Developmental Language Dysfunctions Flashcards
Why are language dysfunctions studied by cognitive psychologists?
Can be used to disentangle nature and nurture
To see if a “language module” exists or is independent from other cognitions
What is Williams Syndrome, and what is it characterised by?
- Very rare form of retardation of known genetic etiology
- 1/20,000 births
- 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 ~7),
Severely impaired planning, problem solving, spatial and numerical reasoning
• Oriented to social world (faces and voices, vs objects); Good social skills and facial recog
• Language acquisition slow, but much better lexical and grammatical development than expected from their intelligence
How does Williams Syndrome affect the adult brain?
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
What is the difference between people with Down syndrome, Williams Syndrome and healthy people?
- Williams Syndrome: Language better than cognition
- Down Syndrome: Cognition better than language
- Discrepancy between cognitive capacity and language abilities
- Supports idea of an innate language module (Pinker, 1999)
What are the diagnostic criteria for Specific Language Impairment?
- Language sig below level expected for age and IQ (i.e. lowest 10%) on standardised testing of expressive and/or receptive language
- Nonverbal IQ and non-linguistic (e.g. self-help, social) develop in normal range
- Not caused by hearing loss, physical abnormality of speech organs, envr deprivation or brain damage
What are the presenting features of Specific Language Impairment?
- Delay in talking (e.g. first words at 2 years or later)
- Immature/deviant speech sound production in early speech
- Use of simplified grammatical structures (e.g. omit past tense, “is”) past the age when grammatical forms are usually mastered
- Restricted vocab in both production and comprehension
- Weaker STM (word or sentence repetition)
- Poor understanding of complex lang (esp when speaker talks rapidly)
What did studies on the KE family reveal about the heritability of SLI? What evidence is there against their findings?
KE family: 50% of children of affected parents diagnosed with SLI
- Identical genetic abnormality (FoxP2 gene on chromosome 7)
- Varied in intelligence – often average or above
- Not associated with general cog deficiency
- Specific deficits in application of grammatical rules relative to naming of objects
However: Most people with SLI do NOT Have FoxP2 abnormality – may be due to multiple genes/envr risks
In a more tightly selected of SLI children with above average nonverbal IQ, 78% had first degree relative with lang impairment.
Difference between Williams Syndrome and SLI, from Nativist perspective?
Nativist view:
• Williams Syndrome: Lang better than expected for cog capacity
• SLI: Lang specifically impaired, compared to other cog capacities
• Double dissociation –> Innate, domain-specific language module that is independent of general “intelligence”