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Neuropsychology > Lecture 2: Child Neuropsychology > Flashcards

Lecture 2: Child Neuropsychology Flashcards

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1
Q

The brain starts to develop by

A

21 days after conception

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2
Q

neural tube

A

a cylinder of cells that develops
into the nervous system

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3
Q

The developing brain looks like a human brain by
about

A

100 days after conception

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4
Q

Sulci and gyri form at about

A

28–30 weeks

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5
Q

Neurons are formed (where)

A

near the walls of the ventricles
and migrate to their destinations

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6
Q

Brain development involves a massive overproduction of cells and connections, followed by

A

apoptosis, or programmed cell death, to remove the excess cells

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7
Q

apoptosis

A

a polite cell say goodbye, to remove
the excess cells

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8
Q

neuro generation

A
  • stem cell -> another stem (1) and progenitor cell
  • progenitor cell -> glioblast and neuroblast
  • glioblast -> glia: supporting and cleaning brain
  • neuroblast -> neuron: thinking

the stem cell (1) -> help fix brain injuries but not easy

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9
Q

neuro constantly generated through lifespan in

A

hippocampus and olfactory bulb (to smell)

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10
Q

as we get older, the brain generate

A

The brain makes fewer new neurons.
And the new neurons might not work as well as the ones from when you were little.

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11
Q

brain generate cells in the

A

subventricular zone

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12
Q

subventricular zone contains a

A

map to instruct cells going to a specific part of the cortex

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13
Q

neurons climb

A

radial glia like a ladder to other regions

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14
Q

cortex is built from

A

the inside-out, so the deepest layer,
VI, forms first, then V, and so on until layer I is formed

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15
Q

Neurogenesis

A

brain cells are born 👶 (mostly before birth)

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16
Q

Myelination

A

The process of forming a myelin sheath (fatty insulation) around axons

Myelin increases the speed and efficiency

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17
Q

Synaptogenesis

A

new brain connections (synapse) are made

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18
Q

Pruning

A

old/unused connections are cut away ✂️ (to keep the brain tidy)

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19
Q

the sequence of brain growth

A

sensorimotor cortex -> parietal and temporal cortex -> frontal cortex

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20
Q

what are dendrites for

A

receive information (neurontransmitter) from other axons

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21
Q

dendrites development in neural maturation

A
  • Dendritic arborization involves branching
  • Dendritic spines (dinh) are the targets for the synapses
  • Dendrites start to form prenatally, and this continues
    long after birth
  • Dendrites grow slowly, only micrometers per day
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22
Q

Plasticity after Early Brain Injury

A

the effects of injury depends on different points in development

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22
Q

axons growth in neuron maturation

A

Axons grow toward the appropriate targets
- Axons grow at a fairly constant rate of 1 millimeter
per day
* The faster axon growth means axons reach their
targets before dendrites have developed, so can
influence dendritic development

