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social science
psychology 2e
Introduction To Abnormal Child And Adolescent Psychology 3rd Edition Robert Weis - Solutions
3. What are some of the particular challenges and difficulties in conducting research on people with paraphilias? How could this affect what we know about paraphilias?
4. Pete disclosed to his therapist that he had been having affairs. Do you think the therapist should have encouraged him to confess this to Helen? Why? Would it help or hurt?
1. How could Bill’s ASPD have emerged from the combination of genes and environment?What specific environmental factors were important in Bill’s life? Was there any evidence for his father having antisocial traits?
2. Which symptoms of ASPD did Bill have?
3. The most effective treatment for ASPD is to prevent cases in the first place by focusing on children and adolescents at risk for the disorder. What are the obstacles to doing this?
4. The lack of effective treatment for ASPD poses great challenges for our society. Given their rates of violence and criminal behavior, some have advocated keeping people with the disorder incarcerated until they are older in an attempt to prevent their future crimes.What do you think about this?
5.1. Describe the key features of intellectual disability and the way in which children with this condition can vary in terms of their adaptive functioning.Differentiate intellectual disability from global developmental delay.List and provide examples of challenging behaviors shown by some children
5.2. Distinguish between organic and cultural–familial intellectual disability.Explain how genetic, metabolic, and environmental factors can lead to developmental disabilities in children.
5.3. Identify evidence-based techniques to prevent and treat developmental disabilities.
ID is characterized by significant deficits in intellectual and adaptive functioning that emerge early in life. Both intellectual and adaptive functioning deficits are necessary for the diagnosis.
Adaptive functioning refers to a person’s ability to cope with day-to-day tasks. DSM5 identifies three dimensions of adaptive functioning: (1) conceptual, (2) social, and(3) practical.
DSM-5 allows clinicians to classify individuals with ID based on their adaptive functioning: mild, moderate, severe, or profound.
In contrast, the AAIDD classifies individuals with ID based on their needed supports—that is, assistance that helps these individuals function in society.
Levels of needed supports include intermittent, limited, extensive, or pervasive.
GDD is characterized by significant delays in several developmental domains (e.g., motor, language, social, or daily living skills) prior to age 5 years. It is a temporary diagnosis used when clinicians suspect ID but the child it too young to administer an intelligence test.
Between 1% to 3% of infants and toddlers meet criteria for GDD.
The American Academic of Pediatrics recommends CMA as a first-line test to identify genetic abnormalities in children with GDD?
It can be physically harmful.
It can strain relationships with parents and cause children to be rejected by peers.
It can limit children’s access to developmentally appropriate social experiences, such as birthday parties, sleepovers, and sports.
It can interfere with learning and cognitive development.
It can place a financial burden on families and the public.
Approximately 25% of youths with ID exhibit challenging behaviors such as stereotypies, SIBs, or physical aggression.
Challenging behaviors can be harmful to the child or others, strain social relationships, limit children’s access to educational or social opportunities, and place a financial burden on families.
Approximately 40% of youths with ID have a comorbid mental disorder. Comorbid conditions are easily overlooked in youths with ID.
The term organic ID was used to describe children who had identifiable causes for their intellectual and adaptive disabilities. Usually, they had genetic disorders, earned very low IQ and adaptive functioning scores, experienced medical complications, and had no family history of ID.
The term cultural–familial ID was used to describe children with no identifiable cause for their intellectual and adaptive disabilities. Usually, they earned IQ and adaptive scores in the 50–70 range, were physically healthy, and had family members with ID.
Most research supports the similar sequence hypothesis—that is, youths with ID progress through the same stages of cognitive development as typically developing peers, albeit at a slower pace.
In contrast, there is limited support for the similar structures hypothesis. Some causes of ID are associated with behavioral phenotypes—that is, specific patterns of behavior and cognitive strengths and weaknesses.
Down syndrome (trisomy 21) is associated with moderate ID, characteristic appearance, weakness in verbal skills and language, strength in visual–spatial reasoning, and sociability.
PWS is caused by missing paternal genetic material on chromosome 15. It is associated with mild ID, weakness in short-term memory, strength in visual–spatial reasoning, hyperphagia, and obsessive–compulsive behavior.
Angelman syndrome is caused by missing maternal genetic material on chromosome 15. It is associated with moderate to severe ID, sporadic/jerky movements, lack of spoken language, hyperactivity, and persistent social smile.
WS is caused by deletions on chromosome 7. It is associated with mild ID, welldeveloped spoken language, strengths in auditory memory, weakness in visual–spatial reasoning, hyperactivity, anxiety, and friendly demeanor.
Fragile X syndrome is an inherited, X-linked disorder that adversely affects boys more than girls. It is characterized by mild to moderate ID, characteristic appearance, strengths in simultaneous processing, weakness in sequential processing, and social deficits.
