Table Of ContentTREATMENT OF
PERSONALITY DISORDERS
TREATMENT OF
PERSONALITY DISORDERS
Edited by
Jan Derksen
University of Nijmegen
Nijmegen, The Netherlands and
Free University of Brussels
Brussels, Belgium
Cesare Maffei
Vita-Salute San Raffaele University
and Scientific Institute San Raffaele
Milan, Italy
and
Herman Groen
Forensic Psychiatric Institute "Oldenkotte"
Rekker, The Netherlands
Springer Science+Business Media, LLC
Library of Congress Cataloging·in·PubHcation Data
Treatment of personality disorders/edited by Jan Derksen, Cesare Maffei, and Herman Groen.
p. cm.
"Including contributions from the First European Congress on Disorders of Personality,
held June 14-17, 1994, Nijmegen, The Netherlands, and the Second European Congress
on Personality Disorders, held June 26-29, 1996, Milan, Italy"-T.p. verso.
Includes bibliographical references and index.
ISBN 978-1-4419-3326-3 ISBN 978-1-4757-6876-3 (eBook)
DOI 10.1007/978-1-4757-6876-3
1. Personality disorders. I. Derksen, Jan, 1953- II. Maffei, Cesare, 1951- III. Groen,
Herman.
RC554.T72 1999
616.85'8-dc21
99-047601
Including contributions from the First European Congress on Disorders of Personality, held June 14-17, 1994,
Nijmegen, The Netherlands, and the Second European Congress on Personality Disorders, held June 26-29,
1996, Milan, Italy
ISBN 978-1-4419-3326·3
© 1999 Springer Science+Business Media New York
Originally published by Kluwer AcademicIPlenum Publishers, New York in 1999
http://www.wkap.nl
10987654321
A C.I.P. record for this book is available from the Library of Congress
All rights reserved
No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any
means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission
from the Publisher
PREFACE
It has been almost twenty years since DSM-III created a major shift in psychi
atric classification procedures and in diagnostic and treatment practice by introducing
the multi-axial system and, for our patients specifically, the Axis II: Personality
Disorders.
Researchers and clinicians were forced to focus on many issues related to the field
of personality and its disorders. This meant an immense impetus for research, both
empirical and theoretical. Many recent developments are described in this book, as
reviews or as original articles. This book also covers developments in Europe as well
as in North America.
Important questions still remain unanswered, such as: What is the relationship
between the different clusters: A, B, & C? Are we talking about dimensions, categories,
or typologies? What can be done for patients who have more than one personality
disorder? Is a pro typical approach required? Consequently, is a multiconceptual
approach in treatment and research required? The authors contribute to this discus
sion and provide guidelines for further thinking in research and treatment planning.
For clinicians, it is of major importance to know whether the disorder can be influ
enced by treatment, and whether permanent change is really possible. A very impor
tant question is whether a person indeed has a personality disorder, and how this
diagnosis affects clinical practice.
We have to differentiate between the genotypical and phenotypical, between bio
logical and psychological, nature and nurture, trait and state. Differentiation implies
the use of diagnostic procedures, which as you will find, are promising. It also implies
different treatment strategies, depending on the phase of treatment for the same dis
order, and the orientation of the therapist.
Accurate diagnoses can allow us to distinguish between different treatment
strategies for various disorders. Within the framework of a DSM personality disorder,
further differentiation then becomes possible. For example, good diagnostic procedures
will allow distinction between an impulsive and a dissociative borderline personality
disorder. Research is suggesting the first might better be influenced by biological!
psychopharmacological treatment, and the latter by focusing in a cognitive or psycho
dynamic way on early childhood (sexual) trauma. It is also important to find out
whether the symptomatology we meet in clinical practice is caused by the personality
disorder itself, (an Axis I disorder) or whether this is the result of the interaction
between the two, complicated by problems and dysfunctioning on Axes IV and V.
v
vi Preface
Once we have established an accurate diagnosis, we can offer a range of treat
ments, simultaneously or separately: psychopharmacological treatment together with
psychoanalytical and/or cognitive treatment.
