Child Psychopathology Study Guide

Chapter 3: Basic Psychological Theories

Be able to write an essay comparing the lecture material on implicit and explicit processing to Freud’s ideas on the id and the superego.  What’s the difference between implicit processing and Freud’s idea of the unconscious? What’s the difference between the superego and explicit processing/effortful control?

Behavioral  Theories:  Know definitions of classical conditioning, operant conditioning, extinguishing behaviors; negative versus positive reinforcement

p. 73: Focus on behavior:  How does this contrast with psychoanalysis? Cognitive therapy?

What was Watson’s experiment on fear?

p. 74: Behaviorists “do not see humans as automatons.” How does this passage relate to the lecture material on explicit processing/effortful control?

p. 76: How did Wolpe treat phobias? (What is reciprocal inhibition?)

Cognitive Theories: p. 80: What are schemata? P. 81: why do they develop?  How can they create problems? (Note especially the example on pp. 81-82.) p. 82: How can cognitions influence emotion? What is Ellis’s ABC model of behavior? What are automatic thoughts? (This relates to implicit processing as discussed in the lecture. In lecture I emphasized that automatic thoughts may be the result of modules for aggression or sexuality. However, the point here  is that things that we have learned really well  (i.e., by repeated experiences), it becomes automatic—such as when a girl repeatedly experiences rejection at a dance, thoughts of rejection will be automatically triggered by the dance context.) What is the role of therapy regarding automatic thoughts?  Notice that therapists challenge irrational thinking. (Give example.)

Attachment theory

pp. 86-87: How is attachment an evolutionary adaptation?

p. 87: Be able to give the analysis from the attachment lecture of what’s going on in the second full paragraph (i.e., the secure base idea).

p. 87: What evidence is there that attachment is a human universal? P. 87: When do babies become particular about who is caring for them? What are the functions of attachment (i.e., the section on the Importance of Attachment).

p. 88: Know the three attachment classifications. How do the babies behave in the Strange Situation? P. 89: Define the Internal Working Model and how it influences later relationships. What is the therapeutic process for attachment disorders.  (In class it was mentioned that the sensitive period may make it difficult to alter the IWM. Remember, the IWM is a special schema—not easily changed, and this may especially true after infancy.)

Family Systems Theory

p. 92: Describe Lewin’s research.  What’s the point of the Jackson & Weakland (1959) study? P. 93-94: In class we talked about several different personality systems and the theory of psychopathology presented was based on individual characteristics. How does this contrast with the approach to childhood anxiety or childhood aggression on p. 94? What is homeostasis as it applies to families? What are linear and circular causation? (Give examples.) Be able to describe an example of family therapy.

Common Features

p. 98: What are the three similarities among the theories? What is their common goal? (Note the goal of “conscious, self-directed life.” How does this relate to the lecture material on explicit processing/effortful control?

p. 99: How does the author discuss the question of which theory is best? Is any one strategy the best for all clients?

Chapter 4: Quantitative Behavior Genetics

Know definitions: Gene; allele; genome, genotype, phenotype, eugenics, concordance, covariation,  heritability, shared and unshared environmental influences; heritability;  active, gxe interactions; passive, and evocative g-http://www.macleans.ca/canada/opinions/article.jsp?content=20080312_5744_5744&page=2e correlations. Reaction range (from lecture notes)

p. 103-104: What did Galton find? What did Jensen find and what were its effects on the field of behavior genetics? Note the importance of the Minnesota Study on Twins Reared Apart.

p. 106-107: Be able to describe the different methodologies represented in Figures 4.1 and 4.2. What is co-variation? P. 108: Describe Gottesman’s family study for schizophrenia.  What ‘s the main problem with family studies?

p. 108-09: Know the logic of twin studies. What is the questionable assumption of twin studies?  Does research show that the assumption is violated? (i.e., see Plomin et al., 2001). What systematic differences are there in twin studies based on self-reports versus reports from parents and teachers? According to the book, why does this happen?  P. 110: Note the power of the twins reared apart design.

p. 110: Know the logic of the adoption study. What are the two problematic assumptions of these studies?

