Social cognition and schizophrenia: Observing others’ actions, rewards and errors By Elliot Clayton BROWN A thesis submitted in partial fulfilment of the requirements for the degree of Philosophiae Doctoris (PhD) in Neuroscience from the International Graduate School of Neuroscience Ruhr University Bochum June 7th th 2013 This research was conducted at the Research Department of Cognitive Neuropsychiatry, Psychosomatics and Preventative Medicine, at the LWL University Hospital, within the Faculty of Medicine at Ruhr University under the supervision of Prof. Dr. Martin Brüne Printed with the permission of the International Graduate School of Neuroscience, Ruhr University Bochum
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Social cognition and schizophrenia: Observing others’ actions, rewards and errors
By
Elliot Clayton BROWN
A thesis submitted in partial fulfilment of the requirements for the degree of
Philosophiae Doctoris (PhD) in Neuroscience
from the International Graduate School of Neuroscience
Ruhr University Bochum
June 7thth 2013
This research was conducted at the Research Department of Cognitive Neuropsychiatry,
Psychosomatics and Preventative Medicine, at the LWL University Hospital, within the
Faculty of Medicine at Ruhr University under the supervision of Prof. Dr. Martin Brüne
Printed with the permission of the International Graduate School of Neuroscience, Ruhr University Bochum
Statement
I certify herewith that the dissertation included here was completed and written
independently by me and without outside assistance. References to the work and
theories of others have been cited and acknowledged completely and correctly. The
“Guidelines for Good Scientific Practice” according to § 9, Sec. 3 of the PhD regulations of
the International Graduate School of Neuroscience were adhered to. This work has
never been submitted in this, or a similar form, at this or any other domestic or foreign
institution of higher learning as a dissertation.
The abovementioned statement was made as a solemn declaration. I conscientiously
believe and state it to be true and declare that it is of the same legal significance and
value as if it were made under oath.
Elliot Clayton BROWN
Bochum, 07.06.2013
PhD Commission
Chair:
1st Internal Examiner: Prof. Dr. Martin Brüne
2nd Internal Examiner: Prof. Dr. Boris Suchan
External Examiner:
Non-Specialist:
Date of Final Examination:
PhD Grade Assigned:
Table of Contents
I. List of Figures
II. List of Abbreviations
III. Abstract
1. General background
1.1. Preamble 1
1.2. Social cognitive neuroscience and “mind-reading” 2
1.3. Action observation and mirror neurons 3
1.4. The EEG mu rhythm suppression and action observation 4
1.5. Processing the outcomes of others’ action 7
1.6. Social approach and avoidance motivations 9
1.7. Deficits in social cognition in schizophrenia 12
1.8. Broken mirrors and the observation of others in schizophrenia 14
1.9. General aims of the thesis work 17
2. The relevance of self and other in mirror motor activity
2.1. Introduction 19
2.2. Method
2.2.1. Participants 20
2.2.2. Task design 20
2.2.3. Procedure 22
2.2.4. EEG data acquisition 23
2.2.5. EEG data analysis of the mu rhythm 24
2.3. EEG mu rhythm results 25
2.4. Summary of results 26
3. The influence of reward and punishment on the motor mirror system
3.1. Introduction 28
3.2 Method
3.2.1. Participants 30
3.2.2. Task design 30
3.2.3. Procedure 31
3.2.4. EEG data acquisition 32
3.2.5. Behavioural data analysis 32
3.2.6. EEG mu rhythm suppression analysis 32
3.2.7. Time-course analysis of EEG mu power 33
3.3. Results
3.3.1. Behavioural results 34
3.3.2. EEG mu rhythm suppression results 35
3.3.3. Time-course analysis of EEG mu power results 36
3.4. Summary of results 37
4. Reward-related modulation of the mirror motor system in schizophrenia
4.1. Introduction 39
4.2 Method
4.2.1. Participants 40
4.2.2. Task design 41
4.2.3. Behavioural tests 41
4.2.4. Procedure 42
4.2.5. EEG data acquisition 42
4.2.6. Data analysis
4.2.6.1. Behavioural data analysis 43
4.2.6.2. EEG mu rhythm suppression analysis 43
4.3. Results
4.3.1. Behavioural results 44
4.3.2. EEG mu rhythm results 45
4.4. Summary of results 49
5. Processing the outcomes of others’ action –
sharing others’ rewards, losses and errors
5.1. Introduction 51
5.2 Method
5.2.1. Participants 52
5.2.2. Task design 53
5.2.3. Procedure 55
5.2.4. EEG data acquisition 56
52.5. EEG data analysis 56
5.3. Results 58
5.4. Summary of results 62
6. A possible neurobiological basis of social approach and avoidance
behaviour in schizophrenia
6.1. Introduction 63
6.2 Methods
6.2.1. Participants 66
6.2.2. Tasks and procedure
6.2.2.1. The Approach-Avoidance Task (AAT) 66
6.2.2.2. The AAT effect scores 68
6.2.2.3. Facial emotion recognition and discrimination test 68
6.2.2.4. State and trait anxiety scale 68
6.2.2.5. Plasma oxytocin assessment 69
6.2.3. Data analysis 69
6.3. Results 70
6.4. Summary of results 73
7. General Discussion
7.1. Overall summary of findings 75
7.2. Detailed discussion
7.2.1. Self and other in the mirror motor system 77
7.2.2. Reward and punishment in the motor mirror system 79
7.2.3. Reward-related modulation of the mirror motor system in
schizophrenia 82
7.2.4. Sharing others’ errors, rewards and losses 85
7.2.5. Social approach and avoidance behaviour
and oxytocin in schizophrenia 89
7.3. General conclusions and implications of findings 91
7.4. Limitations 96
7.5. Synthesis 98
7.6. Open questions and future suggestions 107
8. References 109
9. Appendices
9.1. Curriculum Vitae 127
9.2. List of publications 130
9.3. Acknowledgements 133
I. List of Figures
1.1. An illustration of cortical areas found to be homologues of the
mirror neuron system in humans 4
1.2. Plot showing the mu rhythm suppression 6
1.3. A simplified overview of a distinction between 3 categories of
motivation and the associated behaviours 10
2.1. A pictorial description of the experimental design showing
snapshots of the action observation (video) and
action execution parts 23
2.2. Bar chart showing the EEG mu rhythm suppression pooled over
electrodes covering motor cortex, with self and other conditions
shown for action execution and action observation 26
3.1. Subjective ratings of pleasantness, arousal and ease of paying
attention for rewarding, punishing and neutral observed actions 34
3.2. EEG mu rhythm suppression during the observation of rewarding,
punishing and neutral actions pooled over electrodes 36
3.3. Plot showing the change in EEG mu power, averaged from electrodes
over sensorimotor areas over the course of the video,
showing the different reward conditions 37
4.1. Subjective ratings of pleasantness, arousal and ease of paying
attention for rewarding, punishing and neutral observed actions,
showing ratings for the schizophrenia patient group
and healthy control group 45
4.2. Mean mu suppression for schizophrenia patient group and
matched healthy control group during action observation,
pooled across conditions and central electrodes 46
4.3. Mu suppression pooled over electrodes for schizophrenia patients
group and healthy control group during the observation of
rewarding, punishing and neutral actions 47
4.4. Scatter plot for data from only the healthy control group, to
demonstrate the relationship between mean mu rhythm suppression
and empathy scores in the perspective-taking domain 48
4.5. Scatter plot for data from only the schizophrenia patient group,
to demonstrate the relationship between mean mu rhythm
suppression and negative psychotic symptoms, as indicated
by the PANSS 49
5.1. Illustration of experimental design and stimuli for active part,
showing the potential outcomes of either a gain or a loss 54
5.2. Illustration of experimental design for observational / passive
learning part showing the potential outcomes of
either a gain or a loss 55
5.3. Grand-averaged event-related potentials (ERPs) for onset of
positive (wins) and negative (losses) feedback received 59
5.4. Grand-averaged event-related potentials (ERPs) for onset of
response in the passive condition in the 100% condition 60
5.5. P300 amplitudes for active and passive parts showing results of
pairwise comparisons of high and low expectancy condition 61
6.1. a) A bar plot of reaction times from the social approach
avoidance task (AAT).