Rett syndrome is usually caused by a genetic mutation in a portion of the X chromosome. It almost always affects girls. It is characterized by typical development in early infancy followed by rapid deterioration in social functioning and language, severe ID, hand-wringing stereotypies, and seizures.
Serum screening is a maternal blood test that can be conducted 15 to 18 weeks’gestation to detect the presence of some developmental disorders.
Amniocentesis and CVS are more invasive procedures that may be used when there is an elevated possibility of a developmental disability.
Physicians can use ultrasound to detect structural abnormalities in the fetus that might indicate Down syndrome.
Clinicians can use functional analysis to identify and alter the antecedents or consequences of challenging behavior. Most challenging behavior is maintained by positive social reinforcement, negative reinforcement, or automatic reinforcement.
Differential (positive) reinforcement is usually the first-line behavioral treatment to reduce challenging behavior in youths with ID. Negative punishment strategies include extinction, time-out, and response cost. Positive punishment is used only when other interventions are unsuccessful, when the
Atypical antipsychotics like aripiprazole (Abilify) and risperidone (Risperdal) are effective in reducing aggression in some youths with ID.
1. When many people think of ID, they think about a child with Down syndrome. To what extent do children with Down syndrome reflect all children with IDs?
2. How does the treatment for PKU illustrate the interaction of genes and environment in child development?
3. Why are children of lower-SES backgrounds at greater risk for certain types of ID? Why might low-SES children with IDs have poorer prognoses than middle-class children with IDs?
4. Why would clinicians probably not use extinction (i.e., planned ignoring) to reduce SIBs in a young child with a developmental disorder?
5. What might be the benefits and drawbacks of academic inclusion on a typically developing child?
6.1. Describe the key features of autism spectrum disorder (ASD) and explain how the disorder exists along a “spectrum.”Show how the prevalence of ASD varies as a function of children’s gender, socioeconomic status (SES), and ethnicity.
6.2. Identify the genetic, epigenetic, and brain abnormalities associated with ASD in young children.List and describe early deficits in social cognition typically shown by infants and toddlers who are later diagnosed with ASD.
6.3. Describe several evidenced-based treatments for ASD and differentiate these treatments from interventions that lack empirical support.
1. Stereotyped or repetitive behaviors including speech (e.g., repeating words or phrases), movements (e.g., hand gestures), or use of objects (e.g., lining up toys)
2. Excessive adherence to routines or resistance to change (e.g., need to dress, eat, or bathe at a certain time or in a certain manner)
3. Restricted, fixated interests that are abnormal in intensity or focus (e.g., constantly talking about idiosyncratic hobbies)
4. Hyper- or hyporeactivity to sensory input (e.g., indifference to pain, unusual sensitivity to certain tastes, textures, or sounds).
Approximately 44% of school-age children with ASD may meet criteria for ID.
Approximately 25% of children with ASD are mute and approximately 50% more youths with ASD show problems with speech or language.
Children who show deficits in social communication but do not display restricted or repetitive interests or behaviors would be diagnosed with social (pragmatic)communication disorder rather than ASD.
Approximately 70% of youths with ASD have a comorbid mental disorder (e.g.,
ADHD, anxiety) and 70% have an associated medical problem (e.g., GI problems, seizures).
Approximately two-thirds of children eventually diagnosed with ASD display signs of the disorder by age 18 months. Early indicators include a lack of eye contact, failure to initiate social interactions, and problems with joint attention.
Approximately one-third of children eventually diagnosed with ASD do not show signs of the disorder until after age 2, when social communication deficits and restrictive, repetitive behaviors or interests emerge.
Prognosis for youths with ASD is variable. The best outcomes are seen in children with (a) higher intellectual ability, (b) better language skills, and (c) greater social engagement.
Prevention programs seek to improve the early social communication skills of children at-risk for ASD.
RIT teaches imitation skills. Therapists imitate children’s play and reinforce children for imitating gestures and other actions.
JASPER relies on discrete trial training to improve joint attention and symbolic play in young children with ASD. Treatment can be delivered by therapists, parents, or teachers.
1. What does it mean when professionals refer to autism as existing on a “spectrum”?
2. In retrospect, many parents recall that their children with ASD exhibited problems with social communication and behavior in infancy and toddlerhood. However, in most cases, ASD is not diagnosed until the preschool years. Why?
3. Explain the concept of discrete trial training. How might a therapist use discrete trial training to teach a child with ASD and ID to identify a penny, a nickel, and a dime?
4. Imagine that you are a third-grade teacher. You have learned that a transfer student, a boy with ASD and ID, will be beginning your class in 2 weeks. What might you do with the other students in your class to prepare them for their interactions with this newcomer?
5. Your neighbor has a son with ASD. She is considering flying herself and her son to another state to participate in a 1-week sensory integration therapy program that promises to improve his social functioning. What might you say to your neighbor regarding her plan?
