lecture eight - differences in perception in autism spectrum disorder Flashcards

(32 cards)

1
Q

Why be interested in perception in autism?

A
  • Perception is the interpretation of sensory input – what we
    see, hear, smell, taste and touch.
  • Theory of Mind (ToM) and Executive Functions (EF) are ‘higher
    order’ mental processes.
  • Perception is a fundamental building block of more complex
    cognitive and behavioural processes.
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2
Q

Enhanced Perceptual functioning
(Mottron et al., 2006)

A

The hypothesis:
Perceptual processing is superior in autistic people as they are very sensitive to the environment. This
superiority is hard to control and disrupts the development of
other behaviours and abilities.

a theory devised specifically to help us understand autism - as general models and theories were in place before we started thinking about autism

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3
Q

Pitch discrimination
(Bonnel et al., 2003)

A
  • Same/different judgement - listened to two tones and have to say if they were the same or different
  • High/low categorization - had to say which beep they heard was a low one or a higher one
  • Autistic individuals showed
    superior performance.
  • 12 autistic adolescents and 12
    comparison adolescents. - very few ptps
  • Both groups intellectually high
    functioning. - overlooked those with autism who have a lower IQ
  • Only looked at pitch - only one domain of auditory perception
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4
Q

Auditory discrimination
(Jones et al., 2009)

A
  • broadened it beyond pitch
  • Intensity Discrimination task
    “which dinosaur makes a louder sound?”
  • Duration Discrimination task
    “which dinosaur makes a longer sound?”
  • Frequency Discrimination task
    “which dinosaur makes a higher sound?”
    72 autistic adolescents and 48
    non-autistic adolescents
    Wide range of intellectual ability - covered the full spectrum of IQ

ptps saw a circle appear around each dinosaur as it made a sound and has to identity which was either louder, longer or higher.
- at a group mean level there was no significant differences between the groups
- so looked to see if there was a subgroup among the 72 autistic ptps who had exceptionally good auditory discrimination - as theres lots of variability within autistic people

subgroups with superior performance (1.65 SD above the non-autistic mean)
- subgroup of autistic people who are really good at pitch discrimination - the subgroup also had on average a higher IQ than their peers and they also had delayed language

in autism research or other types of neurodevelopment conditions - heterogeneity is a factor thats not always accounted for

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5
Q

Auditory discrimination

A
  • 1 in 5 autistic adolescents had enhanced frequency
    discrimination
  • They were characterised by average intellectual ability and
    delayed language
  • Possible subgroup whose language development had been
    impaired due to over-focus on perceptual cues (such as pitch) - if sensitive to changes in pitch may be distracting so maybe missing out on content/ semantics - trying to generate a theory for why the entrance pitch perception would Map on to the language delay
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6
Q

Putting EPF theory to the test
Universal?

A

Jones et al. (2009) suggest this is not the case. Further, there is
evidence of impaired as well as enhanced perceptual processing
in autism (e.g. Milne et al., 2002).
Unique?
Largely untested in other developmental disorders.

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7
Q

Putting EPF theory to the test
Explanatory power?

A

Good at explaining sensory sensitivities - restrict receptive behaviours (e.g. hypersensitivity to
sound).

Relies on a developmental ‘knock on’ effect of EPF on higher-order
social and cognitive abilities to explain the majority of autistic
behaviours. More research is needed (e.g. longitudinal studies) to
establish these links.

doesn’t describe all different types of symptoms and features of autism

enhanced perceptual functioning might stop you developing language skills, might stop you paying attention your peers which would then lead to difficulties in friendships

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8
Q

Weak central coherence (WCC)

A

Central coherence: a natural tendency to process stimuli as a
whole.
Weak central coherence: a bias for processing the parts of any
stimulus at the expense of the global whole.

example
“Red wheel” - autistic children called a red tractor a red wheel

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9
Q

WCC in autism
(e.g. Frith, 1989; Frith & Happé, 2006)

A

The hypothesis:
Autistic people have a local processing bias (i.e. features) at the
expense of processing the ‘whole’ (i.e. not getting the ‘gist’;
not seeing the ‘bigger picture’).
This has been framed as a superiority for perceiving details and
features. A different ‘cognitive style’. - enhanced ability to notice details

