the New York Academy of

Sciences 931, 113–139.

Riccio, C.A., Reynolds, C.R., Lowe, P., Moore, J.J., 2002. The continuous performance test: a window on the

neural substrates for attention? Archives of Clinical Neuropsychology: The Official Journal of the

National Academy of Neuropsychologists 17, 235–272.

Ross, R.G., Harris, J.G., Olincy, A., Radant, A., 2000. Eye movement task measures inhibition and spatial

working memory in adults with schizophrenia, ADHD, and a normal comparison group. Psychiatry

Research 95, 35–42.

Rosvold, H.E., Delgado, J.M., 1956. The effect on delayed-alternation test performance of stimulating or

destroying electrically structures within the frontal lobes of the monkeys brain. Journal of

Comparative and Physiological Psychology 49, 365–372.

Rubio, G., Jimenez, M., Rodriguez-Jimenez, R., Martinez, I., Iribarren, M.M., Jimenez-Arriero, M.A., Ponce,

G., Avila, C., 2007. Varieties of impulsivity in males with alcohol dependence: the role of Cluster-B

personality disorder. Alcoholism, Clinical and Experimental Research 31, 1826–1832.



106

CHAPTER 5

Ruocco, A.C., Laporte, L., Russell, J., Guttman, H., Paris, J., 2012. Response inhibition deficits in unaffected

first-degree relatives of patients with borderline personality disorder. Neuropsychology 26, 473–482.

Schecklmann, M., Ehlis, A.C., Plichta, M.M., Dresler, T., Heine, M., Boreatti-Hummer, A., Romanos, M., Jacob,

C., Pauli, P., Fallgatter, A.J., 2012. Working memory and response inhibition as one integral phenotype

of adult ADHD? A behavioral and imaging correlational investigation, Journal of Attention Disorders.

Schoechlin, C., Engel, R.R., 2005. Neuropsychological performance in adult attention-deficit hyperactivity

disorder: meta-analysis of empirical data. Archives of Clinical Neuropsychology 20, 727–744.

Seidman, L.J., Doyle, A., Fried, R., Valera, E., Crum, K., Matthews, L., 2004. Neuropsychological function in

adults with attention-deficit/hyperactivity disorder. The Psychiatric Clinics of North America 27,

261–282.

Servan-Schreiber, D., Cohen, J.D., Steingard, S., 1996. Schizophrenic deficits in the processing of context.

A test of a theoretical model. Archives of General Psychiatry 53, 1105–1112.

Sheehan, D.V., Lecrubier, Y., Sheehan, K.H., Amorim, P., Janavs, J., Weiller, E., Hergueta, T., Baker, R., Dunbar,

G.C., 1998. The mini-international neuropsychiatric Interview (M.I.N.I.): the development and

validation of a structured diagnostic psychiatric interview for DSM-IV and ICD-10. The Journal of

Clinical Psychiatry 59 (Suppl. 20), 22–33. (quiz 34-57).

Sonuga-Barke, E., Bitsakou, P., Thompson, M., 2010. Beyond the dual pathway model: evidence for the

dissociation of timing, inhibitory, and delay-related impairments in attention-deficit/hyperactivity

disorder. Journal of the American Academy of Child and Adolescent Psychiatry 49, 345–355.

Stavro, G.M., Ettenhofer, M.L., Nigg, J.T., 2007. Executive functions and adaptive functioning in young adult

attention-deficit/hyperactivity disorder. Journal of the International Neuropsychological Society 13,

324–334.

van Dijk, F., Lappenschaar, M., Kan, C., Verkes, R.J., Buitelaar, J., 2011. Lifespan attention deficit/hyperactivity

disorder and borderline personality disorder symptoms in female patients: a latent class approach.

Psychiatry Research, 190, 327–334.

van Dijk, F.E., Lappenschaar, M., Kan, C.C., Verkes, R.J., Buitelaar, J.K., 2012. Symptomatic overlap between

attention-deficit/hyperactivity disorder and borderline personality disorder in women: the role of

temperament and character traits. Comprehensive Psychiatry 53, 39–47.

Volker, K.A., Spitzer, C., Limberg, A., Grabe, H.J., Freyberger, H.J., Barnow, S., 2009. Executive dysfunctions

in female patients with borderline personality disorder with regard to impulsiveness and depression.

Psychotherapie, Psychosomatik, Medizinische Psychologie 59, 264–272.

Volkow, N.D., Wang, G.J., Fowler, J.S., Gatley, S.J., Logan, J., Ding, Y.S., Hitzemann, R., Pappas, N., 1998.

Dopamine transporter occupancies in the human brain induced by therapeutic doses of oral methyl-

phenidate. The American Journal of Psychiatry 155, 1325–1331.

Weertman, A., Arntz, A., Kerkhofs, M.L.M., 2000. Structured Clinical Interview for DSM-IV Axis II

Personality Disorders. Swets & Zeitliner BV, Lisse, the Netherlands.

Wargin, W., Patrick, K., Kilts, C., Gualtieri, C.T., Ellington, K., Mueller, R.A., Kraemer, G., Breese, G.R., 1983.

Pharmacokinetics of methylphenidate in man, rat and monkey. Journal of Pharmacology and

Experimental Therapeutics 226, 382–386.

Woods, S.P., Lovejoy, D.W., Ball, J.D., 2002. Neuropsychological characteristics of adults with ADHD: a

comprehensive review of initial studies. The Clinical Neuropsychologist 16, 12–34.

Zanarini, M.C., Gunderson, J.G., Frankenburg, F.R., 1990. Cognitive features of borderline personality

disorder. The American Journal of Psychiatry 147, 57–63



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Under review as:

Van Dijk FE, Mostert, Onnink, Dammers, Arias Vasquez, Kan, Verkes, Hoogman,

Franke, Buitelaar. (2016). Five Factor Model personality traits relate to adult attention-

deficit/hyperactivity disorder but not to their distinct neurocognitive profiles.

Five Factor Model personality traits relate to adult attention-deficit/

hyperactivity disorder but not to their distinct neurocognitive profiles

6



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Abstract

Objective: To investigate whether personality traits are related to neurocognitive

profiles in adults with ADHD.

Method: Neuropsychological performance and Five Factor Model (FFM) personality

traits were measured in adults with ADHD (n= 133) and healthy controls (n= 132).

Three neuropsychological profiles, derived from previous community detection

analyses, were investigated for personality trait differences.

Results: Irrespective of cognitive profile, participants with ADHD showed

significantly higher Neuroticism and lower Extraversion, Agreeableness, and Con-

scientiousness than healthy controls. Only the FFM personality factor Openness

differed significantly between the three profiles. Higher Openness was more

common in those with aberrant attention and inhibition than those with increased

delay discounting and atypical working memory / verbal fluency.

Conclusion: The results suggest that the personality trait Openness, but not any

other FFM factor, is linked to neurocognitive profiles in ADHD. ADHD symptoms

rather than profiles of cognitive impairment may have a determining influence on

personality trait outcome.



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FFM TRAITS RELATE TO ADHD BUT NOT TO THEIR COGNITIVE PROFILES

6

Introduction

Attention-deficit/hyperactivity disorder (ADHD) is a common neuropsychiatric

disorder that is characterized by symptoms of inattention, hyperactivity, and

impulsivity. ADHD often persists into adulthood (Faraone 2015). Current research

does not support a single core (neuro)cognitive deficit of ADHD, but rather

demonstrate that both childhood and adult ADHD are characterized by strong

heterogeneity in cognitive underperformance with multiple cognitive pathways

(Sonuga-Barke, Bitsakou et al. 2010; de Zeeuw, Weusten et al. 2012; Fair, Bathula et

al. 2012; Coghill, Seth et al. 2014; Mostert, Onnink et al. 2015). The main domains

of neuropsychological dysfunction in ADHD are: memory, inhibitory control,

delay aversion, decision making, timing, and response variability. The levels of

deficiency in each of these domains differ more or less independently within

patients with ADHD, and there is considerable overlap between neuropsychologi-

cal performance in patients with ADHD and normal controls (Coghill, Seth et al.

2014). Use of multivariate classification techniques has led to the identification of

subgroups of individuals with ADHD based on a similar neurocognitive profile,

both in children and in adults (Fair, Bathula et al. 2012; Mostert, Hoogman et al.

2015; van Hulst, de Zeeuw et al. 2015). Such results provide some structure to the

heterogeneity in ADHD. However the clinical utility of subgrouping based on neu-

ropsychological characteristics in ADHD needs to be explored.

Contributing to the heterogeneity of ADHD is the presence of temperament

and personality traits. Temperament traits can be described as a set of biologically

based behavioural and emotional tendencies covering negative and positive

emotion systems as well as attentional capacities (Rothbart 2011). A recent study

used the technique of ‘community detection’ to cluster children with ADHD into

subgroups based on temperament dimensions of the Temperament in Middle

Childhood Questionnaire. The results suggested three novel types of ADHD that

were independent of existing clinical demarcations, including DSM-5 presentations

(Karalunas, Fair et al. 2014). Type 1, the mild type, had milder impulsivity, inhibition,

and attentional control impairments compared with the other two ADHD types.

Type 2, the surgent type, had increased impulsivity, activity levels and assertiveness,

decreased shyness coupled to high intensity pleasure seeking than the other two

types. Type 3, the irritable type, had increased impulsivity and attentional control

impairments than type 1 and increased negative emotionality compared to the

other two types. Personality research in general has mostly used the Five Factor

Model (FFM) (Costa and McCrae 1992) as a well-supported organizing framework

that has been characterized with respect to underlying temperament dimensions

(i.e. the initial state of emotional, motor, and attentional reactivity from which

personality develops in interaction with experience) (Rothbart 2007). A recent



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review of findings on ADHD and FFM personality suggests that, in general, ADHD

has associations with the FFM traits of Neuroticism (positive), Agreeableness

(negative) and Conscientiousness (negative). Mixed findings (positive, negative, and

no associations) have been reported for Extraversion and Openness (Gomez and

Corr 2014).

Prior research, mostly assessing the relationship between single tasks or facets

of executive function and single FFM traits in healthy participants, suggests that

significant associations also exist between FFM traits and neurocognitive

functioning, especially executive functioning (for an overview, see (Williams,

Suchy et al. 2009)). Three more recent studies extended that early research by

considering all five FFM traits in relation to a more fully characterized domain of

executive functioning. A first study among 58 healthy older adults investigated

four tests assessing all core aspects of executive functioning (cognitive flexibility,

initiation, inhibition, response selection, working memory, generative fluency,

and attentional vigilance) (Williams, Suchy et al. 2010). The results showed that

the executive functioning factor, that emerged from four executive functioning

scores (one for each executive functioning test), was negatively correlated with

Neuroticism and positively with Openness and Agreeableness. But although high

Neuroticism was associated with poorer executive functioning, both the middle

and high executive functioning groups were in the average range for Neuroticism

(compared to normative values). Individuals with better executive functioning

were characterized by high Openness and Agreeableness and average levels of

Neuroticism. Executive functioning was not associated with Extraversion or

Conscientiousness in this study.

A second study, including 182 students, examined three separate core executive

function factors (i.e. inhibition, updating/monitoring information in working

memory, and cognitive flexibility) as predictors of the five FFM traits (Murdock,

Oddi et al. 2013). Higher Neuroticism and lower Openness were associated with

poor updating/monitoring, and Openness was positively associated with cognitive

flexibility (the ability to shift one’s attention between multiple tasks or mental

sets). The authors suggested that Neuroticism and Openness may share some

common underlying cognitive mechanism, in particular working memory.

Connections between executive functioning and Extraversion, Agreeableness, and

Conscientiousness did not emerge in this study.

A third study examined associations between FFM traits and cognitive

performance to 1) uncover the specific facets of each trait that are most closely

related to cognition, and 2) examine, how these associations may vary by age in

154 healthy older and younger adults. The cognitive domains measured were

processing speed, reaction time, verbal fluency, inductive reasoning, and working

and episodic memory. Neuroticism (trait) and in particular ‘depression’ (a facet of



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Neuroticism) were negatively associated with performance on cognitive tasks that

require effortful processing. The results suggested that individuals, who are more

angry and depressed, have slower processing speed and lower reasoning scores.

Openness (trait) and ‘ideas’ (a facet of openness) were positively associated with

verbal fluency, indicating that ‘ideas’ may be a key characteristic in the association

between Openness and cognition. Those open to ideas are likely to spend more

time exploring intellectual pursuits, which could translate into a greater facility

with words. Extraversion (trait) and ‘assertiveness’ (a facet of Extraversion) were

negatively related to reasoning and reaction time, indicating that extraverted

individuals may be faster, but are less likely to take time to think thoroughly

about a task. The FFM traits and their facets did not predict working memory or

episodic memory in this study. The association between Neuroticism and cognitive

performance was found primarily among younger adults. In older adulthood,

better performance was associated with positive aspects of personality (Graham

and Lachman 2014).

So far, the studies of cognitive performance and personality did not take the

presence of psychopathology into account. In the present study, we follow-up on

this previous work regarding the subtyping of ADHD by cognition and

temperament. Specifically, we examined, whether adults with ADHD and healthy

controls, who share similar neurocognitive profiles, also share specific personality

traits, or, alternatively, whether ADHD is related to personality irrespective of a

specific neurocognitive profile. To this end, we built on our earlier work, in which

we had identified by community detection analysis three subgroups of patients

and healthy controls based on cognitive profiles characterized by (1) poor

performance on attention and inhibition, (2) high scores for impulsive behaviour

on the delay-discounting task (delay aversion), (3) impairment on working memory

and verbal fluency (Mostert, Hoogman et al. 2015). Given the recent evidence for

the relationship between executive functions and FFM trait outcome as outlined

above, we anticipated that our previously identified profiles 1 and 3 would be

associated with higher Neuroticism and lower Openness. Further, in keeping with

previously found associations between Extraversion and higher delayed

discounting rates (Hirsh, Morisano et al. 2008), we also anticipated that Extraversion

would be positively related to our cognitive profile 2. Alternatively, if it would be

the ADHD symptoms that accounted for FFM trait outcome rather than the

cognitive profiles, we expected to find associations of the FFM traits with diagnostic

group, irrespective of cognitive profile membership. Such associations could be

expected for Neuroticism, Conscientiousness, and Agreeableness. The results can

add to the understanding of the associations between FFM traits and executive

functioning, in particular in an adult ADHD population.



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Methods

Participants A total of 265 participants (133 adults with ADHD and 132 healthy controls)

between 18 and 65 years old were included in this study. All participants were part

of the Dutch node of the International Multicentre persistent ADHD Collaboration

(IMpACT - 6 http://impactadhdgenomics.com (Franke, Vasquez et al. 2010)).

Participants had been recruited from the Department of Psychiatry of the Radboud

University Medical Center (RadboudUMC) in Nijmegen and through advertisements.

Patients were included if they had previously been diagnosed with adult ADHD

by a psychiatrist according to the Diagnostic and Statistical Manual of Mental

Disorders (4th edition; DSM-IV-TR; American Psychiatric Association, 2000).

Exclusion criteria were psychosis, alcohol, or substance addiction in the last six

months, current major depression, full-scale IQ estimate < 70 (assessed using the

Wechsler Adult Intelligence Scale-III), neurological disorders, sensorimotor

disabilities, non-Caucasian ethnicity, and medication use other than psychostimu-

lants, atomoxetine, or bupropion. Additional exclusion criteria for healthy

participants were a current or lifetime neurological or psychiatric disorder in

either the participant or his/her first-degree relatives.

Ethical standards This study was approved by the regional ethics committee (Centrale Commissie

Mensgebonden Onderzoek: CMO Regio Arnhem – Nijmegen; Protocol number

III.04.0403). Written informed consent was obtained from all participants. The

authors assert that all procedures contributing to this work complied with the

ethical standards of the relevant national and international and institutional

committees on human experimentation and with the Helsinki Declaration of

1975, as revised in 2008.

Psychiatric assessment Both patients and controls were assessed using the structured diagnostic interview

for adult ADHD (DIVA 2.0.; www.divacenter.eu (Kooij 2010)). This interview focuses

on the 18 DSM-IV symptoms of ADHD and uses concrete and realistic examples to

thoroughly investigate whether a symptom is currently present or was present in

childhood. Additionally, a self-report questionnaire on current symptoms was

obtained using the ADHD Rating Scale-IV (Kooij, Buitelaar et al. 2005). Lifetime

DSM IV axis I and II disorders were assessed with the Structured Clinical Interview

for DSM disorders I and II (SCID I and SCID II) (Groenestijn, Akkerhuis et al. 1999;

Weertman, Arntz et al. 2000). With regard to the Axis II personality disorders,

participants first filled out the SCID II self-report questionnaire, and when



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applicable, according to the SCID II manual, the clinical interview followed.

Further measurements included an MRI scanning session and blood withdrawal for

DNA analysis. These data are described elsewhere and are not part of the current

analyses (Franke, Hoogman et al. 2008; Franke, Vasquez et al. 2010; Hoogman,

Aarts et al. 2011; Hoogman, Onnink et al. 2013; Onnink, Zwiers et al. 2014).

Neuropsychological testing batteryNeuropsychological performance was measured using a test battery that included

measures tapping into executive functioning (working memory, attention,

inhibition, set-shifting, fluency) and delay discounting, deficits of which have been

earlier reported in ADHD. Details about tasks and main outcome measures are

described in Supplementary Table 1 and our previous reports (Mostert, Hoogman

et al. 2015; Mostert, Onnink et al. 2015). The tests were always administered in the

same order. In total, 21 variables in seven tasks were analysed. Outliers were

defined as having a score higher than four times the standard deviation above or

below the mean per group (Leth-Steensen, Elbaz et al. 2000; Nigg, Stavro et al. 2005).

This threshold guarded against artefacts, while still including cases performing

at the extreme of the normal distribution (i.e., including low performing cases

that might have more severe ADHD symptoms). If a participant’s score was an

outlier on one outcome variable of a task, his/her scores on all outcome variables

from that task were excluded. All data was transformed in such a way that higher

values indicated worse performance. To estimate IQ, subtests of the Wechsler Adult

Intelligence Scale (WAIS) were administered (vocabulary and block design)

(Wechsler 1997).

Neurocognitive profiles In our previous report, Confirmatory Factor Analysis (CFA) was used to reduce

neurocognitive data to six cognitive factors: reaction time and variability,

delay discounting, verbal fluency, working memory, attention and inhibition.

Subsequently, factor scores were correlated across subjects to form networks.

Further, a community detection algorithm was used to cluster these networks into

subgroups. The ADHD and the control group each separated into three profiles

that differed in cognitive performance. Profile 1 was characterized by aberrant

attention and inhibition, profile 2 by increased delay discounting, and profile 3

by atypical working memory and verbal fluency. The same profiles were observed

in the control and ADHD sample. Details about the method, sample sizes, results

are described in (Mostert, Hoogman et al. 2015).



