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ASC Flashcards

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1
Q

ASC is a Neurodevelopmental Condition

A
  • Genetic origin characterised by abnormalities in:
    • social interaction and communication (inc language and NVC)
    • repetitive and restricted interests and behaviour
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2
Q

Why is ASC on a spectrum?

A
  • used to be 5 diagnosis of ASC but distinctions between categories were shaky so now there is a continuum
  • ASC with high or low functioning specs
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3
Q

Pathological Demand Avoidance (PDA)

A
  • high IQ and high functioning but deficits in social understanding and communication skills
  • children diagnosed with PDA because of the way their anxiety EXPLODES over the above points
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4
Q

PDA Symptoms

A
  • need to be in control, fight instructions/requests/demands of everyday life
  • impulsive mood swings
  • enigmatic and charming when in control

PDA describes a pattern of behaviour in response to autism-spectrum conditions

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5
Q

Symptoms of Severe Autism in a Child

A
  • language absent or minimal - possible echolalia
  • 30% of kids with ASC are minimally verbal when they reach school age (Tager-Flusberg, 2013)
  • may ignore other people or use them as props to get things they want e.g. manipulate their hands
  • insist on routine e.g. travelling the same way, eating same food etc
  • meltdowns and tantrums
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6
Q

Symptoms of High-Functioning Autism in a Child

A
  • Asperger (1944) described them as ‘little professors’
  • may be disinterested in social contact or may be ‘active but odd’ - socially motivated but struggle to socialise appropriately and maintain relationships
  • obsessive interests:
    • odd things e.g. cataloguing bus tickets
    • normal but unusual for age e.g. Ancient Rome
    • normal for age but to an abnormal extent
  • no appreciation for listener
  • may lack facial expressions and vocal tones
  • need for routine - need warning of changes
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7
Q

Genetic Origins of Autism

A
  • concordance rates between 73-95% in MZ twins and siblings are at a substantially greater risk to develop ASC (Geschwind, 2011)
  • autistic traits occur to extraordinary extent in undiagnosed relatives (Losh et al, 2009)
  • but… genetic contributions to autism are complex, heterogenous and multi-factoral (Persico and Napolioni, 2013)
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8
Q

What does a Theory need to be to be a Good Explanation?

A
  • universal - covers everyone on spectrum
  • specific - to autism, sets people with autism apart from other conditions
  • explanatory power - explains all aspects of the condition
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9
Q

3 Dominant Sociocognitive Models of ASC

A
  • ToM Hypothesis
  • Weak central coherence (WCC) hypothesis
  • EF hypothesis
  • all causal models: they identify particular symptoms and suggest those may be the cause of the autistic phenotype (rest of symptoms)
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10
Q

What is ToM?

A
  • beliefs, desires, intentions used to understand why someone acts a certain way/predict how someone will act (Kloo et al, 2010)
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11
Q

Evidence for ToM Impairment in Autistic Children

A
  • autistic children perform poorly on story tasks involving an understanding another’s beliefs (Baron-Cohen, 1986)
  • struggle on smarties task (Perner et al, 1991)
  • commit social faux pas (Happe, 1994)
  • struggle recognising facial expressions (Baron-Cohen, 2001)

The suggestion is that the other autism symptoms (language and social difficulties) arise from difficulty with ToM. Autism = mind blind

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12
Q

Assessing ToM Thoery

A
  • universal? no. some autistic children and adults pass ToM tasks (Tager-Flusberg, 2007)
    maybe? eye tracking showed that even when answers were correct they had poor understanding of mental states (Senju, 2013)
  • specific? no. ToM deficits shared by deaf children and clinical populations e.g. anorexia, schozophrenia
  • explanatory power? good for symptoms related to social impairment and communication/language difficulties
    but.. doesn’t cover whole phenotype inc detail-focus abd repetitive behaviours (Tager-Flusberg. 2007)
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13
Q

Baron-Cohens (2009) ‘Empathizing - Systemizing Theory

A
  • suggests what sets ASC apart from other disorders with impaired ToM is lower than average empathy and above average systemising
  • cognitive ToM: the ability to identify/recognise another persons mental state
  • affective ToM: having appropriate reaction to other peoples thoughts/feelings

splitting up components can help differentiate ASC from other conditions marked with ToM deficits

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14
Q

Weak Central Coherence (WCC) Hypothesis

A
  • central coherence is the ability to process things globally and meaningfully
  • poor performance in WCC paradigms e.g. Happe and Frith’s (2006) visual spatial paradigms
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15
Q

How Does WCC Explain ASC?