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10
Q

The embedded figures test

A

Autistic children are better and
quicker at finding the
‘embedded figure’ than non-
autistic children
(e.g. Shah & Frith, 1983).
Autistic children are less distracted by the whole image.

child has to work out where in image is the small triangle

the embedded figures test - harder version for adults

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11
Q

Planning/drawing test

A

Autistic children draw in an
atypical, fragmented way
and focus on details - more likely to start with window etc
(Booth et al., 2003).

if you draw the walls and frame first more typically you see the whole picture

if you draw the windows, chimney, door = more piecemeal

roof first = somewhere in the middle

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12
Q

Putting WCC theory to the test
Explanatory power?

A

WCC does not explain all symptoms:
* May interfere with social interaction e.g. focusing on an item
of clothing or object in the room may disrupt recognition of
facial emotion or processing on social information. - could detail development in some way or mean your not interacting in a typical way
* May explain some restricted and repetitive behaviours e.g.
intense preoccupations and attention to parts of objects - you may see things others may not necessarily notice

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13
Q

Atypical social orienting

A

(e.g. Dawson et al., 1998)
The hypothesis: Autistic individuals show reduced orienting to
social information, particularly the face and eyes. They
therefore fail to become ‘face experts’, which leads to reduced
ability to perceive face identity and emotional expression. - not same fundamental inputs as typical children in terms of development

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14
Q

Atypical looking to the face
(Klin et al., 2002)

A

Autistic and non-autistic adolescents and young
adults were filmed watching ‘Who’s afraid of
Virginia Woolf’.
An eye tracker monitored eye gaze.
The autistic group showed significantly less looking
to the eyes, and focussed more on mouths, bodies
and objects.
Increased looking to objects correlated with poorer
social skills.

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15
Q

Atypical looking at the eyes
(Kliemann et al., 2010)

A

Fixation cross led to first focus on face being on eyes or
mouth. - image was moved up or down so were forced to look at eyes or mouth
Subsequent eye gaze was monitored.
The non-autistic group showed significantly more shifts
towards the eyes rather than away from the eyes.
The autistic group showed significantly more shifts away
from the eyes rather than towards the eyes.
This suggests active avoidance of eye gaze, and not just a
lack of orienting.

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16
Q

typical looking to the eyes - Rutherford and towns 2008

A

they had to make an emotional judgement - this may affect what they naturally do

they measured looking to the eyes or the mouth

finding - autistic adults showed no difference in the amount of looking to the eyes and mouth when making emotion judgements

17
Q

Putting atypical social orienting to the
test
Universal?

A

There are many studies that do not show impaired looking to the
face/eyes in autistic people (e.g. Rutherford & Towns, 2008).
Unique?
Individuals with Williams syndrome also show impaired looking
at faces, although there are condition-specific differences.

18
Q

Putting atypical social orienting to the
test
Explanatory power?

A

Atypical social orienting aligns well with the social
communication difficulties seen in autism.
However, it does not adequately explain restricted and repetitive
behaviours.

19
Q

The multiple deficit account
(Happé et al., 2006)

A

Single atypicality accounts make an assumption that the core
behaviours of autism occur together more often that would be
expected by chance as a result of a single underlying aetiology.
The multiple deficit account proposes that the behavioural
symptoms have distinct aetiologies.

multiple explanations will account for lots of the different behaviours of autism and if you have lots of different causes and lots of these different behaviours you will have a diagnosis of autism. if you just have one of those causes and only one behaviours you wont get a diagnosis of autism.

19
Q

Towards a new explanation

A

Historically, researchers have focused on identifying a single
primary cognitive atypicality, which could account for the full
range of autistic behaviours.
Yet the “single-deficit” models proposed have all struggled to
provide complete explanatory accounts of autism. - with both social communication differences and restrictive and passive behaviour differences
So, where to go from here…?

