Causal Models and Neuroconstructivism
Developmental Disorders
Correlation and Cause
Castles et al (2014)
Problems for this Perspective
Neuroconstructivism
Can be genetically defined > known genetic cause
Brain changes over time
Regional differences in neonate cortex = not innately specified, they are domain relevant
'Modules' are the outcome of development through processes of learning + emergent specialisation
Neuroconstructivism is a more dynamic model of development
Genetic risk factors
Specific widespread effects
- Nature of genetic risk (single/multiple genes; dosage effects)
- Timing of developmental perturbation
- Interactions with environmental risk
Environment is dynamic
Can be affected by child's, cognitive + behavioural interactions
Encompasses all non-genetic influences
Can affect gene expression
Disruptions to pre- and post-natal neurological development - importance of plasticity, early brain characterised by domain relevant predispositions
Cog important mediatory between brain and behaviour
'Innate' representations rare
Importance of emergent specialistion
Domain general computational/perceptual abilities become fine-tuned for more specific tasks
Importance of developmental timing + downstream effects
Behavioural phenotype is variable
Both syndrome-specific + general behavioural outcomes are important
Must explain associations and dissociations
- Interactions between all levels of explanation
- Timing = important
- Longitudinal studies = paramount
- Not just what children can/can't do but how they do it
Can be defined by observable behaviour > behaviourally defined, markers but no genetic cause
Decide behaviour is atypical
Age
Culture and environment
Impact of everyday life
Other behaviour
Normal distribution - if behaviour falls outside the range = atypical, disorder if lower
Cut offs = arbitrary
Developmental Trajectories
Not just how they perform now
Idealised
Deviate from usual?
Concerned with describing/explaining
Behaviour
Cognition
Brain
Genes
Environment
Correlation of ToM and Lang
ToM > Lang, Lang > ToM, 3rd confound variable
Longitudinal research + experiments (intervention + random)
Morton and Frith's Causal Frame work
4 Levels of explanation
Causal underpinnings of any disorder
Framework
Neurobiology: differences in brain structure or function that are associated with particular disorders
Cognition: Differences in how children perceive and think about the world
Behaviour: Overt characteristics that define disorder
Aetiology: genetic and environmental influences that shape brain development, cognition and behaviour
Feed into each other > other ways they can interact
Are developmental disorders like adult cases of brain damage?
Cog Neuropsychology
Study of brain damage
Focus on modularity
Modules in brain for specific things
Domain specificity
Information encapsulation
Selective deficits
Fixed neural architecture
Characteristic pace and sequencing
Focus on single case studies > damaged part of brain connected to impairment - provide support
Look for dissociations in cog/behavioural profile
Applied framework of acquired disorders to development
Neuroconstructivism as an alternative
Focus on static behaviour
Neuroconstructivism emphasises developmental and the need for longitudinal studies
Suggests 'hard-wired, innate' abilities
Focus on bottom-up processing
Focus on double dissociations
Neuroconstructivism focuses on learning
Neuroconstructivism highlights interactive and top-down processing
Neuroconstructivism argues these are rare in development, and that associations are just as important
Focus on outcome of behaviour
Neuroconstructivism focuses on the process - how people solve various tasks
Double dissociations
Single dissociations = difficulties in somethings but not the other
Impaired? More than one way to fail a task
Spared or relatively spared? more than one way to pass a task
Can something still be learned from cognitive neuropsychology?
Dissociations and double dissociations can inform developmental disorders but sophisticated methodological approaches
Dissociations are used in developmental research outside of cognitive neuropsychology (e.g. diagnosis)
Cognitive neuropsychology is interested in associations
Case studies can be informative - Group means can be misleading for heterogeneous developmental disorders
Data from acquired cases can inform developmental disorders
Needs to be done in the context of strong, testable theory and hypotheses
Karmiloff-Smith (2009) - Genetic disorders focus on innate specification of dissociated modules in human bring to neuroconstructivist approach
Important for informing theories of cog/describing nature of acquired cog disorders
Development = key to understand developmental disorders
Karmiloff-Smith (1998)
Contributions from genes/enviro.
Theories differ - role they attribute affect ways are researched
Nativist = abnormal phenotypes - impairment to domain specific cog. modules + reported juxtaposition of impaired/intact abilities
Neuroconstrctivist
Differs
Indirect, lower level causes of abnormality rather than impaired cog modules
Modules emerge through developmental process of modulation
Innately specified starting points > domain relevant, becoming specific with development/enviro interactions
Disorders on continuum, rather than specific
Development itself = crucial role in phenotypical outcomes
Bishop (2006)
Deve neuropsychology = uncovering underlying basis of deve disorders (SLI, DD, Autistic disorder)
Twin/family studies> genetic influence
Conventional diagnosing criteria > measures of underlying cog mechanisms
Psych informs genetics - dimensions for heritable phenotypes
Genetic informative designs - causal relationships
Low level auditory deficits = phonological problems in SLI
However, both types of deficits with different origins (enviro = auditory, genes = phonological)
morphosyntactic deficits in SLI = heritable BUT different genetic origins from phonological STM impairments
Genetic perspective = misguided - complex + heterogenous + assoicated with multiple risk factors
Fisher (2006)
Rise of molecular genetics = perverse influence > neurodevelopment disorders
Determine role of genetic factors in aetiology
Deceptive simplicity with correlations between genetic + phenotypic variation > misattribute straightforward linear relationships
Genes do not specify behaviours or cog processes
Embrace complexity of biological systems to understand genes > cog