Developmental Language Dysfunctions

Question 1

Why are language dysfunctions studied by cognitive psychologists?

Answer 1

Can be used to disentangle nature and nurture

To see if a “language module” exists or is independent from other cognitions

Question 2

What is Williams Syndrome, and what is it characterised by?

Answer 2

• 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

Question 3

How does Williams Syndrome affect the adult brain?

Answer 3

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

Question 4

What is the difference between people with Down syndrome, Williams Syndrome and healthy people?

Answer 4

• 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)

Question 5

What are the diagnostic criteria for Specific Language Impairment?

Answer 5

• 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

Question 6

What are the presenting features of Specific Language Impairment?

Answer 6

• 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)

Question 7

What did studies on the KE family reveal about the heritability of SLI? What evidence is there against their findings?

Answer 7

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.

Question 8

Difference between Williams Syndrome and SLI, from Nativist perspective?

Answer 8

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”