Heritability:  Heritability is the proportion of the total variation in a particular population that is the result of genetic influences.  It’s not a characteristic of an individual, but rather of a population. Since it is a proportion, it varies between 0 and 1. Notice that the heritability statistic is specific to the specific population studied and can’t be generalized to other populations (e.g., other races) or ages.

What are pair-wise and probandwise concordance? When are concordance rates used and when are correlations used? How is the heritability of height calculated in a study of twins reared apart? In pairs of MZ and DZ twins?

What are shared environmental influences?  Know the four characteristics of shared environmental influences.  What are nonshared environmental influences?

Notice that a lot of the variation in psychological research is the result of error. Unfortunately, this often gets interpreted as unshared environmental variation.

Be sure you know the three types of g-e correlations.

Chapter 5: Classification, Diagnosis, and Assessment

p. 122: note that it is wrong to say children are depressives, etc. This is the same point I made in my personality lecture: It’s wrong to say someone is the shy type. We all have all of the systems, and there are many other traits on which to classify people.

p. 124: note definition of a disorder. What part of it relates to conduct disorder? Depression? Notice the caveat on cultural differences.

p. 125: Note classifications promote research. How?

p. 129: Categorical vs. dimensional: On the basis of the lecture material, which do you think I prefer? pp. 129–130: Notice the way in which categories are created. P. 130: Are classifications arbitrary? Note the contrasts between the last two paragraphs. p. 131: What drawbacks to categorization does the text mention?

Define: disorder not otherwise specified. Note that this is advanced as a solution to a problem created by the categorization system.

Define interrater reliability; Concurrent validity; predictive validity

The DSM: p. 133: know what inclusion criteria, exclusion criteria are; notice that there is no attempt to understand the causes and DSM does not impose any theory (although the categorization process itself might be said to imply a theory).  What are Axis I disorders? Axis II? Comorbidity?

pp. 137–138: Notice all the different areas of assessment and that the point is to get information on specific dysfunctions and specific strengths.

pp. 139: define structured versus unstructured interviews. What is the advantage of a structured interview?

p. 140: Note the various question areas in the section on developmental history. All of these issues are backed up by research showing the importance of these variables.

p. 142: Name three limitations of clinical interviews.

p. 143–145: Behavioral assessment: What are the two main techniques of behavioral assessment and what are their limitations?

p. 147: What are the two main limitations of psychological testing with clinical populations?

Chapter 6: Conduct Disorder and Oppositional Defiant Disorder

p. 151: Note basic definitions of CD and ODD; notice the developmental sequence at the bottom of p. 151–152.

p. 152: What is the main variable by which different groups of children with these disorders are classified?

pp. 153–154: What strikes you as significant about Darren’s temperament in terms of the lecture material? What parenting factors are suggested? What were his peer relations like? Note the ADD symptoms early as well as in the fifth grade.

pp. 154–156: What strikes you as significant about Joleen’s temperament in terms of the lecture material? What parenting factors are suggested? What were her peer relations like?

What differences between Darren and Joleen strike you as important? (There is one very important one in terms of diagnosis in DSM-IV.)

p. 156: Define undersocialized and socialized delinquents.

p. 157: What is the main variable on which DSM-IV diagnoses CD? P. 158: Childhood onset versus adolescent onset CD.

Table 6.1: Notice that the criteria must be repetitive and persistent to count. Which of the systems covered in lecture would seem to be implicated?

 Notice that severity doesn’t count (p. 158)

p. 160: CD as normative in some neighborhoods?

Table 6.2: Which of the systems covered in lecture would seem to be implicated in ODD? Note that criteria for CD supersede criteria for ODD in that if the ODD criteria are found with CD, the child would just get the CD diagnosis.

p. 161: What feature distinguishes ODD from normal oppositional behavior by children? Note the cultural caveat.

p. 162: Be able to discuss the issue of whether CD and ODD are distinct. In favor of a distinction, note the data on sex differences. The continuous view is compatible with the systems perspective I discussed in class. Why?

