Are the brain mechanisms that process and represent ... · If the brain is a general purpose...
Transcript of Are the brain mechanisms that process and represent ... · If the brain is a general purpose...
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An important (but difficult to investigate) question
• Are the brain mechanisms that process and representlanguage dedicated to language or employed in lots ofcognitive domains?
• Relates to the larger question about modularity: Is themind/brain organized into separate modules, responsible fordifferent cognitive functions, or is the brain an”generalproblem solver”?
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MODULARITY
• What’s a module?Fodor:– not assembled from more primitive processes– of fixed neural architecture (specified genetically)– domain-specific (a module computes a constrained class of
specific inputs bottom-up, focusing on entities relevant only to itsparticular processing capacities)
– fast, autonomous, mandatory (a module's processing is set inmotion whenever relevant data present themselves)
– automatic, stimulus-driven, and insensitive to centralcognitive goals.
– informationally encapsulated. In other words, other parts of themind can neither influence nor have access to the internalworkings of a module, only to its outputs.
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MODULARITY
• Selective loss of a specific cognitive function via brain damage issupport for the modularity view.• But the modularity thesis doesn’t necessarily predict that there shouldbe specific brain areas dedicated to specific cognitive functions. Somodularity could be true even if there was no selective languageimpairment via brain damage.
Fodor:– of fixed neural architecture (specified genetically)
• However, the way brains are is determined by genes and so selectiveloss or sparing of language genes should lead to selective loss orsparing or language.
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MODULARITY
• What would we expect of a person who’s lost their language? Orspared their language?
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DEVELOPMENTAL DISORDERS WITH A GENETIC BASIS
• Specific Language Impairment (SLI):– Language problems without any obvious cause.– fifty to seventy percent of children with SLI have at least one other
family member with the disorder
• Williams Syndrome (WS):– (more or less) general cognitive retardation except in language– Results from the deletion of the long arm of chromosome 7.
If the brain is a general purpose problem solver, one’sgeneral intelligence should be predictive of abilities such aslanguage.
For people affected by WS or SLI that’s simply not true.
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SLI and genetics
• For the SLI population at large, we do not know what geneticmutations cause SLI.
• That there is a genetic basis to SLI is supported by– the fact that It runs in families.– The proportion of pairs where both twins are affected with SLI
is significantly higher for identical (monozygotic – single egg)than for non-identical (dizygotic – separate eggs) twins.
• However, there is one famous SLI family for whom the geneticmutation is known, the KE family in Britain.
– The affected members of this family are clearly not just languageimpaired.
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On the general SLI population
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Specific Language Impairment (SLI)
• Developmental language disorder in the absence of neurological,sensori-motor, non-verbal cognitive or social emotional deficits
• Affects about 7% of the population, males more often thanfemales
• A delay or deficit in the use of function morphemes. Omission offunction morphemes long after age-matched children with typicallanguage development show consistent production of theseelements.
• Diagnosis based on behavioral evaluation but is likely to have agenetic basis.
• Control group is either age-matched, IQ-matched or language-matched (usually MLU(mean length of utterance))-matched.
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Hypotheses about what goes wrong in SLI
• Gopnik: It’s a grammar problem. SLI individuals are impaired intheir ability to use grammatical morphemes.
• Wexler (& Rice): It’s a grammar problem. SLI individuals areimpaired in specific type of verbal inflection.
• Tallal: It’s not a grammar problem! It’s a problem in rapidauditory processing (which has consequences for language).
• Fundamental problem: Since the SLI individuals are aheterogeneous group, these research groups are not necessarilystudying the same types of individuals.
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Gopnik: problem with functional morphology
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Gopnik: problem with functional morphology
Inflection
Derivation
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Gopnik: problem with functional morphology
• Gopnik has data from lots of different languages and for lots ofdifferent types of morphology.
• Gopnik’s hypothesis that SLI is an impairment in grammaticalmorphology predicts that SLI individuals should make lots ofmorphological mistakes.
• But they mostly seem to make one type of mistake, droppingmorphemes. They don’t swap past tense morphology for pluralmorphology, for example. This doesn’t follow from Gopnik’saccount.
• Wexler has an approach to this, kinda.
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Rice & Wexler:SLI are stuck in the “Optional Infinitives Stage”• Wexler (1990, 1992, 1994): In language development, kids go
through the Optional Infinitive (OI) Stage.
– lasts in normal children from birth to around 3;0.
• Infinitive: uninflected form of the verb. Some verbs select forinfinitives as their complements (direct objects), but on their own,infinitives are ungrammatical.
(i) OK: Daddy wants to walk to work.
(ii) Bad: Daddy walk to work.
• In the Optional Infinitive Stage:
a. Root infinitives (as in ii) are possible grammatical sentences
b. These infinitives co-exist with inflected (finite) forms
c. Apart from tense and agreement, the children know relevantgrammatical principles
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• In Dutch, infinitives are always sentence-final:– I want shoes to wash.
• But inflected verbs come in second position, beforethe object:
– I washed shoes.