Given the state of the art of the psychobiological foundations involved, we
analyze genetics, with a view to finding out how the carriers of our existence influence
our being. TIle genetic loading can explain some, but not all of the characteristics influ
encing personality disorders. This has implications for biological research, especially
when foeuse d on treatment and in examining the psychobiology of personality disor
ders. If we accept that phenotypical characteristics represent the same genetic pattern
as influenced by its environment, and if we accept that the relevant environment for
human species is not only biological but also psychological, then psychobiology gets
a far more existential meaning and therefore is of great interest to clinicians and
researchers interested in personality disorders from all perspectives.
Within this genotypical/phenotypical perspective, considerations on the psycho
logical foundations of development and psychodynamic research will become dynamic
in itself. Attachment and the development of the self, vis-a-vis the disorders of per
sonality, is of great importance, as is the occurrence of psychological, sexual, and phys
ical trauma in early childhood. These issues are of clinical importance because human
beings grow through childhood and adolescence and beyond. As is shown by PET
scanning even the brain can change functionally through psychological treatment. So
we are not a victim of our genes and the phenotypical outlook created in childhood.
Even with animals, this is not the case.
It is important for researchers and clinicians to decide on which position to take.
This position should be clear so that patients are aware of how their therapist views
their disorcer, and what outcomes for treatment are perceived. Consequently, our
therapeutic acts are affected by this position. Categorical thinking almost always intro
duces the handicap model; dimensional and typological thinking creates room for opti
mism with possible change from severe to less severe.
We have created an empirical and theoretical framework, aware that we were not
primarily interested in conceptual answers to questions such as: Is a personality disor
der defined by 5, 9, 12 ... factors? Are personality disorders within the continuum of
Axis I disorders and therefore, by definition an Axis 1 disorder? among others. We
created a framework for clinical practice, trying to give clinicians a colorful background
on which basis they might be better able to give their work more depth using innova
tive and creative therapies for these complex patients and their psychopathologies.
We think that with more alternative approaches, treatment will be less frustrat
ing. One should and cannot adhere to one ideology, especially not with the very serious,
rigid, personality-disordered patient. Such a patient does, with respect to his psy
chopathology, everything possible to preserve his homeostasis; not doing so is fearful,
as well as dangerous because of the lack of other possibilities in feelings and behavior.
Finding a way, creating a safe, holding environment, requires flexibility.
There is no final advice, nor concluding remarks, because we think that the
theoretical orientation and the way the therapist is trained, is too diverse throughout
Europe as well as throughout North America. Instead, the framework that we have
created, consisting of elements/modules for each individual patient is to be used by
every individual therapist according to his own frame of reference.
Jan Derksen
Cesare Maffei
Herman Groen
CONTENTS
Part I: Biological Foundations of Personality Disorders
1. Genetics of Personality Disorders ................................. 1
Svenn Torgersen and Marco Battaglia
2. Psychobiology of Personality Disorders: Implications for the Clinic 17
Larry 1. Siever
3. The Implications of Recent Research on the Etiology and Stability of
Personality and Personality Disorder for Treatment ............. 25
W. John Livesley
Part II: Psychological Foundations of Personality Disorders
4. Psychodynamic Research Can Help Us to Improve Diagnosis and
Therapy for Personality Disorders: The Case of Defense
Mechanisms ................................................ ' 39
1. Christopher Perry, Vittorio Lingiardi, and Floriana Ianni
5. Attachment, the Development of the Self, and Its Pathology in
Personality Disorders ....................................... 53
Peter Fonagy
6. Trauma and Personality .......................................... 69
Fabio Madeddu and Adolfo Pazzagli
7. Adolescence and Personality Disorders: Current Perspectives on a
Controversial Problem ...................................... 77
Enrico de Vito, Fran~ois Ladame, and Alvise Orlandini
Part III: Diagnostic Models of Personality Disorders
8. Integrative Perspectives on the Personality Disorders 97
Theodore Millon
vii
viii Contents
9. A Multidimensional Approach to Personality Disorders and Their
Treatment ................................................. 107
Joel Paris
10. The Structure of DSM-IV Borderline Personality Disorder and Its
Implications for Treatment ................................... 119
Cesare Maffei and Andrea Fossati
