Social cognition and metacognition in schizophrenia : psychopathology and treatment approaches

331 Pages·2014·4.301 MB·English

by  Paul H Lysaker, Giancarlo Dimaggio, Martin Brüne

Social Cognition and
Metacognition in Schizophrenia
Psychopathology and Treatment Approaches
Social Cognition
and Metacognition
in Schizophrenia
Psychopathology and Treatment Approaches
Edited by
Paul H. Lysaker
Richard L. Roudebush VA Medical Center,
Indianapolis, IN, USA
and
Indiana University School of Medicine, Indianapolis, IN, USA
Giancarlo Dimaggio
Center for Metacognitive Interpersonal Therapy, Rome, Italy
and
University La Sapienza, Rome, Italy
Martin Brüne
LWL-University Hospital Bochum, Bochum, Germany
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List of Contributors
Ahmad Abu-Akel University of Birmingham, Birmingham, UK
Elisabeth Bacon Strasbourg, France
Ryan Balzan Flinders University, Adelaide, SA, Australia
Rebecca Bargenquast Queensland University of Technology, Brisbane, QLD,
Australia
Michael R. Basso The University of Tulsa, Tulsa, OK, USA
Sune Bo Psychiatric Research Unit, Region Zealand, Denmark
Benjamin K. Brent Beth Israel Deaconess Medical Center and Massachusetts
Mental Health Center, Boston, MA, USA; Massachusetts General Hospital, Harvard
Medical School, Boston, MA, USA; Harvard Medical School, Boston, MA, USA
Martin Brüne LWL-University Hospital Bochum, Bochum, Germany
Elliot C. Brown LWL-University Hospital Bochum, Bochum, Germany;
International Graduate School of Neuroscience (IGSN), Ruhr-University Bochum,
Bochum, Germany
Benjamin Buck University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Kelly D. Buck Richard L. Roudebush VA Medical Center, Indianapolis, IN, USA
Dennis R. Combs The University of Texas at Tyler, Tyler, TX, USA
Sarah Daniel University of Copenhagen, Copenhagen, Denmark
Birgit Derntl RWTH Aachen University, Aachen, Germany
Nadia Di Sturco Center for Metacognitive Interpersonal Therapy, Rome, Italy
Giancarlo Dimaggio Center for Metacognitive Interpersonal Therapy, Rome, Italy;
University La Sapienza, Rome, Italy
Emily Drake The University of Texas at Tyler, Tyler, TX, USA
João M. Fernandes Centro Hospitalar de Lisboa Ocidental, EPE, Lisbon, Portugal
Peter Fonagy University College London, London, UK
Cristina Gonzalez LWL-University Hospital Bochum, Bochum, Germany;
Ruhr-University Bochum, Bochum, Germany
Michael F. Green David Geffen School of Medicine at UCLA, Los Angeles, CA,
USA; VISN 22 Mental Illness Research Education and Clinical Center,
Los Angeles, CA, USA
Andrew Gumley University of Glasgow, Glasgow, UK
Jay Hamm Indiana University School of Medicine, Indianapolis, IN, USA
xiii
xiv List of Contributors
Susanne Harder University of Copenhagen, Copenhagen, Denmark
Ilanit Hasson-Ohayon Bar-Ilan University, Ramat-Gan, Israel
Jaclyn Hillis University of Indianapolis, Indianapolis, IN, USA
William P. Horan David Geffen School of Medicine at UCLA, Los Angeles, CA,
USA; VISN 22 Mental Illness Research Education and Clinical Center, Los
Angeles, CA, USA
Marie Izaute LAPSCO - UMR 6024 CNRS, Clermont-Ferrand, France
Katja Koelkebeck University of Muenster, Muenster, Germany
Mickey Kongerslev Psychiatric Research Unit, Region Zealand, Denmark
Marina Kukla Richard L. Roudebush VA Medical Center, Indianapolis, IN, USA
Bethany L. Leonhardt University of Indianapolis, Indianapolis, IN, USA
Paul H. Lysaker Richard L Roudebush VA Medical Center Indianapolis, IN, USA;
University School of Medicine, Indianapolis, IN, USA
Amanda McCleery David Geffen School of Medicine at UCLA, Los Angeles, CA,
USA
Hamish J. McLeod University of Glasgow, Glasgow, UK
Mahesh Menon University of British Columbia, Vancouver, BC, Canada
Steffen Moritz Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
Paolo Ottavi Center for Metacognitive Interpersonal Therapy, Rome, Italy
Manuela Pasinetti Center for Metacognitive Interpersonal Therapy, Rome, Italy
Raffaele Popolo Center for Metacognitive Interpersonal Therapy, Rome, Italy
Christina Regenbogen RWTH Aachen University, Aachen, Germany; Karolinska
Institutet, Solna, Sweden
David L. Roberts University of Texas Health Science Center, San Antonio, TX, USA
Giampaolo Salvatore Center for Metacognitive Interpersonal Therapy, Rome, Italy
Matthias Schwannauer University of Edinburgh, Edinburgh, UK
Robert D. Schweitzer Queensland University of Technology, Brisbane, QLD,
Australia
Cumhur Tas LWL-University Hospital Bochum, Bochum, Germany;
