Reading difficulties Flashcards

1
Q

what are reading difficulties?

A
  • encompasses range of diagnoses & cog/beh profiles
  • dyslexia
  • DLD
  • poor comprehenders
  • other reading difficulties or deficits
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2
Q

dyslexia

A
  • learning difficulty affecting skills involved in accurate & fluent word reading, and spelling (British Dyslexia Association, 2009)
  • associated with a range of difficulties (Bedias et al., 2013) e.g. speed of word processing & these are broad at cog level
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3
Q

who has dyslexia

A
  • 9-12% of population (European Dyslexia Association)
  • sim prevalence across ranges of IQ & SES: isn’t associated with social circumstance or general IQ
  • more frequent in males - might be due to more variance in reading behs of males (Arnett et al., 2017) or that females better at masking symptoms possibly
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4
Q

multi deficit model level of analysis

pennington (2006)

A
  1. aetilogical risk & protective factors
  2. neural systems = biological expression e.g. brain structure, comm between diff neural systems
  3. cog processes
  4. behavioural expression/disorders (also comorbidity & variability between disorders)
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5
Q

pennington (2006)

further reading

A
  • need for a measure deficit model arises partly from advances in understanding the complex genetics of behaviourally defined developmental disorders like dyslexia, ASD, ADHD
  • emerging etiological model for developmental disorders e.g. dyslexia, is probabilistic & multifactorial
  • prevailing cognitive model has been deterministic & often focused on a single cognitive cause e.g. phonological deficit as the cause of dyslexia
  • potential contradiction in our explanatory frameworks for understanding developmental disorders
  • resolve contradiction by presenting a multiple cognitive deficit model of developmental disorder
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6
Q

genetic basis of dyslexia?

multi deficit model

A
  • reading abilities appear to be heritable
  • ~40-60% (Raskind et al., 2013)
  • child at greater risk if parents have dyslexia (Schuite-Korne et al., 1996)
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7
Q

stevenson et al. (1987)

genetic basis of dyslexia?

A
  • studied 285 twin pairs
  • heritability 29% for reading abilities
  • 73% spelling abilities

all once intelligence was controlled for

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8
Q

examples of candidate genes of dyslexia

A
  • KIAA0319
  • DCDC2
  • DYX1C1
  • ROBO1
  • FOXP2
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9
Q

KIAA0319 on chromosome 6p

candidate genes for dyslexia

A
  • affects neural migration & radial glia adhesion - specialised cells involved in dev of nervous system
  • v from genetic pooling of 223 ppts with DD (dyslexia) & 273 controls
  • explanation of dyslexia at genetic level

(Cope et al., 2005)

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10
Q

DCDC2 in DYX2 locus

candidate genes for dyslexia

A
  • particularly associated with severe phenotype of dyslexia (Schumacher et al., 2006)
  • longitudinal study found that genetic risk from DCDC2 strengthens the link between pre-reading maze learning & subsequent reading impairment (Gabel et al., 2021)
  • this gene responsible for skills involved in finding a way around a maze but also reading showing particular skills helpful for learning to read
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11
Q

pleiotropy

A
  • one gene many effects
  • not one-to-one mapping
  • not on/off
  • gene has multiple effects across multiple domains
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12
Q

polygenicity

A

many genes contribute to a single trait

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13
Q

generalist genes hypothesis

plomin & kovas (2005)

A
  • genes for LD are same as those for normal variance
  • genes for symptom A are same as those for symptom B
  • genes for one LD are same for another LD e.g. dyslexia & ADHD
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14
Q

how do genes influence dyslexia?

A
  • high rates of comorbidity with other types of neurodiversity & psychiatric disorders
  • genome-wide association study found associations between dyslexia risk & risk for ADHD, bipolar disorders & SZ (Gialluisi et al., 2021)
  • genes interact with environment: higher influence when SES is high (Friend et al., 2008) in the expression of dyslexia
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15
Q

dilnot et al. (2017)

A
  • investigated risk factors for predicting att, beh & reading readiness in 251 children at risk of dyslexia (parent has dyslexia)
  • home literacy env & child’s health predicted reading readiness
  • home literacy env & family stresses predicted att & beh
  • no main effect of family risk once environmental factors controlled for so heritability no longer predicting factor
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16
Q

cog theories for dyslexia

A
  • phonological deficit theory
  • automisation hypothesis
  • double-deficit theory
  • magnocellular deficit theory
17
Q

phonological deficit theory

A
  • deficit in phonological awareness
  • e.g. ability to recognise spoken parts of sentences & words
  • sounds same, rhyme patterns, repeated sounds (sc,sk), ability to segment between words, syllabic breakdown of words
18
Q

swan & goswami (1997)

phonological deficit theory

A
  • groups: dyslexia, ‘poor readers’, CA control with typical reading ability, reading age MA (younger children)
  • measured picture naming & phonological abilities
  • picture naming: children with dyslexia poorer performance
  • children with dyslexia performed similarity to reading-age controls for syllable & onset-rime measures
  • children with dyslexia had poorer performance than reading-age controls for phonemic tasks
  • both children with dyslexia & poor readers had better performance for high frequency words on the phoneme tasks
19
Q

