Chapter 16 : Sirois , S. & Karmiloff -Smith, A. Ontogenetic development matters (pp. 312-334).

1. Chapter 16: Sirois, S. & Karmiloff-Smith, A. Ontogenetic development matters (pp. 312-334). Historical Preformationism: the notion that egg and/or sperm contained a little preformed human (homunculus) which over time became grew into adult. Modern preformationism: ideas that genes or sets of genes encode for specific cognitive functions which simply emerge with maturation (called the “canonical view.”)

2. Problems with canonical view: • Genetic (lossy) compression: Too few genes – too many connections. Given that there are around 30,000 genes in human genome, and over 100 billion neurons in brain connecting to upto 10,000 others, the wiring complexity problem is beyond having genes specifically code for neural circuits. Data compression – gene instructions can only utilize very general heuristics (e.g. over-wire and cut back) • The fallacy of innate knowledge: Evolutionary continuity dictates that if other animals have inborn innate knowledge (specified genetically), then humans should too. Reply: Continuity is not in the presence of innate knowledge, it is in the presence of behavioral biases. Ex: newborn geese do not know who their mother is and therefore imprint on here. They are bias to follow a signal with certain physical/sensory characteristics. Similarly, human infants are behaviorally biased to attend to face-like visual signals, though they know nothing of human faces. • Failures of parsimony: Studies claiming to show that infants “understand” certain properties of physics, theory of mind, or language can all be challenged by simpler interpretations based on behavioral biases.

3. Problems with the canonical view • Important implication of overturning canonical view: • “…brains of atypically developing infants should not be conceptualized as normal brains with parts intact and parts impaired. Rather, they should be viewed as brains that have developed differently throughout embryogenesis and postnatal development” (p. 325). • Nota normal brain minus …. But a different brain because…

4. Canonical view: brain as pre-specified cognitive modules, some intact some deficient • Authors’ view: brain as interactive collection of parts where a genetic defect with be variably expressed across a number of different cognitive functions (ripple effects; rather than modular knockout).

5. Example: Development of face processing. • Given adaptive significance a dedicated face processing model seems likely. But such is not the case. • Progressive modularization: • First few months: face processing associated with wide areas of brain across both hemispheres • Six months: face processing more restricted to right hemisphere, where certain biases in info processing make the processes more efficient. • End of first year: increasingly specialized face processing in temporal lobe of right hemisphere which continues to be refined for many years to come.

6. Face processing • No pre-specified face model, but • Behavioral biases (attention to face-like stimuli; maybe subcortically driven recall Johnson chapter) • linking to general but variable patterns of computational processing in brain (right deals better with general configurational patterns) • leading to predicable patterns of brain specialization (fusiform face area receives inputs from visual system and hippocampus for efficient recognition and storage of face patterns.).

7. Effect of genetic disorder: Williams Syndrome Symptoms Delayed speech that may later turn into strong speaking ability and strong learning by hearing Developmental delay Easily distracted, attention deficit disorder (ADD) Mild to moderate mental retardation Personality traits including being very friendly, trusting strangers, fearing loud sound Short stature Unusual appearance of the face • Cause: deletion of 28 genes on one copy of chromosome 7 • Effect: low IQ; hypersociality including normal to better face recognition. • On the surface this seems to support the pre-specified modular view; intact face processing module but defective “intelligence” module

8. Williams Syndrome: evidence for modularity? • Authors argue face processing is not unaffected by Williams Syndrome, face recognition is different and affected by genetic disorder. • WS: more bilateral face processing; more holistic and featural processing; same brain areas used for recognizing cars as faces. • Typically developing controls: processing in typical RH face area; configurational processing (assessing differences in featural locations; how wide apart the eyes, how far mouth from nose, etc); different brain areas for face and cars.  

9. Possible lesson: • brains of atypically developing children may remain more “interconnected” than normal. Less evidence of the same degree of progressive modularization. Or, as in autism, may commit too quickly to specialized areas of processing.   • New view of developmental process: • Development is not a special case of learning • Development is a trajectory toward a certain type of processing state. Critical question is what is controlling or influencing the developmental trajectory and how might it be modified?