p. 163: Note the statement that there are no differences in total problems (aggressive and non-aggressive) between boys and girls before about age 6. Bad argument? Have a general idea of how the sex ratio changes with development. What’s the explanation for why school-age girls have lower rates of conduct problems than when they get to adolescence? But note that there is disagreement about whether girls do less bullying (Pepler and Craig, 1995).

p. 164: What is relational aggression? Note Zahn-Waxler’s view.

p. 169–171: What are the associations of CD with IQ, social cognition (4 points), and personality (focus on impulsivity and callous-unemotional personality). How do these personality traits fit into the systems from the lecture material? What two systems seem to be involved with callous-unemotional personality? P. 171: Re peers: there are two main findings (points 1 and 3).

p. 172: What attachment category do you think most CD children would have?

p. 172: From the systems perspective discussed in lecture, what is surprising about the finding that 50% of CD children with depression had depression before onset of CD?

p. 174: note distinction between life-course persistent and adolescent limited CD. Looking at the last paragraph, could the distinction just be a matter of how extreme the child is on a single dimension?

p. 175: Be able to discuss Figure 6.2 and understand the distinction between overt and covert CD. P. 176: Note the role of anger in distinguishing these to categories.

p. 177: Note difference between predatory (instrumental) aggression and affective (reactive) aggression. Recall the related discussion in the lecture on Conscientiousness/effortful control. How does the overt/covert distinction apply to these? Which category is more likely to come from families with frequent physical punishment?

p. 179–182: Notice the three different courses for CD. Which one is like Darren? Which one is like Joleen? Notice the very large sex difference in the Early Onset, continuing problems category. According to Caspi et al, what is the outcome at age 26 for in the Early Onset, Discontinuation group? In the late onset group, what is the explanation for the increase in problems for girls according  to Silverhorn and Frick? How would this be analyzed from a behavior genetic perspective on g.e correlations? But see the discussion of Moffitt et al. In general, could these three groups possibly be on a continuum of severity of one underlying trait?

pp. 182–183: What kinds of stress are CD families under? (Include having a CD child in the list!) What kinds of g.e correlations will show up in CD families? (See first full paragraph on p. 183.) What is the family background correlate of female delinquents? And note that parents are more likely to be criminals and antisocial—obviously suggesting a genetic link.

p. 184: Note that CD children fail to show the normal decline in aggressive behavior. In terms of the lecture material, what does that suggest? p. 185: Be able to discuss Figure 6.3.

p. 186: Note range of heritability estimates and the mean estimate of 37%. In plain English, what does this 37% figure mean? Note that genetic influences stronger for early-onset conduct disorder. Last paragraph: this is often called difficult temperament. What system(s) from the lectures might be involved?

p. 187: What happens if you control for temperament and study the outcomes of different parenting practices? Gerald Patterson’s research is important. Note Figure 6.4 on p. 188.

p. 189: What is the expected effect on parenting of children who are genetically prone to CD? Be able to summarize the findings of the two studies discussed at the bottom of the page.

pp. 190-191: Be able to understand Figure 6.5 and the distinction between direct and indirect effects on early behavior problems.

p. 192: What might one add to Figure 6.6 based on the lecture material?

p. 192: What are the general findings on the cognitive biases of aggressive children (1^st para)? What developmental course does the textbook suggest (2^nd para)?

P. 193: How do aggressive children respond when asked about what sorts of behaviors would be appropriate as responses in hypothetical vignettes?

p. 195: Table 6.5: A laundry list of factors: “All bad things tend to go together, but the more bad things you have, the more likely you are to be diagnosed as CD.” How do you think these factors interact? That is, starting with the child factors, how would they tend to lead to the rest or at least be correlated with the rest?

p. 196: Note people believe that adolescent onset conduct problems think that environmental influences are the story. But are the data consistent with them being lower than early onset CD children on the critical systems discussed in the lecture material, in combination, perhaps, with an upsurge of testosterone (or analogous female hormones for girls) (which may be genetically influenced)? These biological factors might also interact with the social learning environment discussed on p. 197. Describe this environment.

p. 199: Does the material on the top of p. 199 excuse bad parenting in some groups?

p. 201: Notice that parent-training programs less effective for lower-income families. How does the text account for this? Any other ideas? P. 201: Notice training for good social interactions takes advantage of explicit processing. How is the basic model is consistent with the lecture material on Conscientiousness/Effortful control?

p. 202: Notice that interventions for  school-age children are most effective for reactive rather than instrumental aggression. How is that consistent with the basic model from the lecture material on Conscientiousness/Effortful control?

p. 203: Notice that multisystemic therapy is basically like adopting the child into a better family and removing him completely from his old environment. Notice on p. 204 that it’s not very successful. What does that suggest to you?