A
  • the cognitive style of autistic people is said to explain elements of the autistic phenotype e.g. their insistence on sameness and upset at a minute change
  • also explains language difficulties e.g. inability to understand irony/jokes - could be the result of being unable to consider the wider context - stuck processing the very literal words (Roland et al, 2002)
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16
Q

Assessing the WCC Hypothesis

A
  • universal? no. autistic people can process wholes (faces, homographs)when prompted to process at global level (Happe and Frith, 2006)
  • specific? no. weak central coherence has also been seen in other conditions e.g. eating disorders and schizophrenia
    explanatory power? good job at explaining insistence on sameness and detail focus. weak at explaining social domain
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17
Q

Counterarguments for Criticisms of WCC?

A
  • Happe and Frith (2006) say the WCC account isn’t claiming to fully explain ASC, rather one aspect of cognition alongside ToM
  • WCC should be seen as a cognitive bias towards local processing
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18
Q

EF Account

A
  • suggested that people with autism resemble patients with ‘dysexecutive syndrome’ - inflexible, perseverative cognitive style (Baddeley and Wilson, 1988)
  • people with autism have trouble planning. set-shifting, inhibition and generativity
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19
Q

How can EF Deficits Explain ASC?

A
  • impaired generativity - struggle to generate a new plan when routine is disrupted
  • impaired mental flexibility and inhibition - problems understanding non-literal language as cannot switch between literal and non-literal meanings (Mashal and Kasirer, 2011)
  • possible that EF deficits could explain failure in ToM - unable to disengage what you know is in the box (perseverating) and switch to the other persons perspective (Ozonoff et al, 1991)
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20
Q

Assessing EF Account if ASC

A
  • universal? no. autistic people don’t fail all EF tasks (Hill, 2004). they often pass (Pellicano et al, 2006)
  • specific? least specific of all 3 theories, if ASC was simply due to EF deficits then we would see autistic symptoms in all brain damaged patients with dysexecutive syndrome and clinical groups e.g. OCD, ADHD
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21
Q

Issues with Trying to Explain Autism Causally

A
  • autistic people do have problems with ToM and EF, and do show WCC but it doesn’t mean all these problems are causal. ToM, EF and language are closely intertwined so it is hard to establish causal primacy of problems
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22
Q

Integration

A

Child with ASC placed in mainstream school with no extra support - expected to adapt to curriculum and class environment

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23
Q

Inclusion

A

Educational provision adapts to the child’s need (Batten, 2005)

24
Q

Stats of ASC in Mainstream Schools

A
  • over 32,500 students with ASC in primary and secondary mainstream education
  • more likely to be excluded, due to noisy, inappropriate behaviour or aggression (Barnard et al, 2000)
  • more likely to be bullied (Humphreys and Levis, 2008)
  • more likely to develop psychiatric problems (Evan et al, 2005)
25
Q

What is School like for Autistic Children?

A
  • because of their experiences they view their condition negatively ‘I have a bad brain’
26
Q

Language and Communication Difficulties in School

A
  • struggle to pick up teachers:
    • eye-contact/signals
    • gestures
    • tonal changes
    • facial expressions
  • ‘can you draw another triangle like this one? yes.’
    • hears meaning of the word, not what the teacher means (link to WCC hypothesis)
27
Q

How can the School Help with Language and Communication Difficulties?

A
  • staff: trained in autism awareness, communication etc

- student: training in school situations, strategies to communicate upset and confusion

28
Q

Social Difficulties in Mainstream Schools

A
  • may be unintentionally rude or inappropriate - upsets or scares other children
  • struggle to reciprocate - unable to pick up signals that another child wants to take/share/give
  • difficulty joining play groups
  • difficulty distinguishing good-natured teasing from malice
29
Q

Friendships

A
  • inborn difficulty establishing social skills which means they are denied access to peer relationships. results in them being unable to learn social skills - a vicious circle
  • many autistic children feel lonely and want friends (Bauminger and Kasari, 2000)
  • they are less accepted and spend more time alone (Chamberlain et al, 2007)
30
Q

Bullying

A
  • because of problems with ToM they are less likely to report bullying, may assume the teacher already knows
  • less socially impaired students report more bullying - possibly more vulnerable because of their willingness to approach others ?
  • more socially impaired students tend to hide away during breaks - less chance of bullying? (Wainscot et al, 2008)
  • biggest predictor of bullying is ‘social vulnerability’ - how gullible etc the child is (Sofronoff et al, 2010)
31
Q

How can Bullying of ASC Children be Tackled in Mainstream Education?

