Lecture 5 - Atypical Reading Flashcards

1
Q

WHO ICD-11 developmental dyslexia definition

A
  • A developmental learning disorder with impairment in reading that is defined by significant and persistent difficulties in learning academic skills related to reading, such as word reading accuracy, reading fluency, and reading comprehension.
    It markedly affects performance in reading and is not due to a disorder of intellectual development, sensory impairment (vision or hearing), neurological disorder, lack of availability of education, lack of proficiency in the language of academic instruction, or psychosocial adversity.
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2
Q

main characteristics of DD

A
  • Most common and carefully studied specific learning disorder
    • Dissociation
      • Usually both reading and spelling affected
      • Reading and spelling abilities can also be affected separately
    • Comorbidity
      • High comorbidity with other disorders (e.g. speech and language disorders, dyscalculia, ADHD)
    • Specific
      • Low performance only in the domain of reading that is out of line with age/IQ-related expectations
      • Usually 1.5-2SD below the mean
    • Exclusion
      • Inadequate educational opportunities
      • Neurological or primary visual/auditory impairment
      • Low general cognitive abilities (IQ<70)
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3
Q

prevalence of DD

A
  • One of most common childhood disorders: 5-16% in school children (depending on the criteria used for diagnosis)
    • Higher prevalence in boys (2:1)
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4
Q

stability of DD

A
  • Early onset, persists into adulthood
    • Often restricted progress in learning to read and no/limited catch-up with peers despite extra help
    • Doesn’t grow out
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5
Q

heritability and DD

A
  • Dyslexia runs in families: the risk for a child to develop dyslexia is estimated between 40% and 60% if one parent is affected (higher in case other family members are also affected)
    • Heritability: higher concordance rate of dyslexia in monozygotic twins compared to dizygotic twins
    • Some specific genes have been identified that play a role (but no genetic fix is on the horizon; also: there in no one single dyslexia gene)
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6
Q

primary symptoms of DD

A
  • Persistent difficulties in reading
    - Often also persistent difficulties in reading comprehension & writing
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7
Q

secondary symptoms of DD

A
  • Low motivation, increasing frustration
    - Avoidance, anxiety
    - Lack of self-confidence, low opinion of own capabilities
    - Psychosomatic symptoms
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8
Q

grapheme to phoneme conversion in DD

A
  • Word/pseudoword reading
    - Slow and laboured
    - Rule-based decoding (sounding-out) instead of lexical access, more errors
    - Restricted lexicon
    • Reading comprehension/sentence reading
      • Restricted (too busy with reading)
      • Word recognition as a precondition
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9
Q

stability of primary symptoms

A
  • Learning to read and write is effortful for all children
    • All children make errors when they first learn to read and write
    • The difference: errors/difficulties persist
    • Behavioural symptoms vary with age/experience and differ from person to person
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10
Q

causes of DD

A

Multiple analysis levels:
1. Behaviour (symptoms, defining behaviours)
2. Cognition (cognitive difficulties/resources)
3. Neuronal signature (structural and functional)
4. Genetics (genes and heritability)
- Environment effects all

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11
Q

early cognitive predictors of DD

A
  • Phonological skills, phonological awareness
    - Difficulties with rhymes, letter segmentation, letter replacement, skipping a phoneme
    • Rapid Automatized Naming (RAN)
      • Slower in naming things (colours, objects) quickly
    • Early language skills
      • Difficulties with sentence comprehension, general listening comprehension, limited vocabulary knowledge
    • Letter-name knowledge
      (e.g. Thompson et al., 2015)
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12
Q