Ruhr-University Bochum, Bochum, Germany
Jenifer L. Vohs Indiana University School of Medicine, Indianapolis, IN, USA
Christine Wilhelm School of Medicine, University of Muenster, Muenster, Germany
Todd S. Woodward BC Mental Health and Addictions Research Institute, Vancouver,
BC, Canada; University of British Columbia, Vancouver, BC, Canada
Preface
Seemingly, as much as any subject in the field of medicine and mental health,
our contemporary understanding of schizophrenia has been subject to vigor-
ous debate and significant ongoing revision. Since the late 1990s (or the past
few decades), we have witnessed fundamental changes in our ideas about the
incidence and prevalence of schizophrenia, its natural course, and the validity
of long-held subtypes. In our opinion, one of the most remarkable develop-
ments is the accumulation of evidence that schizophrenia may be character-
ized by relatively specific problems related to being aware of and reflecting
upon one’s own thoughts, feelings, and intentions, and the thoughts, feelings,
and intentions of other people. In other words, schizophrenia, contrary in part
to the direction provided by diagnostic manuals, may be more than a diffuse
set of unrelated decrements in mental processes. As a disorder, it may more
specifically involve difficulties in noticing and making sense of the things that
allow people to experience themselves as unique beings in the world.
Different names have been used to refer to these deficits. They have been
called impairments in social cognition, theory of mind, metacognition, emotional
intelligence, mind-reading, and mentalization, just to name a few. While each
construct emphasizes a slightly different phenomena, to have deficits in any of
them suggests some form of difficulty in recognizing what one and others think,
feel, and intend. In addition, each construct, whether it states it directly or just
infers it, is concerned with the capacities that allow us to know and scrutinize
self-experience and link our experience in the moment with some larger picture
of who we, and others, are across the histories of our lives. Applied to schizophre-
nia, the implication is that this core element of disability interferes with a person’s
ability to form the types of ideas about the self and others that are needed to nego-
tiate the demands of life itself, as well as the challenges posed by schizophrenia.
One limitation we see to date is that there has been a lack of integration of
the work in this area. Many of the papers published, for instance, have been
confined within their own ‘silos’. One example of this is that work on social
cognition has not been integrated with work on metacognition. Work on meta-
cognition has not been integrated with social cognition, and so forth. This book
thus seeks to bring together the developments on these related constructs, which
often is not found in the same volume. We have included chapters on both
social cognition and metacognition without waiting for an agreed-upon defini-
tion about how exactly these constructs overlap and diverge with the hope that
discussing them in the same volume will speed along that process. We have
chosen these two constructs given that each potentially functions as an umbrella
term, with others seen as fitting under the umbrella. Social cognition, for
xv
xvi Preface
instance, often includes constructs such as theory of mind while metacognition
refers to a spectrum of activities which involves thinking about thinking and
stretches from consideration of discrete psychological phenomenon to the syn-
thesis of discrete perception into an integrated representation of self and others.
A further limitation of work in this area has been the bifurcation of clinical and
academic research. Work on schizophrenia offered by clinician scholars has not
been integrated with the science performed by more traditional laboratory-based
scientists. To address this, this book will also include chapters by scholars who are
primarily researchers and others who are clinicians and have spent years in con-
versations with people with schizophrenia. There are chapters that offer rich case
reports and others that present statistical analyses of large and diverse samples.
Finally, much work in schizophrenia can be classified as focused either on psycho-
pathology or treatment, with the two literatures rarely informing one another. This
book thus includes sections dealing with both psychopathology and treatment.
