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Fall, 2014
Psychology 354
Psychopathology I: Child and Adolescent Psychopathology
Instructor: Rex Forehand, Ph.D.
Tuesday 8:30 – 11:15
Overview
This course will provide an introduction to the field of psychopathology during childhood and
adolescence. Topics will include systems of classification and taxonomy in psychopathology,
research methods in developmental psychopathology, epidemiology, etiology, course, risk and
protective factors, and specific problems and disorders of childhood and adolescence.
Throughout the course a developmental perspective will be emphasized by examining
psychological problems and disorders within the context of biological, psychological, and social
developmental processes. The importance of empirical research in studying psychopathology
will also be emphasized. You should leave this course with (a) a solid foundation in research in
child and adolescent psychopathology, and (b) the ability to apply research in this field to
understanding individual cases and to your own research.
Books and Readings:
The text for the course will be:
1. Mash, E.J., & Barkley, R.A. (2014). Child Psychopathology (3rd Edition). New
York: Guilford.
2. A duplicated book of course notes and outside readings.
3. DSM-5
Class Structure
Most (but not all) classes will be structured as follows:
1. Description of Disorder
2. Causal Factors
3. Model Development
Course Evaluation and Grades
Course grades will be based on the following:
1. Class participation (students are expected to be on time, attend all classes, to complete all
assigned readings before the class, and to participate in class). I need to know before
class if you have an illness or emergency that prevents you from attending.
2. A weekly report on the percent variance accounted for by each of four categories of
correlates/risk/marker/causal risk factors (See Table 1 in Kazdin et al. distributed article)
and page 8 for each of 10 disorders (ADHD, ODD, Conduct Disorder, Adolescent
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Alcohol Abuse, Depression, Enuresis, Anxiety, Anorexia, Intellectual Disability,
Autism). The report (see last 4 pages of syllabus for 2 examples) should be a singlespaced (with double spacing between paragraphs) typed paper which includes: (a) a
summary of the percent variance accounted for by each of the 4 categories; and (b) a
justification of why you assigned the percent variance to each category. Your
justification should be based on the DSM-5, the Mash and Barkley assigned reading, any
outside readings assigned, and any additional articles you may choose to read on the
disorder. You will turn these in each week and selected class members will present each
week. Please bring a copy of your summary to class for me, the “coordinator” of the
week, and yourself.
You will email your percent variance to the “coordinator” by Monday noon before class.
The “coordinator” will put the percent variance for each of you on the template sheet,
calculate means, pass out to everyone during class, and summarize. See page 6 for a list
of coordinators by week.
3. Class presentations: Each student will make two additional kinds of presentations.
a. Summary of a research article I distribute (see page 6 for list of presenters and
articles). Your presentation should be 7 to 10 minutes, and include the study title,
journal, authors, purpose, hypotheses, brief methodology, results, and
conclusions. IMPORTANT: Point out why this study is important for the
particular disorder we are examining. You can either do a PowerPoint
presentation (have a copy of the slides for each class member) or summarize the
study verbally with a summary page of the study for each class member.
Individuals presenting were randomly determined.
b. A 20- to 30-minute PowerPoint presentation (see page 7 for time and date for
each student presentation) in one of the last two classes on an assigned chapter.
Your presentation should consist of: definition and description of disorder or topic
area, prevalence, causes, and developmental models on disorder(s). Distribute
your slides to all class members. Your presentation should be a “formal” one
(e.g., Power Point).
4. Second-year students (those who have had assessment) also will make a 2-minute
presentation of the primary assessment instruments used for each disorder. You should
be able to do this based on your assessment classes and discussing with graduate students
and faculty members who are experts in the area. Prepare a ½-page handout (12 copies)
to hand out in class. This is to introduce first-year students to the primary assessment
instruments for children. See page 6 for date of your presentation.
5. Exams: There will be two exams involving the application of course material. Each
exam will consist of one or, more likely, two vignettes and you will answer them in 4
typed pages (and double spaced) in a take home exam.
6. Course Grade: Number 1 above:
Number 2 above:
Number 3 above: A
B
15%
20%
(part of Number 1: Class Participation)
15%
2
Number 5 above:
50% (25% per exam)
7. NOTE: There is one “extra class” at the end in case we don’t get through all the material
or in case I have to “call off” a class. If the latter occurs, we will move everything back
one week except Rob Althoff, who has to come on 10/28.
