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Developmental psychology > Chapter 21: atypical development > Flashcards

Chapter 21: atypical development Flashcards

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1
Q

What is typical development? Name 4 aspects

A
  • absence of disorder
  • statistical (within 2 SD from mean)
  • desired situation
  • successful adaptation
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2
Q

What is the gold standard?

A

Compare clinical group to 2 control groups (one matched on chronological age, other one matched on mental age)

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3
Q

When do you have a delay and when do you have a difference in development considering the Gold standard test?

A

Delay: underperformance clinical group to only control group chronological age, not mental age

Difference: underperformance clinical group compared to both control groups chronological age & mental age

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4
Q

Which 4 advances were important for studying atypical development?

A
  1. Understanding impact of prenatal events
  2. Understanding how genotypes of specific disorders map onto phenotypes and associated atypical pathways –> genetic deficit means exclusion of other reasons!
  3. Research methodology
  4. Brain imaging + eye tracking
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5
Q

What is developmental delay and what is developmental difference?

A

Delay: a delayed but normal path of development
Difference: qualitatively different path of development

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6
Q

What is an inclusion criterion and how large is it often?

A

The boundary of atypical to typical in a statistical sense

Usually it’s 1,5 SD below the mean

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7
Q

What is an atypical trajectory and why do we study it (name 2 reasons)?

A

Atypical trajectory = sequence of development that departs from the typical sequence

  1. Design better interventions
  2. Studying atypical can give us information on typical
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8
Q

What is the Human Genome Project? What did it indicate?

A

Research that found that the number of genes was fewer than previously thought.

Indication that there was more to humanity than action of genes in isolation

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9
Q

What is a risk of the following concept: genetically normal and genetically abnormal?

A

It doesn’t value genetic diversity and can lead to the prevention of atypical development (Down syndrome)

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10
Q

What are chromosomal structural abnormalities?

A

An atypical number of chromosomes or a structural abnormality in one or more chromosomes
–> e.g. down syndrome with 3 copies of chromosome 21

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11
Q

What is amniocentesis?

A

Medical procedure used to look for chromosomal abnormalities and fetal infections

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12
Q

What are neuroimaging techniques?

A

Technique for localizing brain activity that enables us to understand more about the pathways associated with atypical development

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13
Q

What is a benefit of using eye-tracking technology?

A

Measuring saccades with no overt task demands or explicit language requirements

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14
Q

What is William’s syndrome and which 4 difficulties do they show?

A

Rare disease caused by deletion of 26 genes from chromosome 7

  1. Speech is overly dependent on adult’s contributions
  2. Difficulties leading conversation
  3. Inability to add new info and respond to requests for new info
  4. Inability to use pragmatics (socially appropriate manners)
    –> But: no language impairment
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15
Q

What was Stojanovik’s finding in comparing children with William’s syndrome and children with specific language impairment (SLI)? How does that relate to Pinker’s point of view?

A

Stojanovik found support that language skills can’t develop independently from cognitive abilities.
–> Levels of cognition interfere with social aspects of communication

Goes against Pinker’s notion

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16
Q

Which 2 criteria need to be met to get a diagnosis of ASD according to the DSM-5?

A
  1. Problems with social interaction / communication
  2. Limited stereotyped repetitive patterns of behavior
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17
Q

Why is the prevalence of ASD increasing? Name 4 things

A

More diagnoses:
- More knowledge about ASD
- Different diagnostic tools (more specific measurements)
- Early identification
- Assortative mating: tend to find a partner that’s quite similar to yourself –> increase in chance of pairing recessive alleles

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18
Q

What is comorbidity? How is this in children with ASD?

A

Simultaneous presence of multiple disorders

70% of children with ASD meet criteria of other disorders

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19
Q

What are the 3 cognitive theories about the explanation of ASD?

A
  1. Theory of mind hypothesis: difficulty understanding others have thoughts and beliefs
  2. Central coherence hypothesis: integrating information by pieces and not by wholes
  3. Executive function hypothesis: deficits in planning, attention, inhibition of responses
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20
Q

What task result was evidence for the central coherence hypothesis? How does this task work? What is the difference between field dependent and field independent?

A

Embedded figures test: locate a hidden figure from a larger complex design.
–> Field independent: locating shape very quickly
–> Field dependent: processing whole, therefore slower

Children with ASD tend to be more field independent, which is evidence for the central coherence hypothesis

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21
Q

What are the two main symptoms of ADHD in DSM?

A
  1. Inattention / organizing tasks and activities
  2. Hyperactivity-impulsivity: can’t sit still, blurts out answer before question has been asked
22
Q

What are the 3 subtypes of ADHD?

A
  1. Combined type
  2. Predominantly inattentive
  3. Predominantly hyperactivity
23
Q

Why is there a small decline in prevalence of ADHD between youth and adults?

A

Hyperactivity part of ADHD can disappear with age, inattention can stay

24
Q

Why is ADHD diagnosed more often in boys?

A
  • Signs of hyperactivity are more visible
  • More research to male gender
25
Q

Which type of ADHD is most dominant in girls?

A

Inattentive type

26
Q

How is the comorbidity in children with ADHD? Which diseases often go together?

