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21 Cards in this Set

  • Front
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4. What does the research suggest regarding the course and outcome of Autism?
Autisim outcome is variable:
-1 to 3% do great
-5 to 25% can support themselves and live independently
-60 to 75% or more are not doing so well. They will need to be dependent upon others for their entire lives.
-Initial severity, IQ, and early language ability are predictors of autism outcome
- If an autistic kid can speak by 4 yrs, the prognosis will be better than if they don't
-The more severe the early symptoms, the worse the prognosis
-If there is an institutional placement or clear organic medical condition for the autistic kid, prognosis is worse.
-parent's commitment to rigorous treatment improves autism prognosis.

Howlin (2004)
- the findings also showed that, although
having an IQ of at least 70 is a crucial
prognostic factor, above this level outcome can still
be very variable
-Thus, although having a childhood IQ within
the normal range is clearly a crucial factor in determining
outcome, within this sub-group the presence
of ritualistic and/or stereotyped behaviours may still
prevent individuals from attaining an optimal level of
-One of the most significant factors determining
outcome appears to be level of intellectual functioning
in childhood, and IQ scores, tend to remain relatively stable over
time. Nevertheless, even within this higher
functioning group, outcome tends to be very variable
and it seems that the fundamental deficits associated
with autism, in particular the degree of ritualistic
and stereotyped behaviours, may at times
swamp the effects of a relatively high IQ
-In addition,
despite the relatively small changes in IQ
overall, in a minority of cases there were considerable
changes in IQ levels (both upwards and downwards)
over time.
-Finally, the ability to function adequately in
adulthood life may depend as much on the degree of
support offered (by families, employment and social
services) as on basic intelligence
10. NEED TO LOOK AT THIS FURTHER There are 4 possible explanations for "true" comorbidity. (Angold**) Make an empirically informed argument for precisely how each of these 4 explanations may account for the comorbidity of depression and Conduct Disorder/delinquency, ODD/antisocial behavior.
The four possible explanations for true comorbidity:
1. shared risk factors
2. separate but co-occurring risk factors
3. one disorder creates the risk factor for the development of the other disorder
4. the comorbid pair is different from both pure groups (and should consequently be considered a separate disorder.

1. Shared RF: genetic influences, parent's psychopath
-Subbaro (2008)- It seems that CD and depression share genetic RF (and non-shared environmental influence).
-Parents Psychopath: Parents of CD kids tend to have high rates of mom depression, antisocial PD in eaither parent, father's substance abuse
-Ollendick (2006)-Overall,
according to the model, common risk factors give rise
to either disorder, while unique factors differentiate
between these conditions. Various combinations of
these unique and common risk factors may contribute
to comorbidity
Marmostein and Iacano - looked at family relationship risk factors and tried to determine which were common to CD and depression. The three common risk factors that they discovered were: mom's depression, dad's antisocial, and parent-child conflict.
-In a study that used depr and CD checklists the two biggest risk factors (in girls and boys) for co-occuring depression and delinquency were: stressful life events, early childhood externalizing behavior. The also found that >60% of the covariation between these symptoms was due to common risk factors.

2. Seperate but co-occuring RF:
-(For example: Depression RF from mom & Antisocial RF from dad = Comorbid depression & Conduct disorder)
-In Kopp & Beachaine (2007):
Both mom's depression and dad's antisocial were independently related to kids Depression & to Kid's CD; An interaction was evident in which Dad's antisocial was related to CD no matter what mom's level of depression; kids in the depression group did not differ in mom's depression from those in CD group which suggests that depression may be a common RF.
*Seperate but co-occuriing RF- kids in comorbid depress/CD grp were more likely to have dads with antisocial and moms w/ depression relative to CD only, controls, or depression only.

3. One disorder predates the risk for another one.
(For example, CD->peer reject->depression)
In Ingoldsby (2006): Kids in the CD & depression comorbid group had poorer academic and social competence over 2 yrs; their sxn persisted over time, had more severe sxn and worse outcomes than kids with just CD or just depr
-(Kreager: looked at genetic and environmntal influences on substance abuse and found common genetic factors accounting for substance abuse and antisocial). Not so sure about this one.

Here is info for the the comorbid pair is different from both pure groups idea:
How does comorbid pair differ from both the pure groups??
Ezpeleta et al. 2006: (disorders in outpatient 8-17 year olds in
Spain; DEP only; CD/ODD only; and BOTH CD/ODD and DEP)
Review Past studies:
Comorbid in comparison to DEP: more substance abuse; worse
outcomes; fewer emotional problems/symptoms
Comorbid in comparison to CD: More suicide attempts, substance
abuse, worse outcomes (but many studies say similar outcomes),
less aggressive;
Comorbid in comparison to pure CD or DEP: More impaired, poorer
school achievement, lower social competence.
-Few differences in other disorders (ADHD, SEPAX, GAD) between gps. In other words, Comorbid grp did not have higher rates of ADHD or sep anxiety.

Comorbid grp Higher than DEP on 8/11 CBCL scales; but Comorbid
group only higher than CD on a few (anx/dep, somatic, and
--Comorbid more impaired than CD on all global
impairment/functioning measures, psychopathology, mood, and selfharm;
Comorbid more impaired than DEP on only one of the 4
impairment/functioning measures, school, home, relationships with
See Table, page 710, for summary:
--Comorbid in comparison to CD: More angry and resentful, used
weapons less, set fires more, more somatic complaints and anxiety
and more functionally impaired
--Comorbid in comparison to DEP: less sleep problems, more
somatic complaints, more severe anxiety symptoms, and more
impairment at school, home, and in relationships.

They concluded: Comorbid CD and DEP do NOT constitute a disorder
separate from either pure CP or DEP. There really were not
different patterns in the pure and comorbid groups; disorders
manifested with similar numbers of symptoms whether they were
present alone or comorbidly. Impairment differences were NOT
caused by severity of symptoms or higher levels of symptoms.
All in all, "comorbid disorders did not differ dramatically from
either pure depression or pure conduct problems" (page 711) .
Supports DSM-IV having separate CD and DEP and not depressive
conduct disorder (mixed category) as in the ICD-10
What does our research suggest regarding the course and outcome of childhood or early-onset schiz? What variables does the literature suggest are, and are not, related to adult outcome for children with early-onset schizophrenia?

The variables that predict outcome are drawn mostly from adult schizophrenia, but are partially supported in early onset child schizophrenia studies.

The variables that negatively effect outcome are
-early or insidious onset
-poor premorbid functioning
-negative symptoms
-no precipitating event
-family history of Schizophrenia
-nonfluctuating course

Werry et al studies: Follow up of child Sz

-90% on meds in young adulthood
-17% well at follow up, employed or attending school
-15% dead from suicide
-3% in remission (no schizophrenic episodes during follow up interval)

Abnormal premorbid adjustment/personality (past personal and social functioning) and degree of recovery after initial hospitalization were best predictors of outcome

All the predictors (including family history) had some effect on outcome and they are the same for those found in adults. Therefore, showing similarity between the adult and child onset disorder. Age and sex had little impact on the outcome.