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Five Factor Model Personality Measurement The participants completed the NEO-FFI (Costa and McCrae 1992), a 60 item self-

report assessing each of the 5 FFM personality domains: Extraversion, Agreeableness,

Conscientiousness, Neuroticism, and Openness to experiences. Each domain

includes 12 items. The NEO-FFI was not intended to provide definitive measurement

of the five personality factors, but was designed as a brief instrument that would

yield reasonable estimates of the factors, useful in exploratory research. In over a

decade of use, it has shown itself to be reliable, valid, and useful in a variety of

contexts and cultures (McCrae and Costa 2004). Extraversion reflects being

sociable, outgoing, optimistic, sensation seeking, and talkativeness. Agreeableness

refers to the tendency to be agreeable, trustworthy, friendly, and cooperative with

others, rather than suspicious and antagonistic towards others. It is also a measure

of whether a person is generally well tempered or not. Conscientiousness reflects

a person’s tendency to be well organized, responsible, and task-focused in pursuing

goals. Neuroticism indicates the tendency for proneness to unpleasant experience,

such as anger, anxiety, depression, and maladjustment. Neuroticism also refers to

the degree of emotional stability and impulse control and is sometimes referred to

by its low pole, “emotional stability”. Openness to experience reflects a person’s

tendency for being imaginative, creative, and interested in cultural and educational

experiences.

Statistical analysis In the current study, we tested for FFM trait differences between the three

neurocognitive profiles using analysis of variance (ANOVA). For this, a two (group:

ADHD vs. Control) by three (the cognitive profiles: inattention and inhibition

[profile 1] vs. delay aversion [profile 2] vs. working memory and verbal fluency

[profile 3]) ANOVA was performed on the scores of each of the five factors of the

FFM, with group and cognitive profile as between-subject factors and the FFM

factors as dependent variables. These calculations were done using SPSS (version

20; SPSS, Chicago, IL).

Results

Demographics of the sample are described in Table 1. Adults with ADHD and

healthy controls did not differ in age , gender, or IQ, but controls had a higher level

of education. Table 2 presents the scores (mean and SD) of all six groups analysed

in the ANOVA on all factors of the FFM.

The analyses of the Neuroticism scale did not reveal a main effect of cognitive

profile (F(2, 246) = 0.26, p = .77), but a main effect of diagnostic status was observed,



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with a significantly higher score on Neuroticism for the ADHD than the control

group (F(1, 246) = 124.09, p = .0001). Furthermore, the interaction effect of group

and cognitive profile was significant (F(2, 246) = 4.25, p = .02). Using a one-way

ANOVA to localize this effect revealed no significant differences between any of

the profile groups for the ADHD-group (F(2, 121) = 1.18, p = .31), whereas the same

analysis on the control group yielded a significant effect, F(2, 125) = 3.50, p = .03.

Within the ADHD group profile 1 had the highest average score on Neuroticism,

whereas in the control group profile 1 was associated with the lowest score on

Neuroticism. However, these findings did not survive Bonferroni correction. 9

On the Extraversion scale a main effect of group was found (F(1, 247) = 7.76,

p = .006) with significantly higher scores for the healthy control group. There was

no main effect for cognitive profile (F(2, 247) = 2.03, p = .13), nor was a significant

Table 1 Demographics of the participants

ADHD patients(N=133)

Healthy controls(N=132) Statistics

Gender M/F 56/77 53/79 χ² (1, N = 265) = 0.10, p = .75

Age Mean (SD) 35.56 (10.40) 36.30 (11.75) t(258,7) = 0.54, p = .59

IQ1 Mean (SD) 107.84 (14.34) 109.97 (14.90) t(263) = 1.19, p = .24

Education2 Mean (SD) 4.70 (0.80) 5.16 (0.81) t(263) = 4.66, p < 0.001

1 Estimated IQ based on performance on the WAIS-III block pattern and vocabulary tasks.2 Education levels were coded from 1 (unfinished primary school) to 7 (post-university).

Because Levene’s test for equality of variances was significant in the t test for the differences in ages,

degrees of freedom were adjusted accordingly.

Table 2 Outcome of Five Factor Model traits for the ADHD and healthy control groups in Profile 1, 2, and 3

Profile 1 (N=98; 53% ADHD)



ADHD (SD) HC (SD) ADHD (SD) HC (SD) ADHD (SD) HC (SD)

Neuroticism 39.8 (8.9) 24.0 (7.1) 36.9 (9.8) 28.3 (10.1) 38 (6.8) 27.4 (6.7)

Extraversion 41.7 (7.4) 44.6 (6.2) 40.1 (6.7) 42.1 (6.5) 40.9 (6.7) 42.9 (4.5)

Openness 43.6 (6.1) 41.6 (4.8) 38.4 (6.8) 39.5 (5.1) 41 (5.4) 38.9 (5.5)

Agreeableness 42.8 (5.7) 46.2 (6.2) 40.7 (6.7) 46.2 (5.4) 43.6 (5.4) 46.7 (4.5)

Conscientiousness 34 (6.4) 44.9 (6.5) 35.2 (6.2) 45.9 (5.3) 34.5 (6.5) 46.4 (4.4)

Profile 1: poor performance on attention and inhibition; Profile 2: high scores for impulsive behaviour

on the delay-discounting task (delay aversion); Profile 3: impairment on working memory and verbal

fluency. HC= healthy control.



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interaction effect of group and cognitive profile observed (F(2, 247) = 0.15, p = .87).

The analysis of the Openness scale revealed a main effect of cognitive profile

(F(2, 247) = 9.10, p = .0001), showing that the participants in profile 1 scored

significantly higher than the participants in profile 2 and profile 3. Effects of

group and the interaction of group with cognitive profile were non-significant

(F(1, 247) = 1.92, p = .17; F(2, 247) = 1.76, p = .17).

On the Agreeableness scale, a significant main effect for group was found,

with significantly higher Agreeableness scores for the healthy controls (F(1, 247) =

30.68, p = .0001). No effects of cognitive profile (F(2, 247) = 1.71, p = .18) or the

interaction of group and cognitive profile (F(2, 247) = 0.95, p = .39) were observed.

Lastly, there was a significant main effect for group on the Conscientiousness

scale, with significantly higher scores for the healthy controls compared to the

ADHD patients (F(1, 247) = 214.50, p = .0001). There was no significant main effect

for cognitive profile (F(2, 247) = 0.89, p = .41), and no interaction effect of group and

cognitive profile were observed (F(2, 247) = 0.23, p = .80).

Discussion

The present research investigated, whether FFM traits are significantly related to

neurocognitive profiles in adults with ADHD and controls or are related to ADHD

irrespective of a specific neurocognitive profile. Our main findings are: 1) that

there is no particular relationship between personality traits and cognitive

profiles for most FFM traits; 2) that a relationship between Openness to experience

and inattention / disinhibition is observed; 3) that we can confirm a relationship

between ADHD and personality traits.

Irrespective of cognitive profile, participants with ADHD were found to have

higher scores for Neuroticism and lower scores for Extraversion, Agreeableness,

and Conscientiousness than healthy controls. Cognitive profile was significantly

related to Openness, which was higher in participants with profile 1 (inattention

and disinhibition) than in participants with one of the other two cognitive profiles

(2 (delay aversion / impulsivity) and 3 (working memory / verbal fluency) in both

ADHD patients and controls. No additional associations between FFM measures

and cognitive profiles were found. Previously, it has been proposed that ADHD

originates from a primary cognitive deficit in a specific executive functioning (EF)

domain such as response inhibition or working memory or a more general

weakness in executive control (Pennington and Ozonoff 1996; Barkley 1997;

Schachar, Mota et al. 2000; Castellanos and Tannock 2002). The current study

demonstrates that personality and cognitive performance are mainly separate

domains that apparently do not share similar etiological factors or underlying



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mechanisms in adult ADHD. Our study also documents that personality may be

more closely related to clinical symptoms than the cognitive profiles. Treating the

cognitive domains may therefore not necessarily be the most useful therapeutic

approach in ADHD. However, the cognitive profiles may be more closely related

to functional impairments (Mostert, Hoogman et al. 2015). In any case, it seems

important to look at other factors such as personality beyond cognition in considering

what are the most clinically useful options for patient management. Although

this aspect was outside the scope of the current study, it would be useful to know

if patient stratification on personality profile could inform treatment response.

With regard to the relationship between personality and cognitive domains in

ADHD, we only found a higher score on openness to experiences in participants

with cognitive profile 1 (poor performance on attention and inhibition) than in

participants with profiles 2 and 3. Individuals high in openness tend to be

unconventional, explorative, and interested in novelty. This would suggest that

openness is associated with active and impulsive behaviour. Indeed, this would

suggest that disinhibition may underlie openness. This relationship has been

observed before by DeYoung and coworkers, and indeed in that study the authors

controlled for cognitive abilities in order to reveal an association of openness with

externalizing behaviour (i.e. aggression, opposition, and hyperactivity) (Deyoung,

Peterson et al. 2008). In that case, the variance in openness was related to the meta-

trait plasticity (i.e. the shared variance of Extraversion and Openness appearing to

reflect the tendency to explore both behaviourally and cognitive). Plasticity was

positively associated with externalizing behaviour, whereas variance due to

cognitive ability was negatively associated with such behaviour. In other words,

the findings of that study indicated that if one examines individuals equal in the

meta-trait stability (i.e. the shared variance of Neuroticism reversed, Conscientious-

ness, and Agreeableness) and cognitive ability, those higher in plasticity are likely

to show higher levels of externalizing behaviour. In our current study, this may

underline the relatively higher Openness outcome in profile 1, since it is characterized

by inhibition deficits (as measured by a go/no go task). Interestingly, when the

number of self-reported hyperactivity/impulsivity symptoms was examined in our

previous study defining the cognitive profiles, those symptoms were shown to be

unequally distributed across the three cognitive profiles: The patients in profile 1

(and 2) had indeed significantly more hyperactivity/impulsivity symptoms than in

profile 3 (Mostert, Hoogman et al. 2015). While DeYoung et al. also found a

relationship between Extraversion and the cognitive profiles, we did not observe

this link.

The basis for the association found for Openness but not for Extraversion may

be related to the choice of instrument chosen for personality profiling, i.e. the NEO

FFI. Within the literature, there is currently a debate over the basis of personality



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traits. Some emphasise the phenotypical aspects of the FFM traits (Saucer and

Goldberg 1996), whereas others emphasize the neurobiological bases of the FFM,

such as cognition and affect (McCrae and Costa 1907 1999). Research on the levels

of affects (A), behaviours (B) and cognitions (C) included within the operational

definitions of each of the FFM traits has been conducted. They demonstrate that

Openness within the NEO FFI inventory emphasizes cognition and affect over

behaviour. Thus, the association we found between Openness and cognitive profile

1 may also simply reflect the fact that poor attention and inhibition within profile

1 is in line with the used definition of cognition (i.e. thought, beliefs, patterns, or

modes of thinking) in Openness. In contrast, for Extraversion (for which we have

not seen a relationship with cognitive profiles), there is a striking lack of cognitive

content within its NEO FFI definition and instead a substantial emphasis on its

affective aspects (i.e. internal, motivational, and evaluative ‘valenced’ states

including patterns of feelings, emotions, and preferences) and some behavioural

content (i.e. observable actions, including both active and passive behaviours, but

not including mental events) (Pytlik Zillig, Hemenover et al. 2002). Therefore, it

may be not surprising that no relationship is found with cognitive profile.

The finding that the presence of ADHD rather than cognitive profile is

associated with personality traits is in keeping with previous research questioning

the mediating role of cognition in ADHD. It is in line with the thinking that the

relationship between cognitive deficits and symptomatic aspects of ADHD is more

complex than previously recognized (Coghill, Hayward et al. 2014; Mostert,

Hoogman et al. 2015; Mostert, Onnink et al. 2015). Indeed, we observed several

direct links between personality and ADHD diagnosis. More specifically, we noted

lower Agreeableness, Conscientiousness and Extraversion and higher Neuroticism

in the ADHD participants than in the controls, irrespective of cognitive profile

and similar to previous findings on ADHD and personality (Gomez and Corr 2014).

The implications of the lack of significant interactions between adult ADHD,

cognitive profiles and personality deserve discussion. Theoretically, personality

and psychopathology can relate to one another in three different ways (Widiger

2011). Personality and psychopathology can influence the presentation or

appearance of one another, commonly referred to as a pathoplastic relationship.

They can share a common, underlying etiology, referred to as a spectrum

relationship, touching upon the possibility that personality and psychopathology

may themselves fail in some instances to be distinct entities. They may instead

exist along a common spectrum of functioning. All personality disorders may in

fact be maladaptive variants of general personality traits, and some personality

disorders could be early onset, chronic, and pervasive variants of other mental

disorders. Finally, they can have a causal role in the development or etiology of one

another. Unfortunately, the current study cannot tell us, which of the three is



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applicable to ADHD and personality, as it is a cross-sectional study in adults.

Moreover, it also suggests that personality and cognition are independent entities

without significant influence on each other. Future studies should therefore

characterise, whether the NEO FFI personality profiles are related to innate

temperament or behavioural responses. This may clarify, whether the relationship

between personality and ADHD is based on latent temperamental aspects and/or

the ability to behaviourally respond to changing internal and external cues.

Although we used data from a large sample of adults with persistent ADHD

and healthy controls, the interpretation of the results of our study should be

viewed in the context of some limitations. Firstly, the neuropsychological

measurements did not cover exactly the same cognitive domains that were used in

other studies investigating links between personality and cognitive performance.

Secondly, we focused on previously obtained cognitive profiles that were created

using a specific clustering method; different clustering methods may result in the

creation of different cognitive profiles. Thirdly, we employed the NEO FFI, which

is the shortened version of the NEO-PI-R and not intended to replace the full NEO

PI-R. As such, the NEO FFI measures a reduced range of constructs, which could be

argued not to represent the full spectrum of personality profiles. However, despite

these limitations, the current study confirms that ADHD patient show different

levels of personality traits compared to controls.

Conclusion

Our study suggests that the presence of ADHD is strongly connected to personality

traits, as four out of five factors of the FFM Model differed between ADHD patients

and healthy controls. Moreover, a link between personality and cognitive profile

was observed for Openness. Openness was significantly related to a neurocognitive

profile of poor performance on attention and inhibition tasks in ADHD patients as

well as in healthy controls. In sum, our data suggest that personality and cognitive

performance are mainly separate domains that do not share similar etiological

factors or underlying mechanisms in ADHD.



122

CHAPTER 6

Conflict of interest The authors report no conflicts of interest. Jan Buitelaar has been in the past 3

years a consultant to/member of advisory board of/and/or speaker for Janssen Cilag

BV, Eli Lilly, Shire, Novartis, Roche and Servier. He is not an employee of any of

these companies, and not a stock shareholder of any of these companies. He has no

other financial or material support, including expert testimony, patents, and

royalties. Barbara Franke has received educational speaking fees from Merz and

Shire. Jeffrey Glennon has been in the past 3 years a consultant to Boehringer

Ingelheim on a topic not related to the content of this manuscript. Cornelis Kan

has participated in adult-ADHD Advisory and Consultancy Boards of Eli Lilly

(2011-2014) and presented the ADHD Academy of Eli Lilly (2014-2015).

Acknowledgements We thank all the participants in this study. Prof. dr. Anna Bosman and Dr. A.R. den

Otter are gratefully acknowledged for contributing their expert knowledge to the

study. This study used the sample of the Dutch node of the International Multi-

centre persistent ADHD Collaboration (IMpACT). The Dutch IMpACT study is

supported by grants from the Netherlands Organization for Scientific Research

(NWO), i.e. the NWO Brain & Cognition Excellence Program (grant 433-09-229) and

a personal Vici grant to BF (grant 016-130-669), and by grants from the Netherlands

Brain Foundation (grant 15F07[2]27) and BBMRI-NL (grant CP2010-33). The research

leading to these results also received funding from the European Community’s

Seventh Framework Programme (FP7/2007 – 2013) under grant agreements n° 278948

(TACTICS), n° 602805 (Aggressotype), n° 603016 (MATRICS), and n° 602450

(IMAGEMEND), and from the European Community’s Horizon 2020 Programme

(H2020/2014 – 2020) under grant agreements n° 643051 (MiND) and n° 667302

(CoCA).



123


6

Sup

ple

men

tary

Tab

le 1

Ta

sks

and

ou

tcom

e m

easu

res

of t

he

neu

rop

sych

olog

ical

tes

t ba

tter

y

Task

(Co

gnit

ive

do

mai

n)

Des

crip

tio

nO

utc

om

e m

easu

re

1. B

asel

ine

Spee

d ta

sk1

(Mot

or s

pee

d &

rea

ctio

n t

ime)

A fi

xati

on c

ross

is s

how

n o

n a

com

pute

r sc

reen

, wh

ich

in

vari

able

inte

rval

s ch

ange

s in

to a

blo

ck. T

he

par

tici

pan

t is

ask

ed

to r

eact

as

fast

as

pos

sibl

e to

th

is b

lock

by

pres

sin

g a

key.

Bot

h

the

non

-dom

inan

t an

d do

min

ant

han

d ar

e as

sess

ed. S

core

s ar

e av

erag

ed o

ver

dom

inan

t an

d n

on-d

omin

ant

han

d.

Mea

n R

T SD

of R

T

2. W

AIS

-III D

igit

Spa

n t

ask

2

(Exe

cuti

ve f

un

ctio

nin

g:

Wor

kin

g m

emor

y)

Dig

it-s

trin

gs a

re r

ead

alou

d by

th

e ex

per

imen

ter.

In

th

e fo

rwar

d

con

dit

ion

, th

e pa

rtic

ipan

t is

ask

ed t

o re

pea

t d

igit

s in

th

e sa

me

orde

r. In

th

e ba

ckw

ard

con

dit

ion

, th

e pa

rtic

ipan

t is

ask

ed t

o re

pea

t th

e d

igit

s in

th

e re

vers

e or

der.

Forw

ard

dig

it s

pan

sco

reBa

ckw

ard

dig

it s

pan

sco

re

3. S

ust

ain

ed A

tten

tion

Dot

s

(SA

-dot

s) t

ask3

(Exe

cuti

ve f

un

ctio

nin

g:

Att

enti

on &

inh

ibit

ion

)

Part

icip

ants

are

ask

ed t

o re

act

to a

ser

ies

of d

ots

on t

he

scre

en;

ther

e ca

n b

e ei

ther

3, 4

or

5 do

ts p

rese

nte

d si

mu

ltan

eou

sly.

