NEUROBEHAVIORAL SIGNATURES IN CHILDREN-VICTIM OF BULLYING
Transcript of NEUROBEHAVIORAL SIGNATURES IN CHILDREN-VICTIM OF BULLYING
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NEUROBEHAVIORAL SIGNATURES INCHILDREN-VICTIM OF BULLYINGIsabel SolisUniversity of New Mexico
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Recommended CitationSolis, Isabel. "NEUROBEHAVIORAL SIGNATURES IN CHILDREN-VICTIM OF BULLYING." (2018).https://digitalrepository.unm.edu/psy_etds/257
Isabel Solis Candidate Psychology Department This thesis is approved, and it is acceptable in quality and form for publication: Approved by the Thesis Committee: Kristina R. Ciesielski, Ph.D., Chairperson Bruce Smith, Ph.D. Julia Stephen, Ph.D. Steve Verney, Ph.D.
NEUROBEHAVIORAL SIGNATURES
IN CHILDREN-VICTIM OF BULLYING
by
ISABEL SOLIS
B.S., PSYCHOLOGY, UNIVERSITY OF NEW MEXICO, 2012
THESIS
Submitted in Partial Fulfillment of the Requirements for the Degree of
Master of Science
Psychology
The University of New Mexico
Albuquerque, New Mexico
July, 2018
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DEDICATION
To my mother, Silvia Vargas, who has always shown me what a strong woman looks like. Thank you for all of your hard work and sacrifices. I am truly blessed to be your daughter.
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ACKNOWLEDGEMENTS
First and foremost, I praise God for making the impossible possible. Next, I would like to thank my faculty mentor Dr. Kristina Rewin Ciesielski for all her time, guidance and unwavering support. Her dedication to children and science is inspiring and I will forever be grateful to be her student. I also wish to thank my thesis committee members, Dr. Julia Stephen, Dr. Bruce Smith, and Dr. Steve Verney, for providing invaluable support during this process. I sincerely appreciate their time and interest not only in this study but in my professional development. I would also like to thank Dr. Paul Lesnik for his assistance with the statistical analysis. Next, I would like to thank my research assistants Charlene McGinnis and Yesol Kim for all of their time, hard work, and dedication. I really could not have done this project without their assistance. I am deeply grateful to all the children and families who participated in this study. Their willingness to be part of this work is truly motivational. Finally, I would like to thank my family for all of their encouragement and endless love during this process.
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NEUROBEHAVIORAL SIGNATURES
IN CHILDREN-VICTIM OF BULLYING
by
Isabel Solis
B.S., Psychology, University Of New Mexico, 2012
M.S., Psychology, University Of New Mexico, 2018
ABSTRACT
Experiencing bullying victimization can lead to detrimental damage to a child’s
life potential, reduced long-term contributions to society, and in severe cases, to suicide
or desperate acts of defensive aggression, such as school shootings. The current study
aimed to examine risk factors that may increase the vulnerability of a child to become a
target of bullying victimization and the related consequences of victimization, using
rigorous neuropsychological and EEG measures. The end-goal is to translate these
findings into a program of preventive intervention increasing the child’s resilience and
improving social culture among youth in the academic environment. We propose a two-
component novel model for examining child-victim characteristics: Trait Signatures, as
crystalized, long-term neurobehavioral and brain neurophysiology (EEG) markers and
State Signatures, the psychological, somatic, and cognitive acute consequences of
bullying victimization. Results from 16 Children-Victim (VC) and 16 non-exposed to
bullying, Control Children (CC), ages 6-17 are presented. Our key findings in VC as
compared to CC show: In Trait Signatures significantly higher scores on measures of
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anxiety and compulsivity, significantly reduced skills in visual-spatial perception and
attention, but no significant group differences in oscillatory brain activity (alpha power)
during visual cognitive tasks demanding top-down inhibitory control of response. In State
Signatures significantly higher levels of depressive moods, significantly reduced
visuospatial memory and visually mediated conceptualization, and a significantly higher
rate of life-long traumatic experiences, including bullying victimization. Our findings
implicate a prime significance of emotional-social difficulties in VC that may impact
visual cognitive proficiency in complex social problem-solving interactions. The
identified emotional-social-cognitive composite of difficulties in VC must be addressed
in future studies and in prospective programs of prevention.
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TABLE OF CONTENTS
LIST OF FIGURES................................................................................................... viii
LIST OF TABLES ......................................................................................................ix
LIST OF ACRONYMS ................................................................................................ x
INTRODUCTION ........................................................................................................ 1
Definition of Bullying ......................................................................................... 1
New Model of Children-Victim: Trait Signatures and State Signatures ............... 2
Reported Consequences of Bullying.................................................................... 2
Report on Etiology of Being a “Bully” or a Child-Victim ................................... 9
Aims & Hypotheses ...........................................................................................15
METHODOLOGY ......................................................................................................16
Participants ........................................................................................................16
Measurements/Tasks ..........................................................................................16
Data Analysis ....................................................................................................22
RESULTS ....................................................................................................................25
Demographics ....................................................................................................25
Trait Signatures .................................................................................................28
State Signatures .................................................................................................33
DISCUSSION ..............................................................................................................37
Study Limitations ..............................................................................................41
Summary ...........................................................................................................42
APPENDICES .............................................................................................................43
APPENDIX A - Trait Signatures: Neurobehavioral Measurements .........................43
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APPENDIX B - Trait Signatures: Resting State Alpha Power ..................................44
APPENDIX C - Trait Signatures: Neurobehavioral Correlations in Control
Children .......................................................................................................................45
APPENDIX D - State Signatures: Neurobehavioral Measurements .........................46
REFERENCES ............................................................................................................47
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LIST OF FIGURES
Figure 1. Schematic of Blue Man-Stop Response Task ..................................................19
Figure 2. Contrasts in Trait Signatures between Children-Victim and Control Children .29
Figure 3. Alpha Power Correlograms.............................................................................31
Figure 4. Contrasts in Neurocognitive State Signatures between Children-Victim and
Control Children............................................................................................................34
Figure 5. Contrasts in Clinical State Signatures between Children-Victim and Control
Children ........................................................................................................................35
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LIST OF TABLES
Table 1. Participant Demographics ................................................................................27
Table 2. Trait Signatures: Alpha Amplitude for BM-SRT ..............................................30
Table 3. Trait Signatures: Neurobehavioral Correlations in Children-Victim .................32
Table 4. State Signatures: Neurobehavioral Correlations in Children-Victim .................36
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LIST OF ACRONYMS
ASD Autism Spectrum Disorders BM-SRT Blue Man–Stop Response Task BVS-I Bullying Victimization Severity Index (IBS, History of bullying victimization) CC Non-bullied, Control Children CDRS-R Children’s Depression Rating Scale-Revised CFT-C Rey-Osterrieth Complex Figure Test– Copy CFT-DR Rey-Osterrieth Complex Figure Test– Delayed Recall CY-BOCS Child Yale–Brown Obsessive-Compulsive Scale FAS Benton Oral Word Fluency Test/FAS H-DSM History of DSM-5 Disorders IBS Illinois Bully Scale LF Left Frontal Region LP Left Parietal Region NIH-FICA NIH Toolbox - Flanker Inhibitory Control and Attention Test OCS OC-Spectrum Disorders OCD Obsessive-Compulsive Disorder PTSD Posttraumatic Stress Disorder QTE Questionnaire on Traumatic Experiences in Early Childhood RF Right Frontal Region RP Right Parietal Region SCQ Social Communication Questionnaire SI-I Social Interactions Index (SCQ, Peer Interaction History) SS State Signatures SS-PV Current state of peer victimization TS Trait Signatures VA-I Visual Attention Index (CFT-C, NIH-FICA) VC Children-Victim of bullying VE-I Verbal Expression Index (WASI-S, FAS) VS-I Visuo-Spatial Index (CFT-DR, WASI-BD, WASI-MR) WASI-BD Wechsler Abbreviated Scale of Intelligence-II – Block Design WASI-MR Wechsler Abbreviated Scale of Intelligence-II – Matrix Reasoning WASI-PRI WASI-II Perceptual Reasoning Index WASI-S Wechsler Abbreviated Scale of Intelligence-II – Similarities WASI-V Wechsler Abbreviated Scale of Intelligence-II – Vocabulary WASI-VCI WASI-II Verbal Comprehension Index
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INTRODUCTION
Definition of Bullying
Bullying has considerably increased in American schools within the last two
decades, resulting in physical and psychological harm to the young victims’
development, including loss of personal potential, school shooting tragedies, increased
risk of suicide and severe family distress (Nishina, Juvonen & Witkow, 2005; Ranney et
al., 2016; Srabstein, 2013; Rigby & Slee, 1999). Bullying is an aggressive and
persistently repeated act of behavior with an intention to harm, and primarily related to
social power differential (Olweus, 1978; 1993). Forms of bullying include social
aggression (e.g., spreading rumors, social exclusion), verbal aggression (e.g., threats,
name calling), physical aggression (e.g., pushing, hitting), and cyber bullying (e.g., using
electronic means to hurt the reputation of another person; Olweus, 1993). Bullying
transcends across age, gender, race/ethnicity and SES, and among all other environments,
is most frequently recorded in academic institutions.
Bullying occurs in 30% of children and adolescents in the United States (Nansel
et al., 2001; Wang et al., 2009). Other industrialized countries (e.g., Germany, United
Kingdom, Spain, Australia) report a similar prevalence, ranging from 20-30% (Zych et
al., 2017). Importantly, prevalence rates increase among children with special healthcare
needs, as seen in children with Autism Spectrum Disorder (ASD). Their rates of
victimization range from 46% to 80% of (Cappadocia, Weiss & Pepler, 2012; Sterzing et
al., 2012).
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New Model of Children-Victim: State Signatures and Trait Signatures
Considering the clinical and social assessment reports below and first
neuroimaging studies on children-victim (VC), we propose a novel model of
investigation of children-victim characteristics: (i) Trait Signatures (TS), i.e., long-term
characteristics of emotional, cognitive and social development related to pre-existent,
permanent changes in basic neural functions underlying top-down inhibitory control of
cognition and emotions; and (ii) State Signatures (SS), as all psychological, somatic and
neuropsychiatric consequences of being a target of bullying, as compared to control
children (CC). Presented below is our original study aiming to define the distinct SS and
TS in the VC population in children between the age of 6-17. Understanding the
significance of different TS will help us to understand the relationship between TS and
SS and predict the effects of bullying on individual children. Our ultimate goal is to
design well informed and effective methods for prevention of bullying victimization.
Reported Consequences of Bullying in Children of Different Age Groups
Bullying rates and forms of aggression differ across developmental stages.
Contrary to popular belief, bullying begins in early childhood (Kochenderfer & Ladd,
1996; Pepler, Jiang, Craig, & Connolly, 2008; Alsaker & Gutzwiller-Helfenfinger, 2010).
Pre-school aged children can identify bullying behavior, rumor spreading and social
exclusion in their peers when assessed with developmentally appropriate methods
(Alsaker & Nägele, 2008). Victims as young as four years of age, have reported higher
levels of somatic complaints and peer problems, whereas, bullies at this age have been
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more likely to have conduct problems, hyperactivity and poor pro-social behavior (Ilola,
Lempinen, Huttunen, Ristkari, & Sourander, 2016).