A

70% has different disorder as well

  • Learning disorders
  • Sleep disorders
27
Q

What are the two main hypotheses about the cause of ADHD?

A
  1. Castellanos: symptoms may be associated with different brain pathways that are associated with executive function
  2. Deficit in inhibitory control
28
Q

How was deficit in inhibitory control in children with ADHD measured? What could be an alternative explanation?

A

With a stop task: children with ADHD were less able to inhibit responses

Evidence for proof of deficit in inhibitory control in ADHD kids

Alternative: children didn’t remember the task instructions

29
Q

What are 4 types of prenatal factors associated with an increased risk of ASD?

A
  • Maternal diabetis
  • Prenatal infections/inflammations
  • Prenatal exposure to drugs/chemicals
  • Vitamin D / folic acid deficiency
30
Q

What are 4 types of prenatal factors associated with an increased risk of ADHD?

A
  • Maternal stress during pregnancy
  • Heavy metals
  • Cigarette smoking
  • Alcohol
31
Q

How is heritability of ASD in monozygotic twins? What does this tell you about the heritability of ASD?

How is the heritability of ADHD?

A

H = 0,98
–> very high heritability, which indicates that genes play a large role in ASD

ADHD: H=0,74

32
Q

What is a polygenic disorder? Give an example of such a disorder

A

When there are many genes associated with a disorder

E.g. ASD (>800 different genes) and ADHD

33
Q

What does the polygenetic essence of ASD mean?

A

It explains the heterogeneity of the disease
Multiple different genes are affected, so it’s also a broader somatic condition (e.g. heart defects, vision problems, gastrointestinal)

34
Q

What is the clinical relevance of genetic findings? State 4 things

A
  1. Referring to additional services
  2. Gain of knowledge for family
  3. Genetic counselling voor people with ASD when planning on having a child
  4. Genetics can inform pharmacotherapy
35
Q

What kind of somatic complaints are associated with ADHD? Why would that be?

A

Complaints related to lifestyle, such as obesity, lung cancer, artery disease

It has to do with impulsivity

36
Q

How can you best describe differences in the brain of ASD people?

A

Large individual differences, very diverse brain differences if there are any at all compared to individuals without ASD

37
Q

What did Gilbert’s research on brain activity in children with ASD show?

A

For one specific executive functioning test there was greater brain activity in mPFC (important in social interaction) but there were no different behavioral scores

This indicates there is not one thing that reflects someone has ASD

38
Q

What were the results of an MEG study on children with ASD?

A

There is a delay in response when listening to tones
–> Encoding deficit in auditory perception

39
Q

Which task was well suitable for measuring inhibitory control in children with ADHD? How was it measured and what were the results?

A

Stop signal task, measured by EEG

Results: reduced activity in dlPFC, related to inhibitory control

40
Q

What did eye tracking techniques reveal in ASD?

A

People with ASD + no language impairment –> less fixating on eyes

People with ASD + language impairment –> similar results as controls

Showed heterogeneity of ASD

41
Q

What did eye tracking techniques reveal in ADHD? What is an intervention that is derived from this?

A

ADHD show premature saccades, so very fast eye movements

Intervention: extend attention span of ADHD children with eye tracker that gives feedback when the child is losing attention –> adaptive user interface

42
Q

Why is the theory of mind explanation for ASD not completely right?

A

Some children with ASD do well on ToM task, but show poor social functioning nevertheless
Some children also perform poorly on non-social tasks –> maybe more general reasoning as well

43
Q

With which task is the executive functioning hypothesis measured?

A

Wisconsin Card Sorting Test (sort by colour or sort by shape)

Requires cognitive flexibility –> difference ASD vs controls arises

Children with ASD often stick to old rule

44
Q

What were the results of a longitudinal study of Pellicano on children with ASD?

A

Executive function predicts ToM 3y later, not other way around

Central coherence predicts ToM 3y later, not other way around

Conclusion: first executive functioning and central coherence problems and then later ToM problems

45
Q

What are the cause of ToM problems according to Pellicano’s longitudinal study? What can we conclude from this?

A

Caused by executive functioning and central coherence problems

So: ToM isn’t the core of ASD but a consequence of other problems

46
Q

What was the original explanation of ADHD and why did it have to be extended?

A

Original: core deficit in inhibitory control can explain both impulsivity and hyperactivity

There is more to ADHD than just inhibitory control deficit

47
Q

What is the latest model of explaining ADHD?

A

Dual pathway model of ADHD –> sonuga-barke

48
Q

What is Bronfenbrenner’s ecological model and which 5 systems does it have?

A

Model that places individual development into wider context of interaction with environment

  1. Microsystem: individual
  2. Mesosystem: relation between microsystems
  3. Exosystem: Family, friends, mass media, neighbors
  4. Macrosystem: society, culture
  5. Chronosystem: time
49
Q

What are 4 types of interventions for children with ASD?

A
  • Cognitive behavioral therapy
  • Social skills training
  • Modeling
  • Picture exchange communication system for non-verbal clients
50
Q

What are 3 types of interventions for ADHD?

A
  1. Ritalin
  2. Behavioral parent training
  3. School based contingency management

Developmental psychology (19 decks)

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