Dot

s ap

pea

r in

a r

ando

m o

rder

in a

pac

ed t

emp

o. W

hen

3 o

r 5

dots

ap

pea

r on

th

e sc

reen

, th

e p

arti

cip

ant

has

to

reac

t w

ith

, th

e ‘n

o-

key’

(th

e ke

y h

and

led

by t

he

non

-dom

inan

t h

and)

an

d w

hen

4

dots

app

ear

the

part

icip

ant

is a

sked

to

reac

t w

ith

th

e ‘y

es-k

ey’

(th

e ke

y h

and

led

by t

he

dom

inan

t h

and)

. Pre

ssin

g th

e ‘n

o-k

ey’

wh

en 4

dot

s ap

pea

r is

cal

led

a fa

lse

alar

m. P

ress

ing

the

‘yes

-key

’ w

hen

3 o

r 5

dots

app

ear

is c

alle

d a

mis

s. F

or a

nal

ysis

, th

e ta

sk is

sp

lit

up

into

10

bloc

ks,

or

seri

es, i

n o

rder

to

com

pute

var

ian

ce in

p

erfo

rman

ce o

ver

tim

e.

Mea

n s

erie

s co

mpl

etio

n t

ime

SD s

erie

s co

mpl

etio

n t

ime

SD s

erie

s er

rors

(SD

of t

he

erro

rs m

ade

acro

ss b

lock

s)R

esp

onse

bia

s (t

he

dif

fere

nce

bet

wee

n t

he

nu

mbe

r of

mis

ses

and

the

nu

mbe

r of

fals

e al

arm

s ac

ross

th

e en

tire

tas

k).

4. F

lan

ker

task

4

(Exe

cuti

ve f

un

ctio

nin

g:

Inh

ibit

ion

)

The

part

icip

ant

is p

rese

nte

d a

mat

rix

of 9

blo

cks

and

has

to

resp

ond

by in

dic

atin

g if

th

e co

lor

of t

he

mid

dle

blo

ck is

blu

e or

ye

llow

(lef

t or

rig

ht

butt

on p

ress

). In

par

t 1

of t

he

task

, th

is b

lock

is

flan

ked

by o

ther

blo

cks

in t

he

sam

e co

lor

as is

th

e m

idd

le

bloc

k (c

onsi

sten

t tr

ial),

or

in a

dif

fere

nt

colo

r (n

eutr

al t

rial

, gre

en

bloc

ks)

. In

par

t 2,

th

e m

idd

le b

lock

is fl

anke

d by

blo

cks

of t

he

sam

e co

lor

(con

sist

ent

tria

l), o

r by

blo

cks

that

hav

e th

e co

lor

of

the

alte

rnat

ive

resp

onse

(in

con

sist

ent

tria

l), fo

r ex

ampl

e, a

yel

low

bl

ock

flan

ked

by b

lue

bloc

ks

or v

ice

vers

a.

Tota

l mea

n R

T (a

vera

ge o

ver

part

1 a

nd

2)To

tal S

D o

f RT

(ave

rage

ove

r pa

rt 1

an

d 2)

In

hib

itio

n R

T (d

iffe

ren

ce in

RT

on

con

sist

ent

and

inco

nsi

sten

t tr

ials

in p

art

2)

Inh

ibit

ion

err

ors

(dif

fere

nce

in e

rror

rat

e be

twee

n c

onsi

sten

t an

d in

con

sist

ent

tria

ls

in p

art

2)



124

CHAPTER 6

Sup

ple

men

tary

Tab

le 1

C

onti

nu

ed

Task

(Co

gnit

ive

do

mai

n)

Des

crip

tio

nO

utc

om

e m

easu

re

5. S

ust

ain

ed A

tten

tion

to

Res

pon

se T

ask

(SA

RT)

5 (E

xecu

tive

fu

nct

ion

ing:

A

tten

tion

& in

hib

itio

n)

Ada

ptat

ion

of t

he

Go/

NoG

o ta

sk. A

str

eam

of d

igit

s (r

angi

ng

from

1

to 9

) is

pres

ente

d on

th

e sc

reen

. Th

e p

arti

cip

ant

is a

sked

to

reac

t on

th

ese

by p

ress

ing

a bu

tton

(on

a b

utt

onbo

x). T

he

stim

uli

en

sure

th

at r

eact

ion

s fo

llow

a c

erta

in p

ace.

Wh

en t

he

dig

it 3

was

pr

esen

ted,

th

e pa

rtic

ipan

t h

ad t

o w

ith

hol

d a

resp

onse

.

A c

omm

issi

on e

rror

is m

ade

wh

en t

he

part

icip

ant

pres

ses

the

butt

on w

hen

a 3

is p

rese

nte

d. A

n o

mis

sion

err

or is

mad

e w

hen

th

e pa

rtic

ipan

t do

es n

ot p

ress

th

e bu

tton

wh

en a

dig

it t

hat

is n

ot

3 is

pre

sen

ted.

Nu

mbe

r of

com

mis

sion

err

ors

Nu

mbe

r of

om

issi

on e

rror

sM

ean

RT

hit

s SD

of R

T h

its

6. T

rail

mak

ing

task

6 (E

xecu

tive

fu

nct

ion

ing:

M

otor

con

trol

& s

et-s

hif

tin

g;)

In p

art

A, p

arti

cipa

nts

are

ask

ed t

o d

raw

lin

es t

o li

nk

nu

mbe

rs

in c

onse

cuti

ve o

rder

A (1

-2-3

-…-2

5-2

6). I

n P

art

B, t

he

set-s

hif

tin

g co

nd

itio

n, p

arti

cip

ants

are

ask

ed t

o d

raw

lin

es t

o li

nk

nu

mbe

rs

and

lett

ers

in c

onse

cuti

ve o

rder

(e.g

. 1-A

-2-B

-3-…

.-K-1

2-L-

13).

Tim

e to

com

plet

e pa

rt A

Tim

e to

com

plet

e pa

rt B

Dif

fere

nce

in t

ime

to c

ompl

ete

part

B a

nd

ti

me

to c

ompl

ete

part

A.

7. S

eman

tic

cate

gory

an

d

init

ial l

ette

r fl

uen

cy7

(Exe

cuti

ve f

un

ctio

nin

g:

Spee

ch fl

uen

cy)

In t

he

firs

t pa

rt, p

arti

cipa

nts

are

ask

ed t

o n

ame

as m

any

anim

als

as t

hey

can

wit

hin

1 m

inu

te, a

fter

war

ds

they

are

ask

ed t

o m

enti

on a

s m

uch

pro

fess

ion

s as

th

ey c

an w

ith

in 1

min

ute

. In

th

e se

con

d p

art

of t

he

task

par

tici

pan

ts a

re g

iven

a fi

rst-l

ette

r an

d

are

aske

d to

men

tion

as

man

y w

ord

s as

th

ey k

now

th

at b

egin

w

ith

th

at le

tter

. Th

ey h

ave

3 tr

ials

: on

e w

ith

th

e le

tter

‘T’,

one

wit

h t

he

lett

er ‘A

’ an

d on

e w

ith

th

e le

tter

‘D’.

Nu

mbe

r of

wor

ds

men

tion

ed in

ca

tego

ry a

nim

als

Nu

mbe

r of

wor

ds

men

tion

ed in

cat

egor

y pr

ofes

sion

sN

um

ber

of w

ord

s m

enti

oned

in c

ateg

ory

lett

ers

(tot

al o

f 3 le

tter

-tri

als)

8. D

elay

Dis

cou

nti

ng

task

8 (D

elay

ave

rsio

n &

impu

lsiv

ity)

The

part

icip

ant

is r

epea

ted

ly a

sked

to

mak

e a

choi

ce b

etw

een

tw

o (h

ypot

het

ical

) in

cen

tive

s. O

ne

opti

on g

ener

ates

an

ince

nti

ve

(mon

ey) a

t a

shor

t p

erio

d w

hil

e th

e ot

her

opt

ion

gen

erat

es a

n

ince

nti

ve a

t a

late

r ti

me

(i.e.

“D

o yo

u p

refe

r to

rec

eive

30

Euro

s 18

0 da

ys f

rom

now

, or

2 Eu

ros

imm

edia

tely

?”).

Du

rin

g th

e ta

sk, t

he

valu

e of

th

e in

cen

tive

s as

wel

l as

the

tim

e of

th

e de

lay

(wit

h w

hic

h t

he

ince

nti

ve is

gai

ned

) are

var

ied.

Th

e im

puls

ivit

y pa

ram

eter

(k) i

s co

mpu

ted

from

th

e pr

esen

t va

lue

of t

he

dela

yed

re

war

d (V

), th

e re

al v

alu

e of

th

e de

laye

d re

war

d (a

) an

d th

e de

lay

in d

ays

(D) w

ith

th

e fo

rmu

la: V

= a

/ (1+

kD

).

K 1

00

K 3

0 K

10

9. T

ime

Esti

mat

ion

tas

k9

(Tim

ing)

To s

how

th

e le

ngt

h o

f on

e se

con

d,

the

part

icip

ant

is fi

rst

show

n

a pi

ctu

re o

n a

com

pute

r sc

reen

for

one

seco

nd,

th

is is

rep

eate

d

ten

tim

es. N

ext,

th

e pa

rtic

ipan

t h

as t

o re

act

to a

sou

nd

by

pres

sin

g th

e sp

ace

bar

one

seco

nd

afte

r th

e so

un

d is

pre

sen

ted.

Pa

rtic

ipan

ts r

ecei

ve fe

edba

ck a

fter

eac

h t

rial

on

th

e ac

cura

cy o

f th

eir

tim

ing

(‘too

slo

w’,

‘too

fast

’, ‘c

orre

ct’).

Med

ian

res

pon

se t

ime

Abs

olu

te d

evia

tion

of t

he

med

ian

res

pon

se

tim

e fr

om 1

000

ms

AN

T =

‘Am

ster

dam

se N

euro

psy

chol

ogis

che

Test

’ (D

e So

nn

evil

le 1

999)

; RT

= re

acti

on t

ime;

SD

= s

tan

dar

d d

evia

tion

1 P

art

of t

he

AN

T te

stin

g ba

tter

y

2 S

ubt

est

of t

he

Wec

hsl

er A

dult

Inte

llig

ence

Sca

le S

attl

er, J

. M. (

1992

). A

sses

smen

t of

Ch

ild

ren

: WIS

C-I

II a

nd

WPP

SI-R

Su

pp

lem

ent.

La

Mes

a, C

A, U

SA, J

erom

e M

. Sat

tler

,

Pu

blis

her

, In

c, W

ech

sler

, D. (

1997

). W

AIS

-III

—W

ech

sler

Adu

lt I

nte

llig

ence

Sca

le. S

an A

nto

nio

, Psy

chol

ogic

al C

orp

orat

ion

..

3 P

art

of t

he

AN

T te

stin

g ba

tter

y H

uij

breg

ts,

S. C

., A

. J. W

arre

n,

et a

l. (2

008)

. “H

ot a

nd

coo

l fo

rms

of i

nh

ibit

ory

con

trol

an

d e

xter

nal

izin

g b

ehav

ior

in c

hil

dre

n o

f

mot

her

s w

ho

smok

ed d

uri

ng

pre

gnan

cy: a

n e

xplo

rato

ry s

tud

y.”

J Abn

orm

Ch

ild

Psy

chol

36(

3): 3

23-3

33.

4 P

art

of t

he

AN

T te

stin

g H

uij

breg

ts,

S. C

., L.

M.

de

Son

nev

ille

, et

al.

(200

2).

“Th

e n

euro

psy

chol

ogic

al p

rofi

le o

f ea

rly

and

con

tin

uou

sly

trea

ted

ph

enyl

keto

nu

ria:

orie

nti

ng,

vig

ilan

ce, a

nd

mai

nte

nan

ce v

ersu

s m

anip

ula

tion

-fu

nct

ion

s of

wor

kin

g m

emor

y.”

Neu

rosc

i Bio

beh

av R

ev 2

6(6)

: 697

-712

.

5 S

mit

, A. S

., P.

A. T

. M. E

lin

g, e

t al

. (20

04).

“Men

tal e

ffor

t ca

use

s vi

gila

nce

dec

reas

e du

e to

res

ourc

e d

eple

tion

.” A

cta

Psyc

hol

ogic

a 11

5(1)

: 35

-42.

6 K

ortt

e, K

. B.,

M. D

. Hor

ner

, et

al. (

2002

). “T

he

trai

l m

akin

g te

st, p

art

B: c

ogn

itiv

e fl

exib

ilit

y or

abi

lity

to

mai

nta

in s

et?”

Ap

pl

Neu

rop

sych

ol 9

(2):

106

-109

, Stu

ss, D

. T.

and

B. L

evin

e (2

002)

. “A

dult

cli

nic

al n

euro

psy

chol

ogy:

Les

son

s fr

om s

tud

ies

of t

he

fron

tal l

obes

.” A

nn

ual

Rev

iew

of

Psyc

hol

ogy

53: 4

01-4

33, Z

akza

nis

, K. K

., R

. Mra

z,

et a

l. (2

005)

. “A

n f

MR

I stu

dy

of t

he

Trai

l Mak

ing

Test

.” N

euro

psy

chol

ogia

43(

13):

1878

-188

6.

7 H

urk

s, P

. P. M

., J.

G. M

. Hen

dri

kse

n, e

t al

. (20

04).

“Ver

bal fl

uen

cy o

ver

tim

e as

a m

easu

re o

f au

tom

atic

an

d c

ontr

olle

d p

roce

ssin

g in

ch

ild

ren

wit

h A

DH

D.”

Bra

in a

nd

Cog

nit

ion

55(

3): 5

35-5

44.

8 D

om, G

., P.

D’H

aen

e, e

t al

. (20

06).

“Im

pu

lsiv

ity

in a

bsti

nen

t ea

rly-

an

d l

ate-

onse

t al

coh

olic

s: d

iffe

ren

ces

in s

elf-r

epor

t m

easu

res

and

a d

isco

un

tin

g ta

sk.”

Ad

dic

tion

101(

1): 5

0-5

9.

9 V

an M

eel,

C. S

., J.

Oos

terl

aan

, et

al. (

2005

). “M

otiv

atio

nal

eff

ects

on

mot

or t

imin

g in

att

enti

on-d

efici

t/h

yper

acti

vity

dis

ord

er.”

Jou

rnal

of

the

Am

eric

an A

cad

emy

of

Ch

ild

an

d A

dol

esce

nt

Psyc

hia

try

44

(5):

451-

460

, R

omm

else

, N

. N

. J.,

M.

E.

Alt

ink

, et

al.

(200

8).

“Sp

eed

, va

riab

ilit

y, a

nd

tim

ing

of m

otor

ou

tpu

t in

AD

HD

: W

hic

h

mea

sure

s ar

e u

sefu

l for

en

dop

hen

otyp

ic r

esea

rch

?” B

ehav

ior

Gen

etic

s 38

(2):

121-

132.



125


6

Sup

ple

men

tary

Tab

le 1

C

onti

nu

ed

Task

(Co

gnit

ive

do

mai

n)

Des

crip

tio

nO

utc

om

e m

easu

re

5. S

ust

ain

ed A

tten

tion

to

Res

pon

se T

ask

(SA

RT)

5 (E

xecu

tive

fu

nct

ion

ing:

A

tten

tion

& in

hib

itio

n)

Ada

ptat

ion

of t

he

Go/

NoG

o ta

sk. A

str

eam

of d

igit

s (r

angi

ng

from

1

to 9

) is

pres

ente

d on

th

e sc

reen

. Th

e p

arti

cip

ant

is a

sked

to

reac

t on

th

ese

by p

ress

ing

a bu

tton

(on

a b

utt

onbo

x). T

he

stim

uli

en

sure

th

at r

eact

ion

s fo

llow

a c

erta

in p

ace.

Wh

en t

he

dig

it 3

was

pr

esen

ted,

th

e pa

rtic

ipan

t h

ad t

o w

ith

hol

d a

resp

onse

.

A c

omm

issi

on e

rror

is m

ade

wh

en t

he

part

icip

ant

pres

ses

the

butt

on w

hen

a 3

is p

rese

nte

d. A

n o

mis

sion

err

or is

mad

e w

hen

th

e pa

rtic

ipan

t do

es n

ot p

ress

th

e bu

tton

wh

en a

dig

it t

hat

is n

ot

3 is

pre

sen

ted.

Nu

mbe

r of

com

mis

sion

err

ors

Nu

mbe

r of

om

issi

on e

rror

sM

ean

RT

hit

s SD

of R

T h

its

6. T

rail

mak

ing

task

6 (E

xecu

tive

fu

nct

ion

ing:

M

otor

con

trol

& s

et-s

hif

tin

g;)

In p

art

A, p

arti

cipa

nts

are

ask

ed t

o d

raw

lin

es t

o li

nk

nu

mbe

rs

in c

onse

cuti

ve o

rder

A (1

-2-3

-…-2

5-2

6). I

n P

art

B, t

he

set-s

hif

tin

g co

nd

itio

n, p

arti

cip

ants

are

ask

ed t

o d

raw

lin

es t

o li

nk

nu

mbe

rs

and

lett

ers

in c

onse

cuti

ve o

rder

(e.g

. 1-A

-2-B

-3-…

.-K-1

2-L-

13).

Tim

e to

com

plet

e pa

rt A

Tim

e to

com

plet

e pa

rt B

Dif

fere

nce

in t

ime

to c

ompl

ete

part

B a

nd

ti

me

to c

ompl

ete

part

A.

7. S

eman

tic

cate

gory

an

d

init

ial l

ette

r fl

uen

cy7

(Exe

cuti

ve f

un

ctio

nin

g:

Spee

ch fl

uen

cy)

In t

he

firs

t pa

rt, p

arti

cipa

nts

are

ask

ed t

o n

ame

as m

any

anim

als

as t

hey

can

wit

hin

1 m

inu

te, a

fter

war

ds

they

are

ask

ed t

o m

enti

on a

s m

uch

pro

fess

ion

s as

th

ey c

an w

ith

in 1

min

ute

. In

th

e se

con

d p

art

of t

he

task

par

tici

pan

ts a

re g

iven

a fi

rst-l

ette

r an

d

are

aske

d to

men

tion

as

man

y w

ord

s as

th

ey k

now

th

at b

egin

w

ith

th

at le

tter

. Th

ey h

ave

3 tr

ials

: on

e w

ith

th

e le

tter

‘T’,

one

wit

h t

he

lett

er ‘A

’ an

d on

e w

ith

th

e le

tter

‘D’.

Nu

mbe

r of

wor

ds

men

tion

ed in

ca

tego

ry a

nim

als

Nu

mbe

r of

wor

ds

men

tion

ed in

cat

egor

y pr

ofes

sion

sN

um

ber

of w

ord

s m

enti

oned

in c

ateg

ory

lett

ers

(tot

al o

f 3 le

tter

-tri

als)

8. D

elay

Dis

cou

nti

ng

task

8 (D

elay

ave

rsio

n &

impu

lsiv

ity)

The

part

icip

ant

is r

epea

ted

ly a

sked

to

mak

e a

choi

ce b

etw

een

tw

o (h

ypot

het

ical

) in

cen

tive

s. O

ne

opti

on g

ener

ates

an

ince

nti

ve

(mon

ey) a

t a

shor

t p

erio

d w

hil

e th

e ot

her

opt

ion

gen

erat

es a

n

ince

nti

ve a

t a

late

r ti

me

(i.e.