Chapter 8: Bipolar Disorders

p. 257: Note the typical number of episodes per year. What is the most typical age of onset? Note that early onset is associated with greater genetic risk. This seems to be generally true. The text mentions schizophrenia, but that was also the case with CD.

p. 258: Note that the author thinks of bipolar as a bridge between externalizing disorders and internalizing disorders. Why?

pp. 258-259: Note May’s behavior and that the teacher thinks she may have AHHD. What are some of the mother’s symptoms that indicate bipolar disorder?

pp. 260-261: What are some of the behaviors of Rudy and his parents that strike you as relevant to bipolar disorder? What emotion seems to be the most salient for Rudy?

p. 262: What is the main reason clinicians did not diagnose bipolar disorder until the 1980s? Notice that now it may be overdiagnosed.

p. 263: List some of the characteristics of a manic episode. How long does it have to last? How does a hypomanic episode differ from a manic episode? In Table 8.1, criteria #6 and #7 would seem to involve the BAS (Behavioral Approach System). Why?

p. 264: How long does a hypomanic episode have to last?

p. 265, Table 8.3: Note especially Criterion A. Note in the text that some may experience both manic and depressive symptoms at the same time. Hmmmm. What’s up with that? Be able to discuss Figure 8.1. This is discussed in the text on p. 266.

p. 269: Note the candidate characteristics that might lead us to think two disorders are the same or different. pp. 269-270: What did Lyoo et al. and Wozniak et al. find and what is the relevance of their data to the issue of diagnosis? Note the point at the end of the first full paragraph on p. 270. How is this point related to the lecture material at the beginning of the course?

p. 270: What disorders are most often co-morbid with bipolar disorder? What is the subtraction/proportion method? What did Biederman et al. find? Pp. 270-271: what two other reasons indicate that ADHD and BP are distinct?

p. 271: What are three reasons that BP in children is the same as in adults? What three reasons suggest that it’s not the same?

P. 271: Note that the difference between children and adults may just be developmental (second bulleted point). This is illustrated in Table 8.4 on p. 273. Write down some thoughts about Table 8.4.

p. 272: Note the “driven” quality of manic behavior.

p. 274: Under irritability and in terms of the lecture material, what’s the significance of the finding that irritability not only occurs during bouts of mania, but also during bouts of depression? Do you think that effortful control (hot executive function) could have a role? What other system from the lecture material would be implied?

p. 275: Grandiosity. Anyone feel he or she wants to conduct the class? What happens during the  hypothetical softball game? Hyperactivity: Note this refers to motor behavior and multitasking but also a lack of focus, racing thoughts and many switches between tasks. Do you think it’s the same kind of attention problem as in ADHD? Dangerous Behaviors: Sensation seeking is common, but note also that disinhibited  (taking off clothes, sexuality) behavior is common. Hot executive function problem?

p. 276: What did Geller et al. find? Do you think the subjects were interviewed during a manic phase? Besides ADHD and CD, what other problems are commonly associated with BP? Why does it make sense that substance abuse would be associated with BP?

p. 278: What is the estimated prevalence of BP? Note it’s much lower than CD or ADHD. Sex difference?

p. 279: Note that earlier age of onset associated with a more severe diagnosis. Notice the association of mother-child warmth with a relative high rate of remission of symptoms. What percentage of children diagnosed with BP continue to have symptoms as adults?

p. 279: What are some of the characteristics of families of BP children? (See also p. 280 at the end of the first full paragraph.) How do you conceptualize these characteristics? The text hints at genetic influences on p. 280. If so (and thinking in terms of systems), how do you think this works? (I.e., what are the genetic influences influencing? Notice the high prevalence of parents with a mood disorder—strongly suggesting genetic influence.

