26.6 - Typical and Atypical Development Flashcards

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1
Q

Describe why the timing of a lesion is important for understanding development and developmental disorders.

[IMPORTANT]

A
  • There are continued developmental changes in cortical regions from childhood into adulthood (Gogtay, 2004)
  • Different systems develop at different times ->The rise and fall of synaptic density differs in timing for visual, auditory and prefrontal cortex systems (Huttenlocher, 2002)
  • This means that lesions at different times will affect different aspects of functioning
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2
Q

Compare lesions of language areas in children and adults.

[IMPORTANT]

A
  • In infants, right hemisphere lesions lead to great risk for delays in word comprehension (Bates, 1997). In adults, it is left hemisphere lesions that cause language problems.
  • In children, left POSTERIOR lesions lead to difficulties with language production. In adults, left ANTERIOR lesions lead to difficulties with language production (and left posterior lesions are associated with comprehension difficulties).

This suggests that there may be a change in language areas in infants through development (i.e. from right to left side).

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3
Q

Can language area lesions recover if they occur in early life or adulthood?

[EXTRA]

A

If the lesion occurs in early life, the language skills usually resolve regardless of the side of lesion. Adults with left hemisphere lesions do not recover. (Bates, 2001)

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4
Q

Compare lesions of visuo-spatial areas in children and adults.

[IMPORTANT]

A
  • Right hemisphere lesions lead to problems with global aspects of visual stimuli in both children and adults.
  • Left hemisphere lesions lead to problems with local aspects of visual stimuli in adults (remember left = local). In children, they lead to problems with both local and global aspects of visual stimuli.
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5
Q

Can visuo-spatial processing area lesions recover if they occur in early life or adulthood?

[EXTRA]

A

In general, they cannot recover (unlike language, for example).

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6
Q

Give two examples of functionally-defined developmental disorders. What is meant by functionally-defined?

A
  • Attention Deficit Hyperactivity Disorder (ADHD)
  • Autistic Spectrum Disorder (ASD)

They are functionally-defined because they show core neurocognitive deficits but they may be heterogeneous in aetiology, unlike acquired lesions.

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7
Q

What the the DSM-IV criteria for diagnosis of ADHD?

A
  • Criterion A: Child must exhibit six (or more) symptoms of either inattention or hyperactivity (see next flashcard) -> These must have persisted for over 6 months.
  • Criterion B: Some inattentive or hyperactive-impulsive symptoms are present before age 7 years -> Changed to 12 years in DSM-V
  • Criterion C: Symptoms are exhibited in two or more settings (e.g. at school or at home)
  • Criterion D: Must be clear evidence of clinically significant impairment in social or scholastic functioning
  • Criterion E: Symptoms do not occur exclusively during the course of, or can not be better accounted for by, another disorder -> Changed in DSM-V
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8
Q

Describe the symptoms of ADHD.

A
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9
Q

Do all patients with ADHD show symptoms of both inattention and hyperactivity?

A

No, and this gives rise to the different types of ADHD.

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10
Q

What is the prevalence of ADHD?

A

3-5% of school children suffer from ADHD (Castellanos & Tannock, 2005)

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11
Q

Describe the neurocognitive theories of ADHD.

[IMPORTANT]

A
  • The classic view is that the symptoms of ADHD are caused by an inhibition deficit that leads to executive dysfunction (e.g. problems with working memory, etc.) (Barkley, 1997)
  • This was suggested to be due to abnormalities in the fronto-striatal circuitry
  • However, this fails to account for the inattention in ADHD (Huang-Pollock, 2006)
  • Therefore newer theories suggest that ADHD may also be underlaid by:
    • Working memory difficulties (Lui & Tannock, 2007)
    • Sustained attention difficulties (Manly et al, 2001)
    • Motivational difficulties (Solanto et al, 2001) -> For example, executive functions may be present, but only when there is high motivation for a task (Liddle, 2011)
  • This means that recently the view of a single deficit has been argued against and there is increasingly consideration of other areas of the brain

NOTE: The terms in bold are those mentioned in the spec.

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12
Q

Describe the symptoms of autism spectrum disorder (ASD).

A
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13
Q

Describe the neurocognitive theories of autism spectrum disorder (ASD).

[IMPORTANT]

A
  • Classically, ASD is thought to be due to a core mentalising deficit (Mentalising is our ability to understand the mental state of oneself or others. This can be thought of as the ability to imagine the mental activity of others and understand their behaviour from it.)
  • However, this is not always seen in all patients with ASD, so new theories suggest that ASD could also be caused by:
    • Executive difficulties (inhibiting true beliefs) (Russell, 1991) -> Executive functions predict later mentalising abilities in ASD
    • Weak central coherence (a human being’s ability to derive overall meaning from a mass of details) (Happe, 1994)
    • Multiple-hit hypothesis -> Multiple mutations contribute to ASD

NOTE: The highlighted terms are mentioned in the spec.

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14
Q

What is meant by a core mentalising deficit in ASD? Give some experimental evidence for the core mentalising deficit theory of ASD.

A
  • Mentalising is our ability to understand the mental state of oneself or others. This can be thought of as the ability to imagine the mental activity of others and understand their behaviour from it.
  • (Baron-Cohen, 1985):
    • Used the Sally Anne test
    • This features a picture story where a girl’s ball is moved and then the subject is asked where she will look for the ball
    • By the age of 4, most children will answer correctly
    • 80% of children with autism fail the test and only gain the ability to answer correctly when they are older
  • This theory can explain the deficit in understanding others’ emotions that patients with ASD present.
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15
Q

What is meant by weak central coherence in ASD?