--Outcome poor, but only slightly worse than in adults

Asarnow et al. outcome studies:

Follow up children originally seen when between 7 and 14 years old

-2 to 7 years of follow ups

--61% showed continuing schizophrenia through adolescence
--67% had either schizophrenia or schizoaffective disorder throughout adolescence

Outcome was defined using Global Adjustment Scores
-Lot of variability
--56% improved
--44% either stayed the same or deteriorated
--28% had "good" outcome (based on psychosocial adjustment (GAS 60 or above)

Their 14-year follow up found:

½ had severe impairment

Premorbid functioning best predictor of outcome

13. Describe three cognitive (or other psychosocial) models of depression AND the research evidence for or agaist them in explaiining the etiology of Depression in youth.
1. Object-loss model
-Depression will result from a separation/loss
-Reinherst - found that parental death was a risk factor for girls but not boys
-Lewinson- death of a parent early in life was not associated with later depression
-The object loss model is not that great be/c loss is not necessarily a sufficient cause.
2. Beck's model
-According to this model, it is one's cognitions - thoughts and beliefs- that shape one's behaviors and emotions. The most prominent proponent of the cognitive model of depression is Aaron Beck. He proposed that depressive symptoms result when people's attributions for external
events are based on maladaptive beliefs and attitudes.The cognitive triad is identified as a pattern of reportable depressive thoughts that consist of :
Negative view of self (perceived as deficient, inadequate, or unworthy);
Negative view of the world (interactions with the environment are perceived as representing defeat or deprivation)
Negative view of the future (current difficulties or suffering will continue indefinitely).
*Beck's model may not apply as well to kids as it does to adults
*Perhaps studies in kids should be done after mood induction so that schemas are activated
*In Lagrange & Cole's lognituidnal study on the cognitive triad in kids, schemas did not predict depressive sxn 1 yr later.
*There's support for the constructs being associated with depression in kids, but the model is not causal.

3.Learned helplessness/hopelessness
-Diathesis stress has larger effect for adolescents than it does for children
-Studies that have looked at this so far have used nonclinical samples
-In studies of learned helplessness, you need to prime kids to pos/neg mood induction (I'm assuming that previous studies haven't done this).
-Cole et al (2008) No support for cognitive-diathesis interaction with life events until between grades 8-9.
At that pt (I think), the relationship between negative life events and depression was moderated by attributional style. There was a relationship between negative life events and depression only for those with a negative attributional style.
4. *Cole's competency based model, the only model developed for kids.
This model focuses upon negative feedback by others,specifically:
negative feedback influences self perception, which in turn influences depression (neg feedback influences depression indirectly thru the intermediate step of self-perception).
-Self-perception of negative feedback mediates the relationship between negative feedback and depression
20. Have Separation anxiety and Social anxiety been found to be distinguishable, and how does age and sample type contribute to the distinction or nondistinction between these 2 types of anxiety?
Separation Anxiety:
-Only anxiety disorder that has to start before age 18.
-There is excessive recurrent anxiety associated with fear of separation from primary caregiver
-Can express anxiety in different ways: clinging, freezing, tantrums, crying
-Separation anxiety is normal from 7 mo - 5 or 6 yrs.
-Sep anx can occur when separation occurs on when it is anticipated; Kid can worry that some kind of harm will befall the caregiver or that some event will lead to separation.
-separation anxiety is one of the more common anxiety disorders
-nightmares are much more common in the younger kids with separation anxiety
-kids with separation anxiety tend to have more symptoms than adolescents
-many kids with separation anxiety outgrow it
-A quarter to 1/3 of kids with separation anxiety will persist over time and/or develop other anxiety or depressive disorders.
-1/3 of kids with separation anxiety have GAD
-1/3 of kids with separation anxiety have depression, which seems to develop after the separation anxiety. Kids whose separation anxiety persists over time tend to have parents with anxiety disorders or depression.
-In the Aschenbrand study,kids with separation anxiety were at greater risk for specific phobia, PTSD, OCD. Kids with sep anx did not appear to be at greater risk for adult panic, agorophobia, GAD, or social phobia.

Social Phobia:
-Involves persistent fear about being scrutinized, doing or saying something that will cause them to be evaluated negatively
-Fear can involve a specific situation or a more general situation
-generalized subtype of social phobia is the most prevalent
-anxiety has to be present in peer settings, not just with adults
-there has to be evidence that the kid has good relationships with familar ppl
-duration has to be at least 6 mo.
(??Kids with generalized soci phobia have earlier onset, more impaired functioning, higher rates of comorbid disorders, higher future risk for developing other comorbid disorders, higher rates of behavioral inhibition (e.g., inhibited temprament)??
-social phobia more common in adolescents than in children
-social phobic kids at risk for depression, dropping out of school, truancy, antisocial/CD, subst abuse

Ferdinand (2006)
1. Effects of referral status -findings
regarding classes of anxiety symptoms in the general population are not necessarily applicable to referred
2.Age effects = the taxonomy of symptoms of separation and social
anxiety was different for children versus adolescents
ALSO in Ferdinand:
The results indicated that symptoms of social anxiety may
discriminate better between high and low anxious individuals, and cast doubt on the usefulness of separately
assessing separation anxiety in these groups.
A separate separation anxiety class was detected in younger referred children, which underscored the
importance of assessing separation anxiety in this group, and demonstrated the validity of a distinct concept of
separation anxiety in younger children.

From class notes:
-The distinction is present only for referred children.
-No combos of low social anxiety, high separation anxiety for referred adolescents and population sample
* There was a distinction between separation anxiety and social anxiety for referred kids, but no distinction for non-referred adolescents or the general population.
Separation anxiety and social phobia are intertwined to a considerable degree, and high comorbidity rates have been
reported. The present study used latent class analysis (LCA) to investigate if classes of children and adolescents with—
simultaneously—high rates of separation anxiety and low rates of social anxiety symptoms, or vice versa, could be
identified. Eight- to 18-year-olds from a large general population (n ¼ 1000) and referred sample (n ¼ 735) were assessed
with the Multidimensional Anxiety Scale for Children (MASC). With LCA, a separate class of referred 8–11-year-old
children with high separation anxiety scores, and simultaneously lower social anxiety scores was identified, next to a class
of children with high scores on separation anxiety and social anxiety. In the other groups (referred 12–18-year-olds and
children and adolescents from the general population), a class with individuals who specifically scored high on separation
anxiety could not be revealed. The results indicated that separation anxiety represents a different construct than social
anxiety in referred children (but not in referred adolescents or in the general population). It can be concluded that, in
referred children, research regarding etiology and treatment outcome of anxiety symptoms should be aimed specifically at
separation anxiety and social anxiety, instead of just investigating a broader anxiety dimension.

The present study investigated which classes of children and adolescents can be identified, according to the
presence or absence of symptoms of separation anxiety or social anxiety. Because the study was conducted
with individuals from the general population, but also with a sample of referred children and youths, the
influence of referral on the constitution of classes could be determined. Further, the samples that were
studied represented a wide age range, which enabled comparison of LCA solutions for older versus
younger individuals. In three of the four subsamples that were studied (8–11 and 12–18 general population,
and 12–18 referred), a 2-class solution was found, reflecting high versus low anxiety levels. The high versus
low classes differed considerably with respect to the probability of social anxiety symptoms, whereas the
differences in probabilities of separation anxiety symptoms were smaller. This indicated that, in general,
scores on the social anxiety items were more important for class membership than scores on the separation
anxiety items.
Effects of referral status
The most remarkable difference between the referred versus the general population sample was found in
8–11-year olds. Whereas a 2-class solution was found in the general population sample, a 4-class solution was
found in the referred sample. These solutions appeared to differ significantly. This indicated that findings
regarding classes of anxiety symptoms in the general population are not necessarily applicable to referred