b) A pictorial illustration of the congruent and incongruent
push-pull responses to angry and happy faces in the
joystick-based AAT. 65
6.2. An illustration of the experimental design for the AAT showing
the order of events in two individual trials 67
6.3. Table showing means and SDs for symptom severity, behavioural
measures and medication between low and high oxytocin groups 71
6.4. AAT effect scores reflecting push minus pull mean RTs for each
condition, comparing RTs for the low and high basal oxytocin groups 72
6.5. Scatter plot showing line of best to demonstrate the relationship
between basal plasma oxytocin levels and the AAT effect score for
angry faces with a straight-gaze 73
7.1. Schematic representation showing the synthesis of topics
explored in this thesis 106
II. List of Abbreviations
AAT Approach-Avoidance Task
ACC Anterior cingulate cortex
ANOVA Analysis of variance
ASD Autism Spectrum Disorder
BCI Brain-Computer-Interface
CLZ Chlorpromazine equivalent
DLPFC Dorsolateral prefrontal cortex
DSM-IV Diagnostic and Statistical Manual of Mental Disorders IV
EDTA Ethylenediaminetetraacetic acid
EEG Electroencephalography
EIA Enzyme immunoassay
EOG Electrooculography
ERN Error-related negativity
ERP Event-related potential
FEDT Face Emotion Discrimination Task
FEIT Face Emotion Identification Task
FFT Fast Fourier Transform
fMRI Functional magnetic resonance imaging
FRN Feedback-related negativity
GLZ General linear model
ICD-10 International Classification of Diseases v.10
IFG Inferior frontal gyrus
IPL Inferior parietal lobule
IPS Inferior parietal sulcus
IRI Interpersonal Reactivity Index
MPFC Medial prefrontal cortex
oERN Observational error-related negativity
OFC Orbitofrontal cortex
oFRN Observational feedback-related negativity
MFC Medial frontal cortex
MNS Mirror Neuron System
PANSS Positive and Negative Syndrome Scale
PCC Precuneus / Posterior cingulate cortex
RT Reaction time
SD Standard deviation
SPF Der Saarbrücker Persönlichkeitsfragebogen
STAI State–Trait Anxiety Inventory
STS Superior temporal sulcus
TMS Transcranial magnetic stimulation
TOM Theory of mind
TPJ Temporoparietal junction
vACC Ventral anterior cingulate cortex
“We may then lay it down for certain that every [mental] representation of a movement awakens in some degree the
actual movement which is its object; and awakens it in a maximum degree whenever it is not kept from so doing by an antagonistic representation present simultaneously to
the mind”
William James - “Principles of Psychology” (1890)
III. Abstract
A fundamental prerequisite for social interaction is the ability to understand the
meaning and intentions of others’ actions. More evidence is emerging to suggest the
presence of shared neural representations of experience in both the first and third-
person stance. Support has come from the discovery of common neural activity during
both action execution and action observation, namely the mirror neuron system (MNS).
The work in this thesis sought to explore shared neural representations of one’s own
and of others’ actions, rewards and errors along a number of different lines, and how
this could be modulated by different contexts. This was also investigated in terms of
schizophrenia, as patients are known to have deficits in social cognition.
In the first three studies, the EEG mu rhythm suppression was used as an index of mirror
neuron-related motor cortex activity. The first two studies demonstrated,
independently, that greater mu suppression was produced when observing actions that
were relevant to the self, as opposed to the other, and to actions that were rewarding as
opposed to those that were neutral. In the third study, it was shown that patients with
schizophrenia also exhibited a reward-related modulation of the mu suppression during
action observation, and furthermore, that the mu suppression was related to psychotic
negative symptoms and empathy. The fourth study also used EEG to investigate reward
and error-related neural activity, and found that the event-related potentials (ERPs)
associated with one’s own rewards and errors (i.e. the feedback-related negativity and
error-related negativity) also resembled the ERPs associated with others’ rewards and
errors. In addition, an ERP associated with others’ feedback (the P300) was substantially
influenced by expectation. Lastly, a study exploring the relationship between the
prosocial neuropeptide oxytocin and social approach and avoidance behaviour in a
schizophrenia population revealed that individual differences in endogenous oxytocin
levels related to the avoidance of negative emotional stimuli.
In conclusion, it is evident that the internal mental and external environmental context
can shape the interpretation of others’ behaviour, and in particular, the perception of
others’ actions, rewards and errors. These studies suggest that some contextual
modulations of the MNS found in previous studies may have been driven by underlying
influences of self-relevance and reward that were intrinsic to the nature of the perceived
stimuli. This also implies that the emergence and development of the MNS, and the
associated cognitive functions related to shared neural representations of one’s own and
of other’s experience, may also be facilitated by the reward-associations made to other
people’s behaviours, which can also be coloured by the context in which other’s actions
are observed. The influence of reward and self-relevance on the MNS may also have
implications on the development and persistence of social cognitive deficits seen in
schizophrenia. To summarize, a synthesis of these findings is put forward that also aims
to integrate other findings and theoretical frameworks related to learning, perception
and action in the frame of social interaction.