Children in elementary school typically report higher rates of bullying compared
to middle school children (Scheithauer, Hayer, Petermann & Jugert, 2006), showing a
peak during school transitions (Pepler et al., 2008). Physical bullying is often reported in
younger children, with the highest reported severity overserved in 8th grade (Scheithauer
et al., 2006), while more sophisticated forms of verbal, social and cyberbullying emerge
during early adolescence (Pepler et al., 2006). However, most of the research has focused
on middle/high school and college students leaving a gap of knowledge in younger
children (Mason, 2013).
It has been documented that early bullying victimization exposure may lead to
long-term negative consequences in adolescence and/or adulthood. Adolescents with a
history of bullying experience report higher rates of depression and emotional problems
(Zwierzynska, Wolke & Lereya, 2013), increased drug and alcohol use (Kim, Catalano,
Haggerty & Abbott, 2011), sleeping difficulties (Fekkes, Pijpers & Verloove-Vanhorick,
2004), and physical problems such as headaches and stomach-aches (Williams,
Chambers, Logan, & Robinson, 1996). Further, Copeland and colleagues (2013) studied
the consequences of childhood bullying in young adults and found that those participants
who experienced bullying during childhood reported higher rates of depressive,
generalized anxiety, panic and agoraphobia disorders in adulthood. Isolation and
exclusion combined with long-term bullying during high school years have been shown
to increase levels of stress and depression during young adulthood (Newman et al., 2005).
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Gender Related Consequences in Victims of Bullying
Findings regarding gender differences are mixed. Some evidence suggests that
gender differences are found in relation to the forms of aggression used, the frequency of
involvement in bullying and coping strategies. Boys tend to bully both girls and boys and
report higher rates of victimization compared to girls, whereas, girls tend to only bully
girls (Nansel et al, 2001; Veenstra et al., 2005; Ma, 2002). Boys tend to engage more in
physical aggression, while girls engage in verbal aggression (Casey-Cannon, Hayward, &
Gowen, 2001; Nansel et al., 2001). Victimized females tend to internalize behaviors
(Broidy & Agnew, 1997), report higher rates of lower self-esteem, risky sexual behavior
and substance abuse (Bouffard & Koeppel, 2016), while victimized males tend to
externalize behaviors (Broidy & Agnew, 1997). However, when the severity of bullying
increases, gender differences are no longer a significant factor (Rivers & Noret, 2010;
Kim, Boyce, Koh, & Leventhal, 2009; Eisenberg, Neumark-Sztainer & Story, 2003).
Participant Role Related Neurobehavioral Characteristics
Bullying incidences are often thought of as only involving a dyad (i.e., bully and
victim). Those who perpetrate, i.e., target individuals, are identified as bullies, while
those who are the targeted are victims (Olweus, 1978). Bully-victims are those who
engage in both behaviors, but it is uncertain if they have a simultaneous origin or if one
occurred before the other. However, bullying is a phenomenon that involves various
social roles. Salmivalli and colleagues (1996) identified and described, aside from bullies
and victims, additional roles such as assistants, reinforcers, outsiders and defenders.
Assistants are defined as those who join in bullying perpetration but have a secondary
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role and reinforcers are those who provide positive feedback to the perpetrators or may
be constantly present and not assist the victim. Outsiders keep their distance and watch
from afar and defenders intervene in behalf of the victim. Boys are socially accepted by
their peers when assisting the bully as reinforcers but are typically rejected when acting
as outsiders. However, those who are defenders may be either rejected or socially
accepted by their peers (Salmivalli et al., 1996). Notably, the prevalence rate of bullying
in typically developing children increases to 66% when considering all these roles
(Rivers, Poteat, Noret & Ashurst, 2009).
Three meta-analyses for bullies, victims and bully-victims, examined the
relationship between participation in bullying and psychosomatic complaints in children,
ages 7 to 16 (Gini & Pozzoli, 2009). Results indicated that both victims and bully-victims
share common medical problems, poor relationships with peers, low emotional adjustments
and had the largest effect sizes for psychosomatic problems. All three groups involved in
bullying had a significantly higher risk than in controls for psychosomatic problems,
however, bullies demonstrated the lowest number of medical health problems compared to
victims and bully-victims.
Witnessing bullying or helping in bullying has been linked to elevated mental
health risks (Rivers, et al., 2009). For instance, children who witness victimization and are
not directly involved, have been found to experience cognitive dissonance (Craig & Pepler,
1998). This results from their desire to intervene but not taking any action. Those who have
witnessed victimization report a higher risk for substance abuse (Rivers et al., 2009),
sensitivity to rejection, and neural activity consistent with distress (Masten, Eisenberger,
Pfeifer & Dapretto, 2013).
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However, the group to display the most significant levels of psychopathology are
bully-victims. These individuals are victimized and display bullying behaviors. They have
the highest risk for suicide attempts, depression and psychosomatic complaints (Rivers &
Noret, 2010; Nansel et al., 2001), medical problems, poor relationships with peers, low
emotional adjustment (Gini & Pozzoli, 2009), substance abuse and hostility (Shepherd,
Sutherland & Newcombe, 2006; Nansel et al., 2001; Juvonen, Graham & Schuster, 2003).
These observations may suggest that bully-victims were originally victims of bullying, and
the course of prolonged abuse developed aggressive behaviors as a mechanism of defense
or hopelessness.
One study found that children who were assessed as bullies and showed theory of
mind (ToM) impairments, were more likely to misinterpret friendly behaviors of others
as aggressive (Van Roekel, et al., 2010). ToM is defined as the ability to predict another
person’s beliefs, intents, desires and knowledge (Baron-Cohen, Leslie & Frith, 1985).
Adolescents with ASD who were victimized, were more likely to misinterpret friendly
behaviors as threatening and bullying (Van Roekel, et al., 2010). This is consistent with
the Victim Schema Model (Rosen, Milich, & Harris, 2007), which states that individuals
who have been victimized, will more often misinterpret non-threatening interactions as
negative or hostile. Thus, bullying becomes a self-sustaining cycle that increases the
probability of future victimization.
Medical and Psychological Consequences of Bullying in Children-Victim
Chronic bullying victimization leads to both severe short- and long-term
consequences in the victim’s physical and psychological health. Prolonged exposure may
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lead to higher rates of anxiety, depression, reduced academic achievement, suicidal
ideations and completion, uncontrolled acts of aggression and increased likelihood to
become chronically bullied in adulthood (Nishina et al, 2005; Ranney et al., 2016; Rigby
& Slee, 1999; Srabstein, 2013; Sharp, 1995).
Victims and bully-victims have reported higher rates of physical and
psychosomatic health issues such as poor appetite, repeated sore throats, and colds
compared to those who bully and non-involved children (Wolke, Woods, Bloomfield, &
Karstadt, 2001). Exposure to bullying was related to frequent health complaints and
absence from school in young children (e.g., 6 to 9 years of age; Wolke et al., 2001;
Fekkes et al., 2004). Adolescents have reported higher frequency and severity of health
problems (e.g., abdominal pain), higher rates of doctor visits and absenteeism
(Vaillancourt et al., 2011).
Neuroendocrinology studies have suggested that bullying victimization has
neurobiological effects in VC. There appears to be a link between bullying and the
dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis (Knack, Jensen-
Campbell, & Baum, 2011; Vaillancourt et al., 2011; Rudolph, Troop-Gordon, & Granger,
2011). The HPA axis promotes rapid secretion of cortisol to prepare the body for the
fight-or-flight response. Further, bullying victimization appears to be a risk factor for
depressive symptoms in children who displayed heightened anticipatory cortical levels,
especially in girls (Rudolph et al., 2011).
Additionally, childhood bullying exposure predicts low-grade systemic
inflammation in adulthood. Copeland and colleagues (2014) examined low-grade
inflammation by measuring C-reactive protein (CRP) in victims, bully-victims, bullies,
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and non-involved children through a longitudinal study. The authors found a positive
relationship between the number of bullying incidences reported by participants and CRP
levels, thus indicating higher susceptibility to inflammation in victims of bullying.
Prolonged exposure to bullying may also lead to increased risk for severe mood
disorders, psychotic symptoms, behavioral adaptive problems and increased severity of
symptoms in developmental disorders, such as ASD and obsessive-compulsive spectrum
(OCS; Schreier et al., 2009). Bullying victimization has been linked with early onset for
social phobia, OCD, and panic disorder with, or without, agoraphobia (McCabe, Antony,
Summerfeldt, Liss & Swinson, 2003). Schreier and others (2009) found that children who
have been severely or chronically victimized were two times more likely to report
psychotic symptoms even after controlling for prior psychopathology, IQ and other
experienced adversity.
Among the most severe consequences of bullying are suicide attempts and
completions. Victims and bully-victims are at increased risk for suicide ideations and
completion compared to the general population (Kaltaila-Heino et al., 1999; Klomek,
Marrocco, Lkeinman, Schonfeld & Gould, 2007; Rivers & Noret, 2010). Male bully-
victims, ages 12-16, are at the highest risk for suicide attempts (Rivers & Noret, 2010).
Young adults who experienced childhood bullying victimization have reported
significantly higher levels of suicidal ideations compared to the population (Copeland et
al., 2013).
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Neuroimaging Evidence: Consequences of Bullying in Victimized Children
Recent studies have examined bullying in terms of social exclusion in children
and adolescents using neuroimaging techniques. A study using functional magnetic
resonance imaging (fMRI) examined chronically, socially rejected adolescents while
playing a virtual ball-tossing game (i.e., Cyberball; Will, Crone, van Lier & Guroglu,
2016). The authors found that rejection was associated with higher activity in the
subgenual anterior cingulate cortex and the anterior insula during peer exclusion
compared to the control group. These regions have been previously linked with the
distress of peer rejection among adolescents. Additionally, chronically victimized
adolescents were found to exhibit increased activity in the dorsal striatum and lateral
prefrontal cortex compared to CC, when demonstrating prosocial behavior towards other
participants. These regions are associated with cognitive control.
Further, Eisenberger and colleagues (2003) also used the virtual ball-tossing game
and found that those who experienced social exclusion in the game, relative to social
inclusion, showed increased activation in the dorsal anterior cingulate cortex and ventral
prefrontal cortex. Both regions are implicated in functions that warn organisms of a
potential predator or other dangers and to regulate distress associated with physical pain
and negative affect. This suggests a neural overlap between social and physical pain
systems.
Reports on Etiology of Being a “Bully” or a Child-Victim
Clinical and psychosocial analyses of individuals engaging in recent school
shootings have shown that in most cases the performing individual, was not a bully but a
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victim of bullying. Events occurring at Virginia Tech (CNN Library, 2016), Sandy Hook
Elementary (Sedensky III, 2013) and Umpqua Community College (Loew, 2015) urge us
to look closely at characteristics of those who were engaged in those violent crimes.
These individuals were described by their community as rejected by peers, odd, with
social difficulties, repetitive, strange behaviors and interests (Hughes & Johnson, 2015;
Sedensky III, 2013). Letters left by the offenders described how isolated and
misunderstood they felt (Keneally, 2015). Victims often displayed symptoms of clinical
depression and anxiety disorders, which all have a high level of heritability (Mai-Duc,
2015). Therefore, we may be able to predict which children will demonstrate certain
cognitive and emotional-social endophenotypes (i.e., elevated psychopathological
markers without a clinical severity) that leaves them susceptible to becoming victims of
bullying (Gottesman & Gould, 2003). However, this effort must be accompanied with
prevention and intervention programs. Currently, even if victims had displayed symptoms
of emotional and cognitive deficits and had been diagnosed earlier with one of the
developmental psychopathological disorders prior to a tragic shooting event, there is yet
no program that exists to prevent bullying victimization of children with such disorders.