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Schedule*
Mash & Barkley
Book Readings
(Chapters)
8/26
Overview, Introduction
9/2
Developmental Psychopathology:
Overview of Causes, Classification
1
9/9
Attention Deficit Hyperactivity Disorder
(Neurodevelopmental Disorder)
2
9/16
Oppositional Defiant Disorder/
3
Conduct Disorder
(Disruptive Impulse-Control, & Conduct Disorders)
9/23
Conduct Disorder Continued and
Development & Psychopathology in
Adolescence: (Substance Related)
4
(Substance-Related & Addictive Disorders)
(Take Home Exam)
Read
DSM-5
Outside Reading
(Assignments are in
Outside Readings Book
each week)
ADHD
ODD, Impulse
Control, CD
SubstanceRelated & Addictive
9/26 (Friday) Grand Rounds: Martha Wadsworth (10:30-11:45)
9/30
Anxiety Disorders
Obsessive-Compulsive Disorder
(Turn in Exam Before Class)
10/7
Tic Disorders & Hair-Pulling
(Justin Parent – 8:30 – 9:10)
Depressive Disorders
8
Anxiety
9 (Just OCD part of chapter) Obsessive-Compulsive
Remainder Chapter 9
5
Depressive Disorders
10/14
Feeding & Eating Disorders
(Anorexia Nervosa & Bulimia Nervosa)
16
Feeding & Eating
10/21
Intellectual Disability
(Neurodevelopmental Disorder)
12
Intellectual Disabilities
10/28
Pediatric Bipolar & Disruptive Mood
Dysregulation
(Dr. Rob Althoff-8:30 – 9:30);
Enuresis, Encopresis
(Elimination Disorders)
6
Bipolar, Enuresis,
Encopresis
11/4
Autism Spectrum Disorders
(Neurodevelopmental Disorder)
11
11/11
Presentations (1 - 3 – see page 7)
19 (5 pages on Encopresis
& Enuresis)
Autism Spectrum
4
11/18
Presentations (4 - 7 – see page 7)
11/25
Thanksgiving
12/2
Make-up class
(Take Home Exam: Due Monday, 12/8, by noon)
___________________
*Note: There is a required colloquium scheduled during the semester (9/26) and may be more scheduled.
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1.
Research Article Presentations*
Date
Topic
Presenter
Research Article
8/26
2.
Overview of
Assessment
Instruments
3,
Coordinators*
Coordinator
% Variance
Sarah
9/9
Developmental
Trajectories
Kelsey
(Miller)
9/16
ADHD
Hannah
(Bauermeister)
Hannah
Sarah
9/23
ODD/CD
Virginia
1 (Lahey)
Kelsey
Emily
(2 articles)
2 (Cunningham)
Elias
1 (Martel)
Elias
Joanna
Ivori
2 (Maumorstein)
9/30
Substance Use
10/7
Anxiety
Geoff
(Feng)
Emily
Kelsey
10/14
Depression
Jonah
Jonah
Hannah
Kerry
1 (Koffler) (Please include 3
models on page 459)
2 (Gallerani)
Geoff
Virginia
10/21
Eating Disorder
Joanna
(Measelle)
10/28
Enuresis
None
None
11/4
Intellectual
Emily
(Einfeld)
Kelsey
Kerry
Sarah
(Landa)
Hannah
Jonah
Disability
11/11
Autism
*NOTE: Research article presentations, overview of assessment instruments, and coordinators for %
variance are independent (i.e., unrelated) activities that were put on the same page to save space.
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Presentations on November 11 (#s 1-4) and December 18 (#s 5-7)*
Name
Topic
Time Allocated
1.
A. Jonah
Chapter 7 (Suicidal & Non-Suicidal Self-Injurious)
30 minutes
2.
A. Virginia
B. Emily
Chapter 10 (Childhood PTSD)
20 minutes
20 minutes
3.
A. Kelsey (Sleep)
B. Kerry
Chapter 14 (Infancy & Toddlerhood: ½ on Sleep)
20 minutes
20 minutes
4.
A. Sarah
Chapter 17 (Early Onset Schizophrenia)
30 minutes
5.
A. Ivori
B. Hannah
Chapter 13 (Learning Disabilities)
20 minutes
20 minutes
6.
A. Joanna
B. Geoff
Chapter 18 (Personality Disorders)
20 minutes
20 minutes
7.