A
  • Humphrey and Symes (2010) suggest all ASC students should have an adult ‘confidante’ with an understanding of ASC
32
Q

How can Schools help Social Inclusion of Students with Autism?

A
  • circles if friends: identify vulnerable child and engage with peer group to establish a small friendship group
    • involves educating and evoking empathy in peer group
    • teacher and group come up with ways to include the child to celebrate positives snd create strategies for negatives

Outcomes of CoF approach:

  • improves social skills in children with ASC (Kalyra and Avramidis, 2005)
  • increase social acceptance by classmates (Frederickson and Turner, 2003)
33
Q

How can we help ASC Children Improve their Social Skills?

A
  • social stories: transcripts describing typical scenarios and what people do/feel (Howley and Arnold, 2005)
  • must keep ‘autistic’ culture in mind - need to be well-structured and predictable, involve home and school so the learning can be generalised (Humphrey, 2008)
34
Q

Sensory Problems in Mainstream Schools

A
  • classroom noise can be distracting and even painful (Mesibor and Shea, 1996)
  • struggle with auditory filtering, hypo- and hyper-sensitivity can lead to withdrawal and poor academic success (Ashburner et al, 2009)
35
Q

Attentional Problems

A
  • ASC often overlaps with ADHD (Sturm et al, 2004)
    • even children without clinical ADHD can have lower level attentional difficulties
    • schools can ‘cherry-pick’ quiet, well behaved classes for children with ASC (Humphrey, 2008)
36
Q

Emotional and Behavioural Problems

A
  • psychiatric comorbidities especially on higher end of the spectrum (Gadow et al, 2005)
  • internalising psychopathology e.g. sadness, anxiety, low self-esteem
  • frequent outbursts of crying if things aren’t perfect (Ashburner et al, 2010)
  • externalising behaviours e.g. aggression, explosive anger, ODD, PDA
37
Q

Considering the Autistic Thinking Style in Learning

A
  • Humphrey (2008): abstract subjects like maths and science can be brought to a concrete level e.g. use models of atoms, use items that can be physically counted etc
  • power cards: cards with visual depiction of sensory integration (SI) and brief description of the problem with 3 or 4 easy to follow steps
38
Q

TEACH

Treatment + Education of Autistic + related Communication Handicapped children (1994)

A
  • create learning space with boundaries e.g. own working space and clear scheduled activities
  • use visual supports to show the sequence of daily activities and to breakdown individual tasks
  • set clear working system so child is aware of what is expected of them

success of TEACH?
- panerai et al (2009): children had significantly greater improvement on TEACH than children with non-specific inclusion programmes

39
Q

Does Integration Work?

A
  • improves quality of life, educational performance and social development (Osborne et al, 2011)
  • increases tolerance and inclusion in neurotypical children
    • but… sometimes students do better in specialist schools socially and emotionally, whilst no academic difference (Reed et al, 2010)
  • integration into mainstream can create a different type of segregation when obvious support is needed (Mesibou and Shea, 1996)
  • can increase isolation and rejection (Ochs et al, 2001)
40
Q

How do Specialised Staff feel about Integration?

McGregor & Campbell, 2001

A
  • 47% of specialist staff are in favour for full integration
  • 39% thought children were better in mainstream school
  • 83% thought degree of autism was the biggest factor in success of integration
  • 78% of successful integration depends on staff attitude
41
Q

How do Mainstream Staff feel about Integration?

A
  • 47% thought ASC students should be integrated with adequate help
  • 46% of experienced teachers thought they had the skills to teach autistic children
  • 89% of inexperienced teachers thought they did not have the skills

Emam & Farrell (2009):
- teachers made it clear that TAs are crucial for successful integration due to extra attention that ASC children need

42
Q

What is a Neurodevelopmental Condition?

A
  • brain is considered to develop differently from the very beginning
43
Q

What is the Mirroring System?

A

HOW are you doing that? WHAT are you doing?

