What Neurodevelopmental Disorders Can Reveal about Cognitive Architecture

1
What Neurodevelopmental Disorders Can Reveal
about Cognitive Architecture

• Helen Tager-Flusberg
• Boston University

2
Outline

• Discussion of whether neurodevelopmental
  disorders has potential to inform debates about
  cognitive architecture (methodological issues and
  complications)
• Example of research on theory on mind in NDD
  autism and Williams syndrome
• Reinterpretation of the classical evidence

3
Defining Neurodevelopmental Disorders (NDD)

• Focus on genetically-based NDD
• NDD divide into gene/chromosome disorders (e.g.,
  Down, Turner, Williams, PKU) and
  polygenic/complex disorders (e.g., autism, SLI)
• Genetic abnormalities (absence, mutation) disrupt
  normal development of brain
• Lead to different phenotypes that are syndrome
  specific

4
Role of Disorders in Cognitive Science

• Lengthy tradition of using data from people with
  brain/cognitive damage to inform cognitive
  theory, and organization of cognitive system
• Examples from aphasia, amnesia, agnosia etc.
• A for Acquired disorders - provides rich
  information about dissociations between cognitive
  modules from the end state

5
Can Individuals with Abnormal Brain DEVELOPMENT
Inform Cognitive Science?

• Disruption in brain development affects the
  ACQUISITION of cognitive systems
• Studies thus provide data on developmental
  processes can study end state of this
  developmental process in adults with NDD
• Controversial whether NDD can provide evidence
  about cognitive architecture, even from a
  developmental perspective

6
Arguments Against Karmiloff-Smith (1998)

• Because brains develop DIFFERENTLY in NDD
• But little evidence for major differences in
  developmental processes
• Not a logical argument against using NDD evidence

7
Arguments Against (contd 2)

• NDD does not create localized lesion no simple
  intact/impaired cortical circuits that map
  directly onto cognitive modules
• May be true for some disorders but not others
• Depend on the NDD, the cognitive system, the
  individual

8
Arguments Against (contd 3)

• Developmental changes in the phenotype lead to
  fundamentally different organization plasiticity
  in structure /function
• Data on phenotypic changes from infancy are
  controversial and suspect
• Plasticity is highly constrained the brain is
  not a blank slate!

9
Alternative View -

• Arguments proposed by K-S not compelling.
• May depend on which NDD investigate
• Striking difference in children with different
  NDD - and subgroups within syndromes
• Depends on which cognitive module
• Identifying specific cognitive module that has
  been disrupted in NDD has been elusive

10
Methodological Issues in Studying NDD

• Heterogeneity in expression of phenotype within
  each syndrome
• Individual differences related to genetic
  variation related to NDD
• Individual differences related to genetic
  variation NOT related to NDD
• Differences related to experience
• Age effects
• Remediation/Compensation

11
Effects of Retardation and Language Limitations

• Task performance will be a function of
• MR (g - cognitive efficiency?) - non-modular
  influences
• Language (comprehend instructions task content)
• These effects will potentially obsure
  syndrome-specific effects on cognitive module
• At the least, include subjects in limited age
  range, measures of IQ and language ability

12
Example Theory of Mind (ToM)

• Since ToM entered the cognitive cannon evidence
  from NDD has been central in arguments about its
  organization, modularity and innateness
• Classic studies of autism more recent studies of
  other syndromes e.g., Williams

13
ToM in Autism

• Baron-Cohen, Leslie Frith (1985) demonstrated
  failure on FB
• Many studies replicate their findings on FB and
  other related tasks compared to control subjects
  and control tasks
• Support for view of selective impairment to ToM
  in autism
• Taken as evidence that ToM in unitary module
  under genetic influence with unique
  neurobiological substrate

14
Significance of ToM Hypothesis of Autism

• Provides a unified explanation for core social
  and communication symptoms in terms of an
  underlying cognitive module
• Selectivity of cognitive deficit identifies the
  specificity of impaired cognitive module
• Conforms with what is known about neurobiological
  substrate

15
ToM in Williams Syndrome

• Contiguous gene deletion (25-30 genes on
  7q11.32)
• Constellation of physiological, cranio-facial and
  cognitive profile (including MR) forming a unique
  phenotype
• Unusual interest in people, sociable, good
  language and face recognition
• Suggests spared ToM
• Karmiloff-Smith et al (1995) offer supporting
  evidence

16
ToM in NDD

• Claim for double dissociation in ToM
• Autism impaired ToM module
• Williams spared ToM module