1. GENERAL BACKGROUND
1
Chapter 1
General background
1.1. Preamble
Humans are social animals. The evolution of the modern human brain has likely
emerged from the increasing complexity of our social environment over the generations
of our ancestors. Like many other species in the animal kingdom, we spend the majority
of our lives engaged in a social environment, interacting with others, and such that our
actions and behaviours are shaped by socially-driven motivations. We also depend upon
social interaction to maintain our mental wellbeing, as social isolation can lead to
severely detrimental consequences on one’s mental health. Social interaction involves a
multitude of socially-relevant cognitive processes including, to name a few, social
perception, understanding others’ actions, observational learning and social decision-
making. More evidence is emerging that shows “shared neural representations” of
experience when observing others’ behaviours, whereby similar brain activation
patterns are seen for the processing of both one’s own and of others’ experiences, which
may provide the underlying neural basis for understanding, predicting, and empathising
with others’ behaviour. This proposal has largely been fuelled by the discovery of the
mirror neuron system, which is a network of brain regions that are activated both when
performing and observing others’ actions. An important aspect of social interaction is
the context in which social information is processed, as the social context can colour the
interpretation of other people’s behaviour. There is substantial work to indicate that
there is a top-down contextual influence of social information on the modulation of
1. GENERAL BACKGROUND
2
neural activity associated with action observation and observational learning. These
contextual influences on the processing of others’ behaviours have direct and broad
implications on real-world social interaction, but have only begun to be explored in the
field of neuroscience. Dysfunctional social behaviours are often linked with psychiatric
illnesses such as schizophrenia, and impaired social functioning also has strong
associations with deficits in social cognitive skills. Therefore, schizophrenia can act as an
interesting model to explore the neural correlates of social behaviour. By revealing the
neural processes underlying social cognition, we can begin to understand where the
dysfunction is going wrong in schizophrenia, and consequently translate our
understanding of these dysfunctions in the brain to informing therapeutic strategies to
improve social functioning in schizophrenia, and ultimately improve the quality of life of
patients suffering from the illness.
1.2. Social cognitive neuroscience and “mind-reading”
The advancement of modern neuroimaging methods in the last twenty years has opened
up many doors for inquiry in every domain of psychology. The birth of “social
neuroscience” (Cacioppo and Berntson, 1992) uses these newly developed
neuroimaging techniques to reveal the underlying neural mechanisms behind cognitive
processes related to social functioning and behaviour. A seminal paper from Ochsner
and Lieberman (2001) explicitly outlines the emergence of the interdisciplinary field of
“social cognitive neuroscience” that covers a broad scope of investigation. They highlight
the integration of 3 levels of analysis: ‘the social level, which is concerned with the
motivational and social factors that influence behaviour and experience; the cognitive
level, which is concerned with the information-processing mechanisms that give rise to
social-level phenomena; and the neural level, which is concerned with the brain
mechanisms that instantiate cognitive-level processes.’ More generally, the term “social
cognition” often refers to the sum of the cognitive processes required for social
perception and social interaction, and Adolphs (2001) defines social cognition as ‘the
ability to construct representations of the relations between oneself and others, and to
use those representations flexibly to guide social behaviours’.
1. GENERAL BACKGROUND
3
One central concept in the study of social cognition is theory of mind (TOM), or
mentalizing, which is the ability to attribute mental states to others (Premack &
Woodruff, 1978). For someone to be able to understand other people, one must be able
to take the other’s perspective, or put oneself in the “other person’s shoes”. To do this,
one must first understand that other people do not have the same thoughts, opinions,
beliefs or knowledge as oneself. A broad network of brain areas have been consistently
associated with mentalizing / TOM, which includes the medial prefrontal cortex (MPFC),
involving hormones such as cortisol and oxytocin also have a central role in determining
social approach and avoidance tendencies (Roelofs et al., 2005). Deficits in social
motivational drives have substantial relevance in functional recovery in schizophrenia
(Barch & Dowd, 2010). Lower levels of basal plasma oxytocin have previously been
associated with greater symptom severity and poorer social cognition in schizophrenia
(Goldman et al., 2008; Rubin et al., 2010). However, the study presented in this thesis
demonstrates that the effects of the differences in endogenous oxytocin levels on the
motivational and affective systems of social approach and avoidance may be
heterogeneous, with some individuals being affected more than others. Individual
differences in endogenous levels of the neuropeptides related to attachment and social
behaviour are determined by inherited genetic traits (Walum et al., 2012) and past
environmental experiences during development, such as childhood trauma (Heim et al.,
2009). The findings from the study in this thesis imply that these individual differences
in endogenous levels of oxytocin may also play a role in the differences in social
functioning seen across a schizophrenia population. Furthermore, recent interest in the
interactions between the dopaminergic system and oxytocin further underscore this
interaction between rewards, motivation and social behaviour, and the potential
relevance to the psychopathology of schizophrenia (Baskerville & Douglas, 2010;
Rosenfeld et al., 2011; Strathearn, 2011).
Psychosocial interventions that involve imitative and observational learning may benefit
from considering whether an underlying deficit in the processing of reward could
influence the ability to learn by observation. In these cases, differences in reward
processing could also influence the capacity for motor simulation, and therefore also
affect the capacity for social learning and the development of social skills during
childhood, which may also persist into adulthood. The reward or punishment associated
with others’ actions may influence the capacity for understanding others’ actions, their
goals and intentions, and therefore could also directly affect the potential for social
observational learning or its selective breakdown in certain pathological conditions such
as schizophrenia.
7. GENERAL DISCUSSION
96
7.4. Limitations
There were several limitations of the studies included in this thesis, of which some have
already been briefly mentioned, but here will now be discussed in more detail.