A
  • Weak central coherence is a human being’s ability to derive overall meaning from a mass of details.
  • For example, seeing a lot of trees and being able to recognise it as a forest.
  • This may explain why children with ASD may be particularly good at finding details in situations, but not the bigger picture.
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16
Q

Describe acquired developmental disorders of executive function in children and adults.

A

For executive functions, there are a significant range of different outcomes that can result from lesions and these are very hard to predict.

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17
Q

Which brain regions are involved in executive functions?

A
  • Frontal lobe
  • Subcortical regions: integration of sensory info and emotion
18
Q

What are EFs?

A

High-order cognitive abilities including working memory, inhibitory control, planning, reasoning, problem solving

19
Q

In children: how do lesions in either right or left hemisphere affect spatial processing, in contrast with adults?

A

BOTH left and right decrease global spatial processing
Only left causes decreased local processing

20
Q

In adults: how do left PPC lesions affect spatial processing?

A

Decrease local spatial processing (e.g. seeing Ps in image)

21
Q

In adults: how do right PPC lesions affect spatial processing?

A

Decrease global spatial processing (e.g. seeing A in the image)

22
Q

What do early right hemisphere injuries in children lead to?

A

Delays in word comprehension (in contrast with left side for adults)

23
Q

What do left PPC lesions lead to in adults?

A
  • Decreased local spatial processing
  • Hemineglect
  • Decreased word comprehension (Wernicke’s)
24
Q

What do left PPC lesions lead to in neonates?

A
  • Decreased global and local spatial processing
  • Broca’s aphasia! - speech production difficulties (contrast w adult cases)
25
Q

Which adult lesion usually leads to decreased word comprehension?

A

LEFT posterior hemisphere - Wernicke’s area

26
Q

What do perinatal right posterior hemisphere injuries result in?

A

Delays in word comprehension

27
Q

What are the two key differences between perinatal/early childhood and adult focal brain lesions?

A

Increased recovery in neonates/children
Different effects even when occurring in the same location (due to developmental timeline)

28
Q

What is the impact of adverse childhood experiences on capacity to parent in the future?

A

More difficult to provide a safe and nurturing environment

29
Q

What is the impact of adverse childhood events on brain development?

A

Changes in
- Cortical volume - smaller white & grey matter volume
- Functional activity - reduced
- Tract connectivity
- Neurotransmitters
- Impaired development of logical thinking areas (PFC) and memory (hippocampus)
–> higher risk of ADHD

30
Q

What are examples of long term mental health outcomes resulting associated with adverse childhood experiences?

A
  • Poor mental health
  • Suicidal ideation/attempts
  • Depression
  • Tendency for violence/becoming a victim of violence
31
Q

What are examples of long term physical health outcomes resulting associated with adverse childhood experiences?

A
  • Diabetes
  • Heart attack
  • Somatic symptoms
  • Poor dental health
  • Asthma
  • Allergies
  • Increased infections
  • Cancer
32
Q

What are adverse childhood experiences?

A

Potentially traumatic events that occur from 0-17 years

33
Q

What can cause abnormal attachment?

A

Unavailability of normal socialising care and attention in early childhood - neglect, abuse, abrupt separation etc

34
Q

What is an attachment disorder (or abnormal attachment)?

A

A disorder of mood, behaviour and social relationships

35
Q

What is the difference in consequences of pre- and perinatal insults vs insults later in childhood?

A
  • Earlier insults leads to much more significant cognitive deficits when assessed for intelligence, academic ability, and everyday executive function
  • While later insults - perform closer to normal
36
Q

Give three examples of genetic conditions that affect development

A

Down syndrome
Williams syndrome
Fragile X syndrome

37
Q

What are the two types of developmental changes?

A
  • Protracted: gradual changes from childhood to adulthood that continue across cortical areas (e.g. improvement of visuospatial memory)
  • Heterochronous: different timing of development across functional regions (e.g. rise and fall in synaptic density for visual, auditory, PFC)
38
Q

What is meant by the impact of timing on development?

A

How the timing of developmental events interacts across different domains of functioning has significant impact on later behavioural outcomes

39
Q

What are two key factors that affect psychological development?

A
  • Genetics
  • Timing
40
Q

What are genetic syndromes associated with?

A

Genetic syndromes associated with high risk of attention difficulties. E.g. Fragile X

41
Q

What is Fragile X syndrome?

A
  1. Fragile X syndrome:
    * Genetically simple
    * High likelihood of ADHD and autism symptoms
    * Developmental pathways to symptoms are complex
    * Need to investigate person-centred profiles
  2. Clinical relevance:
    * Clinical assessment needs to focus on broad dimensions
    * Assessment over time is needed
    * Sensitivity to how symptoms / cognition changes over time is
    necessary
42
Q

What is normal attachment?

A

the process of developing the first close selective relationship of a child’s life, most commonly with the mother. The relationship acts to reduce anxiety in strange settings and forms a base from which children develop further relationships.
Seriously disturbed attachment is hypothesized to lead to personality disorders, depression, or anxiety in later life.