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23
Q

If cortical injury occurs during neurogenesis (embryonic day 18),

A

ecovery tends to be
complete, even if the destruction of the cortex is complete

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24
Damage during neuronal migration and differentiation (postnatal days 1–5)
permanent damage, regardless of size or location of the lesion
25
Damage after migration (postnatal days 7–12)
results in nearly complete recovery of cognitive functions and partial recovery of motor functions
26
Although every seems to be fine at first (recovery), children can grow up with some problems because
the compensating systems are no longer enough (plasticity))
27
Environment and Brain Organization
1. environment when born 2. environment when nurture (early)
28
early experience to brain structure
born in wild -> bigger brain than born in domestic
29
early experience to neuron formation
nurture in complex environment -> increase brain size, longer dendrites, bigger synapse, thicker spines,...
30
young brain and old brain react to the same experience
differently, young brain is more sensitive -> react more, more changes
31
socioeconomic status and academic achievement
are correlated
32
causes of that correlation
parental education, child health, school quality, stress, and language exposure
33
ngheo = nao be
Lower family income is associated with decreased cortical volume across the frontal, temporal, and parietal cortex, independent of sex or race
34
ngheo = it chu
At age 3, children from high-SES families are exposed to 11 million words per year, while children from low-SES families are exposed to only 3.2 million words per year
35
Neurodevelopmental Disorders
- Characterized by onset between in utero development and the start of formal schooling * Result in deficits in social, personal, or school functioning * Impairments may be specific to one function or more global * Incidence may be as high as 17% of school-age children * Deficits often emerge gradually, making it difficult to identify the disorder * Testing and assessment identify variation in the population, so may fail to identify individuals who have difficulties but are still performing close to standard levels
35
Neurodiversity
everyone’s brain works a little differently — and that’s totally okay!
36
Brain Research in Human Infants: Cortical thickness decreases were related to
higher anxiety and depression (high risk group)
37
Neurodevelopmental disorders contain all aspects: identity, disorder, disability, impairment
- indentity vs disorder: curable - disability vs impairment = social barrier
38
Inattentiveness in ADHD
style of behaviour involving disorganisation and lack of persistence * Distractible, forgetful * Can’t follow directions * Disorganised
39
Hyperactivity
excess of movement * Fidgety * Always on the go * Talking excessively
40
Impulsivity
acting without reflecting * Interrupting people * Blurting our answers
41
Prevalence of ADHD
- 5.9% of youth, 2.5% of adults * 2 times more common in males * Inattentive subtype identified more in girls
42
ADHD might sometimes be over-diagnosed — not because the condition is more common
because age, maturity, and different diagnosis practices can affect how often kids are labeled with it.
43
genetic in ADHD
1. heritability: 0.7-0.8 (=ASD, schizophrenia, bipolar) 2. polygenic
44
Cognitive Theories discussed
1. Executive Function deficit (EF) 2. Delay aversion 3. Multiple decifit models 4. Dual Pathway model 5. Three factor model
45
4 criteria to decide whether a model is the primary deficit in ADHD
1. Consistency: EF weaknesses must be present in ADHD across studies 2. Universality: EF weaknesses must be present in most individuals with ADHD 3. Aetiology: EF and ADHD have the same causes (genetic,...) 4. Explanation: EF can be explained for the differences in symptoms of ADHD
46
is EF a primary cause in ADHD
1. Consistency and Aetiology: yes 2. Universality and Explanation: no evidence
47
Delay aversion
the aversion of delay in rewards: The longer they wait, the less rewarding something feels
48
is delay aversion a primary cause in ADHD
Consistency: yes * Meta-analysis indicated consistent delay aversion in ADHD (Marx et al., 2021, JCPP) Explanation: No * The effect size is moderate to small (ibid.) Universality: No * ADHD subgroups without delay aversion can be identified (Stevens et al., 2018, BPCNNI) Aetiology: yes * Brain regions implicated in reward processing are also implicated in ADHD
49
Multiple Deficit Models
* Recognise that ADHD behaviours can arise from different cognitive deficits * Different models propose different cognitive routes * A common criticism is that the multiple deficits models are difficult to test
50
Dual Pathway model
- Independent contributions of executive function deficits and delay aversion * One or both pathways may contribute in an individual
51
Temporal Processing
Trouble with estimating time, rhythms, and timing actions → Example: can't tap along to a beat or misjudge how long tasks take
52
Three Factor Model
any one of the three cognitive problems — or a combination of them — can contribute to ADHD: 1. EF 2. delay aversion 3. temporal processing
53
Brain structure: subcortical volumes
Some reductions in subcortical volume ▪ Most effects found in children ▪ Effect sizes are very small
54
cortical morphology
Kids with ADHD tend to have slightly smaller surface area and thinner cortex, especially in fusiform and temporal regions, suggesting delayed brain development. But the differences are very small, so they are just one piece of the puzzle
55
brain imaging in ADHD
Despite lots of brain imaging studies, we cannot yet identify a reliable “brain signature” of ADHD using fMRI
56
early signs (<12months) of ADHD
- Lack of eye contact * No orienting to name * Little social engagement
57
Signs (12-24 months)
- Delay in language and/or motor development * Repetitive and stereotyped movements become apparent
58
Genetic in ASD
- high heritability (0.9 in twin studies) -
59
Most ASD cases are idiopathic
we don’t know the exact genetic cause — it’s not just one gene.
60
there might be brain structure differences in certain conditions, especially early in life, but it's complicated because not all studies agree and individual differences matter a lot.
bigger head when being babies but grow up with normal size head -> maybe due to neurogenesis and synaptogenesis in ASD infants
61
hypoconnectivity in autism
Too little connectivity in areas that manage attention and sensory input
62
hyperconnectivity in Autism
Too much connectivity in areas like the DMN (resting, wasdering), which can affect social understanding
63
cognitive theories in autism
No cognitive theory provides a universal explanation of autism
64
Theory of Mind deficit
Impairment in the ability the thoughts, beliefs, and desires of others * Explains social difficulties in some autistic people
65
Weak Central Coherence
Bias towards local instead of global processing (detail-oriented) * Explains some perceptual differences
66
Systematising versus Empathising
* Bias towards systems and objects * Explains higher prevalence of autistic traits among scientists and engineers
67
Weak Perceptual Priors
* Reduced reliance on prior knowledge and experience * Explains perceptual differences and sensory sensitivity

Neuropsychology (6 decks)

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