Developmental Psychopathology Endophenotype
Prevalence rates of bullying are higher among children with behavioral and
emotional difficulties. For instance, children with OCS disorders including ASD and
OCD report rates ranging from 46% to 80% in comparison to 30% among typically
developing children (Sterzing, et al., 2012; Cappadocia et al., 2012). Since both, OCD
and ASD, demonstrate deficits in visual attention, cognition of social cues (Baron-Cohen
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et al., 1985; Van Roekel et al. 2010; Newton et al., 2017; Sterzing et al., 2012), and top-
down inhibitory control (Ciesielski et al., 1997; 2007; Greenberg et al., 2000; Loth,
Gomez & Happe, 2010), the investigation of a marker relying on top-down inhibitory
control is important for identifying children at risk for becoming victims of bullying.
Children with OCS disorders have marked severe social and communication
deficits and display repetitive behaviors (Bejerot, 2007). ASD and OCD share
commonalities in neurological and genetic phenomena and both have visual-spatial
processing deficits, impaired social interactions and communication, have restricted
interests in group activities and deficits related to ToM (Ivarsson & Melin 2008; Chasson
et al., 2011; Zandt et al., 2007; Bejerot, 2007; Anholt et al., 2009). Only recently has
research begun to examine the link between ASD and OCD to identify risk factors for
peer victimization.
Bejerot and Mörtberg (2009) examined autistic traits and previous experiences of
victimization during grade-school years on adult patients with social phobia, OCD and
healthy controls. The authors predicted that autistic traits would increase the likelihood of
being bullied even among those with social phobia and OCD. They found that patients
with OCD had higher rates of autistic traits compared to those with social phobia and
healthy controls. This group also reported higher rates of victimization (50%) compared
to patients with social phobia (20%) and healthy controls (27%). Thus, having autistic
traits increased the likelihood for becoming a victim among patients with OCD.
Children with ASD who reported higher levels of anxiety, hyperactivity, self-
injurious, and stereotypic behaviors were more likely to experience higher levels of
victimization (Cappadocia et al., 2012). These children were five times more likely to
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have major communication difficulties. Victims were found to be much younger than
bullies, have fewer friends at school and were 11 times more likely to have higher levels
of child internalizing disorders (e.g., depression, anxiety).
Developmental Inhibitory Neuro-Endophenotype
Persistent poor inhibitory regulation of emotional and cognitive behavior may
increase the risk for becoming a target of bullying. Behavioral evidence demonstrates that
VC display deficits in top-down inhibitory control of both cognitive and emotional
responses. Studies have found that girls who had difficulty regulating their anger
responses were at higher risk for victimization. Boys who poorly suppressed their sadness
and worry reported higher levels of victimization (Alsaker & Gutzwiller-Helenfinger,
2010). Additionally, children in kindergarten who showed deficits in top-down inhibition
of distractions were at a higher risk for victimization (Alsaker & Nägele, 2008; Alsaker
& Gutzwiller-Helenfinger, 2010).
Evidence suggests that proficiency for top-down attentional modulation at early
stages of sensory processing continues to change during childhood and early adolescence
(Bunge, Dudukovic, Thomason, Vaidya, & Gabrieli, 2002; Taylor, Chevalier, &
Lobaugh, 2003). Similar findings have been reported in studies on top-down attentional
control in children, as reflected in EEG oscillatory activity (Klimesch et al., 2001;
Krause, Salminen, Sillanmaki, & Holopainen, 2001). Parietal-occipital alpha was
reported to be mature in children ages 10 to 12 years (Krause et al., 2001; Krause,
Pesonen, & Hämäläinen, 2010) and found to be a sensitive indicator of cognitive
inhibitory task demands (Gevins, Smith, McEvoy, & Yu, 1997; Nunez, Wingeier, &
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Silberstein, 2001). In our earlier study (Ciesielski et al., 2010), we used
magnetoencephalography (MEG) in 10-year-old children to examine developmental
differences in top-down control reflected in modulation of alpha-band (8–13 Hz) to
different stages of a working memory task with high demand for inhibitory control.
A recent study suggested, that focusing only on single-peak effects or one
frequency band may lead to an incomplete understanding of the mechanisms involved in
signal processing in stop-response tasks (Huster et al., 2014). The authors suggested that
a closer view of cortical activation to stop signal processing may be attained by using the
analysis of connectivity patterns and their dynamic changes over time or spatio-temporal
analysis of spectral oscillatory activity. The authors conclude that the critical time for
observation of effects of inhibitory brain action is prior to 200ms post stop-stimulus
presentation.
Stop-response task paradigms have been applied effectively in studies of
inhibitory control development. The characteristic findings report a sharp reduction in
reaction time of responses between childhood and adulthood (van den Wildenberg & van
der Molen, 2004). Developmental studies have found involvement of the frontal-basal
ganglia networks in response inhibition, both in adults and in children, and corresponding
activation in the frontal and parietal cortex (Cohen et al., 2010). Most developmental
neuroimaging studies use fMRI and mostly focus on the prefrontal cortical component of
the frontal-basal ganglia network. These have reported both increases (Ordaz et al., 2013)
and decreases (Durston et al., 2002) in prefrontal ventral activation related to inhibiting a
response. The contrast, increasing with age, between higher activity in control regions
relevant to inhibition and reduction of activity to non-specific regions has also been
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reported (Ciesielski et al., 2006; Crone & Dahl, 2012; Durston & Casey, 2006; Luna et
al., 2010; Stephen et al., 2006).
Summary
Deficits in inhibitory control are well associated with phenomenology of
psychopathological disorders such as ASD or OCD. Early identification of such visual
inhibitory cognitive deficits, may point to risks for becoming a target of bullying
victimization. We aimed to examine whether abnormal top-down inhibitory control of
cognitive and emotional responses and ERPs, their neurophysiological correlates, may be
the elucidating fundamental neurological characteristic of all children victims and, thus, a
biological marker of children at high risk for becoming a victim of bullying. Defining a
reliable neural correlate of cognitive inhibitory control will be important for studying
developmental changes in the brain mechanism underlying adaptive behavior in the
challenging conditions of bullying victimization (Badre, Kayser & D'Esposito, 2010).
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Aims & Hypotheses
To understand the mechanism of causes and effects of bullying in VC we aimed:
AIM 1: To characterize in VC, as compared to CC, the Trait Signatures
considered in developmental neuroscience to reflect permanent, pre-existing cognitive
and neural functions underlying top-down inhibitory control of behavior. Thus,
considering the clinical and research reports we expected in VC as compared to CC:
H1: Preserved functioning in earlier learned skills (e.g., verbal knowledge) less
susceptible to adverse events, but reduced performance in visual-spatial attention and
memory linked to symptoms of anxiety;
H2: Increased anxiety measures (e.g., CY-BOCS) and a history of poor social
interactions;
H3: Consistent reduction in alpha power and its task-related modulation, particularly in
the frontal and parietal brain regions.
AIM 2: To characterize State Signatures (SS) in VC, as compared to CC by
examining the cognitive, emotional and social effects of exposure to bullying.
Considering the aforementioned studies, we predicted in VC:
H1: Higher levels of depressive symptomology and traumatic experiences;
H2: Significant deficits in visuospatial tasks with high demands for organization and in
verbal and visual memory tasks;
H3: Poor, ineffective and mostly negative peer interactions, most likely related to
cognitive and emotional deficits.
AIM 3: The end goal was to identify risk factors for translational outcomes of this
study to facilitate programs of resilience in children vulnerable to victimization.
16
METHODOLOGY
Participants
A total of 46 children were recruited from the community (81.3%) and others
were invited from a longitudinal, developmental study (18.8%). In total, 17 children-
victim of bullying (VC) and 17 age and sex matched control children (CC) participated in
the study. The parents of the remaining 12 children recruited found it too time consuming
to complete the testing. All participants and their parents signed informed consent and
assent forms according to the guidelines of the Office of the Institutional Review Board
at the University of New Mexico. Inclusion criteria for VC included repeated experiences
with being a target of bullying victimization. Children in both groups were between age
6 to 17 years. Exclusionary criteria for CC included history or current clinical diagnosis
of any DSM-5 disorder and any history of being a bully or a victim of bullying. History
of CNS medication, traumatic brain injury, medical conditions (e.g., seizures,
tuberculous, genetic disorders) were exclusionary.
Measurements/Tasks
Cluster 1. Trait Signatures: Neurobehavioral and EEG Measurements
Consistent with our predictions that anxious children with deficient inhibitory
control would be in the high-risk group for bullying victimization, we clustered the
psychometric tools that reflect these characteristics into CLUSTER 1, the Trait
Signatures cluster. The tests included in this cluster were:
Wechsler Abbreviated Scale of Intelligence (Second Edition; Wechsler, 2011) –
Vocabulary (WASI-V). WASI-V was used to assess well learned and crystalized
17
abilities. It measures the participants knowledge of words and verbal concepts. The
subtest includes three-picture items and 38 verbal items. Participants were asked to define
words presented visually and orally.
Rey-Osterrieth Complex Figure Test (Rey, 1941|1993; Osterrieth, 1944|1993) –
Copy (CFT-C). CFT-C trial was used to assess visual-spatial attention, perception and
organization. Participants were instructed to copy a complex visual construct, which
requires low verbal mediation.
NIH Toolbox - Flanker Inhibitory Control and Attention Test (Hodes, Insel, &
Landis, 2013; NIH-FICA). NIH-FICA was used to measures attention and executive
function. The participant was asked to focus upon an arrow located in the middle of the
screen while inhibiting attention to stimuli nearby (i.e., other arrows). Participants
responded by pressing buttons to congruent and incongruent signals (i.e., 20 mixed
trials). There were four practice trials with audio recording feedback.
Child Yale–Brown Obsessive-Compulsive Scale (Scahill et al., 1997; CY-BOCS).
CY-BOCS was used to measure the severity of obsessive and compulsive symptoms. The
scale was comprised of a symptom checklist, target symptom list and severity rating on
10-items. The scale was administered to parents only.
The Social Communication Questionnaire (Rutter, Bailey & Lord, 2003; SCQ).
SCQ was used to measure ASD symptomatology. The screening questionnaire provided
levels of severity of ASD symptoms across different samples of behavior. Sub-scores
provided information on abnormal social interactions, communication and restricted,
repetitive and stereotyped patterns of behavior. The scale was administered to parents
only.
18
Structured Clinical Interview Parents provided information and records of
demographic data, prenatal and postnatal early development, and medical, personal and
family history. They also provided history of peer and family social interactions for their
child.
The normalized CFT-C and NIH-FICA scores were combined to provide a
composite score i.e., Visual Attention Index (VA-I). Scores indicate the standard
deviations above or below the mean. Responses describing past peer interaction from the
structural clinical interview and SCQ scores were combined to provide a Social
Interactions Index (SI-I) for both VC and CC. Higher scores indicated higher levels of
social interaction difficulties.
Blue Man-Stop Response Task (BM-SRT Task; Ciesielski, 2003; Bouchard et al.,
2018; presented in Figure 1). BM-SRT is a visual-spatial n-back working memory task
with a stop-response signal. It was designed in the form of a computer game for children.
Participants were instructed to concentrate on a fixation point and carefully observe the
Blue Men characters (angle size 2°) that were individually presented on the screen (each
for 200 ms). When the stop-response signal (i.e., blue soccer ball) was presented, the
participants were asked to decide if the two consecutive characters preceding the stop-
response signal were congruent or non-congruent in visual-spatial orientation.