“D

o yo

u p

refe

r to

rec

eive

30

Euro

s 18

0 da

ys f

rom

now

, or

2 Eu

ros

imm

edia

tely

?”).

Du

rin

g th

e ta

sk, t

he

valu

e of

th

e in

cen

tive

s as

wel

l as

the

tim

e of

th

e de

lay

(wit

h w

hic

h t

he

ince

nti

ve is

gai

ned

) are

var

ied.

Th

e im

puls

ivit

y pa

ram

eter

(k) i

s co

mpu

ted

from

th

e pr

esen

t va

lue

of t

he

dela

yed

re

war

d (V

), th

e re

al v

alu

e of

th

e de

laye

d re

war

d (a

) an

d th

e de

lay

in d

ays

(D) w

ith

th

e fo

rmu

la: V

= a

/ (1+

kD

).

K 1

00

K 3

0 K

10

9. T

ime

Esti

mat

ion

tas

k9

(Tim

ing)

To s

how

th

e le

ngt

h o

f on

e se

con

d,

the

part

icip

ant

is fi

rst

show

n

a pi

ctu

re o

n a

com

pute

r sc

reen

for

one

seco

nd,

th

is is

rep

eate

d

ten

tim

es. N

ext,

th

e pa

rtic

ipan

t h

as t

o re

act

to a

sou

nd

by

pres

sin

g th

e sp

ace

bar

one

seco

nd

afte

r th

e so

un

d is

pre

sen

ted.

Pa

rtic

ipan

ts r

ecei

ve fe

edba

ck a

fter

eac

h t

rial

on

th

e ac

cura

cy o

f th

eir

tim

ing

(‘too

slo

w’,

‘too

fast

’, ‘c

orre

ct’).

Med

ian

res

pon

se t

ime

Abs

olu

te d

evia

tion

of t

he

med

ian

res

pon

se

tim

e fr

om 1

000

ms

AN

T =

‘Am

ster

dam

se N

euro

psy

chol

ogis

che

Test

’ (D

e So

nn

evil

le 1

999)

; RT

= re

acti

on t

ime;

SD

= s

tan

dar

d d

evia

tion

1 P

art

of t

he

AN

T te

stin

g ba

tter

y

2 S

ubt

est

of t

he

Wec

hsl

er A

dult

Inte

llig

ence

Sca

le S

attl

er, J

. M. (

1992

). A

sses

smen

t of

Ch

ild

ren

: WIS

C-I

II a

nd

WPP

SI-R

Su

pp

lem

ent.

La

Mes

a, C

A, U

SA, J

erom

e M

. Sat

tler

,

Pu

blis

her

, In

c, W

ech

sler

, D. (

1997

). W

AIS

-III

—W

ech

sler

Adu

lt I

nte

llig

ence

Sca

le. S

an A

nto

nio

, Psy

chol

ogic

al C

orp

orat

ion

..

3 P

art

of t

he

AN

T te

stin

g ba

tter

y H

uij

breg

ts,

S. C

., A

. J. W

arre

n,

et a

l. (2

008)

. “H

ot a

nd

coo

l fo

rms

of i

nh

ibit

ory

con

trol

an

d e

xter

nal

izin

g b

ehav

ior

in c

hil

dre

n o

f

mot

her

s w

ho

smok

ed d

uri

ng

pre

gnan

cy: a

n e

xplo

rato

ry s

tud

y.”

J Abn

orm

Ch

ild

Psy

chol

36(

3): 3

23-3

33.

4 P

art

of t

he

AN

T te

stin

g H

uij

breg

ts,

S. C

., L.

M.

de

Son

nev

ille

, et

al.

(200

2).

“Th

e n

euro

psy

chol

ogic

al p

rofi

le o

f ea

rly

and

con

tin

uou

sly

trea

ted

ph

enyl

keto

nu

ria:

orie

nti

ng,

vig

ilan

ce, a

nd

mai

nte

nan

ce v

ersu

s m

anip

ula

tion

-fu

nct

ion

s of

wor

kin

g m

emor

y.”

Neu

rosc

i Bio

beh

av R

ev 2

6(6)

: 697

-712

.

5 S

mit

, A. S

., P.

A. T

. M. E

lin

g, e

t al

. (20

04).

“Men

tal e

ffor

t ca

use

s vi

gila

nce

dec

reas

e du

e to

res

ourc

e d

eple

tion

.” A

cta

Psyc

hol

ogic

a 11

5(1)

: 35

-42.

6 K

ortt

e, K

. B.,

M. D

. Hor

ner

, et

al. (

2002

). “T

he

trai

l m

akin

g te

st, p

art

B: c

ogn

itiv

e fl

exib

ilit

y or

abi

lity

to

mai

nta

in s

et?”

Ap

pl

Neu

rop

sych

ol 9

(2):

106

-109

, Stu

ss, D

. T.

and

B. L

evin

e (2

002)

. “A

dult

cli

nic

al n

euro

psy

chol

ogy:

Les

son

s fr

om s

tud

ies

of t

he

fron

tal l

obes

.” A

nn

ual

Rev

iew

of

Psyc

hol

ogy

53: 4

01-4

33, Z

akza

nis

, K. K

., R

. Mra

z,

et a

l. (2

005)

. “A

n f

MR

I stu

dy

of t

he

Trai

l Mak

ing

Test

.” N

euro

psy

chol

ogia

43(

13):

1878

-188

6.

7 H

urk

s, P

. P. M

., J.

G. M

. Hen

dri

kse

n, e

t al

. (20

04).

“Ver

bal fl

uen

cy o

ver

tim

e as

a m

easu

re o

f au

tom

atic

an

d c

ontr

olle

d p

roce

ssin

g in

ch

ild

ren

wit

h A

DH

D.”

Bra

in a

nd

Cog

nit

ion

55(

3): 5

35-5

44.

8 D

om, G

., P.

D’H

aen

e, e

t al

. (20

06).

“Im

pu

lsiv

ity

in a

bsti

nen

t ea

rly-

an

d l

ate-

onse

t al

coh

olic

s: d

iffe

ren

ces

in s

elf-r

epor

t m

easu

res

and

a d

isco

un

tin

g ta

sk.”

Ad

dic

tion

101(

1): 5

0-5

9.

9 V

an M

eel,

C. S

., J.

Oos

terl

aan

, et

al. (

2005

). “M

otiv

atio

nal

eff

ects

on

mot

or t

imin

g in

att

enti

on-d

efici

t/h

yper

acti

vity

dis

ord

er.”

Jou

rnal

of

the

Am

eric

an A

cad

emy

of

Ch

ild

an

d A

dol

esce

nt

Psyc

hia

try

44

(5):

451-

460

, R

omm

else

, N

. N

. J.,

M.

E.

Alt

ink

, et

al.

(200

8).

“Sp

eed

, va

riab

ilit

y, a

nd

tim

ing

of m

otor

ou

tpu

t in

AD

HD

: W

hic

h

mea

sure

s ar

e u

sefu

l for

en

dop

hen

otyp

ic r

esea

rch

?” B

ehav

ior

Gen

etic

s 38

(2):

121-

132.



126

CHAPTER 6

References

Association, A. P. (2000). Diagnostic and statistical manual of mental disorders: DSM-IV TR®. Washington,

DC, American Psychiatric Press.

Barkley, R. A. (1997). “Behavioral inhibition, sustained attention, and executive functions: constructing a

unifying theory of ADHD.” Psychol Bull 121(1): 65-94.

Castellanos, F. X. and R. Tannock (2002). “Neuroscience of attention-deficit/hyperactivity disorder: the

search for endophenotypes.” Nat Rev Neurosci 3(8): 617-628.

Coghill, D. R., D. Hayward, et al. (2014). “A longitudinal examination of neuropsychological and clinical

functioning in boys with attention deficit hyperactivity disorder (ADHD): improvements in executive

functioning do not explain clinical improvement.” Psychol Med 44(5): 1087-1099.

Coghill, D. R., S. Seth, et al. (2014). “A comprehensive assessment of memory, delay aversion, timing,

inhibition, decision making and variability in attention deficit hyperactivity disorder: advancing

beyond the three-pathway models.” Psychol Med 44(9): 1989-2001.

Costa, P. T., Jr. and R. R. McCrae (1992). Manual for the revised NEO personality inventory (NEO P-R) and NEO

five-factor inventory (NEO-FFI). Odessa, Psychological Assessment Resources.

De Sonneville, L. M. J. (1999). Amsterdam Neuropsychological Tasks: a computer-aided assessment program.

Cognitive ergonomics, clinical assessment and computer-assisted learning: Computers in Psychology.

B. P. L. M. Den Brinker, P. J. Beek, A. N. Brand, S. J. Maarse and L. J. M. Mulder. Lisse, The Netherlands,

Swets & Zeitlinger. 6: 187-203.

de Zeeuw, P., J. Weusten, et al. (2012). “Deficits in cognitive control, timing and reward sensitivity appear

to be dissociable in ADHD.” PLoS One 7(12): e51416.

Deyoung, C. G., J. B. Peterson, et al. (2008). “Externalizing behavior and the higher order factors of the Big

Five.” J Abnorm Psychol 117(4): 947-953.

Dom, G., P. D’Haene, et al. (2006). “Impulsivity in abstinent early- and late-onset alcoholics: differences in

self-report measures and a discounting task.” Addiction 101(1): 50-59.

Fair, D. A., D. Bathula, et al. (2012). “Distinct neuropsychological subgroups in typically developing youth

inform heterogeneity in children with ADHD.” Proc Natl Acad Sci U S A 109(17): 6769-6774.

Faraone, S. V. A., P. ; Banaschewski, T. ; Biederman, J. ; Buitelaar, J.K. ; Ramos-Quiroga, J.A. ; Rohde, L.A. ;

Sonuga-Barke, E. ; Tannock, R. ; Franke, B. (2015). “Attention Deficit Hyperactivity Disorder. .” Nature

Review Disease Primers.

Franke, B., M. Hoogman, et al. (2008). “Association of the dopamine transporter (SLC6A3/DAT1) gene 9-6

haplotype with adult ADHD.” Am J Med Genet B Neuropsychiatr Genet 147B(8): 1576-1579.

Franke, B., A. A. Vasquez, et al. (2010). “Multicenter analysis of the SLC6A3/DAT1 VNTR haplotype in

persistent ADHD suggests differential involvement of the gene in childhood and persistent ADHD.”

Neuropsychopharmacology 35(3): 656-664.

Gomez, R. and P. J. Corr (2014). “ADHD and personality: a meta-analytic review.” Clin Psychol Rev 34(5): 376-388.

Graham, E. K. and M. E. Lachman (2014). “Personality Traits, Facets and Cognitive Performance: Age

Differences in Their Relations.” Pers Individ Dif 59: 89-95.

Groenestijn, M., G. Akkerhuis, et al. (1999). Gestructureerd klinisch interview voor de vaststelling van

DSM-IV as I stoornissen [structured Clinical Interview for DSM-IV axis I disorders]. Lisse, The

Netherlands, Swets & Zeitlinger.

Hirsh, J., D. Morisano, et al. (2008). “Delay discounting: Interactions between personality and cognitive

ability.” Journal of Research in Personality(42): 1646-1650.

Hoogman, M., E. Aarts, et al. (2011). “Nitric oxide synthase genotype modulation of impulsivity and ventral

striatal activity in adult ADHD patients and healthy comparison subjects.” Am J Psychiatry 168(10):

1099-1106.

Hoogman, M., M. Onnink, et al. (2013). “The dopamine transporter haplotype and reward-related striatal

responses in adult ADHD.” Eur Neuropsychopharmacol 23(6): 469-478.

Huijbregts, S. C., L. M. de Sonneville, et al. (2002). “The neuropsychological profile of early and continuously

treated phenylketonuria: orienting, vigilance, and maintenance versus manipulation-functions of

working memory.” Neurosci Biobehav Rev 26(6): 697-712.



127


6

Huijbregts, S. C., A. J. Warren, et al. (2008). “Hot and cool forms of inhibitory control and externalizing

behavior in children of mothers who smoked during pregnancy: an exploratory study.” J Abnorm

Child Psychol 36(3): 323-333.

Hurks, P. P. M., J. G. M. Hendriksen, et al. (2004). “Verbal fluency over time as a measure of automatic and

controlled processing in children with ADHD.” Brain and Cognition 55(3): 535-544.

Karalunas, S. L., D. Fair, et al. (2014). “Subtyping attention-deficit/hyperactivity disorder using temperament

dimensions: toward biologically based nosologic criteria.” JAMA Psychiatry 71(9): 1015-1024.

Kooij, J. J. (2010). Diagnostic interview for ADHD in adults 2.0 (DIVA 2.0). Adult ADHD. Diagnostic Assessment

and Treatment. Amsterdam, Pearson Assessment and Information BV.

Kooij, J. J., J. K. Buitelaar, et al. (2005). “Internal and external validity of attention-deficit hyperactivity

disorder in a population-based sample of adults.” Psychol Med 35(6): 817-827.

Kortte, K. B., M. D. Horner, et al. (2002). “The trail making test, part B: cognitive flexibility or ability to

maintain set?” Appl Neuropsychol 9(2): 106-109.

Leth-Steensen, C., Z. K. Elbaz, et al. (2000). “Mean response times, variability, and skew in the responding of

ADHD children: a response time distributional approach.” Acta Psychol (Amst) 104(2): 167-190.

McCrae, R. R. and P. T. Costa (2004). “A contemplated revision of the NEO Five-Factor Inventory.” Personality

and Individual Differences 36: 587-596.

Mostert, J. C., M. Hoogman, et al. (2015). “Similar Subgroups Based on Cognitive Performance Parse

Heterogeneity in Adults With ADHD and Healthy Controls.” J Atten Disord.

Mostert, J. C., A. M. Onnink, et al. (2015). “Cognitive heterogeneity in adult attention deficit/hyperactivity

disorder: A systematic analysis of neuropsychological measurements.” Eur Neuropsychopharmacol.

Murdock, K. W., K. B. Oddi, et al. (2013). “Cognitive correlates of personality.” Journal of Individual

Differences 34(2): 97-104.

Nigg, J. T., G. Stavro, et al. (2005). “Executive functions and ADHD in adults: Evidence for selective effects on

ADHD symptom domains.” Journal of Abnormal Psychology 114(4): 706-717.

Onnink, A. M., M. P. Zwiers, et al. (2014). “Brain alterations in adult ADHD: effects of gender, treatment and

comorbid depression.” Eur Neuropsychopharmacol 24(3): 397-409.

Pennington, B. F. and S. Ozonoff (1996). “Executive functions and developmental psychopathology.” J Child

Psychol Psychiatry 37(1): 51-87.

Pytlik Zillig, L. M., S. H. Hemenover, et al. (2002). “What do we assess when we assess a Big 5 trait? A content

analysis of the affective, behavioral, and cognitive proecesses represented in Big 5 personality

inventories.” Personality and Social Psychology Bulletin 28(6): 847-858.

Rommelse, N. N. J., M. E. Altink, et al. (2008). “Speed, variability, and timing of motor output in ADHD:

Which measures are useful for endophenotypic research?” Behavior Genetics 38(2): 121-132.

Rothbart, M. K. (2007). “Temperament, development, and personality.” Current Directions in Psychological

Science 16: 207-212.

Rothbart, M. K. (2011). Becoming who we are: Temperament and personality in development. . New York,

NY, Guidford Press.

Sattler, J. M. (1992). Assessment of Children: WISC-III and WPPSI-R Supplement. La Mesa, CA, USA, Jerome

M. Sattler, Publisher, Inc.

Schachar, R., V. L. Mota, et al. (2000). “Confirmation of an inhibitory control deficit in attention-deficit/

hyperactivity disorder.” J Abnorm Child Psychol 28(3): 227-235.

Smit, A. S., P. A. T. M. Eling, et al. (2004). “Mental effort causes vigilance decrease due to resource depletion.”

Acta Psychologica 115(1): 35-42.

Sonuga-Barke, E., P. Bitsakou, et al. (2010). “Beyond the dual pathway model: evidence for the dissociation of

timing, inhibitory, and delay-related impairments in attention-deficit/hyperactivity disorder.” J Am

Acad Child Adolesc Psychiatry 49(4): 345-355.

Stuss, D. T. and B. Levine (2002). “Adult clinical neuropsychology: Lessons from studies of the frontal lobes.”

Annual Review of Psychology 53: 401-433.

van Hulst, B. M., P. de Zeeuw, et al. (2015). “Distinct neuropsychological profiles within ADHD: a latent class

analysis of cognitive control, reward sensitivity and timing.” Psychol Med 45(4): 735-745.



128

CHAPTER 6

Van Meel, C. S., J. Oosterlaan, et al. (2005). “Motivational effects on motor timing in attention-deficit/

hyperactivity disorder.” Journal of the American Academy of Child and Adolescent Psychiatry 44(5):

451-460.

Wechsler, D. (1997). WAIS-III—Wechsler Adult Intelligence Scale. San Antonio, Psychological Corporation.

Weertman, A., A. Arntz, et al. (2000). Gestructureerd klinisch interview voor DSM-IV as II persoonlijkheids-

stoornissen [The Structured Clinical Interview for DSM-IVAxis II Disorders]. Lisse, The Netherlands,

Swets & Zeitlinger.

Widiger, T. A. (2011). “Personality and psychopathology.” World Psychiatry 10: 103-106.

Williams, P. G., Y. Suchy, et al. (2010). “Five-Factor Model personality traits and executive functioning

among older adults.” Journal of Research in Personality 44: 485-491.

Williams, P. G., Y. Suchy, et al. (2009). “Individual differences in executive functioning: implications for

stress regulation.” Ann Behav Med 37(2): 126-140.

Zakzanis, K. K., R. Mraz, et al. (2005). “An fMRI study of the Trail Making Test.” Neuropsychologia 43(13):

1878-1886.



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Summary and General Discussion

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SUMMARY AND GENERAL DISCUSSION

7

Summary and General Discussion

The current thesis examines both the symptomatic overlap and differences

between ADHD and BPD, and studies the interactions with regard to symptoms,

temperament/personality, and response inhibition (chapter 3-5). Furthermore,

chapter 6 focuses on the relationship between neurocognition and personality

traits in adult ADHD vs controls.

Here we summarize and discuss our findings within the context of the

literature in this field. The clinical relevance and recommendations for future

research are then outlined.

Summary of our main findings

Chapter 2, a literature review, dealt with several concepts and issues concerning

the relation of adult ADHD to personality disorders and traits. One of our conclusions

was that most previous studies on adult ADHD and personality did not account for

co-occurring personality disorders, making it difficult to draw specific conclusions

on the delineation and overlap among ADHD, personality disorders and personality

traits.

In chapter 3 we illustrated that every female with BPD in our sample had some

ADHD symptoms in both childhood and adulthood and that hyperactivity

symptoms appear to be characteristic for both female ADHD and BPD patients. We

suggested that hyperactivity could play a mediating role in the development of

BPD along the path of ADHD.