17
Problems with this Classic Picture

• Criticisms of ToM hypothesis of autism
• Problems with the evidence of impairment in
  autism and sparing in WMS
• Methodological issues
• Role of language and MR
• Question the basic view that ToM is directly and
  selectively affected by NDD

18
Criticisms of ToM Hypothesis of Autism

• ToM deficits are secondary to other domain
  general deficits such as executive functions
• Cannot explain full range of symptoms in autism
• Symptoms of autism predate ToM
• Children with other NDD (e.g., Down syndrome SLI)
  also fail ToM tasks

19
Problems with the Evidence

• Some children with autism PASS ToM tasks (e.g.,
  20 in Baron-Cohen et al., 1985 much higher in
  our studies)
• Our studies on ToM in young children (age 4-8)
  with Williams syndrome show that they are NO
  BETTER (or worse) on FB and related
  metarepresentational tasks than control children
  matched on age, IQ, and language

20
Reconciling the Evidence

• Performance on FB strongly related to language
  level (not nonverbal IQ) in broad range of
  children with NDD (and normal children)
• Computing the contents of propositional attitudes
  (e.g., beliefs) measures a representational
  capacity that can be acquired by language

21
ToM in Autism

• Fundamental impairments in the core module that
  computes information about mental states directly
  from perceptual inputs (e.g., face, voice,
  gesture)
• Impaired in knowledge of concepts of mental
  states
• IF have linguistic knowledge, then can access
  metarepresentational level using this alternative
  route

22
ToM in Williams Syndrome

• Fundamental sparing in the core module that
  computes information about mental states directly
  from perceptual inputs (e.g., face, voice,
  gesture)
• ? Relative sparing of knowledge of concepts of
  mental states
• MR decreases cognitive efficiency therefore,
  metarepresentational level also depends on
  support from language, and therefore not spared
  compared to controls

23
Language and FB

• Role of sentential/tensed complements in the
  acquisition of FB
• Communication verbs - say, tell, whisper
• Cognition verbs - think, know, forget
• John said that he went shopping
• Mary thought that John was sleeping
• Larry believed that John was working
• John went to the movies!

24
Complements and ToM

• Parallels between sentential complements and the
  representational requirements for the contents of
  mental states (propositional attitudes)
• Can mark embedded clause true/false
• Semantic parallels between mental state and
  communication verbs and ToM (Pinker Bloom, 1990
  - evolutionary link)

25
Evidence for Links between FB and Sentential
Complements

• Jill de Villiers et al. (1998) - longitudinal
  study of preschoolers complements acquired
  prior to passing FB tasks
• Hale Tager-Flusberg - training study training
  on complements (communication verbs) led to
  changes on FB task
• Deaf children fail FB tasks - related to language
  ability especially complements (Peter de Villiers
  et al.)

26
Sentential Complements and ToM in Autism

• Battery of ToM tasks (FB Smarties, FB Sally-Anne,
  Perception/Knowledge)
• Extraction of say and think false complements
• General language measure (PPVTEVT)
• Executive functions (spatial and verbal WM, WMIC
  - stroop planning Tower)
• Annual Visits - Year 1 and Year 2

27
Subjects at Time 1

• 40 children aged 5-14, all diagnosed with autism
  using ADI and ADOS (Mean 83)
• IQ assessed using the Differential Ability Scales
• VIQ Mean82 sd19
• NVIQ Mean88 sd 21
• PPVT Mean84 sd20
• EVT Mean79 sd 19

28
Time 1 Variables Correlating with Time 2 ToM

• Age and general language partialled out
• T1 Tower r.51
• T1 Say complements r.56
• T1 ToM r.62
• NB NOT Think complements or any other EF
  measures

29
What Predicts ToM at Time 2

• Hierarchical regression analysis
• Step 1 - force in age, vocabulary and T1 ToM
• R2 .65
• Step in the predictor variables (Say complements
  and Tower) according to significance level
• Say complements R2 .11
• Tower R2 .01 ns

30
Summary of Autism Findings

• Ability to interpret sentential complements FOR
  COMMUNICATION VERBS predicted later ToM ability
• EF not related to ToM (so ToM isnt secondary to
  EF, as claimed)
• ToM at T1 does NOT predict EF or sentential
  complements at T2

31
Implications

• Only linguistic knowledge for communication verbs
  predicts passing FB in autistic children
• Communication verbs do not entail conceptual
  understanding of mental states
• Passing FB does not entail ability to compute
  mental state information from faces/voices
  (evidence from Baron-Cohen, Klin, Meyer TF)
• Language is an alternative bootstrap into ToM