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Neuropsychology > Lecture 8: Child Psychology > Flashcards

Lecture 8: Child Psychology Flashcards

1
Q

What is right hemispherectomy? When is this intervention used and which consequences do you expect?

A

Removing one hemisphere of the brain

Used when there are severe seizures in one part of the brain and no other treatment works

Expect severe disabilities in moving/controlling one side of the body

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2
Q

What are the consequences of hemispherectomy when it’s done as a kid?

A

Subtle motor difficulties, otherwise healthy

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3
Q

When does the brain start to develop?

A

21 days after conception by forming neural tube

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4
Q

What is a neural tube?

A

Cylinder of cells that develops into the nervous system

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5
Q

When does the developing brain sort of look like a human brain?

A

100 days after conception

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6
Q

When do the sulci and gyri form in brain development?

A

28-30 weeks after conceptions

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7
Q

Where are neurons formed in the developing brain and what happens to them after formation?

A

Formed in subventricular zone (near the walls of ventricles)

They migrate to their destination in the cortex

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8
Q

What can you say about the amount of neurons produced during prenatal brain development?

A

Overproduction of cells and connections.

Later in development (postnatal) there is apoptosis to remove excess cells

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9
Q

In which two brain areas can you still find active stem cells in adults?

A

Hippocampus and olfactory bulb

But generally speaking there is no generation of new neurons in adults except these regions

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10
Q

What does the presence of stem cells in adults suggest?

A

It suggests neural injuries could be repaired, but that often doesn’t happen

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11
Q

How does the rate of neurogenesis develop over age? And the function of neurons produced?

A

The rate decreases with age

Function of produced neurons may be different depending on your age

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12
Q

In which two types of cells do neural stem cells divide?

A
  1. Another stem cell
  2. Progenitor cell
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13
Q

What is a progenitor cell?

A

These divide to produce neuroblasts/glioblasts –> develop into neurons of glia

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14
Q

Explain how cortical maps develop in 3 steps

A
  1. Subventricular zone contains map of cortex
  2. Map enables cells to migrate to a specific part of the cortex
  3. Neurons migrate along radial glia to the cortex
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15
Q

How many layers does the cortex have and how is it formed?

A

6 layers

Built from inside out (from subventricular to primitive cortex at the brain surface)

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16
Q

What are radial glial processes?

A

The migration of a neuron from subventricular zone to the brain surface

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17
Q

What happens to the neurons during maturation? (2)

A
  1. Cells produce dendrites to increase surface area for formation of synapses
  2. Axons grow toward appropriate targets
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18
Q

What is dendritic arborization?

A

Branching of dendrites to be better able to form synapses

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19
Q

What is the span of development of dendrites?

A

Form prenatally and continues development until 24 months after birth. They grow very slow

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20
Q

How does fast axon growth influence dendritic growth?

A

The faster axons grow, the faster they reach their targets (dendrites), even before dendrites have developed a lot. In this way dendrites fulfill their function faster

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21
Q

What is the time span of neurogenesis and myelination?

A

Neurogenesis from 21 days after conception until 2 months before birth

Myelination from 2 months before birth onwards through life

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22
Q

Give the order of development of 3 main regions in the cortex

A
  1. Sensorimotor: -2m til 12m
  2. Parietal-tempral association: birth til 8 years
  3. Prefrontal cortex: birth (slow up), peak around 2 years, then down

(see slide 11)

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23
Q

There has been research on rats concerning plasticity after early brain injury. What happened:

  • Cortical injury during neurogenesis
  • Damage during neuronal migration/differentiation
  • Damage after migration
A
  • Complete recovery, even if complete destruction of cortex
  • Permanent damage regardless of size/location of the lesion
  • Nearly complete recovery of cognition, partial recovery of motor
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24
Q

What happens in the brain when a child is growing into deficits?

A

Regions that were previously compensating for lost function can no longer do so

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25
Q

What is the difference between apoptosis and synaptic pruning?

A

Apoptosis: programmed suicide of entire cell
Pruning: cutting branches of neurons and breaking connections (not destroying entire cell)

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26
Q

What is the reason early injury has a good prognosis? And for later recovery 7-12 days after birth?