Ramus et al. 2003 hypotheses

A
  • Phonological deficit hypothesis
    § Impairment in representation, storage and/or retrieval of speech sounds
    § Difficulty with grapheme-phoneme correspondence
    - Double-deficit hypothesis
    § Both phonological and RAN impairments are related to reading difficulties as independent processes
    § Individuals who have both show greater reading impairments
    - Cerebellar deficit hypothesis
    § Impairments in motor control, thus is speech articulation, phonological representations and
    § Impairment in automatization, thus with difficulty with grapheme-phoneme correspondence
    - Magnocellular theory
    § Magnocellular system: part of visual system that projects to or originated from larger neurons in2 most ventral layers (magnocellular layers) of the lateral geniculate nucleus (thalamus). Allows the rapid perception of movement, form, and changes in brightness but is relatively insensitive to stimulus location and colour.
    § Impairment in fast auditory processing, thus impairment in the representation, storage and/or retrieval of speech sounds and letters/words, thus difficulty with grapheme-phoneme correspondence
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13
Q

neural signature and DD

A
  • D’Mello and Gabrieli, 2018
    - Left temporal region specialised for perception of print
    - Parietal area specialised for relating print to sound
    - These areas function differently in people with dyselxia
    • Left occipito-temporal cortex (VMFA)
    • Left temporo-parietal cortex
    • Inferior frontal cortex
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14
Q

functional differences in DD

A
  • D’Mello and Gabrieli, 2018
    - VWFA and temporo-parietal cortex
    § Both regions consistently underactivated (hypoactivation)
    § Occipito-temporal: associated with problems in word identification/rapid naming - perception of print
    § Temporo-parietal: associated with problems in grapheme-to-phoneme mapping - mapping print to sound
    - Inferior frontal cortex
    § Mixed results
    § Increased activation (=hyperactivation); possibly associated with compensatory processes (e.g., covert/subvocal reading) or increased effort
    § Typical readers show age-dependent decreases in activation; readers with dyslexia show increased activation across ages
    § However, other studies show decreased activation (=hypoactivation)
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15
Q

structural differences in DD

A
  • D’Mello and Gabrieli, 2018
    • Differences throughout reading network in regions that typically also show functional differences
    • Less grey and white matter volume in VWFA and temporo-parietal areas
    • Altered white matter integrity in children and adults
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16
Q

DD is not delayed maturation - explain

A
  • Hypoactivation in VWFA & inferior parietal cortex is specific to dyslexia
    • Hypoactivation is also found when compared with skill-matched controls
    • Dyslexia not simply on the lower end of a continuum of reading ability
    • Hyperactivation in inferior frontal cortex related to reading ability
    • Hyperactivation no longer observed when compared with skill-matched controls
17
Q

early identification of DD

A
  • Often late diagnosis/support measures (often only in year 2/3)
    • Can we identify (and act on) risk factors/predictors before children learn to read?
    • Fixing the failure model
      “It’s most likely children are born with a sub-optimal brain for learning to read, but still we wait until they turn nine years old to give them a diagnosis.” (Nadine Gaab)

Early differences in structure (Langer et al., 2017)
- 32 infants (age 5-17 months), with (FHD+) and without (FHD-) familial risk of dyslexia; infants slept in the MRI scanner
- Lower connectivity in the left arcuate fasciculus for FHD+
- Measures of white matter integrity in the arcuate fasciculus correlated with expressive language skills, which are associated with future reading skills
- Deficits associated with dyslexia may result from altered structural connectivity in left-hemispheric regions

18
Q

implications of neuroscientific understanding of DD for educational practice

A
  • Add another level of explanation, expand the evidence base
    - Corroborate (or not) established theory about the neural basis of (typical/atypical)reading
    - Behavioural change through training/symptoms is reflected on the neural level
    • Advance our understanding of causal mechanisms
      • Describe/distinguish underlying causes of the same overt behaviour
      • Potential to predict response to instruction and help identify tailored support to meet children’s needs
    • Improve early identification of children at risk
      • “In the future, if we could identify brain differences near birth, there could be an entire new generation of interventions even done at home.”
      • (Early neuroscientific predictors may complement behavioural or environmental predictors (in the future)