Participants were permitted to respond when presented with the stop-release-signal (i.e.,
green dot). There were four awaiting-for-response periods between the soccer ball and
green dot: 1000ms, 1600ms, 3200ms and 4200ms.
The experiment was presented in six separate runs, lasting about three minutes
each, all consisting of 20 to 22 trials, for a total of 126 trials. All participants practiced
19
the task in a separate room before being prepared for the EEG to ensure familiarization.
They also completed a short practice run (i.e.,12 trials) in the EEG chamber, for which
the data were not recorded.
time
Figure 1. Schematic of Blue Man-Stop Response Task (BM-SRT). BM-SRT is a visual-spatial n-back working memory task with a stop-response signal. The task was to carefully observe individually presented Blue Men characters. When the stop-response signal (i.e., blue soccer ball) is presented, participants must decide if the last two consecutive characters were congruent or non-congruent in visual-spatial direction and respond when presented with the stop-release signal (i.e., green dot). The correct response for the sample trial above is congruent (Ciesielski, 2003; Bouchard et al., 2018).
Electrophysiological Data Acquisition.
Data for BM-SRT was collected with a BioSemi High Density EEG 64-channel
recording system (BioSemi B.V., Amsterdam, Netherlands) in a dimly lit room that was
noise and electromagnetic field shielded. EEG was recorded at a sampling rate of 512 Hz
and pass filtered online with a frequency of 0.16-100 Hz. The 64 channels were placed
Response Delay 1000, 1600, 3200, or 4200ms
Response Button Press
Stop-Response Signal
Stop-Release Signal
20
according to the international 10-20 system using the BioSemi Active2 system. Vertical
and horizontal eye movements were recorded using four electrooculography (EOG)
electrodes, two of which were placed on the outer eye canthi and two below and above
the left eye. Two additional reference electrodes were placed on the left and right
mastoids. All electrode locations were digitized using Polhemus. The experiment was
conducted using the Presentation software (Version 11.3) and responses were collected
using Current Designs 4 button Inline USB response box.
Cluster 2. State Signatures: Neurobehavioral Measurements
Consistent with the reported literature and our own hypotheses about the
depressive traits and related deficits in visual attention and memory, the psychometric
measurements expected to reveal the immediate consequences of victimization of
bullying were clustered into a battery of tasks named CLUSTER 2. These elucidated the
State Signatures of VC, which included:
Rey-Osterrieth Complex Figure Test (Rey, 1941|1993; Osterrieth, 1944|1993) –
Delayed Recall (CFT-DR). CFT-DR trial was used to assess visual-spatial perception,
attention, memory and organization. After participants were instructed to copy an
abstract image, they were asked to draw the image from memory after a 30-minute delay.
Wechsler Abbreviated Scale of Intelligence (Second Edition; Wechsler, 2011) –
Block Design (WASI-BD). WASI-BD was used to assess visual perception and
organization, nonverbal concept formation, and visual motor coordination. Participants
were asked to recreate two-dimensional designs from patterns in stimulus booklet using
21
blocks with red and white coloring. The test was time-limited, with extra-credit points
for fast rate of performance.
Wechsler Abbreviated Scale of Intelligence (Second Edition; Wechsler, 2011) –
Matrix Reasoning (WASI-MR). WASI-MR was used to assess fluid intelligence, visual-
spatial skills, and perceptual organization. The participants were asked to select response
options that complete a matrix or a sequence of stimuli.
Wechsler Abbreviated Scale of Intelligence (Second Edition; Wechsler, 2011) –
Similarities (WASI-S). WASI-S was used to assess verbal concept formation and
reasoning. Participants were given two words that represent similar objects or concepts
and they had to describe in their own words how these two objects were similar to each
other.
Benton Oral Word Fluency Test - FAS (Benton & Hamsher, 1976; FAS). FAS
was used to assess phonemic verbal fluency. Participants were instructed to say as many
words as possible within a minute, when given the letters F, A, or S; excluding proper
names, changing endings, or slang.
Children’s Depression Rating Scale-Revised (Poznanski & Mokros, 1996; CDRS-
R). CDRS-R was used to measure depression and severity of symptoms. The
questionnaire (parent version) was a semi structured interview that provided a cumulative
score for interpretation of scores representing behavioral and mood characteristics of a
child.
Questionnaire on Traumatic Experiences in Early Childhood (Tretiak &
Ciesielski, 2014; QTE). QTE was used to assess the participant’s history of exposure to
22
potentially traumatic life experiences. The 10-item questionnaire assessed direct exposure
to accidents or violence before the age of one, three, five, and ten.
Illinois Bully Scale (Espelage & Holt, 2001; IBS). IBS measured the frequency of
bullying, fighting and victimization by peers in the last 30 days. The psychometrics are
high for all subscales (i.e., bullying= 0.87; fighting= 0.83; victimization= 0.88). The
same questions were used to inquire about the participant’s history of bullying
victimization.
To control for multiple statistical comparisons, the normalized CFT-DR, WASI-
BD, WASI-MR scores were combined into a composite score named Visuo-Spatial Index
(VS-I). A relationship to normative score is provided in number of standard deviations.
The Verbal Expression Index (VE-I) included normalized WASI-S and FAS scores. The
scores obtained from IBS were combined from the assessment of history of bullying
victimization which provided an overall Bullying Victimization Severity Index (BVS-I) for
VC.
Data Analysis
EEG. Data were processed using EEGLAB toolbox for MATLAB (Delorme &
Makeig, 2004), which is an open source toolbox available for EEG signal processing.
Data was re-referenced to the average of the signal from the two mastoid electrodes.
Channel data from frontal and posterior regions were analyzed, which included left
frontal (LF; i.e., F1, F3, FC1, FC3), right frontal (RF; i.e., F2, F4, FC2, FC4), left parietal
(LP; i.e., P1, P3, PO3, O1), and right parietal (RP; i.e., P2, P4, PO4, O2) regions.
23
Only correct and congruent responses during the latency period (i.e., “waiting-to-
respond” window) in the BM-SRT were analyzed. The first 150ms of the first 1000ms
were removed and 150ms to 450ms after the stop-signal were averaged for analysis from
all four waiting latency periods (i.e., 1000ms, 1600ms, 3200ms, 4200ms). A high pass
filter of 0.01 Hz to 0.20 Hz was applied. Noisy channels were removed, and the data were
re-calculated to the average reference. Data were segmented into 2400ms epochs (200ms
pre-stimulus to 1000ms post-stimulus) and baseline corrected to the mean pre-stimulus
baseline. Interference signals resulting from gross body movements were removed from
the continuous data. An independent component analysis (ICA) was then conducted to
remove eye blinks and saccades. Spatial topography maps of the ICA components were
manually inspected to identify physiological activity and noisy components were
removed (Onton, 2010).
For each participant, the average alpha spectral power was calculated across the
four regions (i.e., LF, RF, RP, LP) using a custom written MATLAB script (The
MathWorks, Inc., Natick, MA). The spectral power was calculated using the decibel (dB)
conversion, which is the ratio between the strength of one signal (i.e., alpha frequency
band power) and the strength of another signal (i.e., baseline power of the same
frequency band; Cohen, 2014).
Statistical Analysis
Neurobehavior. Statistical data analysis was conducted using IBM SPSS version
24 and R version 3.4.3. Descriptive and frequency statistics were used to test for any
significant relationship between groups. Two-tailed independent t-tests were conducted
24
to determine statistical significant differences between VC and CC on the
neurobehavioral indices and behavioral reports of symptomology. False discovery rate
(FDR) was calculated to control for multiple comparisons using the Benjamini-Hochberg
(BH) method (Benjamini-Hochberg, 1995), when appropriate. Cohen’s d was calculated
to determine effect size, which was interpreted as .2 for small, .5 medium and .8 or
greater as large effects sizes (Cohen, 1988). Pearson’s r two-tailed correlations were
conducted for within-group analysis.
25
RESULTS
Rationale
The goal of this study was to characterize Trait Signatures (TS) and State
Signatures (SS) displayed by VC in contrast to CC. TS were assessed as representing the
long-term, some permanent and most likely pre-existing characteristics of children (e.g.,
demographics, prenatal and early postnatal development of language and social
interactions) that are vulnerable to becoming a target of bullying. SS, in contrast, were
assessed to identify the cumulative detrimental effects of bullying victimization on
cognitive, emotional and social functioning, as predicted by earlier studies. Our far-
reaching goal is to investigate whether children with a specific pattern of TS may form a
population that is at high-risk to becoming victims of bullying and translate these results
to models of early identification and thus, offering a preventive intervention.
Presented below are three sets of data: i.) demographics of both tested
populations, as a potential variable that may contribute to our understanding of a
differences in pattern of TS in VC population; ii.) TS measures, including scores on
anxiety tests, and pattern of alpha oscillatory activation during inhibitory control of
behavioral response, that were considered a long-term physiological indicator of top-
down inhibition; and iii.) SS data, that involved measures of consequences of exposure to
bullying in the emotional, social and cognitive domain.
Demographics
A total of 34 children (17 VC) completed all study tests and procedures. One
participant from each group were excluded due to their difficulty to follow task rules or
26
disclosure of exclusionary criteria during study participation. A total of 16 VC and 16 CC
were included in the final analyses. Participant characteristics are described in Table 1.
Majority of the participants in the VC group identified as Hispanic (56.3%), while
CC generally identified as non-Hispanic, White (43.8%). The majority of VC were in
middle school (37.4%), while CC in elementary school (56.3%). There were no
significant group differences observed in race/ethnicity identification or SES as reported
in Table 1. The groups did not differ in terms of Verbal Comprehension Index (VCI; t24.7
= -1.53, p = .14) or the Perceptual Reasoning Index (PRI; t30 = -1.74, p = .09), calculated
from WASI-II.
27
Table 1.
Participant Demographics
Children-Victim (n=16) Control Children (n=16) pa
Characteristic n % M SD n % M SD
Age 12.5 3.01 10.4 3.22 .064
SESb 46.3 11.3 47.2 10.9 .81
WASI-VCI 102 8.7 108 12.4 .14
WASI-PRI 96.9 9.4 104 14.4 .09
Sex .73
Female 9 56 8 50
Male 7 44 8 50
Race/Ethnicity .053
American Indian 0 0 1 6.3
Asian 1 6.3 0 0
Bi-racial 3 18.8 0 0
Black/African American 1 6.3 0 0
Hispanic 9 56.3 8 50
Non-Hispanic White 2 12.5 7 43.8
School Grade .30
Elementary School 5 31.3 9 56.3
Middle School 6 37.4 3 28.7
High School or higher 5 31.3 4 25
Note. No group differences in demographic characteristic between Children-Victim and Control Children.
WASI-VCI=WASI-II Verbal Comprehension Index; WASI-PRI=WASI-II Perceptual Reasoning Index aSignifiance was evaluated by independent sample t-tests. bAccording to Hollingshead socioeconomic status
codes (Hollingshead, 1975).
28
Trait Signatures
Between-Group Analysis
Neurobehavioral Measurements. Independent t-tests were conducted to determine
statistical significant differences between VC and CC on the WASI-Vocabulary (WASI-
V) and Visual Attention Index (VA-I). FDR correction was employed to control for
multiple comparisons and the adjusted p-value was estimated using the BH method
(hereinafter, only adjusted pBH-values are reported when appropriate). There was a
statistically significant group difference in performances between groups in WASI-V and
VA-I (as reported in Appendix A).