In three of the four subsamples (both subsamples from the general population, and the referred 12–18
group), a 2-class LCA solution was found. In these subsamples, it was found that the high anxious group
differed from the low anxious group, predominantly with respect to rates of social anxiety symptoms, whereas
differences in rates of separation anxiety symptoms were much smaller. This indicated that, in these three
subsamples, social anxiety symptoms differentiated better between high versus low anxious individuals than
separation anxiety symptoms did. Furthermore, in general, if rates of social anxiety in these three subsamples
increased—that is, if individuals moved from the lowest to the highest LCA class—the probability of
separation anxiety symptoms increased as well, be it to a smaller extent. Hence, the possibility to discriminate
between different homogeneous groups of individuals, according to the presence or absence of anxiety
symptoms, did not seem to profit much from assessment of separation anxiety symptoms.
1. Describe the three core symptom areas or characteristics of autism that are reflected in
the current DSM. What does empirical research find regarding the third domain/area, and
what are the implications of these findings?
III. DSM Core SYmptom Areas/Characteristics of Autism
1. Impaired social development. There is a qualitative
impairment in reciprocal social interaction. There is a lack of
social responsiveness, or interest in, people. They rarely smile
~ or gesture to respond to or signal social intent. Lack of eye
contact and facial responsiveness, don't cuddle, are indifferent
or find aversive, affection and physical contact. Lack of
empathy, no interest in cooperative group play, no interest in
making peer friendships.
2. Language and communication deficits. There is a qualitative
impairment in verbal and nonverbal communication. Language may
be totally absent. Understanding of spoken language is usually
markedly delayed. Nonverbal communication (facial expression,
gesture) is absent or minimal, or, if present it is socially
inappropriate. Even if there are no gross abnormalities in
language skills, communication is often impaired. They fail to
use speech for social communication
Abnormal play patterns. Impairment in imaginative activity, no
symbolic play, no "pretending". Play is ritualistic and lacking
in imagination, play patterns are limited and rigid, with little
variety or creativity.
3. They have a markedly restricted, repetitive patterns of
activities, behaviors, and interests. They are resistant to
changes and have a marked dislike of changes in their daily
routine. There is a lot of perseveration and rigidity in their
behavior. There is often an obsessional attachment and/or
preoccupation with bizarre objects, such as string or rubber
bands. Their use of "normal" objects is abnormal. Most have
stereotyped or repetitive motor mannerisms: body movements, arm
flapping, hand clapping or flicking, spinning, head banging.
Verbal stereotypies include repetition of words or phrases
regardless of meaning or appropriateness of the social context.

Research findings from Szatsmari:
Findings indicate that the Restricted, Repetitive Behaviours and Interests (RRBI) domain is composed of
two distinct factors or dimensions: Insistence on Sameness (IS) and Repetitive Sensory and Motor
Behaviours (RSMB). RSMB is negatively correlated with adaptive skills; that is, lower functioning
individuals tend to have higher levels of repetitive sensory and motor behaviours. On the other hand, IS
is positively correlated with autistic symptoms in the communication and language domain. Further
analyses suggest moderate familial aggregation among affected sibling pairs within the IS but not the
RSMB factor. Conclusions: These results provide evidence for the heterogeneity of the RRBI domain of
the ADI-R in terms of both clinical presentation and other correlates. In addition, the IS factor seems to
be under familial (presumably genetic) control, while RSMB appears to simply reflect variation in
developmental level.
2. What are the similarities and differences between autism and mental retardation (Le.
how are they similar and how can they be distinguished from one another)?
Autism vs. MR
About 40-70% of autistic kids are MR
1. Autism erratic early development, normal in some areas,
markedly delayed in others vs. MR consistent delay in all
2. Autism-normal physical appearance, normal physical/motor
development vs. MR delays in motor development
3. Autism-islets of ability or "Splinter Skills"
-Intact fine motor and spatial skills
-Good rote memory
-Hyperlexia (precocious reading) but they can't comprehend
what they read
-Musical Skills
4. Autism-mechanical stereotypic speech
5. Autism-absence of gross neurological anomalies (vs. MR)
Severe MR-obvious neuropathology vs autism only subtle
6. Social behavior--Autism-lack of responsiveness to or
awareness of others, failure to interpret social and emotional
stimuli and form normal affectional attachments (MR kids do)
7. Although one forth in each group has seizures the MR child's
seizures onset in infancy or early childhood, vs. late childhood
or adolescent onset in autism
8. Slight male preponderance in MR VS. 4:1 in autism
9. Down Syndrome most common genetic/chromosomal cause of MR but
rarely associated with autism
10. Autism-more likely to fail on tasks that require skills in
abstraction, language and the use of meaning
11. Cognitive--autism-scatter, nonverbal and verbal discrepancy
with verbal being lower, MR-globally retarded, pervasive
impairments with little scatter or variation in skills.
12. Outcome--both depend on IQ, but prognosis is less positive ~n
autism than nonautistic individuals with similar IQ levels
Similarities: both autism and MR involve cognitive impairment; both involve similar prognostic features (e.g., job and relational difficulties).
3. What are the similarities and differences between childhood autism and childhood
schizophrenia (i.e., how are they similar and how can they be distinguished from one
Autism vs. Childhood Schizophrenia
Both show social impairment, resistance to environmental change,
impaired communication, and inappropriate affect


2. Differences in social responsiveness (autism none, schizo
3. Specificity of symptoms
Not as well defined in schizo as in autism
5. Sex distribution
Not as clear male preponderance in schizo as with autism 4:1

4. Family characteristics
Schizophrenia tends to run in families more than autism
Parents of autistic tend to be higher than average social class vs. schizophrenia show a more normal class distribution
8. Organic factors; prenatal and perinatal complications and
epilepsy are more common in autism
9. Intellectual differences; MR commonly associated with autism,and much less frequently associated with schizo
11. The development and use of language; autism-failure to
develop complex language; schizo have acquired language, but use
it deviantly.
6. Degree of cognitive impairment (autism worse)
Autism-typical patterns of cognitive dysfunction; not present in
7. No delusions, hallucinations in autism
10. Course and Prognosis--Steady course in autism; schizo
remissions and relapses are common. Schizo prognosis more
positive if meds are effective; autism prognosis is less positive

1. Onset and developmental course
Schiz.-Iater onset, waxing and waning developmental course
Autism-failure of development; early onset of symptoms, steady
developmental course
5. Describe some ways in which early-onset schizophrenia is BOTH similar to and
different from adult-onset schizophrenia.
Adults and children with schizophrenia share similar cognitive, motor and behavioural disorders and the use of magnetic resonance imaging (MRI) indicates there are abnormalities in certain areas of the brain in both child and adult schizophrenics.

Early vs. Adult Onset
More family history in EO schizophrenia
Almost always gradual onset in EO schizophrenia
Kids tend to be weird (i.e., peculiar, strange personality) before the onset of EO schizophrenia.
Kids delusions are not as detailed as those with adult schizophrenia (hard to diagnose before 7…typically occur around 9 or 10). Visual hallucinations are more obvious.
EO schizophrenia cases are more resistant to medication (i.e., medication is less effective for these cases).
EO is typically associated with poorer outcomes.