A. Elias
Chapter 19 (Health-Related & Somatic: Selected Parts)
30 minutes
*When there are 2 presenters, you decide where to divide the chapter.
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Categories of Correlates/Risk/Marker/Causal Risk Factors and Examples of Each
1. Temperament/Genetics: Biological and genetic factors – includes child characteristics such as
gender and race.
2. Family Characteristics
(a) Parenting
(1) warmth/positive dimension
(2) consistent discipline
(3) structure (rules, supervision, monitoring)
(4) psychological control (guilt induction, verbal manipulation)
(b)
(c)
(d)
(e)
SES
# siblings
2 parents vs 1 parent (divorce)
family stress
1. conflict (between parents, between siblings, between parent & child)
2. parent depressive symptoms
3. parent antisocial personality
4. parent physical illness
3. Extrafamilial (peers, school, immediate neighborhood)
(a) peers
(b) school
1. general environment
2. teacher variables
(c) neighborhood
1. risks
2. resources
3. population density (rural/urban)
4. Culture/Society
(a) differences by “cultural” groups
(b) differences
1. across regions of country
2. across countries
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Percent Variance Accounted for By
(1)
Disorders
Temperament/
Genetics/Child
(2)
Family
Characteristics
(3)
Peers/School/Community
(4)
Culture/Society
Total
ADHD
100
ODD
100
CD
100
Alcohol Abuse
100
Depression
100
Enuresis
100
Anxiety
100
Anorexia
100
Intellectual Disability
100
Autism Spectrum
100
NOTE: No Percent Variance for Disruptive Mood Dysregulation, Bipolar, Obsessive-Compulsive, Encopresis, or Bulimia.
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Child Psychopathology
Percent Variance: Eating Disorders
Temperament/
Genetics/Child
50%
Family
Characteristics
20%
Peers/School/
Community
10%
Cultural/Society
20%
Research has pointed to a definite biological and genetic vulnerability in developing eating
disorders. Neuroendocrine studies have shown low levels of norepinephrine in patients with anorexia
nervosa (AN) and bulimia nervosa (BN), although it is not clear if this is a cause or result of the
disorders (Mash & Barkley, 2003). In BN, on the other hand, individuals may suffer from a
hyposerotonergic functioning causing an increase in meal size and the binging behaviors seen (Mash &
Barkley, 2003). The genetic component of eating disorders has been studies through family studies and
an increased risk for eating disorders has been found in relatives of individuals with AN and BN (Mash
& Barkley, 2003). One study’s findings indicate that more than 50% of the risk for developing AN can
be attributed to genetics (Tyre, 2005). Temperament is an impacting factor as well with perfectionism
being the main trait associated with both AN and BN. Individuals with AN also have a tendency to
conform, have an obsessive nature to them and an overcontrol of their emotionality. I think that child
characteristics play a larger role in eating disorders than any of the other disorders that we have looked
at thus far. Females have a much greater likelihood of developing eating disorders than males, with
clinical samples of eating disorder patients showing 90 – 95% female (Mash & Barkley, 2003).
Ethnicity is a risk factor as eating disorders occur mainly in white females, although recent research has
shown that rates in black, Hispanic and Asian populations are rising (Tyre, 2005). Sexual orientation is
another child characteristic that plays a role. Homosexuality is a risk factor for development in males,
while in females this may serve as a protective factor (Mash & Barkley, 2003). In females, an early
menarche is a specific risk factor for BN (Mash & Barkley, 2003). With these findings on the biological
and genetic impact, the influence of temperament and the contribution of child characteristics, I have
placed 50% of the variance in this category.
Additionally, certain family environments put individuals at a greater risk for the development of
eating disorders. In general, modeling of family members in terms of weight preoccupation and dieting,
valuing thinness and having control over weight are all risk factors for the development of eating
disorders (Mash & Barkley, 2003). One study looking specifically at BN found that families who tend
to comment on the patients’ weight, shape or eating habits put these individuals at risk for the disorder,
as well as tension or lack of attendance at family meals (Mash & Barkley, 2003). Research continues to
be done on family interactions, and although most are inconclusive, there does seem to be a greater
enmeshment, or overinvolvement, in families of patients with eating disorders, indicating that this type
of home environment may put individuals at risk (Mash & Barkley, 2003). Fami8ly influences do
appear to play a role in the development of eating disorders, although not to the degree that had been
thought in the past due to the newer research on the biological vulnerability to the disorders. Therefore,
I allotted 20% variance to this category.