p. 281: What is the major neurological hypothesis for BP? But notice that they don’t know how it works. Note the strong evidence of genetic influences. But do we know how the genetic influences work or what systems are involved? What is the “gene-repeats” theory of Huntington’s disease and how does the text suggest it works with BP? Environmental stress: What animal model is suggested? What is a diathesis/stress model? Make a graph depicting genetic predisposition (strong to weak) and environmental stress (strong to weak). Notice also that having a manic episode may sensitize the brain to more episodes—a positive feedback loop. (BTW, I’m getting the impression they really don’t understand BP.)

p. 283: What is the single most important risk factor for BP?

p. 284: Notice that, like ADHD, medication seems indispensable for treatment (but the text also says psychosocial treatments are also “essential”). What are the likely effects of BP on peer relationships? As the text says, the worry is that children will develop a poor reputation before getting treatment and then it is difficult to reverse.

p. 284-285: Medication: Notice that most children don’t respond to any of the three drugs typically used. (Same with adults.) Lots of bad side effects, but is it a good idea to discontinue taking the meds?

p. 286: Note the importance of a warm family environment. How do you conceptualize the effectiveness of such an environment?

Chapter 9: Depressive Disorders

p. 288: Notice DD is underdiagnosed. Why? P. 289: What strikes you as relevant in the vignette about Donald? (Notice particularly the anger and irritability is highlighted.)

What strikes you as relevant about Magda? What are the differences between Magda and Donald?

p. 293: Describe Rene Spitz’s findings. What is masked depression? (Note applicability to Donald.) pp. 294-95: In what two ways do the different depressive disorders differ? What symptom of depression is part of the diagnosis for children but not adults? What are the two differences between major depressive disorder and dysthymic disorder? Be able to discuss Tables 9.1 and 9.2.

p. 299: What observations suggest they are depression and its co-morbid disorders are distinct? Could the co-morbid disorder cause depression? Notice more evidence for distinctiveness in children with more intense depressive systems. So general childhood unhappiness may be appropriate for less intensely depressed children. P. 299: What are some differences between childhood depression and adult depression (i.e.,  sleep patterns, cortisol patterns)? What about the dexamethasone suppression test? Notice that depressed people tend to secrete cortisol even after taking the drug. P. 300: note the unsettled state of ideas on whether the disorder is the same in children and adults. Note especially the third option: They are the same, but … Note the feed forward hypotheses, as with BP.

p. 300: Note the very high percentage of dysthemia overlapping with major depressive episode. But this suggests several hypotheses, as described on p. 301. Note that it may be a matter of degree of impairment.

p. 301: Notice that the case of depression they pay more attention to diagnostic issues. Note the problems with child self-report measures. p. 302: What did Braaten et al. find?

p. 304: Notice that loss of interest in most activities is a general feature of depression, but that two different types of mood also have to be present. Which types? What is anhedonia and how would you conceptualize it in terms of the systems discussed in lecture? What is hypersomnia? What kinds of sleep problems do depressed children have? Note the feelings of worthlessness—the opposite of what happens in mania.

p. 305: Be able to describe typical problems in the area of  peers, parents, and school for depressed children. Notice parents may exacerbate problems because they are upset with the child’s withdrawn behavior. How would you conceptualize their problems in school?

p. 306–307: How does the prevalence of depression change with age?  Does the age curve for depression go up gradually, or are there ages where it shoots up? Note that major depression is quite uncommon in children and that DDNOS is the most common diagnosis. (What is DDNOS?) Why does the text think that depression is becoming more common among children since 1960?

p. 309: Notice that having one depressive episode (how long do they last on average?) predisposes toward more episodes. What are the environmental correlates of relapse?