A

Early: active stem cells can replace damage neurons

Later: other regions are able to compensate for the damage

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27
Q

Why do wild animals have a 10-20% lager cortex than domesticated animals? How does it work for animals born in the wild and then domesticated at young age?

A

Wild animals have a more rich environment, which leads to it being necessary to use the brain a lot –> larger brain

There is a sensitive region to be able to domesticate wild animals. They have brain sizes similar to other wild animals when young, after that more like domesticated animals

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28
Q

What are 4 differences observed in cortex of animals with simple compared to rich environment?

A
  1. Glial cell density
  2. Density of spines
  3. Length of dendrites
  4. Size of synapses
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29
Q

What is the relation between socioeconomic status and academic achievement? Name 5 possible causes

A

There is a relationship between SES and academic achievement

Causes:
- Parental education
- Child health
- School quality
- Stress
- Language exposure

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30
Q

What is lower family income associated with concerning the brain?

A

Less cortical volume across frontal, temporal and parietal cortex

Independent of sex or race

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31
Q

Why are neurodevelopmental disorders hard to identify?

A

Deficits often emerge gradually

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32
Q

What is the incidence of neurodevelopmental disorders in school-age children?

A

17%

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33
Q

When is the typical onset of neurodevelopmental disorders?

A

Between in utero development and start of formal schooling

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34
Q

What is neurodiversity?

A

The idea that everyone’s brain is different and therefore everyone thinks, behaves and feels differently

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35
Q

What are the 2 spectra in neurodiversity?

A
  1. Disability vs. impairment
  2. Identity vs. disorder
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36
Q

What is meant with disability vs. impairment?

A

Impairment: physical difference that creates limitation
Disability: interaction between personal characteristics and societal barriers

37
Q

What is meant with identity vs. disorder?

A

Identity: characteristics that define a sense of self
Disorder: characteristics that could be treated or modified

38
Q

What are the 3 subtypes of ADHD according to DSM 5?

A
  1. Predominantly inattentive type
  2. Predominantly hyperactive-impulsive type
  3. Combined type
39
Q

Name 4 aspects of DSM 5 criteria for ADHD

A
  1. 6 or more symptoms of inattention and/or hyperactivity for at least 6 months
  2. Symptoms present in two or more settings
  3. Symptoms present before age 12
  4. Lead to impairment in social, academic or occupational functioning
40
Q

What is inattentiveness in ADHD?

A

Behavior involving disorganization and lack of persistence

E.g. distractible, forgetful, can’t follow directions

41
Q

What is hyperactivity in ADHD?

A

Excess of movement

E.g. fidgety, always on the go, excessive talking

42
Q

What is impulsivity in ADHD?

A

Acting without reflecting

E.g. interrupting people, blurting out answers in class

43
Q

What is the prevalence of ADHD in youth and adults? How is the gender balance?

A

youth: 5,9%
adult: 2,5%

2x as likely in males
Inattentive subtype more seen in females

44
Q

Are there cultural differences concerning ADHD?

A

There are no large differences in prevalences. Everywhere the number of diagnoses increased in the past 30-40 years

45
Q

What is the heritability of ADHD? What can you say about the genetic mechanism behind it?

A

70-80%

Associated with thousands of genetic variants with a small effect size. There is a high overlap between polygenic risk for ADHD and other disorders (e.g. ASD)

46
Q

What is executive function and what are the 4 tasks?

A

Higher order cognitive processes that guide behaviors in pursuit of a goal

  1. Inhibition
  2. Updating
  3. Shifting
  4. Planning
47
Q

What are 4 criteria for establishing if executive function deficits are a primary deficit in ADHD? Are they met?