11. The Relationship between Anxiety Disorders and Personality Disorders:
Prevalence Rates and Comorbidity Models ..................... 129
Carol 1. M. Van Velzen and Paul M. G. Emmelkamp
Part IV: Treatment of Personality Disorders
12. Psychodiagnostics and Indications for Treatment in Cases of Personality
Disorder: Some Pitfalls ...................................... 155
1. Derksen and H. Sloore
13. The Psychotherapeutic Treatment of Borderline Patients 167
Otto F. Kernberg
14. Functional Analysis of Borderline Personality Disorder Behavioral
Criterion Patterns: Links to Treatment ......................... 183
Jennifer Waltz and Marsha M. Linehan
15. Psychopharmacological Treatment of Personality Disorders: A Review 207
Peter Moleman, Karin van Dam, and Veron Dings
16. New Drugs in the Treatment of Borderline Personality Disorder ....... 229
F. Benedetti, C. Colombo, L. Sforzini, C. Maffei, and E. Smeraldi
17. The Narcissistic Personality Disorder and Addiction. . . . . . . . . . . . . . . . . . 241
PerVaglum
18. Pharmacotherapy for Patients with Personality Disorders: Experiences
from a Group Analytic Treatment Program . . . . . . . . . . . . . . . . . . . . . 255
S. Friis, T. Wilberg, T. Dammen, and 0. Urnes
19. A New Interpersonal Theory and the Treatment of Dependent
Personality Disorder ........................................ 269
John Birtchnell and Giuseppe Borgherini
20. HIV Infection, Personality Structure, and Psychotherapeutic
Treatment ................................................. 289
R. Visintini, E. Campanini, A. Ama, R. Alcorn, S. Corbella, S. Gessler,
D. Miller, L. Nilsson Schonnesson, and F. Staracel
Index 305
1
GENETICS OF PERSONALITY DISORDERS
Svenn Torgersen 1 and Marco Battaglia2
University of Oslo
1
Department of Psychology
Blindern Oslo Norway
University of Milano and the San Raffaele Hospital
2
Department of Neuropsychiatric Sciences
29 via Prinetti Milano Italy
1. INTRODUCTION
When we wonder about whether genetic factors influence the development of a
disorder, we may think about necessary and sufficient conditions for the manifestation
of the disorder.
- Do we need to have some genes to get the disorder, or is it possible to develop
the disorder without the genes?
- Are the genes the full explanation, or do some non-random environmental
factors also have to be present?
- Are genetic factors completely irrelevant, the whole explanation being envi
ronmental?
- Do some genes increase the likelihood of developing the disorder, without
being either sufficient or necessary?
Basically, the genetic influence on the development of a disorder is of two kinds:
1) One or more genes exert an independent influence on the development of
the disorder. This is called non-additive inheritance. The genes may be dom
inant or recessive. If the genes are dominant, a critical allele from either the
mother or the father is sufficient. Recessive genetic transmission claims that
both the allele from the mother and from the father needs to carry the seed
of the disorder. It can be generally stated that while rare, mendelian disor
ders whose inheritance is based on a single gene have traditionally been the
focus of medical genetics, psychiatric genetics, and behavioral genetics are
examining much more common illnesses and behaviors in which an inherited
Treatment of Personality Disorders, edited by Derksen et al.
Kluwer Academic / Plenum Publishers. Ncw York, 1999. 1
2 S. Torgersen and M. Battaglia
liability-or vulnerability-appears to interact with environmental factors in
a complex way, so that the methods of psychiatric genetics and behavioral
genetics are usually closer to those of genetic epidemiology.
2) A number of genes, being recessive or dominant, are adding up. The more
effective genes a person has, the higher liability for the disorder. This is
the basic model for additive inheritance. A multifactorial additive influence
means that a number of physical, psychological, and social factors contribute
in an additional fashion. The implication may be that the more traumatic the
environment, the fewer critical alleles are necessary for the development of
the disorder (Goldsmith and Gottesman, 1996). In principle, it is possible to
develop the disorder even when all at environmental conditions have been
favourable if the genetic load is massive. Conversely, a certain amount of trau
matic experiences, physical, psychological or social, may imply a development
of the disorder even if the genetic basis is weak or absent. Given an average
genetic make-up, a certain amount of negative experiences are necessary. On
the other hand, with an ordinary environment, a lot of critical alleles are nec
essary for the disorder to develop.
In general, it should be remembered that when data show a continuous distribu
tion for a certain trait (a given behavior in our case) in the popUlation, then the trait
is likely to be influenced by several genes, each having a small effect, and environmental
factors, whereas non additive mechanisms are more likely to be involved when a trait
distribution tends to be bimodal, instead of normal (Plomin, DeFries, and McLean,
1990).