20
Q

multiple differences leading to an autism

A

genetic cause X – atypicality A:ToM – social and communicative symptoms

genetic cause Y – atypicality B:EF – restricted and receptive behaviours

genetic cause Z – atypicality C:WCC – attention to detail

21
Q

Support for a multiple differences 1

A
  • If a particular type of cognition (e.g. poor ToM) explains all
    behavioural symptoms then these behaviours should be correlated. - social communication difficulties and difficulties in restricted and receptive behaviours
  • However, twin studies in the general population do not find this
    (Ronald et al., 2006). 10% show atypicality in only one of three
    areas (social impairment, communication impairment, restricted
    and repetitive behaviours). - these are not correlated in the general population you can have difficulty in one area - not one single cause
  • Growing evidence suggests there is very limited genetic overlap
    between the three areas (e.g. Ronald et al., 2006; Robinson et al.,
    2012).
22
Q

Support for a multiple differences 2

A
  • Autism is heritable, but so are subclinical manifestations of
    core behaviours.
  • The ‘broader autism phenotype’.
  • Relatives often show isolated traits but may not have autism themselves (e.g. only restricted and
    repetitive behaviours).
  • Different relatives with different behaviours indicates
    independent genetic inheritance (e.g. Pickles et al., 2000).
23
Q