A
  1. Consistency: consistent demonstration EF deficits across studies
    –> yes: 65% with ADHD poorer in EF
  2. Explanation: EF deficits should account for substantial variance in symptoms
    –> no: variance in EF can’t fully explain variance ADHD symptoms
  3. Universality: EF weaknesses must be present in most people with ADHD
    –> No: not everyone with ADHD shows EF deficit
  4. Aetiology: EF deficits and ADHD symptoms must have common aetiological influences (e.g. genetic)
    –> Yes: overlap between genes and brain mechanisms between ADHD and EF
48
Q

What is delay aversion? Do they meet the 4 criteria to say it’s a primary deficit in ADHD?

A

Faster decline in the effectiveness of reward as the delay between behavior and reward increases

  1. Consistent delay aversion in ADHD
  2. Explanation: no big effect size
  3. Universal: not everyone with ADHD has delay aversion
  4. Aetiology: brain regions in reward prcessing are also involved in ADHD
49
Q

What is the multiple deficits model of ADHD? What is a point of criticism?

A

Model that recognizes that ADHD behaviors can arise from different cognitive deficits. Different models propose different cognitive routes

Criticism: multiple deficits models are difficult to test

50
Q

What is the dual pathway model of ADHD?

A

Independent contributions of executive function deficits and delay aversion to ADHD

One or both pathways may contribute in an individual

51
Q

What is the three factor model of ADHD? What are the three factors?

A

Independent contributions from
1. Executive function
2. Delay discounting
3. Temporal processing

52
Q

What is temporal processing?

A

Rhythm, estimating durations, anticipating stimulus

53
Q

What is delay discounting?

A

Process underlying decision making. It’s the reduction of a value of a reward related to the time that it takes to be released.

54
Q

What can you say about the cortical volume in people with ADHD?

A

Some reductions found in subcortical volume, most in children. However, the effect sizes are very small

55
Q

What can you say about the cortical morphology in people with ADHD?

A

Lower total cortical thickness and regional increase in thickness in the fusiform gyrus and temporal pole in children

Very small effect sizes though

56
Q

What were the results of a resting-state fMRI test in people with ADHD? And a task fMRI test?

A

Resting state: no significant hyper/hypo connectivity of any specific region in ADHD

Task: no consistent differences

57
Q

What are specific learning disorders (SLD)?

A

Disorders that impact the ability to learn and apply reading, writing or math skills

58
Q

What is reading and what are the 3 types?

A

Identifying letters, converting them into sounds, combining sounds and short term memory

  1. Phonological: decode letters of words into sounds
  2. Graphemic: looks at whole word an produces sound of that word from memory
  3. Fluent reading = phonological + graphemic
59
Q

Which brain area are impairments of phoneme use associated with?

A

Left-hemisphere language areas

60
Q

What do we mean with the finding that there is reduced functional connectivity in males with dyslexia?

A

Males had weaker connections between left medial geniculate body (MGB) and left temporal cortex

61
Q

What is the typical time in which most people can separate two sounds? How is this in language impaired people?

A

If they are separated by 10-40 milliseconds

Language impaired people require much longer intervals between tones

62
Q

What are 5 possible causes of reading deficiencies?

A
  1. Reduced functional connectivity
  2. Reduced sound-detection ability
  3. Attentional deficiency
  4. Motor deficiency
  5. Multicausal approach: reading disorder isn’t one single condition but multiple conditions with different causes
63
Q

What is the attentional deficiency in people with reading disorders and what brain region is associated with it?

A

Difficulty shifting attention to relevant cues

Parietal lobe association areas

64
Q

What is the motor deficiency in reading disorders and which brain region is involved?

A

Cerebellum is involved in timing, coordination and attention. Damage to the cerebellum might result in problems with reading

65
Q

What is the multicausal approach to investigating the causes of reading disorders?

A

It’s possible that reading disorders aren’t single conditions, but multiple conditions with different causes

66
Q

What is dyscalculia? What are 3 difficulties experienced by the people who have this?

A

Difficulty representing and processing numbers in a typical way.

Diffficulty with:
- Number sense
- Calculation
- Mathematical reasoning

67
Q

What is the incidence of dyscalculia?

A

5 per 100 students

68
Q

What is the function of neuropsychological testing?

A

Identify individuals with specific cognitive profiles

69
Q

What are IQ tests most commonly used for?