Independent t-tests were used to assess group differences in the Social Interaction
Index (SI-I), CY-BOCS and performance of correct responses on BM-SRT. Significant
group differences were observed in the SI-I (pBH = .018), with VC reporting higher rates
of poor peer relationships, evidenced even in their early school years. CY-BOCS was not
statistically different between VC and CC, however, a medium effect size was observed
in VC. Due to high levels of noise during BM-SRT, one VC and two CC, were removed
from all related analysis, including correct responses. No significant differences were
observed for correct responses in the BM-SRT across both groups (t27 = 1.01, p = .32, d =
.39).
29
Figure 2. Contrasts in Trait Signatures between Children-Victim (VC) and Control Children (CC). There was a significant difference in WASI-V, VA-I, and SI-I between VC and CC, even after adjusting for multiple corrections using the False Discovery Rate. Numerical findings are in Appendix A. WASI-V=WASI-II Vocabulary; VA-I=Visual Attention Index; SI-I=Social Interactions Index; CY-BOCS=Child Yale–Brown Obsessive-Compulsive Scale. Alpha Amplitude for BM-SRT.
The alpha power was assessed during the delay period while awaiting to respond
across four cortical regions (i.e., LF, RF, LP, RP). Independent t-tests were conducted to
test for statistical significant differences between VC and CC spectral alpha power. As
indicated before, one VC participant and two CC participants were removed from further
data processing due to high level of motion noise in data. No significant group
differences in alpha power were observed in any brain region as seen in Table 2.
30
Table 2.
Trait Signatures: Alpha Amplitude for BM-SRT
VC CC t df pa d 95% CI of d
Region M SD M SD LL UL
Left Frontal 0.18 0.24 0.22 0.26 -0.44 27 .67 -0.17 -0.25 0.08
Right Frontal 0.44 0.41 0.51 0.53 -0.44 27 .67 -0.15 -0.32 0.01
Left Parietal 0.56 0.68 0.57 0.85 -0.04 27 .97 -0.01 -0.28 0.26
Right Parietal 0.67 1.00 0.65 1.10 0.07 27 .95 0.02 -0.35 0.39
Note. Significance was evaluated by independent sample t-tests. d = Cohen’s d effect size; CI=Confidence
Interval; LL=Lower level; UL=Upper Level. aUncorrected for multiple comparisons p value
Within-Group Analysis
EEG. Pearson’s r correlations revealed strong power coherence between frontal
and parietal regions in both VC and CC, as indicated in Figure 3. A positive statistically
significant correlation was found between the LP and RP in both VC (Pearson’s r(15) =
.98, pBH < .001) and CC (Pearson’s r(14) = .96, pBH < .001) during the BM-SRT. Further,
there were significant correlations between higher percent of correct responses in BM-
SRT and high alpha power in LP, RF and LF (pBH = .044, pBH = .044, & pBH = .049,
respectively) regions in CC only.
31
Figure 3. Alpha Power Correlograms. Pearson r values are respresented in the correlograms for a) Vicitmized Children (VC) and b) Control Children (CC) between frontal-parietal areas during BMT-SRT awaiting-to-respond period. The size of the circle indicate the strength of correlation (e.g., bigger circle, stronger relationship), while the color represents the direction of relationship (e.g., positive or negative correlation). Both correlograms demonstrante a positive correlation in frontal-parietal regions for VC and CC. Numerical findings are in Appendix B.
Neurobehavioral. Pearson’s r correlations were conducted to determine if alpha
power was correlated with family history of anxious and OCS disorders and severity of
victimization. As seen in Table 3, no significant findings were found, however, there
were medium effect sizes observed in alpha power and history of DSM-5 disorders in
VC. CC did not have signficant findings as seen in Appendix C.
32
Table 3.
Trait Signatures: Neurobehavioral Correlations in Children-Victim
Variables H-DSM BVS-I LF RF LP RP
H-DSM - .20 -.42 -.42 -.38 -.35
BSI-I - -.02 -.09 -.11 -.10 Note. Pearson’s r values presented. H-DSM=History of DSM-5 Disorders; BVS-
I=Bullying Victimivation Severity Index; LF=Left Frontal; RF=Right Frontal; LP=Left
parietal; RP=Right Parietal.
Conclusions: Trait Signatures displayed by VC as compared to CC involved:
(i) Significant deficits in basic cognitive and visual attention abilities;
(ii) Higher levels of anxiety characteristics prior to victimization (e.g.,
displayed more prevalent OCS phenomena);
(iii) No significant group differences in alpha power were recorded during top-
down inhibition of motor act and the correlations between alpha power in
frontal-parietal network were not statistically significant between groups
either.
33
State Signatures
Based on the participant’s reporting, verbal victimization was the most prevalent
(88%), such as being called derogative names or receiving demeaning commands. Other
frequently experienced bullying acts, were social victimization expressed in exclusions
and ridiculing in front of others (19%) and physical victimization including hitting and
pushing (19%). Further, 25% of VC reported having experienced all three forms of
bullying victimization. On average, 63% of VC had been bullied multiple times within
the last 30 days as reported by the Illinois Bully Scale (Espelage & Holt, 2001). The
scores on this scale suggested that severity of bullying victimization phenomena was
within a moderate range.
Between-Group Analysis
Neurobehavioral Measurements. Independent t-tests were conducted to determine
statistical significant differences between VC and CC on the Visuo-Spatial Index (VS-I)
and Verbal Expression Index (VE-I). There were no statistically significant group effects
of bullying victimization on either measure. However, there was large effect size
observed for VS-I according to Cohen’s d effect size (Cohen, 1988).
Independent t-tests, were used to assess group differences in SS of emotional and
social functioning. Significant group differences were observed in CDRS-R (t20.33 = 3.88,
pBH = 0.002, d = 1.47), showing higher depression symptoms in VC relative to CC. There
was a significant difference in the QTE (t24.65 = 2.08, pBH = 0.048, d = 0.76) and BVS-I
(t30 = 6.22, pBH < 0.001, d = 2.22), which indicated VC reported higher number of
34
traumatic experiences and bullying victimization severity than CC. Further, large effect
sizes were observed across all three measures as seen in Appendix D.
Figure 4. Contrasts in Neurocognitive State Signatures between Children-Victim (VC) and Control Children (CC). There was a significant difference in VS-I between VC and CC but was no longer significant after adjusting for multiple comparisons. There was no significant difference found in VE-I between VC and CC. Numerical findings are in Appendix D. VS-I=Visuo-Spatial Index; VE-I=Verbal Expression Index.
35
Figure 5. Contrasts in Clinical State Signatures between Children-Victim (VC) and Control Children (CC). There was a significant difference in CDRS-R and QTE between VC and CC, even after adjusting for multiple corrections using the False Discovery Rate. Numerical findings are in Appendix D. CDRS-R=Children’s Depression Rating Scale-Revised; QTE=Questionnaire on Traumatic Experiences in Early Childhood.
Within-Group Analysis
Neurobehavioral. Pearson’s r correlations were conducted to examine if severity
of cognitive and emotional deficits was correlated with current state of peer victimization
(SS-PV) in VC. No statistically significant correlations were found between VS-I (pBH =
.71), VE-I (pBH = .20), and QTE (pBH = .58). However, there was a significant
relationship in the CDRS-R (r = .68, pBH = .032), indicating higher scores in depression
36
symptomology and severe negative peer interactions. There was a medium effect size
between SS-PV and VE-I (r = -.44) as reported in Table 4 (Cohen, 1988).
Table 4.
State Signatures: Neurobehavioral Correlations in Children-Victim
Variable SS-PV VE-I VS-I CDRS-R QTE
SS-PV - -.44 -.11 .68* .22
Note. Pearson’s r values presented. Multiple comparisons controlled using False Discovery rate. SS-
PV=State Signatures Peer Victimization; CDRS-R=Children’s Depression Rating Scale-Revised;
QTE=Questionnaire on Traumatic Experiences in Early Childhood; VS-I=Visuo-Spatial Index; VE-
I=Verbal Expression Index. *p < .05
Conclusions: Our key findings in State Signatures for VC as compared to CC were:
(i) Significantly higher levels of depressive moods;
(ii) Significant deficits in visuospatial memory and visually mediated
conceptualization;
(iii) Ongoing traumatic experiences including bullying victimization.
37
DISCUSSION
The central aim of the present study was to characterize children-victim (VC) by
peer bullying victimization on two dimensions, Trait Signatures precipitating the abuse,
and State Signatures, the long-term consequences of persistent abuse. The
neurobehavioral and electrophysiological assessment of VC using a battery of tests
representing Trait Signatures showed, in VC as compared to CC, significantly higher
levels of anxiety including social situations, in line with lower visual-spatial attentional
skills and attention to visual details. VC also showed higher compulsivity as reported by
CY-BOCS. This may indicate lower top-down inhibitory control which may further
hinder their social interactions. It is of interest, however, that in this context the event-
related potentials data did not reveal significant group differences in power of alpha
oscillatory activity within the frontal-parietal network, implicated in top-down inhibitory
regulation of behavior (Bressler et al., 2008).
Alpha power is the earliest maturing oscillatory rhythm in the central nervous
system, which becomes relatively stable after the age of 5. This make it an ideal
developmental factor to study as a TS. The above result of no group differences may
result from suppression of alpha relative to baseline as compared to CC. Additionally, we
found large effect sizes in the relationship between alpha power in the left frontal and
right frontal regions in the first-degree familial history of psychiatric disorders in the VC
group. Alpha power in these regions was negatively correlated with familial psychiatric
disorders.
38
The no-group differences in alpha may suggest two additional possible
explanations, considering that there were no group differences on the BM-SRT
performance. The task we were employing to gather EEG spectral oscillatory brain
activity was not specific to the population of VC and relied mostly on controlling a pure
motor response. Including an emotionally charged stimuli in future studies would be
more specific to VC high anxiety characteristics. The second explanation may consider
the severity of anxiety, that in this study was within a mild-to-moderate level, and its
impact on a child’s behavior may be modest, but, yet sufficient to make VC more
susceptible to becoming a target of bullying. Participants in this study represent a healthy
child population with verbal general intellectual abilities and perceptual intellectual
abilities showing no significant group differences and remaining within average-to-high
average intellectual level. The cognitive task we used in the EEG laboratory might have
been relatively easy to take. However, in a socially challenging interaction with their peer
group, these children’s anxiety and poor visual-spatial attention to details may be a
challenge in responding fast and appropriately to the aggressive behavior of others.
Future investigations of the mechanism of bullying in young children must include an
emotionally charged stimuli and include children with higher levels of severity of
victimization.
The description of a child vulnerable to victimization by bullying is
complemented by our findings of State Signatures. VC, as compared to CC, showed
significantly higher levels of depressive moods and, consistent with the depressive
symptoms, increased difficulties in visual-spatial memory and conceptualization. The
scale levels for assessing past and current traumatic experiences including bullying
39
victimization, was significantly higher in VC. Thus, the SS records display a child with
significant depression that adds to primary existing anxious states. The past experience of
traumatic events, and current low social abilities demonstrate a child at high risk for
social victimization.
Of interest, are our findings on consistent visual-spatial attention and memory
problems in the VC group. This abnormality in visuospatial processing is similar to
children who have been maltreated and display symptoms of Posttraumatic Stress
Disorder (PTSD; De Bellis, Woolley & Hooper, 2013; Vasilevski & Tucker, 2016;
Barrera-Valencia, Calderon-Delgado, Trejos-Castillo, & O’Boyle, 2017). Further, both
emotional processing and visuospatial processing are associated with right hemisphere
functioning (Liotti & Mayberg, 2001), which has been suggested to influence the ability
to properly attend to taxing emotional effort due to high levels of negative emotions.