Comorbidities w/ EO Schizophrenia
1) CD or ODD (~30%)
2) Depression or dysthymia (~30-40%)

Early-onset Schizophrenia
Childhood onset schizophrenia can either be a deterioration of functioning or never having developed expected level of functioning. When schizophrenia develops during adolescence, a deterioration is usually obvious. When schizophrenia develops during childhood, we often don’t see a deterioration. Early-onset schizophrenia encompasses both childhood and adolescent onset.
7. How do some of the symptoms of depression, and associated features, vary (or manifest
differently) for children versus adolescents with Major Depression Disorder?
Child MDD:
-more somatic complaints
-more separation anxiety
-more irritability

Adolescent MDD:
-more anhedonia
-more suicidal behavior
-more hopelessness (be/c it is abstract & future oriented)
-more body weight changes
-more substance abuse/eating disorders
-sleep distrubance more likely to manifest as hypersomnia

Birmaher (2004) - Child onset MDD was more similar than different from adolescent MDD in terms of severity, recovery rates, remission, relapse, comorbidity with other disorders, parent's psychopathology; one difference- adolescent onset depression has more genetic influence, higher heritability estimates.
8. What does the empirical literature indicate regarding the similarities and differences in
child-onset versus adolescent-onset Major Depression (in terms of symptoms, correlates,
course, etc.)?
rates: 1-2% prepubescent kids, 3-8% adolescent

Twin studies suggest a greater genetic component in adolescent vs. prepubertal depression

Cognitive distortions are associated with depression in prepubertal children and adolescents, but only in adolescents does evidence show that distortions persist after episode reolves


Similar symptoms - persistent and pervasive sadness, anhedonia, boredom, irritability THAT CAUSE FUNCTIONAL IMPAIRMENT, comorbidity is common.

similar family & environmental risk factors:
family discord and expressed emotion may interact with depression diathesis to predict onset and reccurence; family environmental risk factors include parental ciminality, parental substance abuse, lack of family cohesion, parent-child discord.
9. In what ways is Major Depressive Disorder (MDD) similar to Dysthymic disorder (Le.,
what ways are both of these disorders the SAME, in terms of correlates, etc)? How do
children with BOTH MDD and Dysthymic disorder differ form either disorder alone [i.e.,
how does the comorbid pair (i.e., "double depression") differ from Dysthymia only and
MDD only?]?
-Many kids (35-40%) with MD have dysthymic disorder
-Dysthymia tends to have earlier onset in kids (8yrs) than depression (10-11 yrs).
-Having dysthymic disorder is a risk factor for developing major depression
-70% of kids with dysthymic disorder will develop MD within 5 yrs
-Dysthymia and MDD are more similar in terms of social competence, demographic variables (like gender, ethnicity, and SES), clinical course. They are more similar than different in terms of suicide ideation and attempts.

Combined MDD/Dysthymia vs just Dysthymia vs. Just MDD:
Comorbid pair is more impaired in functioning, has lower social competence, more likely to have comorbidity with anxiety disorders, is associated with less parental monitoring, more likely to be referred for treatment.
11. Describe several research findings ON BOTH SIDES OF the nature (biological/genetic)
versus nurture (environmental/learning) debate on childhood/adolescent Depression?
Rice's Gene-Enviro intxn
To test for gene-environment interaction with depressive symptoms and family conflict. Specifically, to first
examine whether the influence of family conflict in predicting depressive symptoms is increased in individuals at genetic
risk of depression. Second, to test whether the genetic component of variance in depressive symptoms increases as
levels of family conflict increase. Longitudinal twin design was used. Results suggested
significant gene-environment interaction specifically with depressive symptoms and family conflict. Genetic factors were
of greater importance in the etiology of depressive symptoms where levels of family conflict were high. The effects of
family conflict on depressive symptoms were greater in children and adolescents at genetic risk of depression.
Conclusions: The present results suggest that children with a family history of depression may be at an increased risk of
developing depressive symptoms in response to family conflict.

Costello's trajectories
This study used semi-parametric group-based modeling to explore unconditional and conditional trajectories
of self-reported depressed mood from ages 12 to 25 years. Drawing on data from the National
Longitudinal Study of Adolescent Health (N  11,559), 4 distinct trajectories were identified: no
depressed mood, stable low depressed mood, early high declining depressed mood, and late escalating
depressed mood. Baseline risk factors associated with greater likelihood of membership in depressed
mood trajectory groups compared with the no depressed mood group included being female, Black or
African American, Hispanic or Latino American, or Pacific Islander or Asian American; having lower
socioeconomic status; using alcohol, tobacco, or other drugs on a weekly basis; and engaging in
delinquent behavior. Baseline protective factors associated with greater likelihood of membership in the
no depressed mood group compared with the depressed mood trajectory groups included 2-parent family
structure; feeling connected to parents, peers, or school; and self-esteem. With the exception of
delinquent behavior, risk and protective factors also distinguished the likelihood of membership among
several of the 3 depressed mood groups. The results add to basic etiologic research regarding developmental
pathways of depressed mood in adolescence and young adulthood.

Schwartz's peer relationships and academic achievement:
This article reports a longitudinal investigation that examines academic and social difficulties as
predictors of depressive symptoms during middle childhood. Participants were 199 elementary school
children (M  9.1 years) who were followed for 2 consecutive school years. In both years of the project,
children completed a questionnaire assessing depressive symptoms and a peer nomination inventory
assessing friendships and social standing. Grade point averages (GPAs) were obtained from a review of
school records. Low GPAs were predictive of depressive symptoms, but this effect did not hold for
children who had numerous friends. Similarly, children who had relatively few friends tended to
experience depressive symptoms. However, the effect was attenuated for children with high GPAs. Taken
together, the findings suggest that competencies in 1 domain can moderate the risks associated with
difficulties in the other domain.

-genetics-Twin studies - greater concordance among monozygotic twins
-40-65% heritable (with higher rates in adolescence).
-Some twin studies suggest that the effect of a shared enviro is at least as potent as heritable factors. Parental depression may exert it’s effects on child mood disorder not only through genetic mechanisms but also via modeling of cognitive distortions and hostile or passive/withdrawn intxn. Family environmental risk factors that lead to child depression such as parental criminality, parental substance abuse, lack of family cohesion, and parent-child discord, may be most toxic in the absence of a family history of depression.
12. Describe several research findings ON BOTH SIDES OF the nature (biological/genetic)
versus nurture (environmental/learning) debate on childhood/adolescent Anxiety
Family studies have found a large overlap between anxiety disorders in family members. In addition to genetic heritability, a
range of family factors may also be involved in the intergenerational transmission of anxiety. Evidence for a relationship between
family factors and childhood as well as parental anxiety is reviewed. Four groups of family variables are considered: (I) attachment;
(II), aspects of family functioning, such as marital conflict, co-parenting, functioning of the family as a whole, and sibling
relationships; (III) parental rearing strategies; and (IV) beliefs that parents hold about their child. The reviewed literature provides
evidence for an association between each of these family factors and child anxiety. However, there is little evidence as yet that
identified family factors are specific to child anxiety, rather than to child psychopathology in general. Moreover, evidence for a
relationship between child anxiety and family factors is predominantly cross-sectional. Therefore, whether the identified family
factors cause childhood anxiety still needs to be investigated. Further research that investigates mechanisms mediating the
relationship between family factors and child anxiety is also called for. Finally, parental beliefs are identified as important
predictors of parental behaviour that have largely not been investigated in relation to child anxiety disorders.

Anxiety symptoms showed moderate stability during childhood and adolescence
Heightened neonatal biobehavioral reactivity and poor regulation predicted emotion regulation difficulties in preschool, which predicted anxiety symptoms in childhood
Developmental incompetence in childhood predicted anxiety symptoms in preadolescence, and anxiety symptoms in preadolescence predicted incompetence in adolescence
Insecure attachment relationships in infancy predicted negative peer relationship representations in preadolescence, and these representations predicted anxiety symptoms in adolescence.
Compared to males, females showed similar rates of anxiety symptoms and childhood but greater and more stable rates in adolescence; however, males and females showed similar patterns of association between risk factors and anxiety symptoms across childhood and adolescence
The model tested was specific in predicting anxiety symptoms and not psychopathology in general