7.1. Describe the key features of children’s communication disorders.Identify the main causes of communication disorders and their evidence-based treatment.
7.2. Differentiate between a specific learning disorder and a specific learning disability.
1. Tom and Kelly are parents of a 2-year-old girl with late language emergence. At 24 months, their daughter is able to say only a handful of words and communicates mostly through gestures. Tom and Kelly are wondering if their daughter will eventually catch up to other children her age or if her
2. Children’s language problems are sometimes associated with impoverished parent–child interactions.Why can’t we conclude that the quality of parent–child interactions causes these language problems?
3. Some adults try to help children who stutter by encouraging them to “relax” during conversations. Why isn’t this strategy usually effective? What might be a more effective intervention for older children and adolescents who stutter?
4. Why aren’t children who meet diagnostic criteria for ASD also diagnosed with social communication disorder? How might these two disorders be differentiated?
5. Children from low-SES families are at disproportionate risk for being classified with a learning disability.How might school psychologists and other professionals avoid misdiagnosing these children?
8.1. Describe the key features of attention-deficit/hyperactivity disorder (ADHD) and how the signs and symptoms of this disorder vary from early childhood through adulthood.Identify problems associated with ADHD and how these problems vary as a function of children’s age and gender.
8.2. Discuss some of the main causes of ADHD and differentiate among the three neural pathways that underlie the disorder.
1. Nearly all young children show occasional problems with inattention and hyperactivity–impulsivity. How might a psychologist differentiate developmentally expected inattention or hyperactivity–impulsivity from ADHD?
2. Why are children with ADHD at risk for problematic parent–child interactions? Why are children with ADHD at risk for peer rejection? If you were a clinician, how might you prevent these social problems in young children with ADHD?
3. Barkley claims that ADHD is not primarily a disorder of inattention; rather, it is a disorder caused by a lack of behavioral inhibition. How does behavioral inhibition play a critical role in Barkley’s model for ADHD?
4. Under what circumstances might a physician decide to prescribe a nonstimulant medication, such as Strattera, to a child or adolescent with ADHD?
5. Philip is an 8-year-old boy who was recently diagnosed with ADHD, combined presentation. His mother is reluctant to use medication to manage his symptoms; instead, she wants Philip to participate in “talk therapy” with a counselor to help him “learn how to behave.” What might you say to
9.1. Describe the key features of oppositional defiant disorder (ODD) and conduct disorder (CD).Explain how conduct problems vary as a function of children’s age of onset, gender, and capacity for prosocial emotions.
9.2. Discuss some of the main causes of children’s conduct problems across genetic, biological, psychological, familial, and social–cultural levels of analysis.
ODD is a DSM-5 disorder characterized by a pattern of (a) angry or irritable mood,(b) argumentative or defiant behavior, and/or (c) vindictiveness toward others.
Children with ODD differ from typically developing children in two ways: (1) they show a greater number and severity of behavior problems and (2) their behaviors are developmentally unexpected.
CD is a DSM-5 disorder characterized by a repetitive and persistent pattern of behavior in which the basic rights of others or societal norms are violated. Behaviors include (a) aggression, (b) property destruction, (c) deceitfulness or theft, and (d)serious rule violations.
Children’s conduct problems fall into four factors: (1) oppositional and defiant behaviors, (2) aggression, (3) property violations, and (4) rule violations. These factors are identified based on the overtness and destructiveness of the child’s actions.
Aggression can be reactive (in response to threat, frustration, or provocation) or proactive (to achieve some goal).
The Dunedin study showed two pathways for CD based on the onset of conduct problems. Childhood-onset CD was associated with more severe and lasting problems, and placed youths at risk for ASPD in adulthood.
Limited prosocial emotions include (a) a lack of remorse or guilt, (b) callousness or lack of empathy, (c) minimal concern about performance, and (d) shallow or deficient affect. These characteristics overlap with the construct of psychopathy in adults.
ODD and CD are distinct disorders that frequently co-occur. Most youths with
ODD do not develop CD; approximately 31% of youths with CD do not have a history of ODD.
ADHD places children at risk for ODD and CD. Underlying problems with inhibition or emotion regulation could explain the comorbidity of ADHD and these disorders.
Youths with conduct problems begin using substances at an earlier age than typically developing youths and are 6 times more likely to develop a substance use disorder.
As many as 75% of older children and adolescents with conduct problems have anxiety or depression. The dual failure model posits that conduct problems cause academic and peer difficulties that, in turn, contribute to depression.
Approximately 3.3% of youths have ODD and 3.2% have CD.
On average, conduct problems are appropriately 2 to 3 times more likely in boys compared to girls. The gender gap is greatest during middle childhood.
Girls are more likely than boys to engage in relational aggression—that is, harming others’ mood, self-concept, or social status through rumors, lies, and the manipulation of interpersonal relationships ?
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