The study investigating the effect of the self and other framing of actions on the mu
rhythm suppression was largely flawed due to the low sample size, as this study was
intended as a pilot study that was later found to have some important confounding
variables in the experimental design. Firstly, the effect of direct and averted eye-gaze
added an inherent difference in the experimental conditions that could not be separated
out from the findings of the effect of the intended self and other manipulation across
conditions. A second major confounder of this experiment was the difference in the
spatial location of the bowls used in action execution conditions that most likely would
have had an effect on general motor cortex activity. One of the bowls in which the
objects were required to be transferred to was further than the other bowl, and this was
not counterbalanced across self and other conditions. These confounding variables were
taken into consideration in the experimental design of the later studies looking at the
mu rhythm suppression during action observation.
The first study investigating the effects of reward and punishment on the mu
suppression in the healthy group had some limitations associated with the sample
population and the controlling of confounders potentially arising from individual
differences in cognition and behaviour. To be specific, the sample used in the first study
looking at reward and punishment and the mu suppression used a largely homogenous
population of females within a narrow age range, who were all students. This therefore
may have not been representative of a healthy population as a whole. In addition,
individual differences in working memory were not controlled for, which may have
affected the action ratings given after action observation, as participants with better
working memory may have given more accurate subjective ratings of the previously
seen actions, as compared to participants with poorer working memory.
The study looking at the effects of reward and punishment on the mu rhythm
suppression in schizophrenia patients demonstrated that the matched healthy control
group exhibited a different pattern of reward-related modulation of the mu rhythm. This
7. GENERAL DISCUSSION
97
may have related to the limitation of the earlier study, as mentioned, because the
matched control group in the patient study was quite different in terms of age, and
additionally, was a mixed sex group, including both males and females. This therefore
made the two healthy control groups, i.e. the young female healthy group in the first
study and the older mixed-sex healthy group used in the patient study, less comparable.
Another limitation of this study may have come from the differences in neurocognition
between the patient group and the matched healthy control group. Differences in
neurocognition were not controlled for and may have had some influence on the
understanding of instructions, empathy questionnaires and action ratings. Furthermore,
the sample size of the groups used in the patient study may not have been sufficient to
show the full extent of the effects of the experimental manipulation of reward-related
modulation of the mu suppression. This also made the data from the first reward-related
modulation mu suppression study less comparable to the second, as sample sizes were
not matching.
In the study exploring the observational FRN and observational ERN, one limitation in
the experimental design was the order and sequence of trials presented for each
condition. The trials for high expectancy were presented in a separate block to the trials
for low expectancy. This may have caused some subsequent global contextual effects in
terms of the responses to the positive and negative feedback and the response to others’
errors, whereby the randomness of the valence of the feedback could have led to an
impoverishment of ERP responses to the feedback. In fact, this randomness may have
also induced some frustration in participants, particularly in the block for low
expectancy trials, as some participants actually reported that they tried to look for a
pattern or rule in the associations between stimulus cues and the outcomes in order to
maximise their gains. Consequently, participants may have taken a submissive or
helpless attitude towards the outcomes of their choices, and in this case, this would have
likely affected the magnitude and valence-related modulation of the ERP responses to
feedback, especially in the latter part of the low expectancy blocks of trials. Additionally,
the sample size of this study may not have been large enough to reveal the true effects of
the experimental manipulations, and therefore it is hard to draw conclusive inferences
from this data.
7. GENERAL DISCUSSION
98
For the study investigating social approach-avoidance behaviour in schizophrenia, the
main limitation was the lack of a healthy control group for comparing normal AAT
responses of healthy participants, and therefore the possibility cannot be ruled out that
the effect found between oxytocin and the AAT may not have been specific to
schizophrenia. However, given the generally slow response times and positive skewness
in AAT scores, and differences in emotion perception of this schizophrenia population,
the use of univariate comparisons would have exerted a statistical bias for this clinical
population when compared to healthy participants with a normal (faster) processing
speed. Nevertheless it would still be informative for future studies to look for causal
inferences using multivariate analyses between the oxytocin levels and AAT scores in
healthy population to allow for the generalizability of the findings.
7.5. Synthesis
The overarching aim of the work included in this thesis was to investigate some of the
processes involved in social interactions and observational learning, from biology to
cognition to behaviour, and also, how these processes can go wrong in the pathology of
schizophrenia. In studying the brain-basis for social interaction it is becoming more and
more evident that numerous interacting and parallel neural systems are recruited
during social encounters. In light of the findings presented in this thesis, and by
combining some integrative frameworks recently proposed for explaining some aspects
of social cognition, a synthesis of the empirical and theoretical work on the topics
discussed here will now be put forward. However, before this synthesis is outlined, a
number of concepts will be briefly introduced to permit further cohesion between
topics.
The general principles that will now be introduced could be considered to fall under the
umbrella of a currently popular idea of the “predictive brain”. The concept of the
“predictive brain” can be generally stated in that brains are constantly generating
mental representations to predict future states (Bar, 2007; Friston, 2005). It is thought
that these predictive internal representations of forthcoming events are constantly
being compared with the actual perceived outcome of internal mental and external
environmental events. To allow for learning to take place, one must be able to process
7. GENERAL DISCUSSION
99
one’s own errors to learn from one’s mistakes, and consequently update internal
representations of the predicted future. Reward prediction errors are generated in
dopaminergic neurons during learning and are thought to encode the magnitude of the
discrepancy, as a product of the comparison, between expected reward and the
experienced reward, i.e. actual outcome (Schultz and Dickinson, 2000). These reward
prediction errors thus drive decision-making. In addition to basic learning processes,
this predictive coding framework is also evident in perception and motor control
whereby internal models of a predicted outcome of a visual percept or motor command
are generated, and consequently act as top-down modulators of bottom-up sensory
input (Rao & Ballard, 1999; Wolpert & Miall, 1996), and also producing sensory or
action prediction errors as a result of the matching process between predicted and
actual outcome (i.e. bottom-up sensory input). This matching process is thought to
create a sense of agency and ownership for one’s own actions, perceptions and
intentions, and therefore provides the central underlying neural mechanism for
distinguishing between self and other (Frith et al., 2000). Thus a breakdown in this
matching system, i.e. when a mismatch occurs, can have pathological consequences, such
as the disturbances in distinguishing between self and other seen in schizophrenia
(Feinberg, 1978). These general principles of the “predictive brain” have proven to be a
fruitful foundation for investigating the implementation of cognitive processes in the
underlying neural substrates. This also provides a framework on which mathematical
principles can be applied, and therefore opening up the potential for testing hypotheses
about the neural and cognitive mechanisms of learning, action and perception with
biologically-plausible computational models. Despite being grounded in relatively old
ideas (Helmholtz, 1860; von Holst and Mittelstaedt, 1950; Sperry, 1950) much
experimental work has only recently emerged to provide support to this framework, and
has already started to be applied to the realm of social neuroscience (Brown & Brüne,
2012).
