Language Disorders Flashcards
question for language processing
domain-general vs domain-specific:
is there a special cognitive system for language?
modular vs interactive:
is the cognitive system responsible for language “encapsulated” from other cognitive systems i.e. operates independently of other cognitive processes?
williams syndrome
1/20000 birth, genetic mutations on chromosome 7 from conception, reduced protein expression in cortex
Characterised by
• Facial, heart and kidney abnormalities
• Mental retardation (IQ: 50-70~Mental age of 7): severely impaired planning, problem solving, spatial and numerical reasoning
• Oriented to social world (faces and voices vs objects): good social skills and face recognition
• Language acquisition slow, but much better lexical and grammatical development than expected from intelligence
Abnormalities in adult brains
• reduced volume (80%)
•Reduced grey matter
•Abnormal layering, clustering of neurones
•Differences in relative size of many regions
•Abnormal brain chemistry in cerebellum
williams vs down’s
Longitudinal data from 10 children with Williams syndrome compared with matched Down syndrome and healthy children
LANGUAGE •Syllable production •Linguistic imitation •Comprehension and production of single and multiword units NON-LANGUAGE(COGNITIVE) •Non-verbal reasoning (eg object permanence) •Visuo-motor integration (eg formboard, block construction, drawing)
down’s: cognition better than language
williams: language better than cognition
“Decoupling” of language and cognition consistent with innate language module
(Pinker, 1999)
Specific Language Impairment
Diagnostic criteria
• Language significantly below level expected from age and IQ (i.e. in lowest 10%) on standardised testing of expressive and/or receptive language
• Nonverbal IQ, nonlinguistic (eg self-help, social) development in normal range
• Not caused by hearing loss, physical abnormality of speech organs, environmental deprivation or brain damage
Presenting features
• Delay in talking (e.g. 1st words at 2yrs or later)
• Immature/deviant production of speech sounds in early speech
• Use of simplified grammatical structures (eg omit past tense) past the age when
grammatical forms are usually mastered
• Restricted vocabulary in both production and comprehension
• Weak short term memory (eg poor word or sentence repetition)
• Poor understanding of complex language (especially when the speaker talks rapidly)
SLI and gene
KE family: 50% of children of affected parents diagnosed with SLI
• Identical genetic abnormality (FOXP2 gene, chromosome 7)
• Varied in intelligence – often average or above
• Specific deficits in application of grammatical rules relative to naming of objects
BUT most people with SLI do NOT have FOXP2 abnormality
➔ usually due to multiple genes + environmental risks
More tightly selected sample of SLI children with above average nonverbal IQ (van der Lely & Ullman, 1999)
• 78% had 1st degree relative with language impairment
• Very poor in grammatical generalisation eg “wug tests”
• Deficits evident even in child with very high IQ
–> Language much poorer than predicted from cognitive capabilities – particularly for grammatical rules
the nativist view of WS vs SLI
Williams syndrome
• Language better than expected for general cognitive capacities
SLI
• Language specifically impaired relative to other cognitive capacities
➔ Double dissociation consistent with an innate, domain-specific language module that is independent of general intelligence
Challenges to nativist account (Karmiloff-Smith, 1998)
- Williams syndrome language IS unusual AND impaired
• Use uncommon words
• Make grammatical errors on more difficult structures
• French children have difficulty learning gender
• Rely less on intentional gestures in language learning - Face-processing is also atypical
• featural rather than configural processing
• Fail to show gradual specialisation/ localisation of face processing of typical development
➔language and face processing are not ‘intact’ in WS
➔many issues involved in defining ‘intact’/’impaired’
criticisms continued
- dissociation logic is not valid for developmental disorders
•Genetically atypical brains develop differently at multiple levels –
eg neural density/efficiency; firing thresholds; neurotransmitters
•No reason to assume that “cognitive architecture” will be the same as other children at any level
•Similar behavioural outcomes might arise from very different neural/cognitive causes eg poor saccadic planning -> ‘sticky fixations -> featural processing bias
➔’missing modules’ do not validly explain developmental disorders
- Assuming a genetic cause does not mean there is no environmental contribution
•gene expression changes over time and is influenced by environmental conditions ➔epigenesis
•Atypical behaviour influences environmental responses eg parents’
responses to developmental disorders
SLI NOT due to a single gene – multiple potential contributors
•May need a ‘double hit’ for clinically significant impairment
•Multiple routes to successful language acquisition
‘Neuroconstructivist’ approach
Does not rule out modular cognitive architecture in healthy adults
• A modular organisation might emerge through development and practice to solve cognitive demands
• Modularity might explain adult skilled behaviour and acquired disorders BUT NOT developmental disorders
autism
Diagnostic category defined by Kanner (1943)
• incidence ~.05%; 3 times more common in males
• Diagnostic criteria cannot be reliably assessed till ~2 ½
• Diagnosis rates have dramatically increased in in last 5-10 years
Clear biological contribution
• strongly associated with a variety of medical conditions eg epilepsy, major EEG abnormality, perinatal distress
• strongly associated with mental retardation (eg 30-50% do not acquire functional communication skills) BUT not defined by
intellectual disability per se: ~25% with autism are not intellectually disabled (Asperger’s Syndrome)
• Many hypotheses about underlying biological abnormality
– dopamine? retrovirus? immunological? perinatal damage? or combination
core symptom triad of autism
- Socialization
– quality of reciprocal interaction - Communication
– delayed language acquisition; persistent impairments in pragmatic aspects of language - Imagination
– lack of spontaneous/pretend play
Other ‘secondary symptoms’ – social avoidance and anxiety – stereotypic behaviour – preference for routine – ‘savant’ skills – some characteristic cognitive deficits due to general intellectual disability rather than autism
Frith & Happe (1998): General framework for understanding developmental disorders
biological causes: genetic/biological abnormality --> brain abnormalities --> common pathway: deficits in gaze, joint attention, absence of social interaction --> cognitive deficit: mentalising deficit --> core symptoms --> behavioural manifestations: impairments in communication, imagination, social interaction
Mediating cognitive deficit best point for
intervention even for biologically based
disorders
core deficit in autism is mentalising deficit
mentalising
ability to predict and explain the behaviour of others in terms of their mental states eg use/understand mentalising terms: believe, know, wish, pretend
theory of mind account of autism
mentalising depends on specific mechanism (ToM module) that does not manifest at birth, but cannot be explained by learning
Typical development
• age 1: infants internally represent physical states of the world eg object permanence ➔1st order representations
• during 2nd year: children come to represent mental states eg he thinks/pretends the orange is a ball
➔2nd order representations
• by age 4: typically developing child understands concept of “belief” eg people can have different beliefs, beliefs can be false
➔ 3rd order representations, “theory of mind”
Finding on false belief attribution task
All children 100% accurate on “Reality” (where is ball really?) and “Memory” (where was ball initially?) questions
“Belief” question: Where will she look for ball?
down’s 86% correct, healthy 85% correct
autistic 20% correct
