Lecture 9 - Neurodiversity & Developmental Disorders

Question 1

Developmental disorders

Answer 1

• atypical development
• disorders are a brain spectrum including:
  > disabling genetic conditions e.g. Angelman syndrome (severe dev delay, lifelong speech and movement problems).
  > milder more specific conditions e.g. high-functioning autism
• autism rights movement - autism as a variation in functioning rather than disorder to be cured. but, many autistic indivs take opposing view and favour search for treatment.
• autism is both a disability and difference - need to find ways of alleviating the disability whilst respecting and valuing the difference

Question 2

known genetic causes in developmental research

Answer 2

• usually genes or chromosomes
• some e.g. are: down syndrome, turner syndrome, fragile X, williams syndrome, PKU and FOXP2.
• most interested in disorders that affect brain function
• many genetic disorders have mental and other physical characteristics

Question 3

unknown and multiple possible causes in developmental research

Answer 3

• e.g. Autism spectrum condition, dyslexia, specific language impairment, dyscalculia, developmental coordination disorder, adhd, tourette syndrome
• defined by mental/behavioural characteristics
• prevalence difficult to estimate as diagnostic categories change
• all are diagnoses under DSM ‘specific learning disorder’
• no known single bio basis
• possibilities:
  > there is single underlying basis yet to discover
  > there are multiple bases
  > we group multiple conditions into one disorder

Question 4

developmental disorders and modularity

Answer 4

• modularity = complex system that can comprise a set of parts with different specialised functions.
• functions mutually exclusive
• behaviour of the system depends on interactions between specialised modules
• indiv modules can be damaged independently

Question 5

are cognitive systems modular

Answer 5

• many disorders have selective impairment to only some functions
• if impairment really selective this supports modular idea
  e.g. broca & wernicke damage
• also supports idea they normally develop independently
• Fodor (1983) modularity of the mind - domain specificity, mandatory operation, limited central accessibility, fast processing, info encapsulation, shallow outputs, fixed neural architecture, specific and characteristic breakdown patterns, characteristic ontogenetic pace & sequencing
• miller-lyer illusion - illustration of info encapsulation and inaccessibility. knowing lines are the same length does not change percept
  > working quickly/unconsciously using dedicated neural architecture and limited knowledge is useful for low level perceptual and motor skills

Question 6

evidence for modularity in developmental disorders

Answer 6

• some genetic disorders show evidence for uneven cog profile e.g. WS has affected visuospatial skills more
• many non genetic disorders have uneven cog profile by defnition - specific learning disorder

Question 7

implications of modularity in developmental disorders

Answer 7

• implications for treating the disorder - need to understand how the module normally develops and what can cause this process to go wrong
• functions seem dissociable and informs us about how they are normally organised
• similar to role neurological patients can play in understanding brain function
• when something goes wrong it tells you what the area was supposed to do
• studies show TMS can stimulate body movement over specific brain motor cortex - over visual cortex can see light rings. can also overload or knock out area for period of time
• blindsight can occur - wont see it but can interpret emotions from faces = seeing and emotion recognition two different paths

Question 8

the modularity approach to disorders has proponents & critics

Answer 8

• examples of claims for modularity:
  > a module for reading fails to develop in dyslexia
  > theory of mind module does not develop properly in autism
  > module for syntax does not develop properly in some SLI
  > module for editing intentions does not develop properly in tourettes
• probably not this simple
• kamiloff smith (1998) - neuroconstructivist approach - believes there are many indirect low things early in dev which interact = impairment
  > seeks indirect low level causes of abnormality
  > considers how simple low level impairments early on can lead to abnormal developmeny
  > emphasises experience and development

Question 9

williams syndrome

Answer 9

• deletion of genetic material from chromosome 7 region
• 1 in 7,500-20,000.
• deletion of approx 26 genes inc one in elastin production - physical characteristics & heart & joint problems
• uneven cog profile: poor spatial, spared language, hypersociability, hyper sensitive learning
• Bellugi et al (1999) - matched DS and WS on mental age. WS struggle to draw elephant but strong verbal fluency and mental rep. also good word fluency but poor word fluency in DS
  > lower IQ in WS but many tasks inc mental rotation which thet struggle with
  > DS better on corsi block task
  > dissociation between spatial judgement (line orientation) impaured while another (facial recognition) close to normal. WS good at facial recognition so this mental rotation must be different
  > unlike DS who are delayed across domains, WS show uneven cog profile (spatial lowest then vocab and faces highest)

Question 10

williams syndrome - a modular account

Answer 10

• pinker (1991) - focusing on: relative language strengths in WS vs impairments in other domains.
  > language impairments in SLI vs scores in normal range in other domains
  > dissociation = language system is autonomous of other cog processing
• if both WS and SLI are genetic in origin and dev of language and nonverbal cog can be separately impaired perhaps genes influencing are independent

Question 11

Williams syndrome - reasons to doubt the modular account

Answer 11

• language abilities in WS may have been overstated (Brock 2007) and some elements on language better than others
• language abilities that are good are usually relative to mental age
• performance in normal range may be generated by highly practiced skills that rely on atypical underlying cog processes
• simple modular account in which genes have independent effects on cog abilities

Question 12

a neuroconstructivist account of williams syndrome

Answer 12

• relationship between genes and abilities is complex and mediated by lower level building blocks e.g. auditory processing abilities or visual
• basic abilities must develop to allow development of more complex ones and its over the whole course of this development that impairments emerge

Question 13

williams syndrome neuroimaging

Answer 13

• show impaired performance on visuospatial task related to structural & functional abnormality in dorsal visual stream
• genetics > brain dev > cog dev
• Chailangkarn et al (2016) - some genetic difs in WS lead to atypical neural development
• implications for org of brain areas and cog function
• supports neuroconstructivist idea of general low level deficits

Question 14

Autistic spectrum condition

Answer 14

• condition with problems in social skills and communication, repetitive behaviours
• no defined cause

Question 15

asc clinical definition

Answer 15

• DSM-IV: comprises of: autistic disorder, pervasive developmental disorder, aspergers disorder, rett’s disorder & childhood disintegrative disorder.
• 3 areas of impairment:
  > social int e.g. delay/lack of language, repetetive language, one sided, awkward convos
  > communication e.g. joint attention, eye contact, imderstanding facial expressions
  > restricted, repetitive and stereotyped patterns of behaviour, interests & activities e.g. lack of symbolic pretend play, restricted narrow interests, rigid routines, stereotyped motor behaviours

Question 16

ASC theories: ToM deficit

Answer 16

• proposal that ability to understand others’ mental states is impaired in autism
• mind-blindness - autism & ToM supported by failures on false belief task
• high functioning autism more likely to: pass basic ToM test, fail complex tests & not attribute mental states spontaneously
• but proposals that ToM is not enough to explain the whole triad of impairments in autism

Question 17

ASC theories: executive function deficit

Answer 17

• autism shows problems with planning, inhibition, flexibility, attention shifting, problem solving
• ASC do worse and take longer to change rule (cog flexibility) in WCST but inhibition not affected much
• could explain restricted & repetitive behaviours
• limitations: not specific to ASC, does not explain social deficits

Question 18

ASC theories: weak central coherence

Answer 18

• focus on detail rather than integrating info into meaningful wholes - could be part of issue with recognising faces
• people with ASC tend to note detail letters more than the whole image of a letter (in navon figures)
• in embedded figures test, ASC find shapes quicker as focus on details rather than larger image
• style of processing is atypical but not deficit. there are some autistic savants
• = continuum?