  • brain regions which respond to our own emotions, actions and sensations and when we observe these in other people
    • includes frontal gyrus, premotor cortex and intraparietal sulcus
  • lower level system
44
Q

What is the Mentalising System?

A
  • higher level system involving MPFC, posterior cingulate and temporo-parietal junction
45
Q

How do the 2 Systems work Together?

A
  • they are dissociable but it’s thought they probably work together to produce the full ability to understand others aka ToM
  • seems to be abnormalities in both these systems in ASC
  • Fishman et al (2014) found hyper- and hypo-connectivity in ToM network and functional connectivity between ToM (mentalizing system) and mirror neuron system
46
Q

Broken Mirrors Hypothesis (Ramachandran, 2007)

A
  • based on evidence that mirror neurons hypoactive in autism: mirror neurons are a way of mapping other peoples actions onto our own motor repertoire (Rizzolati, 2010
  • mirror neurons can code chains of action e.g. grasping to place and item compared to grasping to eat
    • typical children will show movement in mouth muscles when grasping to eat prior to actually putting food in the mouth
    • ASC children don’t show this ‘action chaining’ effect (Cattaneo et al, 2007)
47
Q

Implications of Broken Mirrors Hypothesis

A
  • Rizzolati et al suggest mirror neurons are the basis of empathy and imitation
    • others query the role of mirror neurons in action understanding, mentalising, imitation and empathy (Hickock et al, 2009)
    • broken mirrors hypothesis doesn’t explain why the mirror neuron system is not always hypoactive in ASC (Hamilton, 2013)
48
Q

Mentalising System in ASC

A
  • brain imaging studies show abnormalities in function of mentalising system
  • can be studied by looking at irrational action i.e. WHY did you do that? - autistic people show different brain responses when viewing irrational actions (Marsh et al, 2014)
  • Lambardo et al (2010) asked participants mental or physical judgements about self and other e.g. ‘how likely are you to have bony elbows?’ and how likely is the queen
    • found overlap in brain regions underlying mentalising about self and others
    • in ASC parts of the brain (VMPFC) failed to discriminate between judgements about self vs. others
    • those with the lowest/no VMPFC activity were the most socially impaired in childhood
49
Q

Neurobasis of EF in ASC

A
  • PFC believed to play dominant role in EF
  • some argue the frontal lobes are especially structurally abnormal in ASC (Pierce and Courchnesne, 2005)
    • and the white matter under the frontal lobes is also abnormal - has been linked to genetics underlying ASC
50
Q

Neurobasis of WCC in ASC

A
  • Lee et al (2007) WCC paradigm tasks: found fewer brain areas involved compared to controls
  • others found equal performance but decreased functional connectivity between frontal and posterior brain regions
51
Q

Neurobasis of Sensory Problems in ASC

A
  • brain is more responsive to sensory stimulation in ASC
  • Green et al (2013): ASC show greater activity in the brain area being stimulated, also showed activity in emotion processing regions
52
Q

The Whole Brain in ASC

A
  • ASC cannot be explained by one dysfunctional region or system, it is a condition where the brain develops differently from the very beginning
53
Q

Studying Autism from an Early Age

A
  • can study high-risk infants aka ‘sibs’
  • Hazlett et al (2017) found sibs who went on to be diagnosed with ASC had ‘hyperexpansion’ of cortical surfaces area from 6-12 months
    • could predict severity of autism
54
Q

Why the Overgrowth in Infancy?

A
  • excessive and premature growth of axons, dendrites or cell bodies
  • excessive and/or premature myelination
  • abnormalities in cell death and pruning
  • excessive number of neurons, synapses, axons, glia cells and minicolumns
  • minicolumn: vertical column through cortical levels of the brain
  • glia cells: small cells surrounding brain cells, perform number of functions inc forming myelin, protection of neurons, removing dead neurons etc
55
Q

ASC as a ‘Systems Disorder’

A
  • popular belief
  • there are abnormalities in the whole-brain and local-level connectivity
  • there are links between connectivity abnormalities and symptom severity
  • tiny neural abnormalities over the course of time and development can lead to wide ranging cognitive processing difficulties which affects multiple domains

SO? we can’t look at isolated problems in brain regions supporting ToM, EF or WCC
- more global abnormality likely to underlie all symptoms

Educational Psychology (9 decks)

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