L6, 7 - Language dysfunctions 1 & 2. Flashcards
What are the characteristics of Williams Syndrome?
- Physically categorised by facial, heart and kidney abnormalities.
- Mental retardation: impaired planning, problem solving, spatial and numerical reasoning.
- Good social skills and race recognition.
- Language acquisition slow, better lexical and grammatical development than IQ (50-70) would predict.
- Reduced grey matter volume, abnormal layering of neurons, differences in relative sizes of regions.
What is involved in Bayley’s Scale of Infant Development and what does it find when comparing William’s Syndrome with Down Syndrome?
Language
- Syllable production
- Linguistic imitation
- Comprehension and production of single and multi-word units.
Non-Language (Cognitie)
- Non-verbal reasoning (e.g. object permanence) - Visuo-motor integration
WS vs DS
- WS: L>C, DS: C>L
- De-coupling of language and cognition consistent with innate language module.
What is included in the diagnostic criteria for Specific Language Impairment (SLI)?
- Language significantly below level expected from age and IQ
- Non-verbal IQ, non-linguistic development in normal range.
- Not caused by hearing loss, physical abnormality of speech organs, environmental deprivation or brain damage.
What are the presenting features of SLI?
- Delay in talking (1st word at 2yrs+)
- Immature production of speech sounds in early speech.
- Use of simplified grammatical structures past age when typically mastered.
- Restricted vocabulary in comprehension and production.
- Weak STM
- Overall, language specifically impaired relative to other cognitive capabilities.
What does the nativist view say about SLI and William’s Syndrome?
The double dissociation between language and cognition suggests an innate, domain-specific language module that is independent of “intelligence”
What are the challenges for the nativist account of Williams Syndrome?
- Language IS unusual & impaired (e.g. uncommon words used, make grammatical errors, rely less on intentional gestures).
- Atypical face processing
- > use featural not configural processing (can’t see face in Thatcher illusion).
- Don’t show typical development of gradual specialisation of face-processing.
- Dissociation logic flawed because cognitive architecture trajectory will be different in children with developmental disorders. Assuming a genetic cause for “missing modules” doesn’t mean there’s no environmental contribution (e.g. parents reacting to disordered children differently).
What are the genetic contributions to SLI?
- Not due to a single gene.
- Many risks:
- > environmental risk -> auditory deficit
- > genetic risk 1 -> phonological STM deficit
- > genetic risk 2 -> morphosyntax deficit
These may combine to contribute to SLI
Describe Autism
- ~0.5% incidence, 3x more common in males.
- Cannot be assessed until 2.5 yrs.
- Clear biological contribution (associated with medical conditions, mental retardation)
- Characteristised by:
- > deficits in social communication,
- > social-emotional reciprocity,
- > poor nonverbal communicative behaviours and
- > developing & maintaining relationships.
What is the Autism Core Symptom Triad?
Three impairments that reliably co-occur in Autism.
- Socialisation (quality of reciprocal interaction)
- Communication (delayed language acquisition and persistent impairments)
- Imagination (lack of pretend play)
- Other “Secondary symptoms” (social anxiety, stereotypic behaviour, “savant” skills).
What is the core deficit in Autism?
- Mediating cognitive deficit which is outcome of biological abnormalities.
- “Mentalising deficit.”
What is meant by mentalising?
- Mentalising is the ability to predict and explain the behaviour of others in terms of their mental states.
- Believe, know, wish, pretend.
What is the Theory of Mind account of Autism?
- Mentalising depends on specific mechanism (ToM module) that does not manifest at birth but can not be explained by learning.
What is the typical development of ToM module?
Age 1:
- Initial representation of physical states of the world
- e.g. object permanence (1st order representations).
During 2nd yr:
- Children come to represent mental states.
- e.g. pretends banana is a phone (2nd order representations).
By age 4:
- typically developing children understand ‘belief’.
- Sally Anne tasks.
What did Baron-Cohen, Leslie and Frith (1985) demonstrate between autistic, downs, and typically developing children?
- Asked ‘reality’ (“where is the ball?”), ‘memory’ (“where was the ball originally?”), and belief questions (“where will she look for the ball?”) about a hidden ball task.
- All children 100% accurate on ‘reality’ and ‘memory’.
- Autistic children significantly worse on ‘belief’ questions.
As mental age is higher than in downs children - not due to IQ - supports failure to develop ToM module.
How does the “Meta-Representational Deficit” explain the 3 core symptoms?
- Communication:
- range of verbal and non-verbal problems -> use language instrumentally, not communicatively. - Socialisation:
- “Treat people and objects alike”, socially aloof, lack of empathy -> not aware of others as mentalising beings. - Imagination:
- “Meta-representational” problems -> impairments in spontaneous/pretend play.