Much controversy still surrounds the mirror neuron hypothesis, as many authors have
questioned the functional specificity of the human MNS (Heyes, 2010a; Hickok, 2009). In
response to these criticisms, some alternative models of the mirror neuron system have
been proposed. One that is relevant here, is a predictive coding account of the MNS
(Kilner et al., 2007a,b), which uses a Bayesian statistical framework for its
implementation. This proposal argues that an internal model of an action (or predicted
7. GENERAL DISCUSSION
100
model of the expected consequence of the action) is generated during the observation of
others’ actions, which in turn transfers an action prediction through backwards
connections, from frontal areas implicated in the mirror system, to action
representations in the temporal and parietal mirror neuron-related areas. This
predicted or generative model is then matched with the sensory input of the observed
action (i.e. the visual input of the seen action), which then results in an action prediction
error. This action prediction error therefore represents the discrepancy between the
predictive model of the observed action and the actual sensory (visual) feedback
received following the observation of the action. As with other predictive systems, the
brain seeks to minimize the prediction error (Friston, 2005). Another alternative
account of the mirror system relevant here is based on associative learning (Heyes,
2001; 2010b), and argues that learned sensorimotor experiences, through self-
observation and the observation of others, actually promotes the formation and
emergence of the human MNS. This is therefore acquired and further refined throughout
development. The learned associations of action contingencies (i.e. the contingency
between actions and their sensory consequences / outcomes) are thought to provide the
basis for action understanding. These models of the MNS, and the concepts surrounding
the predictive brain, and its application in social interactions, provide the basis for the
following synthesis.
Figure 7.1 shows a schematic diagram representing a proposed integration of some of
the topics and associated mechanisms discussed in this thesis. However, this schema is
not intended to illustrate the neural pathways between specific or localised brain
regions, but instead is more of a conceptual cognitive map to display the links between
different cognitive processes. Indeed, these cognitive processes may also be served by
related networks of brain regions, though the pathways shown here are not meant to be
faithful representations of anatomical pathways. For the sake of simplicity, the role of
oxytocin has not been included in this synthesis, as this would require consideration of
other interacting hormones that were not investigated in the work in this thesis.
The diagram illustrates the interplay between two agents in a social interaction, and the
internal cognitive mechanisms underlying this interaction. The pathway labelled (a)
represents the sensory input received from the external environment during an
interaction, which may be through the observation of others’ actions, but could also
7. GENERAL DISCUSSION
101
represent input from other sensory modalities. The coupling of action and perception is
shown here by the pathway labelled (b), which is also portraying the process of motor
resonance and MNS related activity, whereby the perception of others’ actions activates
the observer’s motor cortex. As is shown by the star overlaying the action-perception, or
sensorimotor pathway (b), reward-related processing modulates the activation of motor
cortex when observing others, of which the reward value is tagged to the sensory input
via pathway (i). This tagging (or association) of the reward value to the sensory input is
reminiscent of reward-based perceptual learning (Goldstone, 1998), and also illustrates
the proposal that the reward associated with the perceived stimuli can drive the degree
to which one pays attention or engages with that stimuli. In the social interactive
context, this also encapsulates the idea that rewards can drive social learning through
modulation of sensory and motor cortex activation. The rewards associated with
perceived stimuli in a social interaction, including others actions, is generated as a
product of the predicted model. This predicted model of the expected reward outcome is
subsequently compared or matched with the actual perceived outcome, as shown by
pathways (f) and (c), respectively. This matching process of the expected reward and the
actual reward is represented here by the comparator, which produces the reward
prediction error that subsequently updates the predicted model (pathway (e)). This
updating therefore shapes future reward predictions and the reward associations made
to perceived stimuli.
The reinforcement learning loop represented by pathways (d), (e) and (f), which
receives sensory inputs via pathway (c), has reward intrinsic to its functioning. The
mechanism and neurophysiology underlying this reward-based learning loop is
relatively well-established (Schultz, 2000), though outside of the social interactive
context. This learning mechanism of updating the predicted model of future states of the
external and internal mental environment also extends to the principles of social
observational learning, and learning from others’ behaviour. The work in this thesis
presents data that confirms the similarity between the underlying neural mechanism
responsible for learning from one’s own actions, and from learning through the
observation of others’ actions and behaviours. The similarities seen between the ERN
and FRN, and the oERN and oFRN are clear examples of this, as individuals can either
have empathetic or Schadenfreude-like experiences of others’ errors.
7. GENERAL DISCUSSION
102
As a comparable mechanism, the sensory input received during the social interaction is
also matched to the predicted model of that input, be it for example, from the predicted
outcome of an observed action or a heard speech gesture, producing a sensory or
cognitive prediction error. This feedback mechanism could be comparable to the social
version of the MOSAIC model proposed by Wolpert and colleagues (2003), which
parallels the sensorimotor loop between the predictive model and incoming sensory
information (as shown by pathways (c), (d), (e) and (f)), with the social interactive loop
being between self-generated and observed communicative actions. Communicative
actions are thought to be generated from the actions observed by a confederate, which
consequently causes changes in the observer’s mental state, which in turn initiates
communicative actions from the other person, which are perceived by the observer. This
interpersonal loop of social interaction therefore allows one to make predictions and
learn about the likely behaviour of another person in response to one’s own
communicative behaviour. The internal predictive models of other people are thought to
be decoded and learned through the mappings between our own actions and our own
mental states as a priori information, thereby using one’s own motor system to compute
the internal mental states of others, which is consequently suggested to form a basis for
theory of mind.
In the case of a social interaction, the prediction error produced as a result of the
matching of the expectations of others’ actions, and the actual perceived outcomes of the
other’s actions could be considered more specifically as a “social prediction error” that
serves to update the predicted model of other people’s behaviour. The difference
between a social and non-social prediction error would be that the social prediction
error is mediated by additional factors, including social knowledge and expectations of
others’ behaviour. For example the coding of the social reward prediction error, when
observing the outcomes of others’ actions, may produce a prediction error similar to
that produced when one observes the outcome of one’s own actions, but rather the
reward value would be relative to the consequence of the observed outcome on the
observer, i.e., how rewarding other’s behaviours are to the observer. This social
prediction error could also act as a teaching signal for updating higher-level
expectations of others in a social context, such as those related to predetermined beliefs
and stereotypes about individuals or social categories. In the case of these more high-
level predictions about the state of the world, social prediction errors can be generated
7. GENERAL DISCUSSION
103
as a result of an expectancy violation in a social situation, such as when a person breaks
a promise (Baumgartner et al., 2009) or when a social norm is violated (Harris & Fiske,
2010). Contextual information for social expectancies could come from environmental
cues, and particularly the context of the social situation, or could be generated from
internal contexts such as an individual’s affective state, or from a cognitive bias, such as
an attributional bias, as seen in schizophrenia (Bentall et al., 1994).