There was no difference found in verbal functioning in either group. The FAS
subtest, included in the Verbal Expression Index (i.e., FAS, WASI-S), requires flexibility
but provides the ability for participants to choose their own wording. This indicates that
VC have adequate ability in their expressions when they are cognitive and not emotional,
which is related to relatively intact left hemisphere functions. In consistency, Beers and
De Bellis (2002) also found no difference in FAS and Similarities among children who
had maltreatment-related PTSD.
Parental reports of VC revealed higher levels of depression as compared to CC,
which is consistent with other studies focusing on consequences of bullying in children
(Nishina et al, 2005). Farrington and colleagues (2012) found that bullying victimization
was a significant predictor of depression up to seven years later after controlling for other
40
major childhood adverse traumatic events. Additionally, VC reported higher rates of
traumatic experiences in contrast to CC of other nature, not only victimization by
bullying. This is of significant concern since experiencing trauma can alter
developmental trajectory of a child’s emotional, behavioral, and cognitive growth as seen
with children who have been maltreated or abused. Sensitive periods during development
in early adolescence related to synaptic pruning and development of myelination is
essential to healthy development of networks (Fair et al., 2007; Schaefer et al., 2014;
Meng & Xiang, 2016; Stevens, 2016) and can be severely delayed due to trauma (Wilson,
Hansen, & Li, 2011). This delay of myelination can in turn lead to functional deficits in
attention, executive functions and visual-spatial processing.
Our data indicated that VC displayed TS deficits in verbal memory and
knowledge. This may leave them less effective in verbal communication and more
vulnerable to bullying. However, this finding may be biased due to cultural constraints of
the test such as the predominate mainstream culture acceptable responses. We posit this
shortcoming in vocabulary in children from minority cultures may have a significant
impact in initiation of everyday social communication and may represent actual social
communication in typical contexts. Parents often reported that VC were bullied because
of their poor verbal communication skills.
The TS and SS data are crucial for our understanding of the roots of child’s
vulnerability to becoming a victim of bullying and provide us with markers that we need
to focus on to when aiming for early identification of children at risk for bullying
victimization. Further, the results open a possibility to translate them into an effective
intervention program that could be developed very early before children enter the primary
41
school environment. These preventive interventions must address emotional anxiety
treatment, increase child resilience and assist in perception and interpretation of social
cues.
There are many other risk factors that we need to include in a successful design of
preventive programs, such as gender and SES. Although the racial and ethnic
composition of both groups in our study were diverse and representative of the
population in New Mexico, VC children had slightly higher rates of racial/ethnic
minority backgrounds compared to CC.
Study Limitations
A potential limitation in our study was the variable and relatively moderate levels
of severity and short length of exposure in tested children. This could underlie the modest
spectral power effect size seen during the BM-SRT. Increasing these effects may require
in future studies at least three levels of experienced bullying severity, a low to moderate,
severe and prolonged, and no exposure to bullying. Therefore, it is notable, that although
we tested children with only a mild-to-moderate severity of bullying exposure, children-
victim still revealed high levels of depression, slowness in fluency of verbal expression
and in attention to complex visual attention. Other limitations to our model of Trait and
State characteristics of Children-Victim include a small sample size and relatively broad
age-rage of tested children, that could introduce an extra developmental variance. These
properties of the design could only be addressed within a larger program of studies.
42
Future Studies
The current findings will form a foundation for future translational studies
investigating State and Trait Signatures of victimization by social bullying in
neuroimaging of cognition, psycho-motor coordination, as well as emotional and social
development.
Summary
In conclusion, the study aimed to characterize risk factors for bullying
victimization displayed in Trait Signatures, which were hypothesized to precipitate the
susceptibility to victimization and to State Signatures resulting from bullying. We found
that Children-Victim manifesting Trait Signatures, in visual attention and verbal
communication along with traits of anxiety and obsessive-compulsive phenomena,
although not manifesting differences in alpha power during top-down inhibition of motor
responses, were at a higher risk for bullying victimization. Among State Signatures of
Children-Victim, through rigorous testing of neuropsychological skills, significant
deficits were found in complex visuospatial perception, memory and organization,
dysfunctions that may contribute to poor interpretation of social cues. The ultimate-aim
of this study was to further facilitate efforts toward designing empirically based programs
of resilience against bullying for young children.
43
APPENDIX A
Trait Signatures: Neurobehavioral Measurements
Children-
Victim
Control
Children t df pa d 95% CI of d
Measure M SD M SD LL UL
WASI-V 0.044 0.74 0.61 0.70 -2.23 30 0.33* -0.81 -1.05 -0.57
VA-I -0.79 0.96 -0.12 0.50 -2.28 30 0.019* -0.9 -1.16 -0.65
SI-I 3.93 1.74 2.32 1.37 2.80 28 0.009* 1.06 0.51 1.63
CY-BOCS 1.19 1.56 0.38 0.72 1.89 21.1 0.072 0.69 0.28 1.10
Note. Significance was evaluated by independent sample t-tests. Multiple comparison controlled using
False Discovery Rate. d=Cohen’s d effect size; WASI-V=WASI-II Vocabulary; VA-I=Visual Attention
Index; SI-I=Social Interactions Index; CY-BOCS=Child Yale-Brown Obsessive-Compulsive Scale;
CI=Confidence Interval; LL=Lower level; UP=Upper Level. aUncorrected for multiple comparisons p value. *p = <.05.
44
APPENDIX B
Trait Signatures: Resting State Alpha Power
Regions LF RF LP RP
LF - .83** .71** .70**
RF .89** - .93** .90**
LP .85** .89** - .94**
RP .85** .83** .97** -
Note. Pearson’s r correlations presented for Children-Victim above the diagonal and
Control Children below the diagonal. LF=Left Frontal; RF=Right Frontal; LP=Left
Parietal; RP=Right Parietal. * p < .05 (2-tailed) after False Discovery Rate (FDR) correction; ** p < .01 (2-tailed) after
FDR correction.
45
APPENDIX C
Trait Signatures: Neurobehavioral Correlations in Control Children
Variables H-DSM BVS-I LF RF LP RP
H-DSM - .02 -.06 -.27 -.19 -.16
BSI-I - -.27 -.21 -.38 -.35
Note. Pearson’s r values presented. H-DSM=History of DSM-5 Disorders; BVS-
I=Bullying Victimivation Severity Index; LF=Left Frontal; RF=Right Frontal;
LP=Left Parietal; RP=Right Parietal.
46
APPENDIX D
State Signatures: Neurobehavioral Measurements
Children-
Victim
Control
Children t df pa d 95% CI of d
Measure M SD M SD LL UL
VS-I -0.46 0.54 -0.003 0.61 -2.27 30 0.031 -0.82 -1.01 -0.63
VE-I -0.11 0.85 -0.01 0.76 -0.36 30 0.72 -0.13 -0.40 0.14
CDRS-R 45.13 11.04 32.83 5.4 3.88 20.3 0.001** 1.47 -1.45 4.38
QTE 2.94 2.08 1.67 1.23 2.08 24.7 0.048** 0.77 0.19 1.34
BVS-I 2.06 0.36 1.22 0.41 6.22 30 < 0.001** 2.25 2.12 2.38
Note. Significance was evaluated by independent sample t-tests. Multiple comparison controlled using False
Discovery Rate. d=Cohen’s d effect size; VS-I=Visuo-Spatial Index; VE-I=Verbal Expression Index; CDRS-
R=Children’s Depression Rating Scale-Revised; QTE=Questionnaire on Traumatic Experiences in Early
Childhood; BVS-I=Bullying Victimization Severity Index; CI=Confidence Interval; LL=Lower level;
UL=Upper Level. aUncorrected for multiple comparisons p value. *p = < .05; **p = < .01.
47
REFERENCES
Alsaker, F.D. & Gutzwiller-Helenfinger, E. (2010). Social behavior and peer relationships of victims, bully-victims, and bullies in kindergarten. In S.R. Jimerson, S.M. Swearer, & D.L. Espelage (Eds.), Handbook of Bullying in schools: An International Perspective (pp. 87-99). New York: Routledge.
Alsaker, F., & Nägele, C. (2008). Bullying in kindergarten and prevention. In W. Craig & D Pepler (Eds.) An International Perspective on Understanding and Addressing Bullying (Vol. I, pp. 230-252). Kingston, Canada: PREVNet.
Anholt, G. E., van Oppen, P., Emmelkamp, P. M., Cath, D. C., Smit, J. H., van Dyck, R.,
& van Balkom, A. J. (2009). Measuring obsessive-compulsive symptoms: Padua inventory-revised vs. Yale-Brown obsessive compulsive scale. Journal of Anxiety Disorders, 23(6), 830-835.
Badre, D., Kayser, A. S., & D'Esposito, M. (2010). Frontal cortex and the discovery of
abstract action rules. Neuron, 66(2), 315-326. Baron-Cohen, S., Leslie, A. M., & Frith, U. (1985). Does the autistic child have a “Theory
of mind”?. Cognition, 21(1), 37-46. Barrera-Valencia, M., Calderón-Delgado, L., Trejos-Castillo, E., & O’Boyle, M. (2017).
Cognitive profiles of Post-traumatic Stress Disorder and depression in children and adolescents. International Journal of Clinical and Health Psychology, 17(3), 242-250.
Beers, S. R., & De Bellis, M. D. (2002). Neuropsychological function in children with
maltreatment-related posttraumatic stress disorder. American Journal of Psychiatry, 159(3), 483-486.
Bejerot, S. (2007). An autistic dimension: A proposed subtype of obsessive-compulsive
disorder. Autism, 11(2), 101-110. Bejerot, S., & Mörtberg, E. (2009). Do autistic traits play a role in the bullying of obsessive-
compulsive disorder and social phobia sufferers?. Psychopathology, 42(3), 170-176.
Benjamini, Y., & Hochberg, Y. (1995). Controlling the false discovery rate: a practical and powerful approach to multiple testing. Journal of the Royal Statistical Society, 289-300.
Benton, A. L., & Hamsher, K. D. (1976). Multilingual Aphasia Examination. Iowa City:
University of Iowa.
48
Bouchard, C., Solis, I., Pesko, J., Coffman, B., & Ciesielski, K.T.R. (2018). Top-down
inhibitory control of responses to implied biological body motion in children: Right parietal significance. Manuscript submitted for publication.
Bouffard, L. A., & Koeppel, M. D. (2016). Sex Differences in the Health Risk Behavior
Outcomes of Childhood Bullying Victimization. Victims & Offenders, 1-22. Bressler, S. L., Tang, W., Sylvester, C. M., Shulman, G. L., & Corbetta, M. (2008). Top-
down control of human visual cortex by frontal and parietal cortex in anticipatory visual spatial attention. Journal of Neuroscience, 28(40), 10056-10061.
Broidy, L., & Agnew, R. (1997). Gender and crime: A general strain theory perspective.
Journal of Research in Crime and Delinquency, 34(3), 275-306. Bunge, S. A., Dudukovic, N. M., Thomason, M. E., Vaidya, C. J., & Gabrieli, J. D. (2002).
Immature frontal lobe contributions to cognitive control in children: Evidence from fMRI. Neuron, 33(2), 301-311.
Cappadocia, M. C., Weiss, J. A., & Pepler, D. (2012). Bullying experiences among children
and youth with autism spectrum disorders. Journal of Autism and Developmental Disorders, 42(2), 266-277.