A

Assessment of overall cognitive function and the pattern of performance on subtests

70
Q

What is the ACID profile? When is it used?

A

Arithmetic, Coding, Information, Digit span results on the Wechsler Intelligence Scale for Children (WISC)

It can help tracking a specific learning difficulty in children

71
Q

What is the impact of having a child with learning disabilities on the parents?

A

Parents perceive greater impact of learning disabilities on well-being, happiness and social interaction than the individuals with the disability

72
Q

What are 2 important counselling strategies for children with learning disabilities?

A
  1. Assessment of strenghts and weaknessesses, followed by instruction to address these weaknesses
  2. Focus on strategies to work around the individual’s challenges
73
Q

What are 2 important scientists for describing autism?

A

Leo Kanner and Hans Asperger

74
Q

What is the prevalence of autism? How is it distributed between genders and what could be an explanation for this?

A

Around 17 per 1000 children

More common in males: likely a diagnostic bias

75
Q

What are the 5 DSM criteria for ASD?

A
  1. Deficits in social communication and social interaction
  2. Restricted and repetitive behaviors, interests or activities
  3. Symptoms present early in development
  4. Symptoms cause clinically significant impairment in social, occupational or other areas of functioning
  5. Symptoms not better explained by intellectual disability or global developmental delay
76
Q

What are 3 aspects of difficulties in social communication and interaction in children with ASD?

A
  1. Difficulties in social reciprocity
  2. Difficulties with non-verbal comms
  3. Difficuluties with understanding, maintaining and developing social relationships
77
Q

What are 4 aspects of restricted and repetitive behaviors and interests in people with ASD?

A
  1. Repetitive motor movements (use of objects or speech etc)
  2. Insistence on sameness, inflexible adherence to routines
  3. Highly restricted, fixated interests
  4. Hyper or hypo reactivity to sensory input
78
Q

At what age is often the diagnosis of autism?

A

typically around 3 years, but some signs are there at 12 months as well

79
Q

What are 3 early signs of autism (<12months)?

A
  1. Lack of eye contact
  2. No orienting to name
  3. Little social engagement
80
Q

What are 2 signs in the age of 1-2 years?

A
  1. Delay in language development and/or motor development
  2. Repetitive and stereotyped movements become apparent
81
Q

What can you say about the role of genes in ASD?

  • Heritability
  • Is it the only explanation?
A

H = 90% in twin studies

Most cases are idiopathic (not able to establish cause). Unaffected family members may share traits as well.

82
Q

What are some differences in neuroanatomy between people with ASD and healthy controls? (2)

A

ASD:
1. Head size: larger head in infancy, later typical head size. Perhaps due to differences in neurogenesis and synaptogenesis

  1. Differences in subcortical structures (amygdala / striatum)
    –> Inconsistent!
83
Q

What is sensory and attention hypoconnectivity and DMN (default mode network) / subcortical hyperconnectivity associated with in ASD?

A

Social impairment and more sensory processing

84
Q

What are 2 striking differences in connectivity in people with ASD compared to controls?

A
  1. Hypoconnectivity of sensory and attentional areas
  2. Hyperconnectivity of DMN (default mode network) and subcortical structures
85
Q

What are 4 cognitive theories concerning autism?

A
  1. Theory of Mind (ToM) deficit
  2. Weak Central Coherence
  3. Systematizing versus Empathizing
  4. Weak Perceptual Priors
86
Q

What is the Theory of Mind deficit in ASD?

A

Explains social difficulties in some autistic people. It’s the impairment in the ability of thoughts, beliefs and desires of others

87
Q

What is the Weak Central Coherence theory for ASD?

A

Explains some perceptual differences. It states that someone with ASD has a bias towards local instead of global processing

88
Q

What is the systematizing vs. empathizing theory for ASD?

A

It explains higher prevalence of autistic traits among scientists and engineers. It states that someone with ASD has a bias towards systems and objects

89
Q

What is the Weak Perceptual Priors theory of ASD?

A

Explains perceptual differences and sensory sensitivity. People with ASD have reduced reliance on prior knowledge and experience

Neuropsychology (16 decks)

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