Research done on eating disorders has shown that culture has an influence on their development.
As cultures become more “Westernized,” rates increase indicating the impact of the socially constructed
Western ideal of thinness on the disorders (Mash & Barkley, 2003). The idea of beauty and
interpersonal nature being feminine traits contributes to this socialization and is a function of our society
today (Mash & Barkley, 2003). I consider this cultural influence to have a considerable impact on the
development of AN and BN and have therefore placed 20% of the variance into the category of cultural
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and society factors. Intertwined with this is the role of peers, school and community. Although there
does not seem to be specific research on the impact of these factors, they go hand-in-hand with the
overall social construction of the disorder. Environments where the cultural value of thinness and
beauty are clearly demonstrated (in peers, school and social environments) put the individuals in them at
greater risk for internalizing these values and for developing the disorders. Despite the lack of research
on this category, my beliefs about these influences have caused me to place 10% of the variance in peer,
school and community factors.
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Percent Variance: Generalized Anxiety Disorder
Temperament/Genetics/Child: 50%
Family Characteristics: 30%
Peers/School/Community: 10%
Cultural/Society: 10%
Anxiety is one of the most commonly diagnosed disorders in childhood and adolescence, and research has
demonstrated its complex etiological profile (Mash & Barkley, 2003). As is the case with so many psychological
disorders, the factors contributing to the etiology of anxiety in youth often interact with one another to form
bidirectional and multidirectional causal pathways. Generalized Anxiety Disorder (GAD) is among the commonly
seen types of anxiety disorders; one epidemiological study found a GAD prevalence of 5.9% in a sample of 15
year-old adolescents and another reported rates as high as 10.8% (Mash & Barkley, 2003). The factors associated
with the etiology of GAD are discussed below.
Given the evidence for the considerable contributions of genetics, temperament, and other child-specific
factors to the etiology of GAD, I have allocated 50% of the variance to the Temperament/Genetics/Child
category. Mash & Barkley (2003) discuss the evidence related to genetics and anxiety in general, namely that
although heritability of specific anxiety disorders is unlikely, genes are thought to contribute to a general risk
factor for anxiety proneness. Specifically, Mash & Barkley (2003) indicate that genetics may present a general
risk factor for anxiety disorders, but environmental experiences influence how this vulnerability manifests
(similar to the diathesis-stress model of depression). Evidence for the general heritability of anxiety as it relates to
GAD is presented in the case study of Matthew (Anxiety and Somatoform Disorders). In this example, both of
Matthew’s parents displayed some symptoms of anxiety; while neither parent had GAD specifically, the presence
of genes related to the vulnerability for anxiety in parents may contribute to the development of GAD in children
(psychosocial factors will be discussed below). Furthermore, research has shown that GAD is diagnosed more
commonly in females than in males, and that this finding is stable across cultures (Anxiety and Somatoform
Disorders; Mash & Barkley, 2003). While social factors related to this finding are likely, it is possible that this
reflects a sex-linked characteristic of the genes related to a vulnerability for anxiety. There is also considerable
evidence for the contributions of temperament to the etiology of anxiety disorders. While Mash & Barkley (2003)
present this evidence in the context of anxiety disorders in general, given the pervasive nature of GAD it is likely
that these factors are relevant to this disorder. Behavioral Inhibition has been proposed as a likely underlying
temperamental characteristic of children who present with anxiety disorders (Mash & Barkley, 2003). The
Behavioral Inhibition profile consists of the child’s sociability, physiology, and shy or fearful behaviors, and
Mash & Barkley (2003) cite longitudinal evidence that this temperamental style is associated with those behaviors
consistent with anxiety in children. Again, although these findings are not specific to GAD, the excessive and
uncontrollable nature of worries in GAD may be related to factors that have widespread influence (i.e.,
temperament). Furthermore, Mash & Barkley (2003) discuss the biobehavioral system thought to be associated
with the Behavioral Inhibition temperament, namely the Behavioral Inhibition System (BIS). This is a complex
system of nervous system components that is associated with (among other things) increased caution and
processing of threat-relevant information (Mash & Barkley, 2003). Thus, this system may contribute to the
symptoms of GAD. In addition to the contributions of genetics and temperament, child-specific factors such as
cognitive style may play a role in the etiology of GAD (Mash & Barkley, 2003). Finally, cognitive processes have
been found to contribute to the etiology of GAD in children. Children with GAD tend to overestimate the
likelihood of negative consequences and worry in the absence of objective cause for concern (Mash & Barkley,
2003). These types of thought patterns and information processing biases represent cognitive distortions that may
vary among children, and constitute the psychological vulnerability patterns discussed in Mash & Barkley (2003).