From the notes:
Bio and genetic influences are important for anxiety disorders
-having a parent with an anxiety disorder gives kids risk for anxiety, but specific form/type may not be the same as parents
-there is genetic evidence for comorbidity; genes accoutnt for 60% or more of the link between anxiety and depression
-not all behaviorally inhibited kids end up with anxiety disorders, but they are at higher risk than kids who are not behav inhib
-early anx and withdrawn behavior in kids puts them at risk for anxiety disorders in adolescence and adulthood.
-Classical and operant conditioning - kids can learn fears, avoidant behavior. can learn thru observational learning
-cognitive theories- ppl with anxiety interpret ambiguous situations as being more threatening
-intrusive parenting has been associated with kids anxiety, as has overprotection (be/c these things limit kid's autonomy and ability to control environment.
-attachment, particularly insecure attachment, has been associated with kid's anxiety. Of kids with insecure attachment, 28% develop anxiety disorder relative to 13% of control.
-According to Bosquet, insecure attachment predicts negative peer relationships, which predicts anxiety in adolescence.
14. What are the specific baseline risk factors and specific protective factors found to be
associated with depression (or no depression) from age 12 to 25?? And what risk and
protective factors distinguish various developmental trajectories?
Costello et al. 2008: Examined self-reported depressed mood
trajectories between ages 12 and 25 in a huge sample (12,105
students grades 7-12). Baseline risk and protective measures were
obtained at time 1 (not throughout)! Depressed mood assessed by 3
questions from CES-D, asked 1 year later and 5 years later
Four trajectory groups identified: 1) no depressed mood (29%); 2)
stable low depressed mood (59%); 3) early high declining
depressed mood (9.5%); and 4) late escalating depressed mood
Baseline risk factors for odds of being in three depressed mood
trajectories vs. No depressed mood: ethnic minority, female,
using weekly alcohol, tobacco, drugs, low SES, delinquent
Baseline protective factors for being in no depressed trajectory
vs. depressed groups: 2-parent family, self-esteem, feeling
"cared by" or connected to parents peers and school
Stable LOW VS NO depressed: Risk-female, Black or Asian,
delinquent behavior; Protective-2-parent, perceived connection to
parents, peers, school; high self-esteem and high SES
EARLY HIGH vs. No depressed: Risk-female, any minority,
delinquency, weekly alcohol, tobacco, drugs use; protective-same
as above
LATE escalating vs. No depressed: Risk-female, delinquency;
protective-2-parent, high self-esteem and high SES.
(NOTE: Female and delinquency in all!)
Early HIGH vs. Stable LOW: Risk-female, Black, weekly alcohol,
tobacco, drug more likely to be in EARLY HIGH. Protective--2parent,
greater perceived connection to parents, peers, school;
high self-esteem and high SES, less likely to be in EARLY HIGH
LATE ESCALATING vs. Stable LOW: (NO differences)
alcohol/tobacco/Drug more likely to be in EARLY HIGH vs. Late
Escalating; High self esteem more likely to be in LATE escalating
vs. early high.
15. What is the course and/or outcome of childhood depression in both the teenage years
and adulthood? Include a discussion of the many variables that may, or may not, affect
outcome in terms of: 1) continuing depressive episodes, and 2) general outcome
(impairment, family and social functioning, marital functioning, using mental health
services, etc).
Essau: persistance = cps, nn
not related to persistance = pa gap
Dunn & Goodyear: predicted recurrence = chf; did not predict recurrence = a
Lewison: predicted recurrence= held sf
Birmaher = guilty female with past dep and psychopath parents assoc with worse longitudinal outcome.
1. Course o£ Depression and Depression Episodes:
A. Community samples
B. Clinic samples
C. What happens when depression goes away??
Lewinsohn et al. (1994): When they looked at formerly depressed
adolescents 2 years later:
Formerly depressed adolescents continued to differ significantly
from their never depressed peers on many of the psychosocial
variables. They had most of the characteristics of depressed
adolescents, although somewhat less severe.
--They had lots of internalizing problems and reduced coping
skills; Lots of pessimism, negative attributional style, low
--THUS, the formerly depressed adolescents STILL have these
problems when they are no longer depressed. THIS may set them up
or predispose them to experience future depressive episodes.
Reinhurtz et al., 1999: Those depressed in late adolescence, had
low self-esteem, suicidal behavior, poor overall functioning (int
and ext problems and impairment), dissatisfaction with
work/career, interpersonal (few friends and low social support)
in young adulthood (and all this was true regardless of whether
they had depression when young adults!!).
Essau (2007) and Dunn & Goodyer (2006); both required readings:
Essau (2007)- comorbid T1 disorders tended to persist more; presentce of substance use disorders in kids, parent's alc problems, suicide attempts and ideation, negative school-related events, negative coping all related to persistence. Things not related to persistance in Essau's study were gender, age of onset, parent's psychopathology, perceived competence, attachment to parent's and peers
In Dunn and Goodyear, the things that predicted recurrence were: being female, comorbidity, higher self-report depression scores. (I think that age of onset did not predict recurrence in this study).
Others I will tell you here:
Lewinsohn et al. 2000/2003: predictors of factors in adolescence
that predicted recurring episodes in young adulthood were: social
competence, daily hassles, emotional reliance on others, elevated
depression symptoms, family history of MOD, history of suicide
attempt, longer and more frequent episodes
Birmaher et al. 2004 5-year follow up:
--Predictors of worse longitudinal outcome were: female, guilt
symptoms/feelings, past depression episodes, and parental
psychopathology (depression, alcohol, APD)
Rohde et al., 2005: Parents depression and relations to "formerly
depressed" adolescents' course (Lewinsohn kids) :
--Mothers' depression was associated with: recurrence of
depressions, chronicity, course, and anxiety in young adulthood
--Fathers' depression was associated with recurrences in
daughters, not sons; and lower functioning in both girls and boys
Effects of Other Comorbid Disorders?
Anxiety: Kovacs: Anxiety preceded the depression in about twothirds
of the cases and persisted after the depression went into
remission. Comorbid anxiety disorders did not affect the length
of the MOD in those with primary MOD. Comorbid anxiety did not
affect the risk of subsequent MOD.
Conduct Disorder: DEP with Comobid CD: (see also above) greater
suicide attempts, impairment, criminal behavior versus DEP
without CD
--increased rate of long-term problems (worse prognosis) in terms
of school suspensions, police, courts (like CD) (Kovacs)
--more socially impaired in adulthood; higher risk for adult
criminality, antisocial personality (61% vs. 6%); alcohol
abuse/dependence than DEP without CD (Harrington et al., 1991)
--trend towards DEP/CD LESS likely to have DEP episodes persist
in adulthood (47% versus DEP without CD 69%; Harrington et al.,
1991) But not significant!!
But CD does not affect depressive episodes: above "trend" and
Kovacs: Comorbid CO did not affect the length or severity of
depressive episode or remission period. CD persisted after the
DEP went into remission.
3. General Adult Outcome on OTHER Factors:
Harrin2ton et al.: Depressed kids (followed up when about 30
years old) were at increased risk of being hospitalized for
mental illness, suicide attempts, being prescribed psychotropic
medications, receiving psychiatric services (significantly
differed from nondepressed psychiatric controls)
Lewinsohn et al. 2003: Age 24 follow up of adolescents:
--Adolescent MOD associated with all impairment functioning
measures in unadjusted analyses.
--After accounting for adolescent NONMOOD disorders, adolescent
MOD associated with: low global functioning, low quality family
relationships, small social network, minor hassles, major
adversity, low life satisfaction, and using mental health
treatment services
--After accounting for ALL young adult psychopathology (MOD
recurrence and nonmood disorders in both adolescence and young
adulthood), ALL of those above (except treatment services and
global functioning) remained significant.
--After ALSO accounting for current depression symptoms (in
addition to young adult psychopathology, time 1 functioning,
cormorbid mood disorders, etc), NONE of the associations with
adolescent MOD were significant.
Much of impairment due to psychopathology or problems in general,
not MOD in and of itself.
Gotlib et al. (1998): Adolescent depression related to later
high rates of early marriage (especially for younger women) and
marital dissatisfaction (and this was specific to depression) .
Nonaffective disorders were NOT related to later marital
16. What measurement, assessment, and theoretical issues have been discussed as being
relevant to improving the DSM classification system and criteria for the various anxiety
disorders in youth? What approach has been proposed to deal with the above issues, and
how do components within this approach serve, specifically, to improve the classification of
childhood anxiety disorders?
Weems & Stickle
-In sum, a failure to utilize etiological mechanisms
and theory may contribute to poor validity.
However, although utilization of risk factors and etiological
mechanisms may improve estimates of stability
and long-term outcomes, the mechanisms that
lead to anxiety disorders may differ across individuals
or subgroups of youth who exhibit anxiety. That
is, the most important causal factors and how they
interact to place a child at risk for anxiety disorders
may differ across individuals or subgroups (i.e., equifinality).
Such individual differences in etiology suggest
an approach to assessment that does not rely
solely on etiological mechanisms. Such an approach
would limit the classification system because particular
etiological factors may not necessarily lead to
or be a problem for every child and a useful classification
system needs to have a fairly high degree of
consistency across individuals (Blashfield, 1989). The
challenge is thus to have consistent, reliable diagnostic
criteria, utilize etiological mechanisms to improve
validity, and be able to distinguish symptoms
and signs of the disorder from independent etiological