Casey-Cannon, S., Hayward, C., & Gowen, K. (2001). Middle-school girls' reports of peer
victimization: Concerns, consequences, and implications. Professional School Counseling, 5(2), 138-1 48.
Chasson, G. S., Timpano, K. R., Greenberg, J. L., Shaw, A., Singer, T., & Wilhelm, S.
(2011). Shared social competence impairment: Another link between the obsessive-compulsive and autism spectrums?. Clinical Psychology Review, 31(4), 653-662.
Ciesielski, K.T.R. (2003). Blue Man N-Back Test: Visual-Spatial Working Memory
Paradigm. Laboratory Manual (NMR, MGH 000929/2003). Boston, Massachusetts: MGH/MIT AA Martinos Center for Biomedical Imaging, Massachusetts General Hospital.
Ciesielski, K. T., Ahlfors, S. P., Bedrick, E. J., Kerwin, A. A., & Hämäläinen, M. S. (2010).
Top-down control of MEG alpha-band activity in children performing Categorical N-Back Task. Neuropsychologia, 48(12), 3573-3579.
Ciesielski, K. T., Hämäläinen, M. S., Geller, D. A., Wilhelm, S., Goldsmith, T. E., &
Ahlfors, S. P. (2007). Dissociation between MEG alpha modulation and performance accuracy on visual working memory task in obsessive compulsive disorder. Human Brain Mapping, 28(12), 1401-1414.
Ciesielski, K. T., Harris, R. J., Hart, B. L., & Pabst, H. F. (1997). Cerebellar hypoplasia
49
and frontal lobe cognitive deficits in disorders of early childhood. Neuropsychologia, 35(5), 643-655.
Ciesielski, K. T., Lesnik, P. G., Savoy, R. L., Grant, E. P., & Ahlfors, S. P. (2006).
Developmental neural networks in children performing a Categorical N-Back Task. Neuroimage, 33(3), 980-990.
Ciesielski, K. T., Rowland, L. M., Harris, R. J., Kerwin, A. A., Reeve, A., & Knight, J. E.
(2011). Increased anterior brain activation to correct responses on high-conflict Stroop task in obsessive–compulsive disorder. Clinical Neurophysiology, 122(1), 107-113.
CNN Library. (2016, March 30). Virginia Tech Shootings Fast Facts. CNN. Retrieved from
http://www.cnn.com Cohen, J. (1988), Statistical Power Analysis for the Behavioral Sciences,
2nd Edition. Hillsdale, N.J.: Lawrence Erlbaum. Cohen, M. X. (2014). Analyzing Neural Time Series Data: Theory and Practice.
Cambridge, Massachusetts: MIT press. Cohen, J.R., Asarnow, R.F., Sabb, F.W., Bilder, R.M., Bookheimer, S.Y., Knowlton,
B.J., & Poldrack, R.A. (2010). Decoding developmental differences and individual variability in response inhibition through predictive analyses across individuals. Front. Hum. Neurosci. 4, 47.
Copeland, W. E., Wolke, D., Angold, A., & Costello, E. J. (2013). Adult psychiatric
outcomes of bullying and being bullied by peers in childhood and adolescence. JAMA Psychiatry, 70(4), 419-426.
Copeland, W. E., Wolke, D., Lereya, S. T., Shanahan, L., Worthman, C., & Costello, E. J.
(2014). Childhood bullying involvement predicts low-grade systemic inflammation into adulthood. Proceedings of the National Academy of Sciences, 111(21), 7570-7575.
Craig, W. M., & Pepler, D. J. (1998). Observations of bullying and victimization in the
school yard. Canadian Journal of School Psychology, 13(2), 41-59. Crone, E. A., & Dahl, R. E. (2012). Understanding adolescence as a period of social–
affective engagement and goal flexibility. Nature Reviews Neuroscience, 13(9), 636.
De Bellis, M. D., Woolley, D. P., & Hooper, S. R. (2013). Neuropsychological findings
in pediatric maltreatment: Relationship of PTSD, dissociative symptoms, and abuse/neglect indices to neurocognitive outcomes. Child Maltreatment, 18(3), 171-183.
50
Delorme, A., & Makeig, S. (2004). EEGLAB: an open source toolbox for analysis of
single-trial EEG dynamics including independent component analysis. Journal of Neuroscience Methods, 134(1), 9-21.
Durston, S., & Casey, B. J. (2006). What have we learned about cognitive development
from neuroimaging?. Neuropsychologia, 44(11), 2149-2157. Durston, S., Thomas, K. M., Yang, Y., Uluğ, A. M., Zimmerman, R. D., & Casey, B. J.
(2002). A neural basis for the development of inhibitory control. Developmental Science, 5(4), F9-F16.
Eisenberg, M. E., Neumark-Sztainer, D., & Story, M. (2003). Associations of weight-based
teasing and emotional well-being among adolescents. Archives of Pediatrics & Adolescent Medicine, 157(8), 733-738.
Eisenberger, N. I., Lieberman, M. D., & Williams, K. D. (2003). Does rejection hurt? An
fMRI study of social exclusion. Science, 302(5643), 290-292. Espelage, D. L., & Holt, M. K. (2001). Bullying and victimization during early
adolescence: Peer influences and psychosocial correlates. Journal of Emotional Abuse, 2(2-3), 123-142.
Fair, D. A., Dosenbach, N. U., Church, J. A., Cohen, A. L., Brahmbhatt, S., Miezin, F.
M., ... & Schlaggar, B. L. (2007). Development of distinct control networks through segregation and integration. Proceedings of the National Academy of Sciences, 104(33), 13507-13512.
Farrington, D. P., Lösel, F., Ttofi, M. M., & Theodorakis, N. (2012). School bullying,
depression and offending behavior later in life: An updated systematic review of longitudinal studies. National Council for Crime Prevention.
Fekkes, M., Pijpers, F. I., & Verloove-Vanhorick, S. P. (2004). Bullying behavior and
associations with psychosomatic complaints and depression in victims. The Journal of Pediatrics, 144(1), 17-22.
Gevins, A., Smith, M. E., McEvoy, L., & Yu, D. (1997). High-resolution EEG mapping of
cortical activation related to working memory: Effects of task difficulty, type of processing, and practice. Cerebral Cortex, 7(4), 374-385.
Gini, G., & Pozzoli, T. (2009). Association between bullying and psychosomatic problems:
A meta-analysis. Pediatrics, 123(3), 1059-1065. Gottesman, I. I., & Gould, T. D. (2003). The endophenotype concept in psychiatry:
etymology and strategic intentions. American Journal of Psychiatry, 160(4), 636-645.
51
Greenberg, B. D., Ziemann, U., Cora-Locatelli, G., Harmon, A., Murphy, D. L., Keel, J.
C., & Wassermann, E. M. (2000). Altered cortical excitability in obsessive–compulsive disorder. Neurology, 54(1), 142-142.
Hodes, R. J., Insel, T. R., & Landis, S. C. (2013). The NIH Toolbox Setting a standard
for biomedical research. Neurology, 80(11 Supplement 3), S1-S1. Hollingshead, A. B. (1975). Four factor index of social status. New Haven, CT: Yale
University; 1975. Unpublished Manuscript. Hughes, T., & Johnson, K. (2015, October 2). Official: Oregon gunman left angry note
glorifying mass killers. USA Today. Retrieved from http://www.usatoday.com Huster, R. J., Enriquez-Geppert, S., Pantev, C., & Bruchmann, M. (2014). Variations in
midcingulate morphology are related to ERP indices of cognitive control. Brain Structure and Function, 219(1), 49-60.
Ilola, A. M., Lempinen, L., Huttunen, J., Ristkari, T., & Sourander, A. (2016). Bullying
and victimisation are common in four-year-old children and are associated with somatic symptoms and conduct and peer problems. Acta Paediatrica, 105(5), 522-528.
Ivarsson, T., & Melin, K. (2008). Autism spectrum traits in children and adolescents with
obsessive-compulsive disorder (OCD). Journal of Anxiety Disorders, 22(6), 969-978.
Juvonen, J., Graham, S., & Schuster, M. A. (2003). Bullying among young adolescents:
The strong, the weak, and the troubled. Pediatrics, 112(6), 1231-1237. Kaltiala-Heino, R., Rimpelä, M., Marttunen, M., Rimpelä, A., & Rantanen, P. (1999).
Bullying, depression, and suicidal ideation in Finnish adolescents: School survey. Bmj, 319(7206), 348-351.
Keneally, M. (2015, October 1). Umpqua Community College Shooting Leaves at Least
10 Dead, Police Say. ABC News. Retrieved from http://www.abcnews.go.com Kim, Y. S., Boyce, W. T., Koh, Y. J., & Leventhal, B. L. (2009). Time trends, trajectories,
and demographic predictors of bullying: A prospective study in Korean adolescents. Journal of Adolescent Health, 45(4), 360-367.
Kim, M. J., Catalano, R. F., Haggerty, K. P., & Abbott, R. D. (2011). Bullying at
elementary school and problem behaviour in young adulthood: A study of bullying, violence and substance use from age 11 to age 21. Criminal Behaviour and Mental Health, 21(2), 136-144.
52
Klimesch, W., Doppelmayr, M., Stadler, W., Pöllhuber, D., Sauseng, P., & Roehm, D. (2001). Episodic retrieval is reflected by a process specific increase in human electroencephalographic theta activity. Neuroscience Letters, 302(1), 49-52.
Klomek, A. B., Marrocco, F., Kleinman, M., Schonfeld, I. S., & Gould, M. S. (2007).
Bullying, depression, and suicidality in adolescents. Journal of the American Academy of Child & Adolescent Psychiatry, 46(1), 40-49.
Knack, J. M., Jensen-Campbell, L. A., & Baum, A. (2011). Worse than sticks and stones?
Bullying is associated with altered HPA axis functioning and poorer health. Brain and Cognition, 77(2), 183-190.
Kochenderfer, B. J., & Ladd, G. W. (1996). Peer victimization: Manifestations and relations to school adjustment in kindergarten. Journal of School Psychology, 34(3), 267-283.
Krause, C. M., Pesonen, M., & Hämäläinen, H. (2010). Brain oscillatory 4–30 Hz
electroencephalogram responses in adolescents during a visual memory task. Neuroreport, 21(11), 767-771.
Krause, C. M., Salminen, P. A., Sillanmäki, L., & Holopainen, I. E. (2001). Event-related
desynchronization and synchronization during a memory task in children. Clinical Neurophysiology, 112(12), 2233-2240.
Liotti, M., & Mayberg, H. S. (2001). The role of functional neuroimaging in the
neuropsychology of depression. Journal of Clinical and Experimental Neuropsychology, 23(1), 121-136.
Loew, T. (2015, October 1). Ten killed in shooting at Ore. community college. USA
Today. Retrieved from http://www.usatoday.com Loth, E., Gómez, J. C., & Happé, F. (2010). When seeing depends on knowing: adults with
autism spectrum conditions show diminished top-down processes in the visual perception of degraded faces but not degraded objects. Neuropsychologia, 48(5), 1227-1236.
Luna, B., Padmanabhan, A., & O’Hearn, K. (2010). What has fMRI told us about the
development of cognitive control through adolescence?. Brain and Cognition, 72(1), 101-113.
Ma, X. (2002). Bullying in middle school: Individual and school characteristics of
victims and offenders. School Effectiveness and School Improvement, 13(1), 63-89.