I have allocated 30% of the variance associated with the etiology of GAD to the Family Characteristics
category. The findings related to the heritability of general genetic risk factors for anxiety must take into account
the psychosocial aspects of the family unit, as environmental influences may be at work (Mash & Barkley, 2003).
As discussed above, unique environmental experiences work to determine the expression of this genetic
vulnerability, and in children and adolescences these experiences are likely to stem from the family unit. As
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referenced above, the case of study of Matthew in Anxiety and Somatoform Disorders demonstrates how parental
symptoms of anxiety may be related to GAD in children. While this may be due to genetics, it may also be due to
parenting behaviors or other aspects of the family environment that are common to both parents and children.
Furthermore, Mash & Barkley (2003) discuss the important role of attachment in the etiology of anxiety, and
point to findings indicating that insufficient affection from caregivers played a role in the development of GAD in
children. Parenting behaviors also contribute to the etiology of GAD, as parents can condition processes in their
children—such as cognitive schemas—that increase anxious cognitions (Mash & Barkley, 2003). For example, as
discussed in Anxiety and Somatoform Disorders, when parents model or exhibit anxious responses, or reinforce
any avoidant or anxious behaviors in their children, they may set the foundation for the development of more
persistent or severe symptoms of anxiety. Relating more generally to anxiety, Mash & Barkley (2003) note that
child anxiety disorders are significantly influenced by parents’ anxiety. Furthermore, they discuss how children’s
experience with anxiety may be related to past experiences with control (Mash & Barkley, 2003). For children
and adolescents, situations in which they have felt out of control may have occurred within the family unit (e.g.,
experiences with domestic violence).
Regarding extrafamilial contributions to the etiology of GAD, I have allocated 10% of the variance to the
Peers/School/Community category. The finding that GAD has been found to be unstable over time indicates that
there are environmental factors at work (Mash & Barkley, 2003). This is related to the general finding presented
above that unique environmental influences impact how genetic and psychological vulnerabilities come to
manifest in the presentation of anxiety disorders; it is possible that these environmental influences stem from a
child’s peer group, school, or community (Mash & Barkley, 2003). In addition, events relating to a child’s
experience of control may stem in part from the peer group, school, or community (Mash & Barkley, 2003).
There may also be influences of peer relationships on GAD; these factors might not cause GAD per se but may
work to exacerbate a child’s symptoms. For example, a child with GAD who requires frequent reassurance and
experiences persistent worries regarding peer interactions may actually be rejected by his or her peers, thus
resulting in a bidirectional relationship between child-specific factors and the peer group (Mash & Barkley, 2003).
Given the gender differences found in the diagnosis of anxiety disorders, it is possible that peer groups are
influencing the expression of anxiety symptoms in children (Mash & Barkley, 2003). Finally, Mash & Barkley
(2003) cite evidence that children with OAD (now represented by GAD) come from middle or upper income
families, indicating some effect of SES on GAD in children.
In my opinion, the cultural influences on GAD stem largely from those relating to anxiety in general. I
have allocated 10% of the variance associated with the etiology of GAD to the Cultural/Society category, largely
due to the discussion presented by Mash & Barkley (2003) regarding the acceptability of fear expression across
cultures. These differences may influence the extent to which fears are expressed—and, to some extent, the ways
in which fears are experienced or perceived to be experienced among individuals. Furthermore, the finding that
GAD is diagnosed more commonly in females than males across cultures speaks to the widespread influence of
societally-determined gender norms among a variety of cultures (Anxiety and Somatoform Disorders). Finally, as
discussed in Anxiety and Somatoform Disorders, the presentation of GAD varies by age (i.e., in terms of what
children worry about). Culture may therefore influence the content and severity of worries at a given
developmental stage, which would influence how children experience their own anxiety in addition to the
diagnosis and progression of GAD symptoms over time.
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