This connects with our finding in chapter 4 where we showed that an outspoken

Novelty Seeking temperament suggests a vulnerability for the development of

female ADHD and co-occurring BPD. Here we also pointed out that females with

only symptoms of ADHD (i.e. without BPD symptoms) showed normal character

development and thus absence of a personality disorder.

In chapter 5 we addressed whether the shared hyperactivity symptoms and

impulsivity traits are pointing to the same underlying cognitive processes or whether

ADHD and BPD could be differentiated at the level of cognitive processes. We showed

that, independently of ADHD, response inhibition deficits are also related to BPD.

Moreover, contrary to patients with ADHD, BPD patients may suffer from more

widespread inhibition deficiencies and a specific impairment in context processing.

Thus, it seems that ADHD and BPD share features of hyperactivity and

impulsivity at the level of symptoms, personality traits and neurocognitive

performance. An interesting question following this conclusion is whether such

clinical features, neurocognitive performance, and personality traits are related



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to one another, taking the presence of psychopathology into account. In Chapter 6

we showed that there was no relation between cognitive profile and personality in

the ADHD population, and that the presence of ADHD rather than cognitive profile

is associated with personality traits.

General Discussion

There is no BPD without at least some current and childhood ADHD hyperactivity/impulsivity symptoms The clinical distinction to enable the diagnosis (and treatment) of adults with BPD

(and ADHD) is not clearly defined. In this regard, understanding how ADHD and

BPD are different and/or alike in order to create a clinical distinction is important.

A common underlying trait such as impulsivity can create co-occurrence and obscure

syndrome specific symptoms. Furthermore, not appreciating the comorbidity of BPD

with ADHD could result in inappropriate treatment. Previous studies had already

documented associations between symptoms of ADHD in either childhood or

adulthood and BPD, but rather than showing differences in clinical severity of the

symptoms we have identified qualitatively different symptom profiles for both

childhood and adult ADHD and adult BPD symptoms in female adults with ADHD

and/or BPD (chapter 3).

Whereas adults with a primary diagnosis of ADHD and no BPD showed no

symptoms of BPD, we found that all adults with BPD showed some ADHD symptoms,

with at least hyperactivity/impulsivity. Some adults also showed a symptom profile

with BPD, hyperactivity/impulsivity, and inattention problems. While inattention

symptoms may not be exclusive in ADHD, they may play a role in other diagnostic

cohorts such as BPD. We also showed that the presence of hyperactive/impulsive

symptoms in childhood could possibly play a mediating role in the development of

an adult BPD. This study therefore develops our understanding of the evolution of

BPD in adulthood from childhood ADHD symptoms. Moreover, since we included

only women in this clinical sample and the sex ratio for ADHD is more equally

divided than for BPD (1:1 vs. 1:3 male: female), the results are probably more

representative for the population with BPD. It is not yet determined which factors

mediate whether childhood ADHD progresses to adult ADHD rather than adult

BPD (or both).

In summary, we conclude that hyperactivity/impulsivity has little discriminative

value for ADHD and BPD in women. Most likely, a client with a BPD diagnosis has

already had (and may still retain) hyperactivity/impulsivity symptoms in childhood

similar to that seen in ADHD. Although it is possible that the processes underlying

the expression of any one childhood disorder may increase the likelihood of



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developing BPD in adulthood, we suggest that hyperactivity/impulsivity is one, of

maybe several, unique areas of overlap between BPD and ADHD which warrant

further investigation as to the links between these conditions. Indeed, previous

research has demonstrated that disruptive behavior disorders and ADHD are

predictive of personality disorders (which includes BPD) (Helgeland, Kjelsberg et

al. 2005; Miller, Flory et al. 2008).

Prospective research demonstrated that growth scores in ADHD severity from

10-13 years predicted BPD symptoms at age 14. Additionally, the development of

ODD severity in age 8-10 years also predicted BPD symptoms at age 14 (Stepp, Burke

et al. 2012). Such findings indeed suggest that girls who develop BPD symptoms

may experience many features in common with girls who have ADHD (and ODD).

Furthermore, a recent study revealed a significant association between ADHD and

BPD symptoms and showed that impulsivity, as well as emotion dysregulation,

fully mediated the relationship between retrospectively assessed ADHD symptoms

and current BPD features (Fossati, Gratz et al. 2015). Notably and surprisingly, this

effect was found to be true among only females (vs males). The authors conclude

therefore that gender seems to be an important factor to consider in understanding

the relation between (childhood) ADHD and BPD, at least in clinical populations.

Previous literature mostly suggests that men and women with BPD are more

similar in their clinical presentation than they are different. Gender differences

are found in the type of impulse related disorders that they predominantly display.

For example women are more familiar with eating disorders (internalizing behaviors)

and men with substance abuse and antisocial personality disorder (externalizing

behaviors) (Zanarini, Frankenburg et al. 1998; Zlotnick, Rothschild et al. 2002).

However, it has also been suggested that the few gender differences that are found

in BPD are similar to those found in the general population (Johnson, Shea et al.

2003). Epidemiological research on eating disorders have shown that eating

disorders are more prevalent in women than in men and community studies have

reported higher rates of antisocial behavior in men than in women (Hsu 1996;

Torgersen, Kringlen et al. 2001)

In sum, chapter 3 in this thesis adds to a growing body of literature that

provides support for the notion that ADHD and BPD in women are probably, but

not solely, linked through hyperactivity/impulsivity features. Whether BPD may

emerge as a result of ADHD symptoms is however not clear. It is important to note

that there is likely an interaction between vulnerabilities in emotion regulation,

impulse control, and dysfunctional environment as well as traumatic events that

must occur for BPD to emerge (Crowell, Beauchaine et al. 2009). Additionally, the

developmental progression of childhood ADHD to adult BPD may depend on the

presence of vulnerability and risk factors that have different rates of occurrence

(or different implications) across gender.



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Further research should investigate how developmental risk factors, such as

childhood abuse/neglect and attachment disturbances, may differently interact

with childhood ADHD symptoms in influencing the developmental trajectory of

BPD in females versus males. With regard to the outcome in BPD, it is of interest to

note that prospectively designed studies suggest that a favorable outcome depends

more on the presence of favorable personality traits rather than on the absence of

certain symptoms or syndromes (Stone 2016). Three variables associated with an

earlier time-to-recovery are aspects of temperament: being without the avoidance

and dependency of anxious cluster personality disorders as well as exhibiting

higher levels of extraversion and agreeableness. Besides this, it was also found that

the absence of ADHD also significantly predicted earlier time to recovery in

patients with BPD (Zanarini, Frankenburg et al. 2014). In terms of directions for

future research, it would be important to determine the best predictive model for

the recovery of BPD with co-occurring ADHD.

Extreme Novelty Seeking temperament in ADHD might predispose to later co-occurring BPD

In chapter 4 of this thesis we examined the role of temperament and personality

traits in the co-occurrence of ADHD and BPD. We aimed to identify shared and

unique personality characteristics and to gain greater insight in the possible

pathways from early temperament to future ADHD and/or BPD. Previous studies

had already shown that ADHD and BPD seem to share a number of temperament

and character traits but, at that time, neither the comorbid presence of ADHD in

the BPD samples nor the comorbid presence of BPD in the ADHD samples were

controlled for. Chapter 4 shows that, except for those BPD and ADHD patients that

are characterized by a symptom profile with mostly BPD and ADHD hyperactivity

symptoms, all other patients showed significantly above average scores on a

Novelty Seeking (associated with behavioral activation, including impulsivity)

temperament. Novelty Seeking may therefore be more strongly linked to ADHD

and less to BPD. Later research also illustrated that ADHD and ADHD-BPD patients

differed from BPD subjects by a higher level of impulsivity (Prada and Hasler 2014).

However, the Highest Novelty Seeking was found in those ADHD and BPD patients

with symptoms of BPD and symptoms in all areas of ADHD. Thus, an extreme

Novelty Seeking temperament (i.e. a temperament tendency toward impulsivity in

response to novel stimuli) might suggest a vulnerability for the development of

ADHD and co-occurring BPD. This finding seems in line with previous findings

and our own finding in chapter 3; that impulsivity is an important factor in the

development of BPD, in addition to ADHD.

Furthermore, we showed that Harm Avoidance (which is associated with emotional

sensitivity, negative affectivity, behavioral inhibition in response to danger or



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novelty and trait anxiety) may be specifically linked to BPD, which is a finding in

keeping with previous findings (Joyce, McKenzie et al. 2003). Later work indeed

shows that temperament/personality traits could mediate the relation between

childhood ADHD and adult BPD features. Impulsivity, aggression, novelty seeking,

and juvenile conduct problems altogether completely mediated the relationship

between retrospective ADHD symptoms and current BPD features (Carlotta,

Borroni et al. 2013). Additionally, in a female sample mediation analyses revealed

that both impulsivity and emotion dysregulation fully mediated the relationship

between childhood ADHD symptoms and current BPD features (Fossati, Gratz et

al. 2015). It has also been suggested that emotion dysregulation is prevalent in

ADHD throughout the lifespan and is a major contributor to impairment (Shaw,

Stringaris et al. 2014). Thus, a Novelty Seeking and Harm Avoidance temperament

might indeed predispose for later BPD features. Moreover, adolescents with BPD

show a strong affinity to self-injurious behavior due to experiencing aversive

emotions as intolerable and impulsively attempt to ameliorate those (Kaess,

Brunner et al. 2014).

The basis for the expression of BPD features in those individuals with an

extreme Novelty Seeking temperament is poorly understood. Theoretically it

could be argued that Novelty Seeking may also play a protective role, as aspects of

Novelty Seeking may also dispose to an active coping style. An orientation toward

approaching novel stimuli and overcoming hurdles to achieve goals may run

counter to the avoidance tendencies that have been proposed to underlie self-injury

in BPD (Chapman, Specht et al. 2005). Indeed, there are indications that Novelty

Seeking is negatively associated with future self-injury among females with BPD,

whereas the role of higher levels of Harm Avoidance may need further examination

(Chapman, Derbidge et al. 2009).

Overall, such findings suggest that difficulties with negative emotionality and

behavioral control represent critical elements in the relationship between

childhood ADHD (symptoms) and BPD (symptoms) in adult women. Future research

could concern the role of the interaction between a child’s personality profile and

his/her family environment in the transition from ADHD to BPD. In this regard,

attachment disturbances are of particular interest. On the one hand, because they

represent another developmental risk factor that has been consistently found to be

associated with BPD (Agrawal, Gunderson et al. 2004; Choi-Kain, Fitzmaurice et al.

2009; Fossati, Borroni et al. 2012). On the other hand, when attachment is strong,

individuals may be more likely to experience belongingness, and thereby are less

likely to engage in self-injury (Chapman, Derbidge et al. 2009).



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ADHD and BPD are associated with distinct impulsive phenotypes While it is clear that there is a behavioral overlap in impulsivity in co-occurring

BPD and ADHD, at the level of symptoms and traits, it is unclear if this involves the

same underlying cognitive process. One such process could be response inhibition

deficits, which were assessed in the continuous performance task (CPT) in ADHD

and BPD patients. Previous research has not convincingly established whether or

not BPD is related to response inhibition deficits independently of ADHD. Chapter 5

demonstrated that response inhibition deficits may be related to BPD independently

of ADHD (in both males and females). In fact, patients with BPD performed

significantly worse than ADHD patients on several CPT indices. Therefore, counter-

intuitively, they may suffer from more widespread inhibition deficiencies than

ADHD patients. Moreover, the BPD patients might be specifically impaired in

context processing (i.e. the mental representation, maintenance and updating of

context information). Context processing is an executive ability that refers to

the adaptive control of behavior through use of prior contextual information

that must be mentally represented and maintained to support context-appropriate

behavior (Cohen and Servan-Schreiber 1992). Context processing thus depends on

several cognitive processes including selective attention, working memory, cognitive

control, and response inhibition. In the CPT task representation and maintenance

of antecedent contextual information relevant to an immediate goal is needed to

overcome an established automatic or pre-potent response. Although our work

may contribute to the growing evidence that executive function deficits play a role

in BPD, the specific domains that may account for these contributions are far less

apparent (McClure, Hawes et al. 2016).

Recent studies have suggested that impulsivity symptoms in BPD may be

stress-dependent or linked with high emotionality and therefore variation in

impulsivity may be explained by state changes. Indeed, even under resting state

conditions, BPD patients demonstrated higher trait and state impulsivity compared

to healthy controls and significant correlations between these self-reported

difficulties in emotion regulation and attentional impulsiveness (Cackowski, Reitz

et al. 2014). Such findings might help interpret our data demonstrating differences

in context processing. Moreover, a recent paper, has suggested that top-down regulation

in ADHD differs in comparison to specific emotional instability disorders including

BPD (Sebastian, Jung et al. 2014) which may underlie differential contextual inter-

pretations in both disorders. However, contradictory findings showed no impairment

in inhibitory function in BPD without ADHD and even enhanced response inhibition

after stress induction in patients with BPD without ADHD compared to healthy

particiapants (Krause-Utz, Sobanski et al. 2013).

More globally, whether brain processes associated with “emotion” can be separated

from those involved in “cognition” is debatable (Okon-Singer, Hendler et al. 2014).



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Previous work demonstrates that emotional cues, - states, and – traits can strongly

influence key elements of information processing, including selective attention,

working memory and cognitive control. In turn, circuits involved in attention and

working memory contribute to the voluntary regulation of emotion. The distinction

between the ‘emotional” and the “cognitive” brain is blurry and context dependent

and emotion and cognition seem deeply interwoven together (Okon-Singer,

Hendler et al. 2015). Although ADHD has been classically defined on the basis of

dysfunctional regulation of non-emotional information processing and BPD on

the basis of dysfunctional regulation of emotional processes, it has been recently

proposed that dysregulation in these different dimensions can be incorporated

into one theoretical unified model. This model suggests that ADHD and BPD are

mechanistically related in that they all involve similar dysfunctional top-down

regulation of information processing. The difference is whether this dysfunctional

regulation is related to emotional processing or non-emotional processing. Since

there is substantial overlap between the disorders and a tight relation between

symptoms, in line with a common underlying mechanism for these clinical states,

possibly the best way to describe these states is with traits related to emotional

dysregulation and traits related to non-emotional dysregulation that are combined

to different degrees. Hence, using a dimensional rather than a categorical approach

is recommended, which may both improve our understanding of patients’ needs

and their treatment (Petrovic and Castellanos 2016).

Personality traits are related to clinical symptoms rather than to cognitive profile

In chapter 6 we investigated whether the Five Factor Model (FFM) personality traits

are related to neurocognitive profiles in adults with ADHD and/or healthy controls.

Unfortunately, we could not control for BPD in this study as there was a lack of

sufficient and clear data on BPD diagnosis and symptoms. This impacts on the

ability to discuss the results of chapter 6 in relation to BPD. Therefore, adding to this

discussion, we examined the limited available datasets, i.e. the number of self-

reported BPD symptoms, in relation to the neurocognitive profiles and the FFM traits.

Irrespective of cognitive profile, participants with ADHD showed significantly

higher Neuroticism and lower Extraversion, Agreeableness, and Conscientiousness

than healthy controls. Previous research also showed associations of ADHD with

higher levels of neuroticism and lower levels of conscientiousness and agreeableness

(Nigg, John et al. 2002; Miller, Miller et al. 2008). Findings with regard to extra -

version in ADHD have been inconsistent. Only the FFM personality factor Openness

differed significantly between neurocognitive profiles. Higher Openness was more

common in those with aberrant attention and inhibition than those with increased

delay discounting and atypical working memory / verbal fluency. The results



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suggest that the personality trait Openness, but not any other FFM factor, is linked

to neurocognitive profiles in ADHD. Thus, the presence of ADHD rather than

cognitive profile is associated with personality traits.

With regard to the BPD symptoms, we also found no significant effect of total

number of BPD traits on the cognitive profiles for either the ADHD and the control

group. Of note, 33% of the adults with ADHD had reported five or more BPD features

(compared to 2% of the healthy controls. The cut off of 5 reported traits is used in

clinical practice to initiate full assessment of the existence of BPD. This is in line

with the high frequency of co-occurring ADHD and BPD, as was also the case in

chapter 2 with a frequency of 15% BPD in our ADHD population and 33% ADHD in

our BPD population. The total number of BPD traits showed a significant positive

correlation with Neuroticism, but not with the other four FFM traits. Thus the

more BPD symptoms were reported, the higher the score on the Neuroticism trait.

This finding is consistent with extensive prior literature showing strong positive

associations between phenotypic associations for BPD with Neuroticism. Previous

work also shows that low Agreeableness and low Conscientiousness are consistently

associated with BPD (Widiger and Costa 2002; Kendler, Myers et al. 2011).

With regard to the FFM traits it thus seems that both ADHD and BPD are

associated with high Neuroticism, Low Agreeableness and low Conscientiousness.

Furthermore, there is evidence suggesting genetic correlations for Neuroticism,

Agreeableness and Conscientiousness with BPD characteristics and for Neuroticism

and Conscientiousness with ADHD (Martel, Nikolas et al. 2010; Kendler, Myers et

al. 2011). Thus, ADHD and BPD appear to be linked to similar personality traits.

The underlying basis may however differ. Analyses of the facets of the overall

domains could be quite important and fundamental to the description and

understanding of both ADHD and BPD. For example, it was found that five

personality disorders were meaningfully related to the domain of Neuroticism.

However, facet level analysis indicated that only one of these five personality

disorders correlated significantly with the facet impulsivity (i.e. BPD) (Saulsman

and Page 2004). Therefore, a next step in the understanding of the relation between

ADHD and BPD could be to explore not only domain but also facet scores of the

FFM in both ADHD and BPD patient groups.

Chapter 6 showed no relation between FFM traits and cognitive profile in

adults with ADHD, except for the domain Openness to experience, which was

associated with a cognitive profile mostly characterized by inattention and

disinhibition. This may explain reports, that show that, contrary to the other four

domains of FFM, Openness to experience is poorly related to the DSM personality

disorders and warrants further consideration regarding its conceptualization and

assessment (Samuel and Widiger 2008). Therefore, the finding that Openness is

linked to the cognitive profile in adult ADHD remains to be more fully resolved.



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The lack of significant interactions between the other cognitive profiles (that

were similar in ADHD and controls) and FFM traits deserves more discussion.