-In sum, method variance can result from the
characteristics of the informant, assessment situation,
sample, or the assessment instruments themselves.
Method variance has been observed to account for
twice as much variance as is accounted for by particular
traits in studies of childhood psychopathology
(Stickle & Blechman, 2002). In fact, a majority
of variance in measures in some studies of childhood
psychopathology results from factors other than the
behaviors of interest (Fergusson & Horwood, 1989;
Stickle & Blechman, 2002). This lack of precision
is troubling and underscores the need for improved
measurement strategies. Research on the assessment
and classification of child anxiety disorders will benefit
from continued improvement in measurement and
assessment strategies. Research detailing the characteristics
of individual measures of anxiety and an accounting
of how different modalities of assessment
(e.g., self-report, parent report, interviews, behavioral
observation, physiological measures) relate to
each other is necessary to establish clarity about the
relationships among the different elements of anxiety,
the extent to which various elements are stable,
and how these elements are associated both with initial
impairment and with functional status over time

-Our proposal draws on the recommendations of
past theorists. Kanfer and Saslow (1969) and Noyes
and Kolb (1963), for example, have recommended
using multiple factors in diagnosis including genetic,
psychological, and symptom level information.
Kanfer and Saslow (1969) argued that diagnosis
should be organized along three primary domains
(1) etiology, (2) symptoms, and (3) prognosis

-Their model tries to incorporate biological factors, learning factors, cognitive theories, and whatever else I list below

-In sum, an integrative model of childhood anxiety
disorders must include learning factors in order
to understand how anxious responses develop,
how these behaviors are maintained over time, lapse
and relapse, and are most effectively prevented and
treated (Bouton, 2000, 2001). Learning processes
also imply important anxiety mechanisms such as
avoidance and withdrawal

-In sum, cognitive models emphasize biased interpretation,
judgment, and memory as well as attentional
selectivity in the etiology and maintenance
of anxiety disorders in youth and so implicate
several constructs important to the nomological
net of childhood anxiety. A number of studies
have shown that these cognitive processes are associated
with anxiety and differentiate youth with anxiety
disorders from nonanxious youth. Some longitudinal
data suggest possible etiological roles, however,
additional prospective research is needed to
more firmly establish etiological versus concurrent

-In sum, interpersonal models have demonstrated
long-term prediction of anxiety disorders and
may provide a context for differentiating normal separation
protest from pathological separation anxiety.
Although attachment theory provides a conceptual
model of how interpersonal factors can spark
or exacerbate anxiety problems, research is needed
to replicate the predictive findings and clarify if or
what type of insecure attachment is specifically predictive
of anxiety problems before attachment theory
can optimally inform the nomological net. Research
examining the proposition that interpersonal distrust
(e.g., expectations that other people will be untrustworthy
and rejecting) may exacerbate potentially
threatening events or foster negative anxiety sensations
may be important in this regard (see Weems,
Berman, Silverman, & Rodriguez, 2002).

**Empirical research highlights the need for
improving the childhood anxiety disorder diagnostic
classification system and the techniques used to
identify them. These problems may be addressed by
using the nomological net of childhood anxiety. A
nomological net understanding of childhood anxiety
disorders is not primarily descriptive or etiological.
It represents the theoretical structure of anxiety
disorders and is comprised of numerous domains.
The two major subdivisions of these domains
are (1) the symptoms of anxiety disorders (e.g.,
DSM-IV descriptive diagnostic criteria), and (2) the
mechanisms of anxiety disorders (e.g., physiological
responses, affect, behavior, and cognitive processes).
A nomological approach implies greater inclusion
of the mechanisms of the anxiety disorders and the
use of multiple measures (across informants and
modalities) in defining, refining, and testing the
validity of the classification scheme. There are also
specific implications for measurement, classification,
treatment, and policy.

From class notes:
There is a lot of sxn overlap, poor boundaries between the different disorders, poor informant agreement, inconsistency on outcomes for kids, not very good predictive validity with DSM categories. The criteria are basically descriptive, and don't say anything about the uderlying causal mechanisms. Dx should be based on symptoms, etiology and prognosis because symptoms alone are not related to impairment and prognosis.
17. How do youth with Anxiety Only, Anxiety + Anxiety, Anxiety + Depression, and
Anxiety + Externalizing Disorders differ from one another in terms of demographic (age,
sex, ethnicity, SES), symptomatology (fears, anxiety, depression, internalizing and
externalizing problems), psychosocial (peer relationships, academic performance), and
family (parents' psychological symptoms) variables?
To evaluate the external validity of comorbid patterns of anxiety disorders among youth who presented to
an anxiety disorders clinic, comorbid cases were compared to ‘‘pure’’ anxiety disorder cases. Children and
adolescents (N = 329; mean age = 10.04 years) and parents were administered structured interviews and
four groups were formed, Pure Anxiety, Anxiety + Anxiety, Anxiety + Externalizing, and Anxiety + Depressive,
and compared along with four external validation criteria: sociodemographics, clinical phenomenology,
psychosocial, and family factors. All comorbid groups were more severe than the pure anxiety
group on clinical phenomenology and psychosocial factors. The Anxiety + Depressive Disorders group was
most severe on all criteria except sociodemographics. Results provide evidence for the external validity of
comorbid diagnostic presentations among anxiety disorders, as there was differential meaningfulness in the
diagnostic presentation of a pure anxiety disorder versus anxiety disorder comorbid with other disorders.