The generative internal model of the predicted sensory outcome of an event is also used
in fine motor control, and has been referred to by Friston and colleagues (2011) with the
term “precision”, which is shown in the diagram by pathway (g). The cyclic updating of
the predicted model of an executed action, via comparison with the sensory feedback
(pathway (c), (d), (e) and (f)), is utilised to make fine motor adjustments during the
performance of an action, i.e. contributing to pathway (g). In relation to this, a similar
mechanism involving the predicted reward outcome of one’s own actions could also be
represented conceptually by this pathway and feedback loop. A comparable mechanism
may also be at play in a social interaction, in which this cyclic updating of the expected
outcomes of others actions drives the execution of one’s own actions and behaviour. The
dynamic interplay between the perceived behaviour of others, and the expected
outcome of one’s own and others’ actions, are likely to drive social behaviours, including
social approach and avoidance, as shown here by pathway (j). The motivational aspects
behind social approach and avoidance behaviour are determined by the rewards
associated with one’s own and others actions, and thus the initiation of one’s own motor
actions and behaviour is driven by the interactions between these internal and external
motivational factors in the social scenario.
The figure also highlights some areas of this cognitive map that could potentially be
going wrong in schizophrenia. These are labelled with a red outline. It is known that
people with schizophrenia have some sensory and motor processing dysfunctions
(Javitt, 2009; Schurmann et al., 2007), and thus this is labelled in the diagram. According
to the pathways laid out in this schema, these sensory and motor deficits may also play a
role in the problems in the transmission of reward-related processing in other areas that
are encoding the reward, and thus having more downstream effects that would only be
expressed in motivational signs in behaviour. It has been proposed that differences in
reward-processing in schizophrenia cannot be merely explained by a generalised
7. GENERAL DISCUSSION
104
impairment in the experience of reward, but may be more likely to be a deficit in the
representation of the value of different choices, which can consequently lead to the
impairments seen in decision-making (Gold et al., 2008). Therefore, this deficit in the
representation of value, and the subsequent influence on choice responses, may be
representative of a disturbance in the pathways (b) to (j) illustrated in figure 7.1. Thus, a
breakdown in these pathways could potentially influence social approach and
avoidance, and the initiation of social behaviours. As a result of a breakdown in this
mechanism, motivation to seek social interaction may also be diminished. Eventually,
this is likely to have a detrimental effect on the capacity for successful social functioning
in schizophrenia.
Furthermore, there is a substantial body of work suggesting a disturbance in the
matching process between the predicted outcome or sensory consequence of an event
and the actual sensory input in schizophrenia (Feinberg, 1978; Ford et al., 2001)
Although this work refers instead to the corollary discharge and efference copy, which is
essentially a copy of a motor command, and is represented in the figure by pathway (f).
A dysfunction in the processing of the corollary discharge or efference copy has been
used to explain disturbances in the sense of agency and the generation of auditory
hallucinations in schizophrenia (Ford & Mathalon, 2005). This disturbance in the
processing of the corollary discharge is comparable to a mismatch occurring between
pathways (c) and (f), and is therefore represented in figure 7.1 as a dysfunction in the
comparator. This would therefore also produce inaccurate prediction errors, which may
impact on the reward-related and sensory predictive models. If this was the case in
schizophrenia, then according to this schema illustrated here, a disturbance in the
comparator may have resonating effects on other downstream and connected processes.
In essence, the schematic representation illustrated by figure 7.1 seeks to integrate a
series of cognitive loops associated with the processing of one’s own actions, perception
and learning, and how these processes become extended into the context of social
interaction through the processing of others’ behaviour. The processing of both non-
social and social cognitive mechanisms is represented by these multiple interacting
loops in personal and interpersonal neural systems, which interface at sensory and
motor inputs and outputs. The aim of this schematic representation is also to highlight
the dynamic and parallel nature of the processes that occur during a social interaction
7. GENERAL DISCUSSION
105
between and within two interacting brains. Within the scope of this schema, some areas
are highlighted in which potential breakdowns may be occurring in schizophrenia. In
light of the dynamic and parallel nature of the interactions between personal and
interpersonal cognitive processes, it is therefore easy to see how breakdowns in some
low-level sensory or perceptual sub-processes may propagate downstream, eventually
leading to more overt dysfunctions in high-level social cognition and social functioning.
7. GENERAL DISCUSSION
106
7. GENERAL DISCUSSION
107
7.6. Open questions and future suggestions
It is still under debate as to what degree the MNS is involved in action understanding,
and even whether this activity actually reflects action understanding at all (Hickok,
2009). Evidently, there is still more work to be done to clarify the functional specificity
of the MNS in humans, and to see whether different areas related to the human mirror
neuron network may have more specific subsets of functions related to social cognition.
Further studies exploring the mu rhythm suppression during action observation should
also seek to dissociate the dynamic temporal changes in neural activity when making
inferences about social interaction, which more accurately reflect the dynamic changes
in the environment that occur during everyday social interaction. In light of these new
results, differential “simulated” motor effects may stem from underlying fundamental
situational and contextual differences in the processing of self-relevance, reward or
punishment. More specifically, future studies therefore may need to consider the
potential confounding effects of the associated self-relevance and reward on the
observed action in the experimental condition of interest, and the self/reward-related
associations of actions created by different contexts, whether it is social or not. To gain
further insight into the findings presented here on the mu rhythm, it would be
interesting for a future study to investigate the interaction between self-relevance and
reward in action observation in both a healthy and schizophrenia group. A further
suggestion would be to see if the modulation of motor resonance as a result of the
interaction between self-relevance and reward may be also associated with behavioural
measures of empathy and Schadenfreude.