The first overall set of objectives of the book are thus integration and dia-
logue: the integration and dialogue of research on social cognition and meta-
cognition, the integration and dialogue of work from primarily clinical and
research settings, and the integration of work on treatment and psychopathol-
ogy. Pragmatically, the book opens with chapters regarding the biologic and
social roots of social cognitive and metacognitive activity. The next set of
chapters then focuses on different forms of social cognitive and metacognitive
deficits and their linkages with functional outcomes. Finally, a range of differ-
ent treatment approaches are offered and discussed.
We imagine the readers of this book will come from many different clinical
and academic backgrounds. We anticipate this book will end up in the hands
of clinicians, scientists, students, and even policy makers. And for all, we hope
the book accomplishes two larger goals. First, we hope for a more deeply
human and nuanced portrait of schizophrenia. We believe that the chapters
offered here have the potential to paint a richer picture of how schizophrenia
interrupts the lives of unique human beings via alteration of the basic experi-
ence of one’s own being and the being of others. We believe this picture will
be richer because of the integration rather than the exclusive focus on one con-
struct, one form of evidence, or one type of author. Second, we hope to spur
the development of treatments that help people with this condition to meaning-
fully recover. We explicitly do not want to find ‘the’ new treatment or promote
one universal response to deficits in social cognition or metacognition. We
do not want to privilege one view or one treatment above another but instead
desire to spur on the type of dialogue that will allow for the proliferation of
many different treatments, which could meet the needs of many different types
of people who experience schizophrenia. Finally, we hope to support the devel-
opment of treatments that move beyond a symptom focus and take into account
the whole person and his or her core experience as a unique being in the world.
Paul H. Lysaker
Giancarlo Dimaggio
Martin Brüne
Chapter 1
Neurobiologic Underpinnings
of Social Cognition and
Metacognition in Schizophrenia
Spectrum Disorders
Elliot C. Brown,1,2 Cumhur Tas,1,3
Cristina Gonzalez1,3 and Martin Brüne1
1LWL-University Hospital Bochum, Bochum, Germany, 2International Graduate School
of Neuroscience (IGSN), Ruhr-University Bochum, Bochum, Germany, 3Ruhr-University Bochum,
Bochum, Germany
Chapter Outline
Introduction 1 Action Observation and the
Animal Studies on Basic Social Mirror Neuron System in
Cognition and Social Behavior with Schizophrenia 11
Schizophrenia Models 2 Neuroimaging of Social
Neurotransmitters and Receptors Decision-Making 13
Related to Social Cognition 4 The Neurobiology of
Social Cognition in Schizophrenia: Metacognition 15
Neuroimaging Research 5 Biomarkers for Deficits in Social
Neuroimaging of Emotion Cognition 16
Processing 6 Limitations and Future
Neuroimaging of Theory Suggestions 17
of Mind 9 References 18
INTRODUCTION
As the field of psychiatry is currently becoming more focused on the brain as
the target organ for treatment, it is natural then to search for the neurobiologic
factors that play a role in the pathologic features of mental illness and disorder.
In schizophrenia, potential dysfunctions of the ‘social brain’ provide a tangible
Social Cognition and Metacognition in Schizophrenia.
DOI:http://dx.doi.org/10.1016/B978-0-12-405172-0.00001-6
© 22001144 Elsevier Inc. All rights reserved. 1
2 Social Cognition and Metacognition in Schizophrenia
starting point to explore the underlying neurobiology of deficits in social cog-
nition. This line of inquiry is particularly pertinent due to the growing work on
animal models of schizophrenia, as well as with the rise of social neuroscience
as a discipline that utilizes neuroimaging and brain stimulation techniques to
uncover the neural substrates of the cognitive processes underlying human social
interaction.
The aim of this chapter is to present the current state of research in the neuro-
biology of social cognition in schizophrenia. As animal studies provide the initial
steps that lead to human studies, we first focus on rodents as animal models of
schizophrenia and social cognition. The translation of these findings, as well as the
neurobiologic evidence on social cognition in schizophrenia, is also summarized
with current limitations and future suggestion in the following sections.
ANIMAL STUDIES ON BASIC SOCIAL COGNITION
AND SOCIAL BEHAVIOR WITH SCHIZOPHRENIA MODELS
In order to understand the most fundamental neural underpinnings of social
behavior in humans, many scientists have opted for animal models owing to
the opportunity to explore and alter and measure the brain mechanisms and
the resulting behavior. Furthermore, while sociocognitive tasks for humans
are usually designed in experimental settings and involve large machinery
or cables (e.g., magnetic resonance imaging (MRI) or electroencephalogra-
phy (EEG)), that is in non-natural circumstances, social behavior and basic
social cognition assessed in animals reduces the effects of, or at least controls,
laboratory influence. Lastly, neurotransmitter networks can be more easily
explored in the brains of animals, while brain networks in low- and high-level
social cognition are better investigated in humans.