Of the Cantwell (1995) external validation criteria examined in this study, clinical
phenomenology did particularly well in differentiating comorbid anxiety disorders from pure
anxiety disorders: All comorbid groups were significantly different from the pure anxiety
disorder group when it came to all the indices of clinical phenomenology. That is, youth with a
primary anxiety disorder comorbid with other anxiety disorder, a depressive disorder, or an
externalizing disorder, rated themselves as having significantly higher levels of anxiety, fear, and
depression than youth with pure anxiety disorder. Moreover, these differences showed medium to
large effect sizes. This also was found for parents’ ratings of their child’s behavior problems:
youth with diagnostic presentations of ANX + ANX, ANX + DEP, or ANX + EXTwere rated by
their parents as having significantly higher internalizing and externalizing behavior problems
(using the CBCL subscales) than youth with pure anxiety disorder. These findings suggest that
clinical phenomenology is a robust external validation criterion, and the distinct comorbid
patterns are meaningful with respect to this criterion. Additionally, although it might appear to be
a truism that anxiety disorders when comorbid with other conditions lead to greater clinical
severity among cases, it is important to emphasize that this ‘‘truism,’’ to our knowledge, has not
undergone empirical scrutiny. Establishing empirically many so-called ‘‘truisms’’ is an important
part of the psychology research enterprise, especially because many truisms frequently fail to
hold up empirically. Moreover, our goal in this study was to mainly show that when some of
Cantwell’s external validation criteria are applied to anxiety disorders, differing patterns are
observed between single anxiety disorder cases and cases with comorbid conditions, highlighting
the possibility of the distinctiveness among anxiety comorbid conditions.
Results also indicated that all three psychosocial factors (i.e., extracurricular activities, quality
of peer relationships, and academic performance) differentiated the ANX + DEP and
ANX + EXT groups from the pure anxiety disorder group. This finding speaks to the
importance of assessing beyond clinical phenomenology, as anxious youth with comorbid
conditions of depressive or externalizing disorders show impairment in psychosocial areas that
was not observed in youth with either a pure anxiety disorder or with multiple anxiety disorders.
Interestingly, only one psychosocial factor, extracurricular activities, differentiated the
ANX + ANX group from the pure anxiety disorder group suggesting that the presence of
multiple anxiety disorders particularly serves to limit youths’ resources for extracurricular
When it came to the parent psychopathology variables, the ANX + EXT group had parents
who rated themselves as having more psychopathology symptoms than parents of children in the
pure anxiety disorder group. Future research should be conducted to explore whether parental
distress is a response to the child’s comorbid presentation of an externalizing behavior problem,
perhaps because having a child with an externalizing disorder along with an anxiety disorder
taxes parents’ resources more than having an anxious child.

Of all the external validation criteria of Cantwell (1995), only sociodemographics (i.e., age,
sex, race, SES), did not significantly differentiate among the groups. On one hand, this was
surprising because significant age and sex differences are commonly observed in comparisons of
youth with pure anxiety disorders, pure externalizing disorders, and pure depressive disorders
(Kovacs & Devlin, 1998). On the other hand, Strauss et al. (1988) reported that when children
ages 5 and 6 were removed from the statistical analyses, the significant age differences were no
longer present among all the groups examined (pure anxiety compared to anxiety comorbid with
The study’s findings suggest that there might be meaningful distinctiveness with regard to the
specific comorbid groups suggesting that comorbidity in the present sample is factual rather than
artifactual (Angold et al., 1999; Caron & Rutter, 1991). Significant differences appeared mainly
in terms of the ANX + DEP comorbid group relative to the other comorbid groups. Specifically,
the ANX + DEP group had higher levels of self-rated anxiety than the ANX + ANX group,
higher self-rated depression than the ANX + ANX and ANX + EXT groups, and less
involvement in extracurricular activities than the ANX + ANX group. Strauss et al. (1988)
also found that youth with an anxiety disorder comorbid with depression rated themselves as
having greater anxiety than youth with a pure anxiety disorder diagnosis. Future research is
needed to shed light on potential reasons for the unique pattern of impairment presentation
among different criteria (i.e., clinical phenomenology, psychosocial factors, and parental
psychopathology) found in the ANX + DEP group.
If the present study’s findings are found to be robust in future research, they suggest interesting
possibilities about the handling of comorbid conditions in the DSM. Some incorporation of
comorbid disorders already appears in the latest version of the International Classification of
Diseases (ICD-10) (World Health Organization, 1993), which contains the unitary categories of
anxiety disorders (pure disorders) and the comorbid categories of mixed anxiety and depression
and other mixed anxiety disorders (which allow for ‘‘disorders of conduct’’). Given the greater
severity observed among comorbid conditions of anxiety disorders, the findings further highlight
the importance of conducting thorough and careful diagnostic evaluation in practice.
18. Which specific anxiety disorders are more strongly associated with each of ADHD,
ODD, and CD; and how do these associations vary with respect to children's age and
association between externalizing and anx:

ADHD = soc, gener sep
ODD= specific, soc, gener, sep
CD=specific, soc, gen
Minimal information about the relationship between anxiety disorders and externalizing disorders in
youth is available. This study examined relationships between different specific anxiety and externalizing
disorders and examined whether these associations varied by age and gender. The Methods for the
Epidemiology of Child and Adolescent Mental Disorders (MECA) data set, consisting of youth from
ages 9 to 17 recruited at four sites across the United States using a probability sampling method, was used.
Results indicated that all externalizing disorders (attention-deficit hyperactivity disorder, oppositional
defiant disorder, and conduct disorder) were positively related to a range of anxiety disorders. The
magnitude of these associations tended to be stronger for males than for females (particularly for
associations between social phobia and all externalizing disorders) and at younger, compared to older,
ages (particularly for the association between oppositional defiant disorder and overanxious disorder). The
cross-sectional positive relationships between externalizing and anxiety disorders vary somewhat based on
gender, age, and which specific pair of disorders is examined; this may help explain the discrepant findings
of previous research in this area.

The results of this study support the notion that anxiety and externalizing disorders are
positively associated, and the strength of the associations between these two sets of disorders
differs based on which specific pair of disorders is examined. In addition, the relationships differ
somewhat based on gender and age group. Some of the discrepant findings of past research may
be accounted for by differing pairs of disorders examined, as well as different age and gender
compositions of samples.
Overall, positive relationships were found between most pairs of anxiety and externalizing
disorders. Specifically, ADHD was associated with social anxiety (SOP and AVD), generalized
anxiety (GAD and OAD), and separation anxiety (SAD). ODD was associated with specific fears
(SIP), social anxiety (SOP, AGOR, and AVD), generalized anxiety (GAD and OAD), and
separation anxiety (SAD). CD was associated with specific fears (SIP), social anxiety (SOP), and
generalized anxiety (GAD and OAD).
The associations between externalizing disorders and anxiety disorders tended to be
somewhat stronger and more widespread for males, compared to females. This effect was
particularly pronounced in relation to SOP (where there was a statistically significant interaction
effect between gender and all externalizing disorders): boys with SOP were much more likely to
have ADHD, ODD, and CD than were girls. Perhaps boys with externalizing disorders are more
aware of their social problems, making them more socially anxious. It is also possible that boys
are more likely to express their social anxiety by acting out and/or associating with deviant (e.g.,
delinquent) peer groups; this could result in them exhibiting the symptoms necessary for both
anxiety and externalizing diagnoses.

The relationships between externalizing disorders and anxiety disorders tended to be stronger
for younger, compared to older, youth, though in only one case was this difference statistically
significant. Specifically, the interaction effect found in the association between OAD and ODD
indicated that younger participants evidenced a much stronger link between these two disorders than older participants.

As discussed in Section 1, previous research has yielded contradictory findings regarding the
relationship between CD (and related problems) and general anxiety (GAD and OAD); the results
of this study indicated that there was, in fact, a positive relationship between these two constructs.
19. How do children versus adolescents with Social Phobia differ (or not differ) from one
another in terms of symptomatology (other anxiety disorders, comorbidity, loneliness,
anxiety symptoms, internalizing and externalizing problems, etc.), social problems on
behavioral tasks, impairment, etc.??
Separation anxiety and social phobia are intertwined to a considerable degree. In the other groups (referred 12–18-year-olds and
children and adolescents from the general population), a class with individuals who specifically scored high on separation
anxiety could not be revealed. The results indicated that separation anxiety represents a different construct than social
anxiety in referred CHILDREN (but not in referred ADOLESCENTS or in the general population). It can be concluded that, in
referred children, research regarding etiology and treatment outcome of anxiety symptoms should be aimed specifically at
separation anxiety and social anxiety, instead of just investigating a broader anxiety dimension.