What does childhood depression predict (bulleted list on p. 309). How does the text interpret the tendency for depressed children to have substance abuse problems?

p. 311: What is the bottom line on sex differences in the course of depression?

p. 313-315: Note the sex differences in depression. At what age is the sex difference noticeable? The text suggests girls are subject to more stress or aren’t as able to handle stress as well, especially if early maturing. What kinds of stress are suggested? Buy it? Given our discussion of the BAS, why might girls be more prone to depression than boys? In class I will mention a life history perspective that suggests why early maturation is a problem.

p. 315-316: Why is it sometimes difficult to determine suicidal intent? Prevalence: Note boys twice as high as girls. Note the high rates of suicide attempts and medically significant suicide attempts.

p. 317: What possible explanations does the text give for the association between suicide and substance abuse? What is the most common disorder associated with suicide? Note the genetic influence on suicide. Pp. 317-318: Note that quite a few different stresses are associated with suicide—the child’s version of “things aren’t going well.” Be able to list some of them. P. 318: Emotions: Note that the text treats suicide and depression as separate and interacting—e.g., the suicidal thoughts could increase depression. What is the role of anger in suicide? Cognition: Note the general point that psychological disorders of many kinds are associated with distorted cognitions. What are some distorted cognitions in cases of depression? What are constriction and tunneling? P. 319: Notice that suicides are often violent. pp. 319-320: Is there any evidence for suicidal contagion?

Families: Maternal depression as a risk factor. But even without a depressed parent, families with a depressed parent are problematic. Why?

pp. 321-322: What is the HPA hypothesis? Why might this system be particularly active in depressed people? P. 323: Note the discrepancy between parent reports and twin reports in yielding heritability estimates. What does the text make of it? The results of Rende et al. and Rice et al. are, as the text notes, intriguing. Do these results surprise you? (They surprise me.) Note also that there is more evidence for heritability of depression in adolescence than in early childhood. But it’s all a mess because adoption studies found no evidence of genetic influence. 323: Parenting: What kinds of parenting are associated with childhood depression and by what mechanism is this thought to work?

Pp. 324-325: What is the attachment theory of depression? Notice that affect regulation is the critical issue. How would insecure attachment lead to poor affect regulation?

Separately, how might depression lead mothers to behave in a way that would increase depression in their children?

Cognition: pp. 326ff: Note that depression can bias a variety of perceptions. What is rumination? What is learned helplessness and why is it considered a problem of biased attributions. Understand what it means to say that depressed children attribute negative events as global, internal, and stable and positive events as specific, external, and unstable. Be able to discuss Figure 9.2 and the attributional style of depressed children.

p. 329: Be able to discuss Figure 9.3.

p. 330: What did Sheeber et al. find? How does the author suggest that parents of depressed children act? P. 331: Gotlib & Robinson: How do normal people respond to people with depression in a “get acquainted” session? (Notice the word ‘evoke’ is used here.)

pp. 331ff: The developmental models basically chart typical life course of two types of depressed children.

p. 335: What types of preventive measures are most common? Notice that they all involve explicit processing and conscious control attempts. Are these programs effective in the long run?

p. 337: Figure 9.4: Why is regression to the mean a problem in interpreting the effects of treatments for depression and other psychiatric problems?

pp. 337–338: Therapy: note that some meds that work with adults don’t work with children and the ones that do work don’t work as well. It’s interesting that the SSRI’s are a problem because they promote impulsivity and mania. Think about that in terms of the BAS.

pp. 338–340: Psychosocial Interventions: How is explicit processing recruited in these four different types of treatments? Which of the four treatment types seems to rely least on explicit processing?

p. 340: Note especially the therapy for infants at risk for insecure attachment. Unfortunately, there aren’t methods to treat older children with attachment disorders, or at least the critical/sensitive period makes it very difficult.

Chapter 10: Anxiety Disorders

p. 344: Which of the systems discussed in lecture seems most relevant to this chapter?

p. 345–348: What are the salient facts about Xavier’s case? What do you think is the relevance of the fact that they live in an unsafe neighborhood? What about the  mother’s behavior? Kim: Notice the different reactions of Alex (who was actually bitten) and Kim.

p. 349: Notice (but please do not remember!) Freud’s psychoanalytic analysis of Hans. Is it any wonder that people have not been able to test Freud’s theories? Watson’s Little Albert is a classic.

p. 351: Notice that children who have one anxiety disorder often have others. Why is this more compatible with a dimensional perspective?

