Reading difficulties Flashcards
what are reading difficulties?
- encompasses range of diagnoses & cog/beh profiles
- dyslexia
- DLD
- poor comprehenders
- other reading difficulties or deficits
dyslexia
- 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
who has dyslexia
- 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
multi deficit model level of analysis
pennington (2006)
- aetilogical risk & protective factors
- neural systems = biological expression e.g. brain structure, comm between diff neural systems
- cog processes
- behavioural expression/disorders (also comorbidity & variability between disorders)
pennington (2006)
further reading
- 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
genetic basis of dyslexia?
multi deficit model
- 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)
stevenson et al. (1987)
genetic basis of dyslexia?
- studied 285 twin pairs
- heritability 29% for reading abilities
- 73% spelling abilities
all once intelligence was controlled for
examples of candidate genes of dyslexia
- KIAA0319
- DCDC2
- DYX1C1
- ROBO1
- FOXP2
KIAA0319 on chromosome 6p
candidate genes for dyslexia
- 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)
DCDC2 in DYX2 locus
candidate genes for dyslexia
- 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
pleiotropy
- one gene many effects
- not one-to-one mapping
- not on/off
- gene has multiple effects across multiple domains
polygenicity
many genes contribute to a single trait
generalist genes hypothesis
plomin & kovas (2005)
- 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
how do genes influence dyslexia?
- 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
dilnot et al. (2017)
- 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
cog theories for dyslexia
- phonological deficit theory
- automisation hypothesis
- double-deficit theory
- magnocellular deficit theory
phonological deficit theory
- 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
swan & goswami (1997)
phonological deficit theory
- 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
automisation hypothesis
- 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
moores et al. (2003)
automisation hypothesis
- 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
general resource deficit
automisation hypothesis
inds with dyslexia lack the resources to perform well on the att-shifting task
automisation deficit
automisation hypothesis
inds with dyslexia struggle to automise some skills, & therefore need more resources for these particular skills
moores et al. (2003) investigating general resource deficit and automisation deficit
- 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
double-deficit theory
badain (1997)
- phonological awareness
- rapid naming
- 3rd orthographic deficit?