automisation hypothesis

A
  • dyslexia is as result of a deficit in automatic processing
  • e.g. difficulty ‘automising’ reading behs once learnt
  • might be caused by reduced activation in cerebellum
20
Q

moores et al. (2003)

automisation hypothesis

A
  • ppl with dyslexia & controls took part in tasks that required focusing & shifting att between 2 target types (shapes and colours)
  • dyslexia & control performance was sim for focusing att
  • but dyslexia performed sig worse when relied on shifting att
  • recog doesn’t appear to be automatic
  • 2 hypotheses from this study - general resource deficit, automisation deficit
21
Q

general resource deficit

automisation hypothesis

A

inds with dyslexia lack the resources to perform well on the att-shifting task

22
Q

automisation deficit

automisation hypothesis

A

inds with dyslexia struggle to automise some skills, & therefore need more resources for these particular skills

23
Q

moores et al. (2003) investigating general resource deficit and automisation deficit

A
  • normal & degraded stim (shapes)
  • will increasing attentional load disproportionally affect the dyslexia group?
  • dyslexia group weren’t uniquely affected by degraded stim
  • suggests a general lack of resources doesnt explain performance diffs
  • could be explained by an automisation deficit
24
Q

double-deficit theory

badain (1997)

A
  • phonological awareness
  • rapid naming
  • 3rd orthographic deficit?
25
Q

single deficit models

A
  • 1 to 1 relationship between bio factors or cog deficits & presentation of the disorder
  • e.g. trying to find a singular ‘core’ explanation for dyslexia that fits every diagnosis
26
Q

multiple deficit models

A
  • complex etiology
  • shared & independent factors contributing to a cog skill
  • genes have a probablistic influence (not on/off)
  • pennington & bishop (2009)
27
Q

explanations of comorbidity

A
  • one diagnosis increases likelihood of receiving another diagnosis
  • shared liabilities - could have a genetic, cog, or cellular basis
  • correlated liabilities - associated but distinct risk factors
28
Q

comorbidity within dyslexia

A
  • DLD (Catts et al., 2005)
  • ADHD (Gilger et al., 1992)
  • developmental dyscalculia (Landerl & Moll, 2010)
  • developmental coordination disorder (Kaplan et al., 1988)
29
Q

snowling et al. (2019)

A
  • family risk of dyslexia or DLD vs TD controls
  • observed before entering school (t1,t2) & during school (t3-5)
  • measured range of cog predictors
  • classified in year 3 of school into disorder groups
  • severity changes over time
  • poor lang as preschool precursor of deficits
  • dyslexia & DLD show diff dev trajectories
  • more severe phonological deficits in comorbid cases
  • motor & EF deficits as a marker of wider neural deficits (corr but unrelated to lang performance)
  • improvements in lang dev in comorbid group could be protective
  • very important to examine influence of time on outcomes
30
Q

why does comorbidity occur between dyslexia & other neurodev disorders?

A
  • shared genetic etiology
  • shared cog bases
  • ev points towards sim underlying mechanisms rather than causality (van Bergen, 2023)
31
Q

evidence based interventions

A
  • theory of how a skill develops
  • theory of how a skill is promoted
  • high quality evidence

snowling & hulme (2011)

32
Q

theory-based interventions

A
  • theories inform which skills are targeted by the intervention
  • e.g.:
  • phonological deficit theory identifies phonemic awareness as a key skill
  • intervention based on isolating, identifying & blending phonemes
33
Q

review of phonologival awareness training

A
  • effect sizes reported by the national reading panel (NICHD, 2000)
  • 0.86 on phonological awareness
  • 0.53 on reading outcomes
  • 0.59 on spelling outcomes
  • highly effective across literacy domains
  • not effective outside domain e.g. maths
  • improved in combination with letter knowledge intervention
34
Q

theory of how a skill develops

A
  • ev reviewed to see how a skill is best promoted
  • e.g. phonics instruction can be used to improve letter-sound knowledge
  • different techniques: synthetic phonics, analytic phonics
  • both focus on segmenting & understanding words but do this in different ways
  • both techniques useful, but combined approach with synthetic phonics instruction appears most successful
35
Q

high quality evidence

A
  • rigorous trials
  • educationally realistic trials - able to implement them, reflect types of behs appropriate to classroom & ind
  • randomised controlled trials
  • scaled up classroom research - approaching interventions which are realistic to which they would be implemented and that which would be most helpful
36
Q

things to consider

A
  • cost of intervention - realistic and affordable
  • implementing into educational settings - e.g. how long does it take?
  • accommodating for inds with reading difficulties if interventions aren’t successful - relates to variability in behavioural phenotype of dyslexia, comorbidity. What are the other options?
37
Q

snowling & hulme (2011)

further reading

A
  • decoding difficulties appear to be caused by problems with phonological (speech sound) processing
  • any well-founded educational intervention must be based on a sound theory of the causes of a particular form of learning difficulty, which in turn must be based on an understanding of how a given skill is learned by TD children
  • phonologically based interventions are effective in ameliorating children’s word level decoding difficulties
  • smaller evidence base showing that reading & oral language (OL) comprehension difficulties can be ameliorated by suitable interventions to boost vocabulary and broader OL skills