It is still not clear how deficits in reward-processing may be associated with deficits in
social cognitive processes in psychopathologies such as schizophrenia. Further studies
are required to discern how potential disturbances at the low level of sensory and motor
processing can translate to the poor performance seen in more complex social cognitive
tasks in psychiatric illness. Future work looking at the ERP responses, such as the oFRN
and oERN, in healthy and schizophrenia populations during the observation of others’
behaviour is likely to provide a very useful and informative platform to explore the
underlying neurological causes for higher level social cognitive deficits.
7. GENERAL DISCUSSION
108
There has recently been much attention paid to the potential therapeutic effects of
oxytocin administration in treating pathological deficits in social cognition (Feifel,
2012). However, it appears that much of the research on oxytocin with schizophrenia
populations has largely focused on improvements in high-level social cognitive skills and
social functioning capacity as the primary outcome measure, with many showing mixed
results (Feifel, 2012). However, it may be more feasible and informative to first look at
the effect of neuroendocrinological factors underlying social behaviour at a low-level of
processing, by investigating the neurophysiological effects of oxytocin on social affective
and motivational systems, and how these effects may be translated downstream,
through neural activity, and inevitably into social behaviour. The findings presented
here encourage replication with future studies using oxytocin administration in clinical
groups, while also considering the endogenous individual differences as confounders
when assessing the effect of exogenous neuroendocrinological manipulation on social
behaviours and motivations.
The abnormalities seen in schizophrenia in the underlying neurophysiological and
neurobiological mechanisms associated with the observation of others’ actions, the
outcomes of others’ actions and the relationship with social motivations leading to
approach and avoidance behaviours may help to serve as signs of risk factors in the
development of the illness, and particular symptom clusters. Using these potential
biomarkers of psychotic characteristics may also aid in predicting treatment efficacy.
This could therefore contribute to the development of more specialised treatment
programs for individuals and subgroups of individuals with schizophrenia that aim to
remediate specific sets of social cognitive skills. The use of brain-based assessment
paradigms also provides an extra tool for the clinician to determine the most effective
treatments for patients and to give more accurate prognoses.
8. REFERENCES
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Chapter 8
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Chapter 9
Appendices
9. APPENDICES
127
9.1 Curriculum Vitae
Elliot Clayton BROWN
Research Department of Cognitive Neuropsychiatry, LWL University Hospital
2008 “Transcranial Magnetic Stimulation (TMS) in Plasticity and Rehabilitation”, MAGSTIM TMS Summer
School - Institute of Cognitive Neuroscience, University College London, UK.
2008 Neuroscience in Education Workshop, Institute of Cognitive Neuroscience - University College London,
UK.
AD-HOC REVIEWER FOR
Brain Imaging and Behaviour, Frontiers in Human Neuroscience, Journal of Neurology & Neurophysiology,
Psychological Reports, Schizophrenia Research.
LANGUAGES
English (Native) German (Basic) Cantonese (Intermediate)
9. APPENDICES
130
9.2 List of Publications
Peer-reviewed journals
1. Gonzalez-Liencres, C., Tas, C., Brown, E.C., Erdin, S., Onur, E., Cubukcuoglu, Z., Esen-Danaci, A., Brüne, M. (2013) Oxidative stress in schizophrenia: The effects on social cognition and neurocognition (in preparation).
2. Brown, E.C., Tas, C., Yilmaz, H., Esen-Danaci, A., Roelofs, K., Brüne, M. (2013). A role for resting-state frontal EEG activity as a trait marker for social approach and avoidance behaviour in schizophrenia (in preparation).
3. Tas, C., Brown, E.C., Onur, E., Aydin, O., Brüne, M. (2013). The effects of endogenous oxytocin levels on the perception of emotions in bipolar disorder (submitted).
4. Brown, E.C., Tas, C., Esen-Danaci, A., Roelofs, K., Brüne, M. (2013). Social approach and avoidance behaviour for negative emotions is modulated by endogenous oxytocin in schizophrenia (submitted).
5. Tas, C., Brown, E.C., Imak, S., Aydin, O., Esen-Danaci, A., Brüne, M. (2013). Cortisol response to psychosocial stress predicted by plasma oxytocin levels facilitates social functioning in schizophrenia (submitted).
6. Brown, E.C., Tas, C., Esen-Danaci, A., Brüne, M. (2013). The relationship between the subdomains of social cognition, social functioning and symptomatology in a clinically stable group of schizophrenia patients (under review).
7. Brune, M., Tas, C., Brown, E.C., Armgart, C., Dimaggio, G., Lysaker, P. (2013). Metakognitive und sozial-kognitive Defizite bei Schizophrenien. Funktionelle Bedeutung und Behandlungsstrategien. Zeitschrift für Psychiatrie, Psychologie und Psychotherapie (in press).
8. Brown, E.C., Brüne, M. (2013). Reward in the mirror neuron system, social context and the implications on psychopathology. Behavioral and Brain Sciences (in press).
9. Brown, E.C., Wiersema, J.R., Pourtois, G., Brüne, M. (2013). Modulation of motor cortex activity when observing rewarding and punishing actions. Neuropsychologia 51 (1), 52-58.
10. Tas, C., Brown, E.C., Cubukcuoglu, Z., Aydemir, O., Esen-Danaci, A., Brüne, M. (2013). Towards an integrative approach to understanding quality of life in schizophrenia: The role of neurocognition, social cognition and psychopathology. Comprehensive Psychiatry 54 (3), 262-268.
11. Brown, E.C., Brüne, M. (2012). Evolution of social predictive brains? Frontiers in Psychology 3, (414).
12. Tas, C., Brown, E.C., Esen-Danaci, A., Lysaker, P.H., Brüne, M. (2012). Intrinsic motivation and metacognition as predictors of learning potential in patients with remitted schizophrenia. Journal of Psychiatric Research 46 (8), 1086-1092.
13. Brown, E.C., Brüne, M. (2012). The role of predictive coding in social neuroscience. Frontiers in Human Neuroscience 6 (147).
14. Brown, E.C., Tas, C., Brüne, M. (2011). Potential therapeutic avenues to tackle social cognition problems in schizophrenia. Expert Review of Neurotherapeutics 12 (1), 71-81.