• A Dutch kid in the OI Stage:(8) pappa schoenen wassen
daddy shoes wash-INF'Daddy shoes wash (non-finite)’
(9) ik pak ‘t opI pick it up
'I pick (fin) it up'
Infinitival in final position, as it should be.Although the child substitutes the infinitivefor the inflected form, he/she uses theinfinitival grammar.
Finite verb in second position, as it should be.
Rice & Wexler:SLI are stuck in the “Optional Infinitives Stage”
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• Development of 47 normally developing Dutch children (Wexler,Schaeffer and Bol, 1999).
Rice & Wexler:SLI are stuck in the “Optional Infinitives Stage”
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• Extended Optional Infinitive Hypothesis:
Children with SLI are just like normal children exceptthat they go through the OI period for a much longertime than normal children, perhaps never reallyemerging from it.
Rice & Wexler:SLI are stuck in the “Optional Infinitives Stage”
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• Prediction for children with SLI:Children with SLI:a. Use OI's in languages where younger normalchildren dob. Show the same patterns of grammatical knowledgeas normal children
• Wexler, Schaeffer and Bo:In the 6;00-8;02 year range, Dutch children with SLIstill had 15% OI's (50 of 334). The OI stage persistedmuch longer in the children with SLI.
Rice & Wexler:SLI are stuck in the “Optional Infinitives Stage”
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• Problem:– SLI kids don’t just have problems with verbal
inflection.
Rice & Wexler:SLI are stuck in the “Optional Infinitives Stage”
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SLI – nonlinguistic hypotheses
• Tallal: SLI is a non-language specific deficit inthe rate of auditory processing.– Children with SLI have difficulty processing brief or
rapidly presented auditory stimuli.
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Evidence for auditory processing difficulty in SLI(Tallal)
• Normal children are able to discriminate two 75-msectones separated by an interstimulus interval (ISI) asshort as 8 msec, while individuals with SLI required anISI exceeding 300 msec to perform the samediscrimination at the same level of accuracy.
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Evidence for auditory processing difficulty in SLI(Tallal)
• The degree of auditory processing deficit correlateswith the degree of language comprehension deficit.
• Early deficits in rapid auditory processing abilities bothprecede and predict subsequent language delays:
– At 6-9 months, significant differences in auditory perceptionbetween infants born to families with a history of SLI andchildren without history of SLI
– Threshold for rapid auditory processing at 7.5 months is thesingle best predictor of language outcome.
– At age 3, rapid auditory processing threshold and being male,together predict 39/41% of the variance in language outcome.
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Evidence for auditory processing difficulty in SLI(Tallal)
• So what would be the connection between auditoryprocessing difficulty and having trouble with functionalmorphology?
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Evidence for auditory processing difficulty in SLI(Tallal)
• Leonard: it’s hard to hear little functional morphemeslike –ed or –s!
– As a consequence, there are difficulties in learningmorphological paradigms.
• Predicts crosslinguistic differences in SLI profiles.• In languages where functional morphemes have more
perceptual salience, SLI kids should have less troublewith them.
• Leonard shows that that’s actually true in Hebrew andItalian.
• This is in contrast to Gopnik’s findings that evenphonologically salient morphemes cause trouble.
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KE family
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KE family
• Half of the KE family are affected by SLI.
FemaleMale
Shading = LanguageImpaired
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KE family
• Vargha-Khadem et al (Science, 2001):In the affected members of the KE family,there is a mutation in the gene FOXP2.
• A language gene?
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KE family – behavior on linguistic tasks
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KE family – behavior on linguistic tasks
• The language problems of the SLI members of the KEfamily are much more global than in the general SLIpopulation.
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KE family – behavior• Not just language problems.
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KE family – brains• Watkins et al (2002):
In motor and speech-relatedbrain regions, significantlydifferent amounts grey matter inaffected family members ascompared to unaffected andcontrol groups, which did notdiffer from each other.
• Volume of caudate nucleus(part of the basal ganglia)reduced in affected members.
– Involved in regulatingvoluntary movements
FOXP2 a language gene?
FOXP2 a language gene?
• No, mice have it too and it’s very similar.• Good news: we can study it in mice.• What would happen to mice if they were
given the human version of FOXP2?• What would happen to mice their FOXP2
underwent the mutation that SLIindividuals have?
http://www.cell.com/supplemental/S0092-8674(09)00378-X
Mice with a humanized FOXP2
• Cellular changes in the striatum, a part ofthe basal ganglia.
• Decreased exploratory behavior. Altered ultrasonic (>20KHz) vocalizations.
Mice with SLI-mutated FOXP2
• On isolation from the mother/nest, healthypups emit ultrasounds that elicit retrieval bythe parent (cf. crying baby).
• Mice lacking a functional Foxp2 do notproduce these calls.
SLI upshot• Messy when it comes the general group as the genetic
basis is not known and different research groups may bestudying different types of populations.
• The KE family offers an interesting research opportunity,but it is unclear to what extent the affected members ofthis family are representative of the SLI population ingeneral.
• The gene that is mutated in the KE family, Foxp2, can bestudied in mice, which allows systemic investigation ofcausal connection between Foxp2 and brain&behavior (inmice).