It suggests that personality and cognition are independent entities without

significant influence on each other. The relative influence of emotional processing

on FFM traits may be useful to explore. Given the cross-talk between cognitive and

emotion processing, it would be useful to know to which extent self-reported

symptoms or traits reflect the neurocognitive constructs (that interact with emotion

processing). Recent work in non-clinical samples indicates that self-reports of

executive functioning are minimally related to performance measures of these

cognitive abilities but are consistently associated with Neuroticism (positive) and

Conscientiousness (negatively) (Buchanan 2016). Moreover, exploratory analysis by

the same group showed little to no relationship between FFM traits and objectively

measured executive functions. This may confirm our inability to find associations

between FFM traits and cognitive profiles, in spite of the clear link between ADHD

classification and FFM traits. Research focusing on ADHD also indicate that (self)

ratings of executive problems have greater ecological validity than cognitive tests,

which often do not correlate with the real world problems experienced by the

patient (Barkley and Fischer 2011; Kamradt, Ullsperger et al. 2014). Such findings

lead to the question of the clinical utility of neurocognitive testing and suggest

that it may also be useful to consider personality in the clinical management of

ADHD.

Clinical implications and future directions

Towards a person specific management of their vulnerabilities In this thesis we looked at the symptomatic overlap between ADHD and BPD and

the role of temperament, personality and cognition. Taken together, we may

conclude that the frequent co-occurrence of adult ADHD and BPD can be

understood by the presence of hyperactive/impulsive symptoms and temperament

traits, already inherent in childhood and a probable precursor for a BPD outcome

in adulthood. A difference between both patient groups may reflect the more

harm avoidant temperament in adults with BPD, but both groups are associated

with high Neuroticism traits. Although neurocognitive measurements show

deficiencies in both ADHD and BPD populations, it seems that these cognitive

deficiencies are not so different from those that are found in the whole population.

Rather, they are at a more extreme end of a dimension which can result in

functional problems. Furthermore, specific cognitive profiles do not seem to link

with specific ADHD symptoms nor with personality traits. Hence, the boundaries

between ADHD and BPD remain blurred.



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An interesting line of thinking might be that our results are in line with a

network approach. Meaning that the boundaries between both disorders are

unclear not as a result of methodological limitations, but rather as a result of the

intrinsic structure of disorders. Perhaps we should accept that the reason we have

been unable to find true boundaries is because there are no true boundaries. It

seems that no longer can comorbidity be meaningfully explained as a correlation

between two disorders, nor as a result of a common underlying (neurobiological

dysfunction) or “super disorder”. Instead the causal relations between symptoms

constitute pathways that can connect different disorders (Borsboom and Cramer

2013). Such multiple pathways from one disorder to another might exist in such a

way that there is no objective or “true” point at which to dissect the symptom

network in two, with each part representing a different disorder (Cramer, Waldorp

et al. 2010).

The present thesis also provides knowledge of psychopathology beyond and

outside the DSM. DSM might provide a guide to but can hardly be a replacement

for our rich psychopathological tradition. Part of the process of good clinical care

is to explore the experience of our patients. This helps us better understand them

and this sense of shared understanding can be directly therapeutic. Therefore we

need knowledge outside of the DSM in order to fully enable clinical management

(Kendler 2016).

Given this, it is important to map the individual specific symptoms and vul-

nerabilities that cause someone to seek help and to connect with the need that is

expressed by them. Our data suggest that in case of reported ADHD and/or BPD

symptoms it is important to know that hyperactivity/impulsivity symptoms and

traits are of poor diagnostic value in the differentiation of ADHD and BPD and that

inattention symptoms may also not be particularly unique to ADHD. Thus, the

DSM classification may not always be representative for the experiences of the

individual. In other words, they do not represent all the relevant symptoms that

deserve evaluation. The same seems true for emotional instability; a feature mostly

associated with BPD. However, a harm avoidant temperament can also be seen in

combination with what might be classified as mostly ADHD features. Such a

combination of hyperactivity symptoms with a novelty seeking and harm avoidant

temperament might predispose for poor prognostic outcomes and increased risk

of generalization between ADHD and BPD diagnoses. Since ADHD and BPD may

not be discernable categories, the examination of how networks of ADHD and BPD

symptoms in unselected groups of patients interact with networks of personality

traits would be useful. Such a network model could be used to simulate the

generalization of symptom activity through the network to predict future psycho-

pathological states (Goekoop and Goekoop 2014).



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Treat a person with difficulties, rather than a DSM classification The current thesis may inform clinical assessment and treatment of ADHD and

BPD. Overall, our research, and that from others, show that both ADHD and BPD

are often characterized by regulation problems in behavior (impulsivity) as well as

regulation problems in emotions (emotional instability). Our results indicated

that ADHD combined with an extreme Novelty Seeking and high Harm Avoidance

temperament might predispose for co-occurring BPD. It could therefore be of

critical importance to assess temperament in children with ADHD in order to

identify those that may be particularly vulnerable and at risk of worsening of their

problems. Consequently, it may be valuable to add the assessment of temperament

in ADHD children to current diagnostic guidelines. In conjunction with this, the

results in this thesis underline the importance of acknowledging that there are no

clear boundaries between developmental disorders (in youth) and personality

(disorders in adulthood).

Without disregarding the usefulness of the DSM system for diagnosis, we

want to make a plea for a more personal and dimensional approach in the

assessment and treatment of the problems that we encounter in clinical practice,

both in children as in adults. Recognizing the evidence that two DSM categories

show overlap not only in their symptoms, but also with regard to temperament

and personality traits, and neurocognitive functioning undeniably calls for a less

categorical perspective. Indeed, recent work suggested that trait models provide

greater specificity in distinguishing personality pathology among those with

childhood and adulthood ADHD (Smith and Samuel 2016).

This thesis also suggests that there is no clear relationship between cognition

and the Five Factor model personality traits in ADHD (with the exception of

Openness). It may be worth determining whether markers of emotional processing

rather than cognitive processing may offer a better match to the FFM scores in

ADHD. In contrast to the accepted role of emotion dysregulation as one of the

primary mechanisms underlying BPD, the role of emotional processing in ADHD

remains relatively unexplored. However, recently emotion dysregulation has been

emphasized as a core feature of ADHD and a significant contributor to the

functional impairment suffered by youth and adults with ADHD (Bunford, Evans

et al. 2014). Generally, emotion dysregulation occurs when an individual fails to

modify an emotional state so as to promote adaptive behaviors that are necessary

to accomplish his/her goals (Thompson 1994). Within the ADHD literature,

emotion dysregulation has been conceptualized as emotional impulsiveness,

difficulty in effortful regulation of induced emotions, and /or difficulty inducing

more acceptable mood states (Bunford, Evans et al. 2015). Meta-analysis of ADHD

and emotion dysregulation in children and adolescents document significant and

strong links between ADHD and emotion reactivity and emotion regulation and to



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a lesser degree emotion understanding (Graziano and Garcia 2016). The link

between emotion dysregulation and ADHD was found to be similar in strength for

boys and girls. Despite the extensive research documenting an association between

emotion dysregulation and BPD, there is also a need to elucidate the precise

emotion regulation deficits that are most relevant (Gratz, Moore et al. 2016). Such

knowledge could contribute to future development of clinical interventions that

more directly target emotion regulation as this may be of importance in improving

the impairments in both ADHD and BPD.

Psychotherapeutic strategies for emotion processing difficulties are commonly

found in the treatment of individuals with BPD. For example: targeting emotional

dysregulation is a key element of Dialectical Behaviour Therapy (DBT). This DBT

treatment has shown to be effective in decreasing inappropriate anger, a reduction

in self-harm and an improvement in general functioning in BPD (Stoffers, Vollm et

al. 2012). Recently it has been recommended that principles of DBT may also

successfully treat ADHD in adults, as adjunct to medication (Asherson, Young et al.

2014). Such skill training approach (i.e. a behavioral approach where painful

emotion can be alleviated through general skills and actions) to emotion regulation

is one that can be applied across distressing situations and largely irrespective of

individual differences (Neacsiu, Eberle et al. 2014). This could therefore be an

important tool that might also help in the coping with some of the ADHD problems.

Another interesting perspective could be that emotional arousal can also be

regulated by qualitatively changing the difficult emotion in question. In this

case, painful emotion is alleviated through the exploration of memories and

idiosyncratic meanings. From this experiential viewpoint, the act of emotion

regulation is essentially a means to another end: allowing one to tolerate emotion

just enough to turn one’s focus inward and complete a distressing but meaningful

task (e.g. exploring and accepting painful material) (Pascual-Leone, Gillespie et al.

2016). Since it is known that attachment difficulties and childhood trauma are not

only related to BPD but also to persistent ADHD (Ferrer, Andion et al. 2016; Storebo,

Rasmussen et al. 2016), this might be a valuable additional strategy in cases that

call for more specific and personal understanding by the patient of their emotions.

Future work should focus on clarifying exactly how, when, and what needs to

be done to help clients to gain the ability to adapt ones responses to match the

situation they are in. This might inform us further on how best to integrate

current research and clinical practice in processing cognitive and emotional

dysregulation in ADHD and BPD.



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Future research recommendations

This thesis has demonstrated a clear symptomatic overlap in ADHD and BPD cases.

It remains to be resolved whether this overlap is present on a biological level. Such

strategies may be useful to further enlighten the relationship between ADHD and

BPD. Currently the association between ADHD and BPD has primarily been

investigated at the phenotypic level and there is still a lack of sufficient information

about the biological etiology of co-occurring ADHD and BPD.

The high rate of co-occurring ADHD and BPD may suggest a shared genetic

architecture. Indeed, genetic effects behind the shared features of ADHD and BPD

have been suggested (Distel, Carlier et al. 2011; Reif, Nguyen et al. 2011; Weissflog,

Scholz et al. 2013; Weber, Scholz et al. 2014). Although this adds to identifying

unique and shared genetic imprints, larger sample sizes are needed for more

robust results. Furthermore, it has been argued that it is important to shift away

from categorical case-control approaches that view psychiatric disorders as

unitary constructs, towards a dimensional approach that incorporate endo-pheno-

types, or intermediate traits, and bottom-up statistical classification methods

(Hawi, Cummins et al. 2015). Such an approach may help to better characterize the

heterogeneous nature of the disorders and the extent of overlap.

Another genetic research strategy that might be successful in the identification

of common versus unique risk factors for ADHD and BPD could be family-genetic

studies. For example, family genetic research in ADHD and autism spectrum

disorder has built on the idea that polygenic and multifactorial causes of disease

will increase symptom levels in most or all members of the family, whereas

sporadic genetic and non-genetic causes will be strictly personal to the patient

(Oerlemans, Hartman et al. 2015). To our knowledge, such particular attempt has

not yet been made for ADHD and BPD. However, twin family data of a large

population based sample was used to determine whether shared (genetic and

environmental) etiology could explain (part of) the comorbidity between ADHD

symptoms and BPD symptoms (Distel, Carlier et al. 2011). The genetic analysis

showed that the high correlation between BPD and ADHD symptoms could be

explained for 49% by additive genetic factors and for 51% by unique environmental

factors. It thus seems that common biological factors influence both ADHD and

BPD. Further research is needed to investigate the underlying sources of the

genetic and (non) shared environmental factors that influence both ADHD and

BPD symptoms.

Another way of further gaining knowledge about the overlap in ADHD and

BPD might be through brain imaging studies. Brain volume abnormalities are

important indicators of pathophysiological processes that likely reflect disorder

etiology. For ADHD, total brain volume and grey matter volume have been found



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to be decreased compared to typically developing controls (Valera, Faraone et al.

2007; Seidman, Biederman et al. 2011; Frodl and Skokauskas 2012; Greven, Bralten

et al. 2015). With regard to BPD there are also indications of abnormalities in gray

matter (Rossi, Lanfredi et al. 2015; Yang, Hu et al. 2016). No studies to date have

investigated structural correlates between ADHD and BPD. It could be of interest

to investigate whether the extent to which ADHD symptoms occur in BPD (or vice

versa) may have an effect on the brain volumes in ADHD (or BPD).

Lastly, we want to highlight the potential use of pharmacological studies in

dissecting ADHD and BPD traits. Case reports and a small scale study of successful

methylphenidate treatment (the first line treatment in adult ADHD) have been

reported in BPD (Golubchik, Sever et al. 2008). Methylphenidate treatment was

associated with a significant improvement not only in ADHD symptoms but also in

BPD severity, aggressive behavior, and self-injurious behavior. However, the effects

of pharmacological treatments for ADHD and/or BPD have not been investigated in

large scale controlled trials which consider effects on the symptomatic overlap.

More generally, it could be suggested that medication strategies that alter response

inhibition such as methylphenidate, citalopram and atomoxetine may be useful in

the comparison of ADHD and BPD (Nandam, Hester et al. 2014).

Given the multitude of biological substrates deserving of investigation as

candidate mechanisms underlying common ADHD and BPD symptoms, it may be

useful to consider applying the NIH Research Domain Criteria (RDoC) approach to

the study of common ADHD and BPD endophenotypes (Cuthbert 2015; Kozak and

Cuthbert 2016).



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References

Agrawal, H. R., J. Gunderson, et al. (2004). “Attachment studies with borderline patients: a review.” Harv

Rev Psychiatry 12(2): 94-104.

Asherson, P., A. H. Young, et al. (2014). “Differential diagnosis, comorbidity, and treatment of attention-

deficit/hyperactivity disorder in relation to bipolar disorder or borderline personality disorder in

adults.” Curr Med Res Opin 30(8): 1657-1672.

Barkley, R. A. and M. Fischer (2011). “Predicting impairment in major life activities and occupational

functioning in hyperactive children as adults: self-reported executive function (EF) deficits versus EF

tests.” Dev Neuropsychol 36(2): 137-161.

Borsboom, D. and A. O. Cramer (2013). “Network analysis: an integrative approach to the structure of psy-

chopathology.” Annu Rev Clin Psychol 9: 91-121.

Buchanan, T. (2016). “Self-report measures of executive function problems correlate with personality, not

performance-based executive function measures, in nonclinical samples.” Psychol Assess 28(4):

372-385.

Bunford, N., S. W. Evans, et al. (2014). “Emotion Dysregulation Is Associated With Social Impairment

Among Young Adolescents With ADHD.” J Atten Disord.

Bunford, N., S. W. Evans, et al. (2015). “ADHD and Emotion Dysregulation Among Children and Adolescents.”

Clin Child Fam Psychol Rev 18(3): 185-217.

Cackowski, S., A. C. Reitz, et al. (2014). “Impact of stress on different components of impulsivity in

borderline personality disorder.” Psychol Med 44(15): 3329-3340.

Carlotta, D., S. Borroni, et al. (2013). “On the relationship between retrospective childhood ADHD symptoms

and adult BPD features: the mediating role of action-oriented personality traits.” Compr Psychiatry

54(7): 943-952.

Chapman, A. L., C. M. Derbidge, et al. (2009). “Temperament as a prospective predictor of self-injury among

patients with borderline personality disorder.” J Pers Disord 23(2): 122-140.

Chapman, A. L., M. W. Specht, et al. (2005). “Borderline personality disorder and deliberate self-harm: does

experiential avoidance play a role?” Suicide Life Threat Behav 35(4): 388-399.

Choi-Kain, L. W., G. M. Fitzmaurice, et al. (2009). “The relationship between self-reported attachment styles,

interpersonal dysfunction, and borderline personality disorder.” J Nerv Ment Dis 197(11): 816-821.

Cohen, J. D. and D. Servan-Schreiber (1992). “Context, cortex, and dopamine: a connectionist approach to

behavior and biology in schizophrenia.” Psychol Rev 99(1): 45-77.

Cramer, A. O., L. J. Waldorp, et al. (2010). “Comorbidity: a network perspective.” Behav Brain Sci 33(2-3):

137-150; discussion 150-193.

Crowell, S. E., T. P. Beauchaine, et al. (2009). “A biosocial developmental model of borderline personality:

Elaborating and extending Linehan’s theory.” Psychol Bull 135(3): 495-510.

Cuthbert, B. N. (2015). “Research Domain Criteria: toward future psychiatric nosologies.” Dialogues Clin

Neurosci 17(1): 89-97.

Distel, M. A., A. Carlier, et al. (2011). “Borderline personality traits and adult attention-deficit hyperactivity

disorder symptoms: a genetic analysis of comorbidity.” Am J Med Genet B Neuropsychiatr Genet

156B(7): 817-825.

Ferrer, M., O. Andion, et al. (2016). “Differences in the association between childhood trauma history and

borderline personality disorder or attention deficit/hyperactivity disorder diagnoses in adulthood.”

Eur Arch Psychiatry Clin Neurosci.

Fossati, A., S. Borroni, et al. (2012). “Predicting borderline personality disorder features from personality

traits, identity orientation, and attachment styles in Italian nonclinical adults: issues of consistency

across age ranges.” J Pers Disord 26(2): 280-297.

Fossati, A., K. L. Gratz, et al. (2015). “The relationship between childhood history of ADHD symptoms and

DSM-IV borderline personality disorder features among personality disordered outpatients: the

moderating role of gender and the mediating roles of emotion dysregulation and impulsivity.” Compr

Psychiatry 56: 121-127.



148

CHAPTER 7

Frodl, T. and N. Skokauskas (2012). “Meta-analysis of structural MRI studies in children and adults with

attention deficit hyperactivity disorder indicates treatment effects.” Acta Psychiatr Scand 125(2):

114-126.

Goekoop, R. and J. G. Goekoop (2014). “A network view on psychiatric disorders: network clusters of

symptoms as elementary syndromes of psychopathology.” PLoS One 9(11): e112734.

Golubchik, P., J. Sever, et al. (2008). “Methylphenidate in the treatment of female adolescents with

cooccurrence of attention deficit/hyperactivity disorder and borderline personality disorder: a

preliminary open-label trial.” Int Clin Psychopharmacol 23(4): 228-231.

Gratz, K. L., K. E. Moore, et al. (2016). “The role of emotion dysregulation in the presence, associated

difficulties, and treatment of borderline personality disorder.” Personal Disord 7(4): 344-353.

Graziano, P. A. and A. Garcia (2016). “Attention-deficit hyperactivity disorder and children’s emotion

dysregulation: A meta-analysis.” Clin Psychol Rev 46: 106-123.

Greven, C. U., J. Bralten, et al. (2015). “Developmentally stable whole-brain volume reductions and develop-

mentally sensitive caudate and putamen volume alterations in those with attention-deficit/

hyperactivity disorder and their unaffected siblings.” JAMA Psychiatry 72(5): 490-499.

Hawi, Z., T. D. Cummins, et al. (2015). “The molecular genetic architecture of attention deficit hyperactivity

disorder.” Mol Psychiatry 20(3): 289-297.

Helgeland, M. I., E. Kjelsberg, et al. (2005). “Continuities between emotional and disruptive behavior

disorders in adolescence and personality disorders in adulthood.” Am J Psychiatry 162(10): 1941-1947.

Hsu, L. K. (1996). “Epidemiology of the eating disorders.” Psychiatr Clin North Am 19(4): 681-700.

Johnson, D. M., M. T. Shea, et al. (2003). “Gender differences in borderline personality disorder: findings

from the Collaborative Longitudinal Personality Disorders Study.” Compr Psychiatry 44(4): 284-292.