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Book chapters
15. Brown, E.C., Tas, C., Gonzalez-Liencres, C., Brüne, M. (2013) Neurological underpinnings of social cognition and metacognition in schizophrenia spectrum disorders. In P. Lysaker, G. Dimaggio and M. Brüne, Social cognition and metacognition in schizophrenia: Psychopathology and treatment approaches. San Diego, CA, USA: Academic Press / Elsevier (contract approved)
16. Tas, C., Brown, E.C., Gonzalez-Liencres, C., Brüne, M. (2013) Experimental usage of oxytocin to combat deficits in social cognition in schizophrenia. In P. Lysaker, G. Dimaggio and M. Brüne, Social cognition and metacognition in schizophrenia: Psychopathology and treatment approaches. San Diego, CA, USA: Academic Press / Elsevier (contract approved)
Published conference abstracts
17. Brown, E.C., Wiersema, J.R., Pourtois, G., Brüne, M. (2012). Catharsis in the motor cortex: Reward and punishment when observing others’ actions. Belgian Brain Congress, Liege, Belgium (Published in Frontiers in Neuroscience. (doi: 10.3389/conf.fnhum.2012.210.00052))
18. Brown E.C., Tas C., Danaci A.E., Brüne M. (2012). How separable are the domains of social cognitive deficits in schizophrenia? 3rd Schizophrenia International Research Conference, Florence, Italy (Published in Schizophrenia Research 136 (S1), 180 (doi: 10.1016/S0920-9964(12)70545-5))
19. Tas C., Brown E.C., Danaci A.E., Lysaker P., Brüne M. (2012). Motivation and metacognition as predictors of occupational functioning in remitted schizophrenia patients. 3rd Schizophrenia International Research Conference, Florence, Italy. (Published in Schizophrenia Research 136 (S1), 180 (doi: 10.1016/S0920-
9964(12)70544-3))
20. Brown, E.C., Brüne, M. (2011). Theory of mind in at-risk stages of schizophrenia. 3rd European Conference on Schizophrenia Research (ECSR): Facts and Visions, Berlin, Germany (Published in European Archives of Psychiatry and Clinical Neurosciences 261 (S1), S26 (TALK))
21. Brown, E.C., Brüne, M. (2011). Social cognition and violence in schizophrenia: Is there a link? 3rd European Conference on Schizophrenia Research (ECSR): Facts and Visions, Berlin, Germany (Published in European Archives of Psychiatry and Clinical Neurosciences 261 (S1), S39 (TALK))
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Other conference abstracts
22. Brown, E.C., Pourtois, G., Wiersema, J.R., Brüne, M. (2013). The influence of reward and punishment in action observation. UCL Conference on “Implications of Research on the Neuroscience of Affect, Attachment, and Social Cognition”, University College London, UK. (POSTER)
23. Brown, E.C., Brüne, M. (2013). Neural evidence for the potential use of rewards in observational learning in schizophrenia? Neurex Symposium on “Cognitive disorders and remediation in schizophrenia and other mental disorders”, Strasbourg, Switzerland. (TALK)
24. Brown E.C., Tas C., Danaci A.E., Brüne M. (2012). Social approach and avoidance in schizophrenia: The relationship with paranoia, social cognition and oxytocin. The German Society for Biological Psychiatry Congress (DGBP), Heidelberg, Germany. (POSTER)
25. Tas C., Brown E., Esen-Danacı A., Brüne M. (2012). The role of plasma oxytocin and cortisol levels and metacognition on social learning and social stress response in schizophrenia patients. The German Society for Biological Psychiatry Congress (DGBP), Heidelberg, Germany. (POSTER)
26. Brown, E.C., Pourtois, G., Wiersema, J.R., Tas, C., Brüne, M. (2012). Reward-related changes in motor cortex excitability during action observation of others. 8th FENS Forum of Neuroscience, Barcelona, Spain. (POSTER)
27. Brown, E.C., Brüne, M. (2011). Mirror neuron activity in schizophrenia. Deutsche
Gesellschaft für Psychiatrie, Psychotherapie, und Nervenheilkunde Kongress
(DGPPN), Berlin, Germany. (TALK)
28. Brown, E.C., Brüne, M. (2011). How ’social’ is the mirror neuron system: Insights from the EEG mu rhythm. Donders Discussions, Nijmegen, Netherlands. (POSTER)
29. Brown, E.C., Cocchini, G. (2010). Perception without awareness: A case study. International Conference on Parietal Lobe Function, European Science Foundation (ESF) Congress, Amsterdam, Netherlands. (POSTER)
30. Brown, E.C., Cocchini, G. (2009). A study of error awareness and insight in schizophrenia using the Sustained Attention to Response Task (SART). British Psychological Society (BPS) Annual Conference, Brighton, UK. (POSTER)
Other Publications
31. Tas, C., Brown, E.C., Enzi, B., Brüne, M. (2013). Social cognitive deficits in schizophrenia: Are they acquired or developmental? IGSN Report (in press).
(“in preparation” refers to manuscripts that are completed and are awaiting submission)
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9.3 Acknowledgements
I would like to dedicate this thesis to my beloved Godfather, Con Conway, who sadly
passed away in September 2012. May he rest in peace.
Firstly I would like to express my utmost gratitude to my Doktorvater, Martin Brüne, for
his positive support and guidance throughout my PhD. I wholeheartedly appreciate the
freedom and encouragement he provided me, which kept me motivated and focused.
Secondly, I would like to give a huge thanks to Cumhur Tas, as without his working
partnership, I would not have been half as productive in the last 3 years, or enjoyed my
work half as much. I feel that I have gained a life-long research collaborator and a new
brother.
I give my thanks to my mother, as without her unconditional and unwavering support
over the last few years (well, last 32 years to be precise), I would not have been able to
have the opportunity to follow my passion and my dream.
I would also like to give my thanks to Manu Schütze for her helpful feedback on my
thesis, but most of all, for all her loving support and care, which gave me strength to
carry on.
My thanks also go to Burak Erdeniz, for all the times we shared talking about the brain,
and everything related to it. His inspiration has been invaluable.
Many thanks also to Cristina Gonzalez for bringing lots of laughter and fresh new ideas
to our office.
I also want to extend my gratitude to my supervisors and collaborators that I have
worked with over the last 3 years, as without them, I would not have been able to write
this thesis. To Christian Bellebaum, Roeljan Wiersema, Gilles Pourtois, Aysen Esen-
Danaci and Karin Roelofs, thank you so much for all of your help and support. Thanks
also to my friends at the Psychology Department of Ghent University, and the Psychiatry
Department at Celal Bayar University Hospital, and particularly Duygu Kuzu for her
incomparable motivation and help with collecting data in Turkey.
I would also like to express my thanks to all my other friends and family along the way
for giving more meaning to my life.
Last, but not least, I would like to extend my appreciation to all of the people that kindly
participated in the studies presented here, as without them I would have no data.