From class notes:

The only thing that kids had significantly more than adolescents was separation. They also had higher scores on MASC. There was no difference on internalizing/externalizing. Kids with social phobia are very similar to adolescents with social phobia.
Although the presentation of social anxiety disorder (SAD) in adults is well documented, less is known about its clinical
manifestation in children and adolescents. To date, most studies have included combined samples of children and adolescents
despite the fact that this age range represents an extensive period of growth and development. This study compares and
contrasts the clinical presentation of SAD among children (ages 7–12) and adolescents (ages 13–17). One hundred and fifty
children (n ¼ 74) and adolescents (n ¼ 76) with a primary diagnosis of SAD participated in the study. The assessment battery
included clinical ratings and behavioral observation as well as parental and self-report. The results indicate that, although the
symptom presentation of children and adolescents with primary SAD shares many features, children tend to present with a
broader pattern of general psychopathology, while adolescents have a more pervasive pattern of social dysfunction and may
be more functionally impaired as a result of their disorder.
This investigation differs from previous studies, however,
in that it is the first to compare and contrast the clinical presentation of SAD in children and adolescents.
The results indicate that although its basic form appears consistent across groups, there are differences
as well.
With respect to similarities, broad measures of social anxiety (SPAI-C, CSR, extraversion) indicate
moderate and equivalent levels of social distress for both children and adolescents. In fact, over 90%
of both groups met criteria for the generalized subtype, a percentage higher than what usually is found
among adult populations (Turner, Beidel, & Townsley, 1992). Furthermore, based on their K-GAS ratings,
both groups experienced equal and moderate impairment as a result of SAD. Thus, although more adolescents
may endorse significant anxiety across a broader range of situations, the disorder’s impact is equal for
both groups.
With respect to group differences, adolescents endorsed a broader pattern of fear and avoidance when
compared to their younger counterparts. Adolescence is a period when engagement with peers and
establishment of friendships is emphasized and encouraged by parents and other adults. For example, in
addition to general social expectations regarding friendships and age-appropriate activities, dating and
heterosocial interactions are also expected adolescent activities. When children are young, interactions with
peers are usually arranged by parents (play dates, dancing lessons, soccer team membership) and the choice to
actively avoid these interactions is limited. However, with cognitive and physical maturity, parents are less
likely to arrange these interactions as that responsibility gradually shifts toward the adolescent (Hartup, 1989;
Hartup & Stevens, 1999) thereby allowing opportunities for avoidance. Thus, for adolescents with SAD,
physical and cognitive maturity, as well as cultural expectations for independence in social encounters, may
result in a broader pattern of social avoidance.
The consequences of increased social avoidance include fewer friendships and a stronger feeling of social
isolation. Indeed, the literature addressing the significance of friendships reveals that people with a satisfying
social network have a greater sense of well-being than those without ongoing social relationships (Hartup &
Stevens, 1999). Thus, this broader pattern of social avoidance in socially phobic adolescents likely accounts for
their higher scores on the LS.
Adolescents also reported significantly higher scores on the MASC Social Anxiety subscale than did
children. Specifically, in contrast to the SPAI-C, where items assess anxiety across various social situations,
the MASC Social Anxiety subscale (on its surface) appears to more directly tap the ‘‘cognitive’’ aspect of SAD
(e.g., I worry about other people laughing at me, I worry about getting called on in class, I worry about what
other people think of me). Thus, the higher scores of adolescents on the Social Anxiety subscale of the MASC
may reflect a cognitive worry component, a dimension that is more likely to reflect the adolescent’s cognitive
maturity. A large community study of adolescents in the Netherlands (Westenberg, Drewes, Goedhart,
Siebelink, & Treffers, 2004) that found a direct link between cognitive maturity and an increase in social
evaluative fears during adolescence, provides further support for this hypothesis.
In contrast, children with SAD had a broader pattern of general psychopathology than adolescents. They
were more likely to worry about doing things correctly and about being separated from their parents. These
data are consistent with the general understanding of fears and anxiety in children, where prevalence rates for
fears and phobias are higher among younger children than adolescents (Beidel & Turner, 2005) with the
exception of SAD. With respect to comorbid disorders, the types of co-existing conditions found among this
sample are consistent with those of Beidel et al. (1999) whereas the pattern among adolescents is quite different
from those among an epidemiological sample of German adolescents, where 41% had a comorbid
somatoform disorder, 29% had a depressive disorder, and 24% had a substance abuse disorder (Essau et al.,
1999). However, this latter study differs from the current investigation on several relevant factors including the
diagnostic instrument and assessment strategy and the fact that in the epidemiological sample, there was no
attempt to determine whether SAD was the primary diagnosis as was the case for the current investigation.
The high rate of comorbid somatoform disorder reported by Essau et al. (1999) is inconsistent with any other
investigations of the psychopathology of SAD in other reported populations.
Furthermore, although both children and adolescents with SAD have significantly poorer social skills than
youth with no disorder (Beidel et al., 1999; Beidel et al., in press; Spence et al., 1999), when compared directly,
children with SAD displayed significantly less skill and more anxiety than their adolescent counterparts. The behavioral assessment used in this investigation was a structured task, requiring responses to one sentence
prompts provided by a same age peer. Although its discriminative validity for both age groups has been
previously demonstrated, it may be that despite their higher level of fear and avoidance, adolescents with SAD
have sufficient skills to respond minimally to these very brief and structured interactions. In fact, unstructured
social interactions are described as much more challenging for adolescents with SAD (Beidel & Turner, 2005)
and future investigations may need to consider the specific conversational format most likely to reveal the
extent of skill deficits in various age groups.
21. What does the empirical literature find with respect to the course and outcome of
childhood anxiety disorders?
Anxiety symptoms showed moderate stability during childhood and adolescence
Heightened neonatal biobehavioral reactivity and poor regulation predicted emotion regulation difficulties in preschool, which predicted anxiety symptoms in childhood
Developmental incompetence in childhood predicted anxiety symptoms in preadolescence, and anxiety symptoms in preadolescence predicted incompetence in adolescence
Insecure attachment relationships in infancy predicted negative peer relationship representations in preadolescence, and these representations predicted anxiety symptoms in adolescence.
Compared to males, females showed similar rates of anxiety symptoms and childhood but greater and more stable rates in adolescence; however, males and females showed similar patterns of association between risk factors and anxiety symptoms across childhood and adolescence
The model tested was specific in predicting anxiety symptoms and not psychopathology in general

In the Aschenbrand study,kids with separation anxiety were at greater risk for specific phobia, PTSD, OCD. Kids with sep anx did not appear to be at greater risk for adult panic, agorophobia, GAD, or social phobia.

Objective: To examine whether separation anxiety disorder (SAD) in childhood is a risk factor for panic disorder and
agoraphobia in adulthood. Method: Patients (n = 85) who had completed treatment for SAD, generalized anxiety
disorder, and/or social phobia 7.42 years earlier (on average) were reassessed using structured diagnostic interviews.
Results: Subjects with a childhood diagnosis of SAD did not display a greater risk for developing panic disorder and
agoraphobia in young adulthood than those with other childhood anxiety diagnoses. Subjects with a childhood diagnosis
of SAD did not more frequently meet full diagnostic criteria for panic disorder and agoraphobia, generalized anxiety
disorder, social phobia, or major depressive disorder in adulthood than subjects with childhood diagnoses of generalized
anxiety disorder or social phobia, but were more likely to meet criteria for other anxiety disorders (i.e., specific phobia,
obsessive compulsive disorder, posttraumatic stress disorder, and acute stress disorder). Conclusions: These results
argue against the hypothesis that childhood SAD is a specific risk factor for adult panic disorder and agoraphobia.

From notes:
Comorbidity - over 1/2 kids with anx disorder have another one. Of kids with anx, depression is most common. Also, 1/3 of kids with anx disorders have been found to have ADHD