Joyce, P. R., J. M. McKenzie, et al. (2003). “Temperament, childhood environment and psychopathology as

risk factors for avoidant and borderline personality disorders.” Aust N Z J Psychiatry 37(6): 756-764.

Kaess, M., R. Brunner, et al. (2014). “Risk-behaviour screening for identifying adolescents with mental

health problems in Europe.” Eur Child Adolesc Psychiatry 23(7): 611-620.

Kamradt, J. M., J. M. Ullsperger, et al. (2014). “Executive function assessment and adult attention-deficit/

hyperactivity disorder: tasks versus ratings on the Barkley deficits in executive functioning scale.”

Psychol Assess 26(4): 1095-1105.

Kendler, K. S. (2016). “The Phenomenology of Major Depression and the Representativeness and Nature of

DSM Criteria.” Am J Psychiatry 173(8): 771-780.

Kendler, K. S., J. Myers, et al. (2011). “Borderline personality disorder traits and their relationship with

dimensions of normative personality: a web-based cohort and twin study.” Acta Psychiatr Scand

123(5): 349-359.

Kozak, M. J. and B. N. Cuthbert (2016). “The NIMH Research Domain Criteria Initiative: Background, Issues,

and Pragmatics.” Psychophysiology 53(3): 286-297.

Krause-Utz A., Sobanski E. et al. (2013). Impulsivity in relation to stress in patients with borderline

personality disorder with and without co-occurring attention-deficit/hyperactivity disorder: an

exploratory study. J Nerv Ment Dis. 201(2):116-123.

Martel, M. M., M. Nikolas, et al. (2010). “Personality mediation of genetic effects on Attention- Deficit/

Hyperactivity Disorder.” J Abnorm Child Psychol 38(5): 633-643.

McClure, G., D. J. Hawes, et al. (2016). “Borderline personality disorder and neuropsychological measures of

executive function: A systematic review.” Personal Ment Health 10(1): 43-57.

Miller, C. J., J. D. Flory, et al. (2008). “Childhood attention-deficit/hyperactivity disorder and the emergence

of personality disorders in adolescence: a prospective follow-up study.” J Clin Psychiatry 69(9): 1477-1484.

Miller, C. J., S. R. Miller, et al. (2008). “Personality characteristics associated with persistent ADHD in late

adolescence.” J Abnorm Child Psychol 36(2): 165-173.

Nandam, L. S., R. Hester, et al. (2014). “Dissociable and common effects of methylphenidate, atomoxetine

and citalopram on response inhibition neural networks.” Neuropsychologia 56: 263-270.

Neacsiu, A. D., J. W. Eberle, et al. (2014). “Dialectical behavior therapy skills for transdiagnostic emotion

dysregulation: a pilot randomized controlled trial.” Behav Res Ther 59: 40-51.



149


7

Nigg, J. T., O. P. John, et al. (2002). “Big five dimensions and ADHD symptoms: links between personality

traits and clinical symptoms.” J Pers Soc Psychol 83(2): 451-469.

Oerlemans, A. M., C. A. Hartman, et al. (2015). “Simplex and multiplex stratification in ASD and ADHD

families: a promising approach for identifying overlapping and unique underpinnings of ASD and

ADHD?” J Autism Dev Disord 45(3): 645-657.

Okon-Singer, H., T. Hendler, et al. (2014). “Introduction to the special research topic on the neurobiology of

emotion-cognition interactions.” Front Hum Neurosci 8: 1051.

Okon-Singer, H., T. Hendler, et al. (2015). “The neurobiology of emotion-cognition interactions: fundamental

questions and strategies for future research.” Front Hum Neurosci 9: 58.

Pascual-Leone, A., N. M. Gillespie, et al. (2016). “Measuring Subtypes of Emotion Regulation: From Broad

Behavioural Skills to Idiosyncratic Meaning-making.” Clin Psychol Psychother 23(3): 203-216.

Petrovic, P. and F. X. Castellanos (2016). “Top-Down Dysregulation-From ADHD to Emotional Instability.”

Front Behav Neurosci 10: 70.

Prada P., Hasler R. et al. (2014). Distinguishing borderline personality disorder from adult attention deficit/

hyperactivity disorder: a clinical and dimensional perspective. Psychiatry Res. 217:107-114.

Reif, A., T. T. Nguyen, et al. (2011). “DIRAS2 is associated with adult ADHD, related traits, and co-morbid

disorders.” Neuropsychopharmacology 36(11): 2318-2327.

Rossi, R., M. Lanfredi, et al. (2015). “Abnormalities in cortical gray matter density in borderline personality

disorder.” Eur Psychiatry 30(2): 221-227.

Samuel, D. B. and T. A. Widiger (2008). “A meta-analytic review of the relationships between the five-factor

model and DSM-IV-TR personality disorders: a facet level analysis.” Clin Psychol Rev 28(8): 1326-1342.

Saulsman, L. M. and A. C. Page (2004). “The five-factor model and personality disorder empirical literature:

A meta-analytic review.” Clin Psychol Rev 23(8): 1055-1085.

Sebastian, A., P. Jung, et al. (2014). “Frontal dysfunctions of impulse control - a systematic review in

borderline personality disorder and attention-deficit/hyperactivity disorder.” Front Hum Neurosci 8:

698.

Seidman, L. J., J. Biederman, et al. (2011). “Gray matter alterations in adults with attention-deficit/

hyperactivity disorder identified by voxel based morphometry.” Biol Psychiatry 69(9): 857-866.

Shaw, P., A. Stringaris, et al. (2014). “Emotion dysregulation in attention deficit hyperactivity disorder.” Am

J Psychiatry 171(3): 276-293.

Smith T.E. and Samuel D.B. (2016). A Multi-Method Examination of the Links Between ADHD and

Personality Disorder. J Pers Disord. 4:1-23.

Stepp, S. D., J. D. Burke, et al. (2012). “Trajectories of attention deficit hyperactivity disorder and oppositional

defiant disorder symptoms as precursors of borderline personality disorder symptoms in adolescent

girls.” J Abnorm Child Psychol 40(1): 7-20.

Stoffers, J. M., B. A. Vollm, et al. (2012). “Psychological therapies for people with borderline personality

disorder.” Cochrane Database Syst Rev(8): CD005652.

Stone, M. H. (2016). “Long-Term Course of Borderline Personality Disorder.” Psychodyn Psychiatry 44(3):

449-474.

Storebo, O. J., P. D. Rasmussen, et al. (2016). “Association Between Insecure Attachment and ADHD:

Environmental Mediating Factors.” J Atten Disord 20(2): 187-196.

Thompson, R. A. (1994). “Emotion regulation: a theme in search of definition.” Monogr Soc Res Child Dev

59(2-3): 25-52.

Torgersen, S., E. Kringlen, et al. (2001). “The prevalence of personality disorders in a community sample.”

Arch Gen Psychiatry 58(6): 590-596.

Valera, E. M., S. V. Faraone, et al. (2007). “Meta-analysis of structural imaging findings in attention-deficit/

hyperactivity disorder.” Biol Psychiatry 61(12): 1361-1369.

Weber, H., C. J. Scholz, et al. (2014). “SPOCK3, a risk gene for adult ADHD and personality disorders.” Eur

Arch Psychiatry Clin Neurosci 264(5): 409-421.

Weissflog, L., C. J. Scholz, et al. (2013). “KCNIP4 as a candidate gene for personality disorders and adult

ADHD.” Eur Neuropsychopharmacol 23(6): 436-447.



150

CHAPTER 7

Widiger, T. A. and P. T. Costa (2002). Five factor model personality disorder research. Personality Disorders

and the Five Factor Model of Personality. P. T. Costa and T. A. Widiger. Washingtin DC, American

Psychological Association: 59-87.

Yang, X., L. Hu, et al. (2016). “Default mode network and frontolimbic gray matter abnormalities in patients

with borderline personality disorder: A voxel-based meta-analysis.” Sci Rep 6: 34247.

Zanarini, M. C., F. R. Frankenburg, et al. (1998). “Axis I comorbidity of borderline personality disorder.”

Am J Psychiatry 155(12): 1733-1739.

Zanarini, M. C., F. R. Frankenburg, et al. (2014). “Prediction of time-to-attainment of recovery for borderline

patients followed prospectively for 16 years.” Acta Psychiatr Scand 130(3): 205-213.

Zlotnick, C., L. Rothschild, et al. (2002). “The role of gender in the clinical presentation of patients with

borderline personality disorder.” J Pers Disord 16(3): 277-282



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Nederlandse samenvattingList of publications

DankwoordCurriculum Vitae



155

NEDERLANDSE SAMENVATTING

Nederlandse samenvatting

ADHDADHD staat voor ‘Attention-Deficit Hyperactivity Disorder’ en is een ontwikkelings-

stoornis die gekenmerkt wordt door de aanwezigheid van een hardnekkig patroon

van onoplettendheid en/of hyperactiviteit en impulsiviteit dat leidt tot functionele

belemmeringen. Lange tijd zag men ADHD als een stoornis in de kindertijd met

beperkt effect op de volwassenheid. Inmiddels weten we dat bij tot wel 50% van de

kinderen met ADHD de symptomen en functionele beperkingen voortduren in de

volwassenheid. Volwassenen met ADHD hebben veelal nog bijkomende psychische

en/of psychiatrische problemen. Dit wordt co-morbiditeit genoemd. Het betreft

vooral andere ontwikkelingsstoornissen zoals autismespectrumstoornissen, maar

ook angst- en stemmingsstoornissen, middelenmisbruik, gedragsstoornissen en

persoonlijkheidsstoornissen. Het begrijpen van de overeen komsten en verschillen

met stoornissen die vaak samen met ADHD voorkomen is van belang om onder-di-

agnostiek (of foutieve diagnostiek) van ADHD te voorkomen en kan bijdragen aan

het inzetten van passende behandelinterventies.

Borderline persoonlijkheidsstoornisDe borderline persoonlijkheidsstoornis (BPS) wordt gekenmerkt door een hardnekkig

en uitgebreid patroon van instabiliteit in de emotieregulatie, interpersoonlijke

relaties en zelfbeeld, en verhoogde impulsiviteit. Hoewel de diagnose BPS per

definitie niet voor de adolescentie gesteld kan worden laat onderzoek zien dat het

klinische beeld ook bij jongeren een valide construct is. Ook bij BPS is sprake van

onder-diagnostiek. Er is een grote overlap van symptomen met bijvoorbeeld

depressieve stoornissen, impulsiviteitsstoornissen en identiteitsstoornissen. Dit

kan het in de praktijk moeilijk maken om vast te stellen of de symptomen horen

bij de BPS of bij een co-morbide stoornis. Ook hier geldt dat het begrijpen van de

overeenkomsten en verschillen met stoornissen waarmee BPS vaak samen

voorkomt van belang is om onder-diagnostiek te voorkomen en bij te dragen aan

het inzetten van passende behandelinterventies.

Overlap tussen ADHD en BPSIn de klinische praktijk kan het soms moeilijk zijn om ADHD en BPS van elkaar te

onderscheiden. Symptomen als impulsiviteit, emotionele instabiliteit, risicovol

gedrag, moeite om boosheid te controleren zijn kenmerken die zowel bij ADHD als

bij BPS worden gezien. Impulsiviteit is een van de meest kenmerkende overlappende

symptomen. Maar ook emotionele instabiliteit en interpersoonlijke problemen,

beiden belangrijke kenmerken van BPS, worden herkend als bijkomende problemen

bij ADHD. Beide stoornissen kennen een chronisch beloop en bovendien komen



156


ADHD en BPS vaak samen voor in de klinische praktijk. De oorsprong van de

relatie tussen ADHD en BPS wordt echter nog niet goed begrepen.

Het doel van het onderzoek in dit proefschriftHet doel van het onderzoek in dit proefschrift is het kritisch beschouwen van de

overeenkomsten (en verschillen) tussen ADHD bij volwassenen en de borderline

persoonlijkheidsstoornis en daarmee een bijdrage te leveren aan het beter

begrijpen van de relatie tussen beide stoornissen. We hebben gekeken naar de

overlap op het gebied van symptomen, persoonlijkheidstrekken, en neurocognitie.

In hoofdstuk 2 presenteren we een literatuurstudie naar ADHD, persoonlijkheids-

stoornissen, en persoonlijkheidstrekken. In hoofdstuk 3 werd er een Latente

Klasse Analyse uitgevoerd bij volwassen vrouwen met ADHD en/of BPS om van

elkaar te onderscheiden groepen met homogene symptoomprofielen te identificeren.

In hoofdstuk 4 onderzochten we de rol van temperament en karaktertrekken in

het onderscheiden van volwassen vrouwen met gelijke ADHD en BPS symptoom-

profielen. Ook keken we naar mogelijke ontwikkelingstrajecten van temperament

naar toekomstig ADHD en/of BPS uitkomsten. In hoofdstuk 5 onderzochten we of

een cognitieve maat van respons inhibitie kon differentiëren tussen volwassenen

met ADHD, BPS en gezonde controles. In hoofdstuk 6 bestudeerden we de interacties

tussen cognitieve profielen in volwassenen met ADHD en persoonlijkheidstrekken.

Belangrijkste bevindingen uit dit proefschriftHoofdstuk 2, een literatuuronderzoek, behandelt en bespreekt diverse concepten

en thema’s die betrekking hebben op de relatie tussen ADHD, persoonlijkheids-

stoornissen en persoonlijkheidstrekken. Een belangrijke conclusie was dat eerdere

studies naar ADHD en persoonlijkheid geen rekening hielden met co-morbide

persoonlijkheidsstoornissen bij de ADHD waardoor het moeilijk is specifieke

conclusies te trekken over de overlap en verschillen tussen ADHD, persoonlijk-

heidsstoornissen en persoonlijkheidstrekken. We concludeerden daarom ook dat

meer onderzoek nodig is om de relatie tussen ADHD en persoonlijkheidsstoornis-

sen (meer specifiek de borderline persoonlijkheidsstoornis) beter te gaan begrijpen

en hun gedeelde kenmerken beter te ontrafelen.

In hoofdstuk 3 hebben we kwalitatief verschillende symptoomprofielen van

zowel ADHD in de kindertijd als volwassen leeftijd en BPS symptomen bij volwassen

vrouwen met ADHD en/of BPS geïdentificeerd. We illustreerden dat elke volwassen

vrouw met BPS in ons onderzoek enkele ADHD symptomen had in de kindertijd en

volwassenheid en dat hyperactiviteit karakteristiek is voor zowel volwassen vrouwen

met ADHD als BPS. Hier hebben we ook laten zien dat hyperactiviteit mogelijk een

mediërende rol speelt tussen ADHD en de ontwikkeling van BPS. Concluderend

stelden we daarom dat hyperactiviteit/impulsiviteit weinig discriminatieve



157


waarde heeft voor ADHD en BPS. Het onderzoek in hoofdstuk 3 heeft bijgedragen

aan een groeiend bewijs dat ADHD en BPS waarschijnlijk, maar niet alleen, aan

elkaar gerelateerd zijn via hyperactiviteit/impulsiviteit kenmerken. Of BPS ook

ontstaat uit de ADHD symptomen is niet helder.

In hoofdstuk 4 hebben we laten zien dat een opvallend uitgesproken ‘Prikkel-

zoekend’ temperament een kwetsbaarheid suggereert voor de ontwikkeling van

een ADHD met co-morbide BPS bij vrouwen. Daarnaast vonden we dat een ‘Leed-

vermijdend’ temperament meer specifiek geassocieerd zou kunnen zijn met BPS.

Deze bevinding komt overeen met later werk waaruit bleek dat impulsiviteit,

maar ook emotie-disregulatie, de relatie tussen ADHD symptomen in de kindertijd

en volwassen BPS kenmerken volledig medieerde. Zulke bevindingen suggereren

dat moeilijkheden met negatieve emoties en gedragscontrole kritische elementen

zijn in de relatie tussen ADHD symptomen in de kindertijd en BPS symptomen in

de volwassenheid.

In hoofdstuk 5 hebben we onderzocht of ADHD en BPS ook overlappen in

onderliggende cognitieve problemen of dat ADHD en BPS van elkaar te

onderscheiden zijn op het niveau van cognitieve processen. We hebben laten zien

dat onafhankelijk van de aanwezigheid van ADHD, respons-inhibitieproblemen

ook gerelateerd zijn aan BPS. Bovendien bleek dat de groep met BPS meer en meer

specifieke inhibitieproblemen had dan de ADHD groep. Hoewel ons werk hiermee

bijdraagt aan groeiend bewijs dat executieve functie beperkingen een rol spelen in

BPS, is nog erg onduidelijk wat aan deze beperkingen ten grondslag ligt.

Samenvattend lijkt het er op dat ADHD en BPS kenmerken van hyperactiviteit

en impulsiviteit delen op het niveau van symptomen, persoonlijkheidstrekken en

neurocognitieve prestaties. Een interessante vraag die hieruit volgt is of deze

klinische kenmerken, persoonlijkheidstrekken en neurocognitieve prestaties aan

elkaar gerelateerd zijn. In hoofdstuk 6 hebben we laten zien dat alleen de persoon-

lijkheidstrek ‘openheid’, maar geen enkele andere persoonlijkheidstrek uit het vijf

factoren model van persoonlijkheid, gerelateerd was aan neurocognitieve

profielen in ADHD. Juist de aanwezigheid van ADHD, en niet het cognitieve profiel,

was geassocieerd met persoonlijkheidstrekken. Onze bevindingen, en die van

anderen, leiden tot de vraag hoe klinisch bruikbaar neurocognitief testen is en

suggereert dat het nuttig zou kunnen zijn persoonlijkheid mee te nemen in de

diagnostiek en behandeling van ADHD.

Klinische implicatiesWe kunnen concluderen dat het frequent samen voorkomen van ADHD en BPS

begrepen kan worden vanuit de aanwezigheid van hyperactiviteit en impulsiviteit

symptomen en persoonlijkheidstrekken die al aanwezig zijn in de kindertijd en

een mogelijke precursor zijn voor BPS in de volwassenheid. Deze kenmerken



158


blijken dus niet uniek voor ADHD. Een verschil tussen beide stoornissen kan een

meer ‘Leedvermijdend’ temperament bij vrouwen met BPS zijn. De rol van emotionele

disregulatie in ADHD is nog relatief onbekend, maar er zijn aanwijzingen dat

emotionele disregulatie, net zoals bij BPS, ook sterk geassocieerd is met ADHD.

Kortom, de afgrenzingen tussen ADHD en BPS blijven vaag.

Het onderzoek in dit proefschrift heeft kennis gegenereerd in aanvulling op

de kennis uit de DSM en dit is van belang voor goede klinische zorg. Het kan helpen

om het individu beter te begrijpen.

Omdat ADHD en BPS niet zo eenvoudig van elkaar te onderscheiden zijn en

de DSM classificatie mogelijk niet altijd representatief voor de ervaring van een

individu is het belangrijk om de individuele symptomen en kwetsbaarheden

waarvoor iemand hulp vraagt in kaart te brengen en hierbij aan te sluiten. Het kan

waardevol zijn om bij de assessment van ADHD ook temperament te onderzoeken.