Mai-Duc, C. (2015, October 2). Gun-obsessed, timid and his mom called him 'baby':
53
What we know of Chris Harper-Mercer's life. Los Angeles Times. Retrieved from http://www.latimes.com
Mason, K. L. (2013). Bullying no more: Understanding and preventing bullying. Barrons
Educational Series, Incorporated. Masten, C. L., Eisenberger, N. I., Pfeifer, J. H., Colich, N. L., & Dapretto, M. (2013).
Associations among pubertal development, empathic ability, and neural responses while witnessing peer rejection in adolescence. Child Development, 84(4), 1338-1354.
MATLAB, U. S. G. The MathWorks, Inc., Natick, MA 01760, 1994–2001. McCabe, R. E., Antony, M. M., Summerfeldt, L. J., Liss, A., & Swinson, R. P. (2003).
Preliminary examination of the relationship between anxiety disorders in adults and self-reported history of teasing or bullying experiences. Cognitive Behaviour Therapy, 32(4), 187-193.
Meng, L., & Xiang, J. (2016). Frequency specific patterns of resting-state networks
development from childhood to adolescence: A magnetoencephalography study. Brain and Development, 38(10), 893-902.
Nansel, T. R., Overpeck, M., Pilla, R. S., Ruan, W. J., Simons-Morton, B., & Scheidt, P.
(2001). Bullying behaviors among US youth: Prevalence and association with psychosocial adjustment. Jama, 285(16), 2094-2100.
Newman, M. L., Holden, G. W., & Delville, Y. (2005). Isolation and the stress of being bullied. Journal of Adolescence, 28(3), 343-357. Newton, V., Solis, I., Aviña, G. E., McClain, J. T., King, C., & Ciesielski, K. T. R.
(2017). Analysis of social interaction narratives in unaffected siblings of children with ASD through Latent Dirichlet Allocation. In International Conference on Augmented Cognition (pp. 357-371). Springer, Cham.
Nishina, A., Juvonen, J., & Witkow, M. R. (2005). Sticks and stones may break my
bones, but names will make me feel sick: The psychosocial, somatic, and scholastic consequences of peer harassment. Journal of Clinical Child and Adolescent Psychology, 34(1), 37-48.
Nunez, P. L., Wingeier, B. M., & Silberstein, R. B. (2001). Spatial-temporal structures of
human alpha rhythms: theory, microcurrent sources, multiscale measurements, and global binding of local networks. Human Brain Mapping, 13(3), 125-164.
Olweus, D. (1978). Aggression in the Schools: Bullies and Whipping Boys. Oxford,
England: Hemisphere.
54
Olweus, D. (1993). Victimization by peers: Antecedents and long-term outcomes. Social Withdrawal, Inhibition, and Shyness in Childhood, 315, 341.
Ordaz, S. J., Foran, W., Velanova, K., & Luna, B. (2013). Longitudinal growth curves of
brain function underlying inhibitory control through adolescence. Journal of Neuroscience, 33(46), 18109-18124.
Osterrieth, P. A. (1993). Psychological examination of traumatic encephalopathy. (J.
Corwin & F.W. Bylsma, trans.). The Clinical Neuropsychologist, 7, 9-15. (Original work published 1944)
Pepler, D. J., Craig, W. M., Connolly, J. A., Yuile, A., McMaster, L., & Jiang, D. (2006).
A developmental perspective on bullying. Aggressive Behavior, 32(4), 376-384. Pepler, D., Jiang, D., Craig, W., & Connolly, J. (2008). Developmental trajectories of
bullying and associated factors. Child Development, 79(2), 325-338. Poznanski, E. O., & Mokros, H. B. (1996). Children's Depression Rating Scale, Revised
(CDRS-R). Los Angeles: Western Psychological Services. Ranney, M. L., Patena, J. V., Nugent, N., Spirito, A., Boyer, E., Zatzick, D., &
Cunningham, R. (2016). PTSD, cyberbullying and peer violence: Prevalence and correlates among adolescent emergency department patients. General Hospital Psychiatry, 39, 32-38.
Rey, A. (1993). Psychological examination of traumatic encephalopathy. (J. Corwin &
F.W. Bylsma, trans.). The Clinical Neuropsychologist, 7, 9-15. (Original work published 1941)
Rigby, K., & Slee, P. (1999). Suicidal ideation among adolescent school children,
involvement in bully—victim problems, and perceived social support. Suicide and Life-Threatening Behavior, 29(2), 119-130.
Rivers, I., & Noret, N. (2010). Participant roles in bullying behavior and their association
with thoughts of ending one’s life. Crisis, 31, 143-38. Rivers, I., Poteat, V. P., Noret, N., & Ashurst, N. (2009). Observing bullying at school:
The mental health implications of witness status. School Psychology Quarterly, 24(4), 211.
Rosen, P. J., Milich, R., & Harris, M. J. (2007). Victims of their own cognitions: Implicit
social cognitions, emotional distress, and peer victimization. Journal of Applied Developmental Psychology, 28(3), 211-226.
Rudolph, K. D., Troop-Gordon, W., & Granger, D. A. (2011). Individual differences in
55
biological stress responses moderate the contribution of early peer victimization to subsequent depressive symptoms. Psychopharmacology, 214(1), 209-219.
Rutter, M., Bailey, A., & Lord, C. (2003). SCQ: The Social Communication
Questionnaire. Torrance, CA: Western Psychological Services. Salmivalli, C., Lagerspetz, K., Björkqvist, K., Österman, K., & Kaukiainen, A. (1996).
Bullying as a group process: Participant roles and their relations to social status within the group. Aggressive Behavior, 22(1), 1-15.
Scahill, L., Riddle, M. A., McSwiggin-Hardin, M., Ort, S. I., King, R. A., Goodman, W.
K., ... & Leckman, J. F. (1997). Children's Yale-Brown obsessive compulsive scale: Reliability and validity. Journal of the American Academy of Child & Adolescent Psychiatry, 36(6), 844-852.
Schaefer, A., Margulies, D. S., Lohmann, G., Gorgolewski, K. J., Smallwood, J., Kiebel,
S. J., & Villringer, A. (2014). Dynamic network participation of functional connectivity hubs assessed by resting-state fMRI. Frontiers in Human Neuroscience, 8, 195.
Scheithauer, H., Hayer, T., Petermann, F., & Jugert, G. (2006). Physical, verbal, and
relational forms of bullying among German students: Age trends, gender differences, and correlates. Aggressive Behavior, 32(3), 261-275.
Schreier, A., Wolke, D., Thomas, K., Horwood, J., Hollis, C., Gunnell, D., ... & Salvi, G.
(2009). Prospective study of peer victimization in childhood and psychotic symptoms in a nonclinical population at age 12 years. Archives of General Psychiatry, 66(5), 527-536.
Sedensky III, S. J. (2013). Report of the state’s attorney for the judicial district of Danbury
on the shootings at Sandy Hook Elementary School. Newtown, Connecticut. Sharp, S. (1995). How much does bullying hurt? The effects of bullying on the personal
wellbeing and educational progress of secondary aged students. Educational and Child Psychology, 12(2), 81-88.
Shepherd, J. P., Sutherland, I., & Newcombe, R. G. (2006). Relations between alcohol,
violence and victimization in adolescence. Journal of Adolescence, 29(4), 539-553. Srabstein, J. C. (2013). News reports of bullying-related fatal and nonfatal injuries in the
Americas. Revista Panamericana de Salud Publica, 33(5), 378-382. Stephen, J. M., Ranken, D. F., & Aine, C. J. (2006). Frequency-following and
connectivity of different visual areas in response to contrast-reversal stimulation. Brain Topography, 18(4), 257.
56
Sterzing, P. R., Shattuck, P. T., Narendorf, S. C., Wagner, M., & Cooper, B. P. (2012). Bullying involvement and autism spectrum disorders: prevalence and correlates of bullying involvement among adolescents with an autism spectrum disorder. Archives of Pediatrics & Adolescent Medicine, 166(11), 1058-1064.
Stevens, M. C. (2016). The contributions of resting state and task-based functional
connectivity studies to our understanding of adolescent brain network maturation. Neuroscience & Biobehavioral Reviews, 70, 13-32.
Taylor, M. J., Chevalier, H., & Lobaugh, N. J. (2003). Discrimination of single features
and conjunctions by children. International Journal of Psychophysiology, 51(1), 85-95.
Tretiak, O., & Ciesielski, K.R. (2014). Questionnaire on Traumatic Experiences in Early
Childhood. Unpublished manuscript, Department of Psychology, University of New Mexico, Albuquerque, New Mexico.
Vaillancourt, T., Duku, E., Becker, S., Schmidt, L. A., Nicol, J., Muir, C., & MacMillan,
H. (2011). Peer victimization, depressive symptoms, and high salivary cortisol predict poorer memory in children. Brain and Cognition, 77(2), 191-199.
van den Wildenberg, W. P., & van der Molen, M. W. (2004). Additive factors analysis of
inhibitory processing in the stop-signal paradigm. Brain and Cognition, 56(2), 253-266.
Van Roekel, E., Scholte, R. H., & Didden, R. (2010). Bullying among adolescents with
autism spectrum disorders: Prevalence and perception. Journal of Autism and Developmental Disorders, 40(1), 63-73.
Vasilevski, V., & Tucker, A. (2016). Wide-ranging cognitive deficits in adolescents
following early life maltreatment. Neuropsychology, 30(2), 239. Veenstra, R., Lindenberg, S., Oldehinkel, A. J., De Winter, A. F., Verhulst, F. C., & Ormel,
J. (2005). Bullying and victimization in elementary schools: A comparison of bullies, victims, bully/victims, and uninvolved preadolescents. Developmental Psychology, 41(4), 672.
Wang, J., Iannotti, R. J., & Nansel, T. R. (2009). School bullying among adolescents in the United States: Physical, verbal, relational, and cyber. Journal of Adolescent Health, 45, 368–375.
Wechsler, D. (2011). Wechsler Abbreviated Scale of Intelligence–Second Edition Manual. Bloomington, MN: Pearson.
Will, G. J., Crone, E. A., van Lier, P. A., & Güroğlu, B. (2016). Neural correlates of
57
retaliatory and prosocial reactions to social exclusion: associations with chronic peer rejection. Developmental Cognitive Neuroscience, 19, 288-297.
Williams, K., Chambers, M., Logan, S., & Robinson, D. (1996). Association of common
health symptoms with bullying in primary school children. BMJ, 313(7048), 17-19. Wilson, K. R., Hansen, D. J., & Li, M. (2011). The traumatic stress response in child
maltreatment and resultant neuropsychological effects. Aggression and Violent Behavior, 16(2), 87-97.
Wolke, D., Woods, S., Bloomfield, L., & Karstadt, L. (2001). Bullying involvement in
primary school and common health problems. Archives of Disease in Childhood, 85(3), 197-201.
Zandt, F., Prior, M., & Kyrios, M. (2007). Repetitive behaviour in children with high
functioning autism and obsessive compulsive disorder. Journal of Autism and Developmental Disorders, 37(2), 251-259.
Zwierzynska, K., Wolke, D., & Lereya, T. S. (2013). Peer victimization in childhood and
internalizing problems in adolescence: a prospective longitudinal study. Journal of Abnormal Child Psychology, 41(2), 309-323.
Zych I., Farrington D.P., Llorent V.J., Ttofi M.M. (2017) School Bullying in
Different Countries: Prevalence, Risk Factors, and Short-Term Outcomes. In: Protecting Children Against Bullying and Its Consequences. SpringerBriefs in Psychology: Springer, Cham.