Support for a multiple differences 3

A
  • A single underlying cognitive/perceptual cause would predict
    atypicalities at the neural level that are observed for the range
    of behaviours.
  • However, a ‘social brain’ network has been identified (including
    frontal and temporal regions - associated with ToM), which is very distinct from the
    atypical subcortical activation associated with restricted and
    repetitive behaviours. - not one single cause as we can distinguish these different neural pathways of these two areas
24
the multiple differences
happe et al 2006 - ToM (Social and communicative symptoms) EF (restricted and repetitive behaviours) WCC (attention to detail) - these all overlap - causing autism? you need to have enough of these different behaviours in the same individual so you're crossing a threshold in terms of amount of behaviours that would lead to a diagnosis
25
A point for reflection
* We have explored whether autistic people have difficulty with Theory of Mind, executive functions and social orienting. * This is a ‘deficit model’ that intrinsically suggests that there is something about autistic people that is not working, is ‘less than’. * Other theories have focussed more on difference (weak central coherence- different processing style), or even enhanced abilities (enhanced perceptual functioning). * All these theories compare autistic to non-autistic people and do not consider other contexts. * Consider the implications of this research focus. To what extent might the dominant neurotypical lens, where autism is compared to the ‘norm’, drive these implicit assumptions of autism as a ‘dysfunction’?
26
neurodiversity - a new (old) framework
neurodiversity - the range of natural diversity that exists in human neurodevelopment neurotypical - a person or people whose neurodevelopment falls within the range usually considered to constitute 'typical' development neurodivergent - a person or people whose neurodevelopment falls outside of (or 'diverges' from) the range usually considered to constitute 'typical' development eg a group of autistic people is a group of 'neurodivergent' people pelicano and den houting 2022
27
The Neurodiversity perspective
* The neurodiversity perspective considers all brains as equal and frames neurodivergent individuals as ‘different’ not ‘impaired’ (e.g. Pellicano & den Houting, 2022) * Finding ToM difficult can cause challenges in a neurotypical- dominant world but what happens when two people with a ToM ‘difficulty’ converse?
28
Crompton et al. (2020)
* Communication difficulties are more pronounced across the neurotype boundary (autistic + non-autistic person conversing) than within. researcher had a story that they told to one person, another person came in the room and they told that person the story and then they left and so on 3 types of chain - autistic chain, non-autistic chain, mixed chain interested to see what would happen if has autistic and non autistic people conversing the autistic and non-autistic chains both did better at keeping the integrity of the story than the mixed chain maps onto the social model of disability - the idea that sometimes its the environment that causes the disability conditions for a person
29
Summary
* Evidence suggests that basic perceptual processing (either in terms of ability or in relation to processing style) is atypical in autism, which influences cognition and behaviour. * This atypical processing is often a strength (i.e. enhanced ability) rather than a weakness, despite leading to difficulties in everyday life. * However, no single-deficit model can offer a complete explanatory account of autism. * The multiple-deficit account is better able to explain the difficulties seen in autistic people. * However, the neurodiversity perspective moves us away from the language of ‘deficit’ and encourages us to understand and embrace difference.
30
reading - Visual Attention and Social Functioning in Autism Spectrum Disorder (ASD): A Systematic Review and Meta-Analysis Riddiford, A. S., McConachie, H., Parr, J. R., Charman, T., & Rodgers, J. (2022)
Aim To test whether visual attention (eye gaze) is linked to: Social functioning, and Autism symptom severity in ASD. Specifically: do people with ASD show reduced gaze to faces/eyes, and does this relate to poorer social outcomes? Background - Social difficulties are core features of ASD. - One explanation is atypical social attention (less looking at faces/eyes → reduced social learning). - Previous findings were mixed, motivating a large-scale meta-analysis. Methodology - Systematic review & meta-analysis (PRISMA). 95 studies (from ~3,000 screened). - Participants: Individuals with ASD vs neurotypical controls. - Measures: Eye-tracking (fixation to eyes, face/head, mouth). - Social functioning (ADOS, Vineland, SRS). - Analyses: Combined effect sizes (correlations). - Moderator analyses (age, task type, rater, emotion). Key Findings - Overall relationship Reduced gaze to faces/eyes → poorer social functioning & greater ASD severity. - Region-specific effects Face/head gaze: strong association (r ≈ −.50). - Eye gaze: moderate association (r ≈ −.19). - Mouth gaze: no reliable association (often nonsignificant). ➡ Face and eye gaze are better predictors of social ability than mouth gaze. Moderating Factors - Stronger effects when: Social functioning rated by clinicians (vs parent/self-report). - Tasks used dynamic, socially rich stimuli. - Eye-tracking calibration was high quality. - Participants were younger (developmental importance). - Faces were emotional or familiar. Interpretation - Supports theories that reduced social attention contributes to social difficulties in ASD. - Gaze patterns may reflect differences in social motivation or social cognition. - Mouth fixation may be adaptive, not deficient (e.g. aiding speech comprehension). - Eye-tracking shows promise as an objective biomarker for social functioning and treatment response. Limitations - High methodological variability across studies. - Mostly cross-sectional → no causal conclusions. - Some small effect sizes (especially eye vs mouth gaze). - Need for longitudinal, standardised, developmental research. Exam-Style Conclusion - ASD is associated with atypical visual attention to social stimuli. - Less face/eye gaze = poorer social functioning and higher symptom severity. - Visual attention patterns are context-dependent, not uniform. - Eye-tracking is useful but requires careful standardisation
31
reading - Happé, F., Ronald, A., & Plomin, R. (2006) Time to give up on a single explanation for autism, Nat. Neurosci., 9, 1218-1220.
Core Argument Autism cannot be explained by a single cause (genetic, neural, or cognitive). The three core domains: - Social interaction - Communication - Restricted/repetitive behaviours These domains are partially independent (“fractionable”), not one unified syndrome. Behavioral Evidence - Twin studies (3,000+ pairs) show only modest correlations between domains (r ≈ .1–.4). - Many children show isolated difficulties: ~59% had impairment in only one domain. ~10% showed a single impairment as severe as ASD. - Suggests autistic traits exist on a continuum and can occur separately. Genetic Evidence - Each domain is highly heritable, but: Influenced by mostly different genes. - Over half of genetic influences do not overlap across domains. - Relatives often show subclinical traits in one domain only. - Indicates distinct genetic pathways for each feature of autism Cognitive & Neural Evidence No single cognitive deficit explains all domains. Different theories explain different features: Theory of Mind deficits → social/communication problems. Executive dysfunction / local processing bias → rigidity/repetitive behaviour. Neuroimaging links different brain regions to different domains. Implications - Research: Stop searching for one autism cause. - Diagnosis: Assess domains separately, not one severity score. - Treatment: Different symptoms need different interventions. - Genetics: Focus on trait-specific genes. Exam Conclusion Autism is not a single disorder with one cause. It reflects multiple overlapping but distinct dimensions, each with its own genetic, neural, and cognitive basis. Best understood using a multifactorial, domain-specific approach