De resultaten van het onderzoek in dit proefschrift onderstrepen bovendien dat

er geen duidelijke grenzen zijn tussen ontwikkelingsstoornissen (in de kindertijd)

en persoonlijkheidsstoornissen (in de volwassenheid). Zonder tekort te willen

doen aan DSM systeem willen we pleiten voor een meer persoonlijke en dimensionele

aanpak in de diagnostiek en behandeling van de problemen waar individuen

zich mee melden in de klinische praktijk.

Toekomstig onderzoekHet onderzoek in dit proefschrift heeft aangetoond dat er een duidelijke

symptomatische overlap is tussen ADHD en BPS. Het is echter nog onduidelijk of

deze overlap ook aanwezig is op een biologisch niveau. Het is gesuggereerd dat er

genetische effecten zitten achter de gedeelde kenmerken van ADHD en BPS, maar

meer onderzoek is nodig voor sterkere resultaten. Naast genetische studies zouden

ook beeldvormend onderzoek (brain imaging studies) en farmacotherapie studies

een bijdragen kunnen leveren aan het beter begrijpen van de relaties tussen ADHD

en BPS. Gezien de diverse mogelijke biologische substraten zou het nuttig kunnen

zijn om de NIH Research Domain Criteria (RDoC) methode toe te passen op de

studie naar ADHD en BPS.



159

LIST OF PUBLICATIONS

List of publications

Articles

Van Dijk, F.E., Mostert, J., Onnink, M., Dammers, J., Arias Vasquez, A., Kan, C., Verkes, R.J., Hoogman, M.,

Franke, B., Buitelaar, J. (2016). Five Factor Model personality traits relate to adult attention-deficit/

hyperactivity disorder but not to their distinct neurocognitive profiles (under review)

Van Dijk, F.E., Schellekens, A.F.A., Van Den Broek, P., Kan, C.C., Verkes, R.J., Buitelaar, J.K.. (2014). Do

cognitive measures of response inhibition differentiate between attention deficit/hyperactivity

disorder and borderline personality disorder? Psychiatry Res 215(3): 733-739.

Van Dijk, F. E., Lappenschaar, M., Verkes, R.J., Kan, C.C., Buitelaar, J.K. (2012). Symptomatic overlap between

attention-deficit/hyperactivity disorder and borderline personality disorder in women: the role of

temperament and character traits. Compr Psychiatry 53(1): 39-47.

Pilgrim, D., Champion, F., Hutschemaekers, G.J.M., Garnoussi, N., Van Dijk, F.E. (2012),”Variations in the

development of psychological therapy in three European Union countries”, The International journal

of sociology and social policy; 32 (1): 70-82

Van Dijk, F.E., Lappenschaar, M., Verkes, R.J., Kan, C.C., Buitelaar, J.K. (2011). Lifespan attention deficit/

hyperactivity disorder and borderline personality disorder symptoms in female patients: a latent

class approach. Psychiatry Res 190(2-3): 327-334.

Van Dijk, F.E. Procesbepalende Factoren in Strategische Allianties tussen Universitair Medische Centra en

Algemene Instellingen voor Geestelijke Gezondheidszorg: een Exploratieve Gevalsstudie. 2008.

Intern gebruik Pro Persona.

Bookchapters

Hutschemaekers, G.J.M. & Van Dijk, F.E. Psychotherapy and Clinical psychology in the Netherlands: The

settlement of five distinctive psy professions. In: Handbook of Counseling and Psychotherapy in an

International Context. Ed. Moodley R, Gielen UP, Wu R. 2012. Routledge.

Van Dijk, F.E. & Anckarsäter, H. ADHD, personality, and its disorders. In: ADHD in Adults: Characterization,

Diagnosis, and Treatment. Ed. Buitelaar JK, Kan CC., Asherson, P. 2011. Cambridge University Press.

Hutschemakers, GJM & Van Dijk, F.E. Klinische psychologie en geestelijke gezondheidszorg. In Psychologie

en Praktijk. Kessels, Hutschemakers, Beckers. 2010. Boom Lemma, Den Haag.

Moene, F.C., Sandijck, P., Spinhoven, P.H., Hoogduin, C.A.L., van Dijk, F.E. & Redert, J.F.M. (2001). Assessment

of conversion disorder, motor type: development, reliability and validity of a video rating scale for

motor conversion symptoms. In: Hypnosis and conversion disorder: assessment and treatment issues.

F.C. Moene. 2001. Cure & Care Uitgeverij, Zeist.

Conference presentations (posters and abstracts)

Van Dijk, FE. Psychotherapie als professie. Oral presentation, Nacholing psychiatrie, PAOG, Januari 2011,

Nijmegen, The Netherlands

Van Dijk, F.E. & Hutschemakers, G.J.M. Psychotherapy in the Netherlands: 1986 - 2010. Oral presentation,

Meeting of CERMES3- CESAMES (La psychothérapie en Europe, spécificités nationales et tendances

communes). September 2010. Paris (ENS), France.

Van Dijk F.E. ADHD bij volwassenen. Oral presentation, Congres NIP. 2006, Utrecht, The Netherlands

Van Dijk F.E. ADHD bij volwassenen: Afgrenzing van en overlap met persoonlijkheidsstoornissen. Oral

presentation, symposium. 2006, Zwolle, The Netherlands

Van Dijk, F.E., Kan C.C., Buitelaar J.K. Temperament en karakter in ADHD en de borderline persoonlijk-

heidsstoornis. Oral presentation, Annual meeting of the Dutch psychiatry association (NVvP), April

2006, The Netherlands.



160

LIST OF PUBLICATIONS

Van Dijk, F.E., Kan C.C., Buitelaar J.K. Borderline persoonlijkheidsstoornis of ADHD? Oral presentation,

Annual meeting of the Dutch psychiatry association, April 2005, The Netherlands.

Van Dijk F.E., Kan C.C., Buitelaar J.K. ADHD and comorbid borderline and antisocial personality disorder.

Poster presentation, European Conference on ADHD and comorbidities in Adults, 2003, Oslo Norway.



161

DANKWOORD

Dankwoord

Dit proefschrift zou nooit tot stand zijn gekomen zonder de hulp van vele anderen.

Ik ben dan ook iedereen heel erg dankbaar die heeft bijgedragen aan een lang

proces waarvan het einde nu in zicht is gekomen. Speciaal geldt dat voor de

proefpersonen die mij hun tijd en inzet hebben gegeven. Mensen met ADHD en/of

een borderline persoonlijkheidsstoornis, die ondanks hun zorgen en problemen

mee hebben willen werken in het belang van de wetenschap. Zonder hen was mijn

onderzoek sowieso niet mogelijk geweest.

Beste promotoren en copromotoren,

Natuurlijk wil ik jullie heel erg bedanken. Zonder jullie was er geen begin en zeker

ook geen eind gekomen aan dit proefschrift.

Jan Buitelaar, wij leerden elkaar kennen toen jij naar Nijmegen kwam. Ik wilde

onderzoek doen naar ADHD en de borderline persoonlijkheidsstoornis en jij bood

me die mogelijkheid. Dat zie ik nog steeds als een groot voorrecht. Toch hadden bij

mij andere werkzaamheden of privé omstandigheden altijd voorrang en zo werd

het een bijzonder lang(zaam) proces waarin het promotietraject mijn ondergeschoven

kindje werd. Ik heb de afgelopen jaren meermalen overwogen om het bijltje erbij

neer te gooien, maar jouw reactie was steeds: je bent er bijna, je moet nu niet

stoppen. Jij was voor mij de constante factor en als ik dan na lange tijd weer met

een zoveelste concepttekst aankwam en het toch wel graag zo snel mogelijk terug

wilde dan kreeg ik dat ook. Heel bijzonder. Jan, dankjewel voor jouw hulp, je geduld,

en je vertrouwen! Het is er uiteindelijk dan toch van gekomen.

Robbert-Jan Verkes, hoewel niet vanaf het begin betrokken bij mijn promotie-

traject heb je een hele belangrijke rol gespeeld op cruciale momenten. Je bleef

geïnteresseerd en steeds bereid om bij te dragen. Ik heb jou als bijzonder steunend

ervaren. Dankjewel daarvoor.

Cees Kan, het is alweer lang geleden, maar wij hebben samen en met anderen de

ADHD/ASS poli op de afdeling psychiatrie vormgegeven. Zo ontstond de mogelijkheid

voor mij om data te gaan verzamelen. Een essentiële samenwerking.

Jeffrey Glennon, wat ben ik blij dat Jan jou in de laatste fase van het schrijven

van mijn proefschrift heeft gevraagd om mij te ondersteunen. Samen met jou is

het snel gelukt om tot een afronding te komen. Dankjewel.

Beste werkgevers,

Dank aan het Radboud UMC (afdeling psychiatrie), GGz Nijmegen (inmiddels Pro

Persona), de Radboud Universiteit (Faculteit Sociale Wetenschappen). Dank voor

jullie bereidheid om me toch steeds wat tijd te gunnen om weer een paar stappen

verder te komen in mijn promotietraject. Dank ook aan mijn huidige werkgevers



162

DANKWOORD

GGNet en Streekziekenhuis Koningin Beatrix. Ook jullie support heb ik gekregen

bij de laatste loodjes.

Beste manuscript- en promotiecommissieleden,

Judith Prins, Paul Hodiamont, en Sandra Kooij. Dank voor jullie bereidheid om

mijn proefschrift te beoordelen en voor de verleende toegang tot de promotie.

Sandra, speciaal dank aan jou. Jij zette me op het spoor van Jan en daar begon het

allemaal mee.

Dank ook aan Anna Bosman, Toon Cillissen en Theo Ingenhoven voor jullie

deelname aan de promotiecommissie.

Beste onderzoeksmaatjes,

Martijn Lappenschaar, Arnt Schellekens en Pieter van den Broek. Dank voor jullie

samenwerking en inzet. Zonder jullie hulp en vooral ook statistische kennis had

ik het echt niet gered. Onderzoeksassistenten Marjan Knippenberg en Marleen

Bastiaanse, dank voor jullie hulp en inzet bij het verzamelen van de data.

Beste (oud) collega’s,

Cees Clarijs en Maurice Bracelly. Opleider en collega’s van het eerste uur in mijn

tijd bij GGz Nijmegen. Dank voor jullie steun en blijvende betrokkenheid. Gelukkig

zien we elkaar nog regelmatig bij de Nijmeegse nascholingen.

Cees van der Staak en Giel Hutschemaekers. Dankzij jullie kreeg ik 2 prachtige

banen binnen het Academisch Centrum Sociale Wetenschappen en maakte daarmee

een geweldige stap in mijn loopbaan. Het heeft me gebracht waar ik nu sta. Dank

voor jullie steun en vertrouwen.

Harold Beckering. Jouw deur stond altijd voor mij open. Een mentor pro bono

zou ik willen zeggen. Jij gaf me de volgende opdracht: “als iemand aan je vraagt

hoe het met je proefschrift staat dan zeg je alleen maar: goed, ik ben er mee bezig”.

En dat hielp! Dankjewel voor jouw steun.

Anna Bosman, lieve Anna, wat ben jij er voor mij geweest de afgelopen 2 jaar.

Dank voor je hulp en steun bij de laatste loodjes.

Dank ook aan alle andere betrokken oud collega’s van GGz Nijmegen, van het

Radboud UMC, van het SPON, van de Faculteit Sociale Wetenschappen, het onder-

wijsinstituut Pedagogische Wetenschappen en Onderwijskunde, en van het

Ambulatorium. Jullie zijn met te veel om op te noemen. Dank voor jullie blijvende

interesse en steun. Maar ook mijn nieuwe collega’s bij GGnet en het Streekzieken-

huis Koningin Beatrix. Wat een warm bad ben ik in terecht gekomen. Dank voor

jullie enthousiasme en vertrouwen.



163

DANKWOORD

Ik wil ook mijn intervisiegenoten bedanken, nieuw en oud. Ik ben heel blij dat

ik altijd bij jullie terecht kan en kon. Dank voor jullie luisterend oor, de steun, en

goede adviezen.

Lieve vrienden,

Wim, heel wat uurtjes hebben we samen doorgebracht en vooral heel veel gelachen.

ADHD bij volwassenen op de kaart van GGz Nijmegen gezet. Samen naar Sandra

om ons te specialiseren in de ADHD. Collega’s zijn we niet meer, maar vrienden

zijn we gebleven.

Rob, het is in al die jaren misschien maar 2 of 3 keer geweest dat ik je mening

vroeg over een analyse, maar bij jou durfde ik mijn ‘domme’ vragen gewoon te

stellen en kon dan weer verder. Dankjewel dat je er op die momenten voor me was.

Mirella, ineens was je daar en hoe! Vriendin en trainer, met een dijk van

een ‘Mindset’. Hoe is me niet helemaal duidelijk, maar zeker is wel dat jij hebt

bijgedragen aan het feit dat ik het proefschrift toch heb afgemaakt, dat ik weer

aan het tennissen ben, en dat er inmiddels een prachtige lieve Collie bij ons woont.

Dankjewel.

Hetty, Hans, en Jeske. Lieve Hetty, wat hebben we veel gedeeld. Helaas maak je

mijn promotie niet meer mee. Maar het is mede jouw kracht en positieve energie

die mij er toe hebben aangezet om het proefschrift nu toch echt eens af te maken.

Dankjewel lieverd voor onze tijd samen. Het was, in jouw woorden, goud waard!

Hans, rots in de branding. Die extra uurtjes om de discussie te schrijven was

precies wat nodig was. Jeske, lieve schat, weet dat ook jij er aan hebt bijgedragen

dat er toch een promotiedag is gekomen. Al jouw fijne knuffels geven mij zoveel

energie dat het toch gelukt is om het proefschrift af te maken.

Dominique. Wat ben ik blij en dankbaar dat ik jou en Ris mag en kan onder -

steunen. Ook dat was een hele goede stimulans om mijn proefschrift uiteindelijk

snel af te ronden. Ik hoop dat we nog veel fijne momenten zullen hebben samen.

Esther, lieve Esther, jou noem ik als laatste, dankjewel dat wij al jaren altijd

lief en leed kunnen delen en dat je nu mijn paranimf wil zijn en me helpt met alle

voorbereidingen voor mijn promotiedag. Heel bijzonder.

Lieve familie,

Peter en Ludie, al 25 jaar mijn schoonouders. Elvira, Gerhald, Floor en Mila; mijn

schoonzusje, zwager en nichtjes. Bedankt voor alles wat jullie voor ons betekend

hebben in al die jaren. Ik ben heel blij met jullie.

Pap en mam, al 43 jaar mijn ouders, en jullie staan nog altijd voor ons klaar.

Dank voor alles wat jullie voor mij betekend hebben, dat is meer dan ik hier

opschrijven kan. Ik ben heel blij en dankbaar dat we mijn promotie samen kunnen

vieren!



164

DANKWOORD

Edwin en Sylvia, broer en schoonzus, we zien elkaar niet veel maar op belangrijke

momenten zijn jullie er. Dankjewel daarvoor.

Robin, mijn grote broer, dank dat je altijd trots op me bent. Dat voelt fijn. Weet

dat ik ook trots op jou ben! Cindy, mijn schoonzus, lief en betrokken, dankjewel.

Lieve Alexander, jij hebt voor mij de prachtige tekening gemaakt voor de

omslag van dit boekje. Je hebt het “verbonden sterren” genoemd. Een titel recht

uit jouw hart van goud. Dankjewel lieve schat dat je zo lief bent, zo betrokken, en

zo enthousiast. Mama’s boekje is nu af. We hebben weer wat meer tijd om samen

te zijn.

Mijn liefste Alain, samen met Alexander ben jij de allerbelangrijkste in mijn

leven. Jij bent de laatste die dank krijgt. Voor de liefste zijn, voor er altijd zijn.

Ik hou van je.



165

CURRICULUM VITAE

Curriculum Vitae

Fiona van Dijk was born in Hardenberg on December 2nd 1973. She graduated in

psychology in 1998 at the Catholic University Nijmegen. She specialized in Clinical

Psychology and finished her specialization in 2008 at the SPON in Nijmegen.

During the post initial educations she worked as a clinician at GGZ Nijmegen

(currently called Pro Persona, mental health care organization) and the Radboud

University Medical Center, department of Psychiatry, where she also started her

research for adults with ADHD and BPD. Between 2009 and 2016 she worked as

vice program director of the post-initial education for healthcare psychologists at

the SPON and as head of the Ambulatorium of the Radboud University in Nijmegen.

Recently she started a new assignment for GGNet (mental health care organization)

and the SKB (Regional hospital Koningin Beatrix) in Winterswijk where she

focusses on health innovation, clinical work, and research. She is shaping the

collaboration between GGNet and SKB; collaborates on a project to dramatically

reduce chronicity in the mental health care; and supervises young specialists.

Besides this she works in her private psychotherapy practice where she offers

supervision and learning-therapy for trainee psychiatrists, clinical psychologists,

and psychotherapists.



167

DONDERS GRADUATE SCHOOL FOR COGNITIVE NEUROSCIENCE

Donders Graduate School for Cognitive Neuroscience

For a successful research Institute, it is vital to train the next generation of young

scientists. To achieve this goal, the Donders Institute for Brain, Cognition and

Behaviour established the Donders Graduate School for Cognitive Neuroscience

(DGCN), which was officially recognised as a national graduate school in 2009.

The Graduate School covers training at both Master’s and PhD level and provides

an excellent educational context fully aligned with the research programme of

the Donders Institute.

The school successfully attracts highly talented national and international students

in biology, physics, psycholinguistics, psychology, behavioral science, medicine

and related disciplines. Selective admission and assessment centers guarantee the

enrolment of the best and most motivated students.

The DGCN tracks the career of PhD graduates carefully. More than 50% of PhD

alumni show a continuation in academia with postdoc positions at top institutes

worldwide, e.g. Stanford University, University of Oxford, University of Cambridge,

UCL London, MPI Leipzig, Hanyang University in South Korea, NTNU Norway,

University of Illinois, North Western University, Northeastern University in Boston,

ETH Zürich, University of Vienna etc.. Positions outside academia spread among

the following sectors: specialists in a medical environment, mainly in genetics,

geriatrics, psychiatry and neurology. Specialists in a psychological environment,

e.g. as specialist in neuropsychology, psychological diagnostics or therapy. Positions

in higher education as coordinators or lecturers. A smaller percentage enters

business as research consultants, analysts or head of research and development.

Fewer graduates stay in a research environment as lab coordinators, technical

support or policy advisors. Upcoming possibilities are positions in the IT sector

and management position in pharmaceutical industry. In general, the PhDs

graduates almost invariably continue with high-quality positions that play an

important role in our knowledge economy.

For more information on the DGCN as well as past and upcoming defenses please

visit: http://www.ru.nl/donders/graduate-school/phd/

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