A variety of animal models of schizophrenia, mostly in rodents, have been
developed and have brought new insights into the neurobiologic underpinnings
that lead to social dysfunction in this psychiatric disorder. One of the great-
est challenges in neuropsychiatric animal research is to reproduce and relate
the clinical characteristics observed in humans to less complex animals. Given
the heterogeneity of symptoms in schizophrenia, most animal models do not
recreate the whole psychopathology of the disease, but instead, present certain
aspects of the disorder (Brüne, 2009). Therefore, some models embody posi-
tive symptoms, while others try to characterize some of the negative symp-
toms, such as social isolation.
Interestingly, some of the behavioral abnormalities common to patients with
schizophrenia also occur and can be assessed in rodents, and these are thus
widely used to determine face and predictive validity of the psychiatric animal
models. These behaviors can be examined by using sensorimotor gating experi-
ments and by measuring social withdrawal. Sensorimotor gating refers to the
filtering of external information that is trivial or unnecessary, such as the back-
ground noise of a party. Deficits in sensorimotor gating lead to an overload of
Chapter | 1 Neurobiologic Underpinnings of Social Cognition 3
sensory and cognitive processes that have been associated with impaired social
behavior in patients with schizophrenia and in rodent models of schizophre-
nia (Duncan et al., 2004; Koh et al., 2007; Lijam et al., 1997). For instance,
Wynn and colleagues showed that patients with schizophrenia who performed
better in a sensorimotor gating test also performed better in a social percep-
tion task (Wynn et al., 2005). Thus, assessing the levels of sensorimotor gat-
ing is greatly informative in terms of social cognition and social behavior in
both humans and animals. Sensorimotor gating impairments have been consis-
tently found in patients with schizophrenia as well as their first-degree relatives
(Kumari et al., 2005), and even though these deficits are not disease-specific,
it has been repeatedly demonstrated to be a key characteristic of this group of
psychiatric disorders. Moreover, most of the literature on sensorimotor gating
has been addressed in schizophrenia given the reliability to replicate the results
in this disease and its relationship to social cognition. However, patients diag-
nosed with other disorders, such as obsessive-compulsive disorder (Ahmari
et al., 2012), Huntington disease (Swerdlow et al., 1995), or bipolar disorder
with acute psychotic mania (Perry et al., 2001) have also been shown to exhibit
deficits in sensorimotor gating, although all of these disorders present dysfunc-
tions in sensory, motor, and/or cognitive information processing (Geyer, 2006).
The most widely used test to assess the levels of sensorimotor gating is through
pre-pulse inhibition (PPI), which occurs when the startle reaction to a particu-
lar stimulus (usually auditory but also visual and tactile) is decreased by pre-
senting a weaker pre-stimulus before. Therefore, animals or people who do not
display a decrease (or inhibition) of their startle reaction when a weak tone pre-
cedes a strong tone, as compared with when only a strong tone is presented, are
considered to have reduced PPI, which is related to deficits in social cognition.
The benefit of this test is that it can be measured in both humans and rodents
and thus offers the possibility for translational approaches. In the case of social
performance, several behavioral measures are used in rodents, such as mating
behavior, nest building, and playful behavior. Hence, animal models that pre-
sent deficits in these behaviors may help us learn the underlying mechanisms
responsible for the social cognitive deficits found in schizophrenia.
Animal studies have found that several factors, including neurodevelop-
ment (during and after pregnancy), brain lesions, genetic predisposition, and
exposure to certain substances, induce abnormalities in PPI responses. For
instance, neonatal rats exposed to epidermal growth factor (EGF), rats with
lesions in the ventral and caudodorsal striatum (Kodsi and Swerdlow, 1995),
rats treated with the adrenoreceptor agonist ciralozine (Carasso et al., 1998),
and rats that are reared in isolation (Wilkinson et al., 1994) present deficits
in this test. Neonatal lesions to the ventral part of the hippocampus (Sams-
Dodd et al., 1997), basal amygdala (Decker et al., 1995; Wan and Swerdlow,
1997), and prefrontal cortex (PFC) (Schneider and Koch, 2005) in rats causes
social interaction abnormalities as well as other schizophrenia-related behavio-
ral malfunctions in juvenile and adults, as occurs in people with this disorder.