p. 353: Table 10.1: Have a grasp of the general thrust of the 8 criteria; know at least one emotion, one cognition, and one behavior included in these criteria. Notice duration of at least 4 weeks. Onset before age 18: suggests that it may not appear during early childhood but then. pp. 354–355: Notice that the disorder become less common as kids reach adolescence, but symptoms increase with age in those who do have it and may continue into adulthood. Notice also that separation anxiety is correlated with generalized anxiety disorder — results congruent with the  dimensional perspective and the view that all of these disorders involve high levels of the BIS. What are the parents like? (Remember Xavier’s mother.) p. 357: Notice the sex difference in specific phobias? How does the text explain the difference? How would the evolutionary theory of sex explain it?

P. 358: Notice that for people with social phobia, increased exposure to the social situation often increases with repeated exposure, while for normal people it decreases. Get the gist of Table 10.3. p. 360: Notice that children with social phobia often cling to adults in social situations. Sounds like separation anxiety. According to the text, what’s the difference? In discussing mania and other examples where children are high on the BAS, we mentioned high self-esteem, etc. How do children with social phobias feel about themselves? Notice also that they tend to be neglected by other children and have few friends.

p. 361: Notice that social phobia is less common than other anxiety disorders. The Chinese example: remember that genetic differences may play a role. The same can be said about the parenting section on pp. 361–362. Notice that the text does not mention sex differences here. This suggests to me that social phobia may be a different kettle of fish than separation anxiety and specific phobias.

pp. 362–363: What are obsessions and compulsions? Notice obsessions technically cannot be about real-life worries. P. 364: Table 10.4: Get the gist of this table. What is the affective component of compulsions? Some data indicate that OCD is associated with the high end of Conscientiousness (Effortful Control/hot executive function). This suggests that it is quite different from separation anxiety, specific phobias, and social phobia. Notice the conflicting data on sex differences. This does not fit with the expectation of higher rates for females based on findings that girls are higher on effortful control and that OCD is a disorder of effortful control. According to the text, why are prevalence rates higher when measured by interviews with the child than by interviews with the parent?

P. 365: Note that the issue of sex differences is unclear. (Recall that in the lecture I noted that girls are higher on effortful control.) Why do you think that there are such low levels of OCD based on parent report?

Generalized Anxiety Disorder: Note Table 10.5 part A, B, & C. As it says in the text (p. 367), the anxiety has to be out of proportion to the threat. P. 368: Notice in the examples of beliefs of GAD children that the worries are about personal threats. Why do you think that GAD children tend to be perfectionists? P. 369: There is possibly a curvilinear relationship between age and GAD. What is it?

Panic Attacks: Notice the emphasis here on the intensity of the fear and specific occurrences rather than generalized anxiety. Notice the physical symptoms in Table 10.6. Know the bold-faced terms on p. 370 and p. 371.  

p. 375: Notice that the heritability of anxiety is only around 33%. Why does the text think that there is less concordance for MZ twins when the twins rate themselves compared to when parents do it? Notice some evidence for the importance of shared environments. This is pretty uncommon. Notice that genetic influence is seen as affecting a general predisposition to anxiety rather than a specific anxiety disorder. P. 378: This material was discussed in the lecture on the BIS (the second personality dimension). What happens differently with behaviorally inhibited children compared to normal children when they enter a novel situation? P 377: Tripartite Model. Be able to discuss Figure 10.2. How does this make sense in terms of the lecture material on personality systems? That is, how were depression and fear conceptualized?

How does Gray’s comparator work? (See Figure 10.4 and text.) Notice this presupposes mutually inhibitory connections between the BIS and the BAS.

p. 382–383: Notice that classical conditioning can lead to fears and phobias. What are some cognitive aspects of anxiety? P. 384: Why is it a bad idea for parents to get anxious children to avoid situations that cause them anxiety. P. 385: How can operant conditioning maintain or intensify anxiety?

pp. 389–390: What is Wolpe’s method and how does it involve reciprocal inhibition? What is CBT? P. 393: What is involved in the parent-training component of the Family Therapy? P. 393: Notice that the same classes of drugs used for depression are used for anxiety disorders. What’s up with that?