Even though understanding precisely how multiple genes with small effects influ
ence behavior can be a very complex task, we have to remember that each of such
many genes is nonetheless submitted to the laws of heredity first discovered by Mendel.
Moreover, with the advent of molecular genetics techniques it has become pos
sible to precisely isolate, identify, and quantify the effect of even a single gene of rela
tively small effect that is able to influence behavior and personality, provided that the
behavioral scales employed to describe the phenotype are reliable and accurately
shaped (Cloninger,Adolfsson, and Svrakic, 1996). Very recent advancements in the field
showing significant associations between some polymorphisms of genes implicated in
the mechanisms of neurotransmission and temperamental, and personologic variants
in the human (Ebstein et aI., 1996; Benjamin et aI., 1996; Lesch et aI., 1996) are inter
esting examples of such possibilities.
Many complications to these simple descriptions exist. Even if a person has seem
ingly sufficient and necessary genes, the disorder does not need to develop. Some
arbitrarily or unknown factors have to be there in addition. This is called reduced pen
etrance. Sometimes also so-called phenocopies exist::a disorder phenomenologically
similar to a normally strongly genetically determined disorder may develop out of
purely environmental reasons. Another important and common aspect in behavioral
genetics is pleiotropism, or the multiple behavioral effects that may be exerted by a
single gene. An example in animal behavior is the finding that the higher emotional
reactivity of the albino mice is partially due to the same gene that influences the coat
color (DeFries and Hegmann, 1970).
More important-and even more complex-is heterogeneity. That means that the
disorder may have many independent causes. Sometimes one gene or one pattern of
non-additive genes are responsible for the development of the disorder, other times
Genetics of Personality Disorders 3
completely different genes, non-additive or additive. Sometimes genes are not involved
at all.
For the same disorders, maybe a combination of non-additive genes and multi
factorial additive genes are necessary.
The possibility also exists that only in interaction with some environmental factors
do the genes have any effect. As we study the phenotypical result of an eventual geno
type and environment, the interaction may be difficult to trace. In fact there is growing
consciousness that a core issue for the understanding of the etiology of mental
ilnnesses-including the personality disorders-is the complex interaction between
genes and environment. It may be too simplicistic to think that one's vulnerability to
a mental illness is merely the sum of the genetic plus the non-genetic risk factors: genes
and environment may well be correlated, in that there can be a genetic predisposition
to selecting some specific environments, given a certain genetic background (see e.g.
Kendler, 1995). In this perspective a simple additive model that predicts the indepen
dence between genotype and the impact of non-genetic factors would be inadequate.
Indeed, recent findings in the field of genetic epidemiology show that the relationships
between genes and environment in shaping normal and abnormal personality variants
need a multivariate, complex approach. Two very important concepts are clearly emerg
ing from research in the gene-environment interaction. First, there may be a genetic
influence in leading people to select high-risk environments: this is what is meant when
we say that genes and environment are correlated. Second, while in a relatively neutral
environment people can be relatively homogeneous in ther levels of psychological dis
tress, when an environmental stressor becomes active, new genes that influence the indi
vidual differences in coping with adverse conditions would "come on line" (Kendler,
1995), so that interindividual differences and symptomatological variability would
become more evident.
2. METHODS
The most straightforward way to prove the genetic influence on the development
of a disorder would be to identify the critical allele of a gene in individuals with a spe
cific disorder. Up to now, the technique of molecular genetics has not developed to a
point where this can be the standard procedure. Moreover, the more genes are involved,
the more the task can be complex.
The linkage method is therefore an approximation. By studying the process of
recombination of alleles in families of more generations, one is not only able to prove
the genetic influence, but also to track down the location of the gene. The technique is
that once a part of the human genome is known, genes in the neighbourhood can be
localised by the fact that they follow each other through generations of recom
binations. However, once more, this method is only realistic when few genes are of
importance.
The more realistic procedure is to apply the twin or the adoption method. The
twin method capitalises on the fact that monozygotic (MZ) twins are genetically iden
tical, while dizygotic (DZ) twins are not more similar in their genetic make-up than
sibs generally.
When the adoption method is applied, the features of the adoptees are compared
to the characteristics of the biological relatives. The social relatives of the adoptees, or
the biological relatives of adoptees without these features, are controls.
