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Psychopathology & Development > Autism > Flashcards

Autism Flashcards

1
Q

HISTORY

A
  • autism = clinically severe/pervasive developmental disorder characterised by impairments in several development areas
  • KANNER & ASPERGER: identified it as recognised clinical disorder over 50Y ago
  • BUT fundamentally flawed perspective aka. “these kids come into world unable to form usually biologically provided affective contact w/others”
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2
Q

WING & GOULD (1979): THE TRIAD

A
  • 3 relevant ability areas:
    1. communication ability
    2. social interaction ability
    3. range of interests/flexibility/imagination
  • lifelong impairment on beh measure in ALL = autistic
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3
Q

WING & GOULD: IMPAIRED SOCIAL INTERACTION

A
  • reduction of non-verbal signs of interest in/pleasure from being w/another person
  • ie. making eye contact (initiating/responding)
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4
Q

WING & GOULD: IMPAIRED SOCIAL COMMUNICATION

A
  • decreased ability to converse non-verbally/verbally w/another ie. sharing ideas/interests
  • manifests as:
    1. no communication
    2. communication of own needs
    3. repetitive/one-sided
    4. formal/long-winded/literal
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5
Q

WING & GOULD: IMPAIRED SOCIAL IMAGINATION

A
  • decreased capacity to think about/predict consequences of your actions for yourself/others
  • manifests as:
    1. handling objects for simple sensations
    2. handling objects for practical uses
    3. copies pretend play of others
    4. limited “pretend play”/repetitive/isolated
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6
Q

NICE CO-MORBIDITY

A

ADLAM & CORMACK (2022)
- NEURODEVELOPMENTAL DISORDERS
- MENTAL/BEHAVIOURAL DISORDERS
- MEDICAL/GENETIC ISSUES & DISORDERS
- FUNCTIONAL ISSUES & DISORDERS

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7
Q

NICE: NEURODEVELOPMENTAL DISORDERS

A

ADLAM & CORMACK (2022)
- global delay/intellectual disability
- motor co-ordination issues/developmental co-ordination disorder
- academic learning issues (ie. literacy/numeracy)
- speech/language disorder
- dif is NOT = issue; issue = exclusive environment

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8
Q

NICE: MEDICAL/GENETIC ISSUES & DISORDERS

A

ADLAM & CORMACK (2022)
- epilepsy/epileptic encephalopathy (4-14%)
- genetic abnormalities incl. fragile X (24-60%)
- cerebral palsy (15%)
- tuberous sclerosis (36-79%)
- Down’s syndrome (6-15%)
- muscular dystrophy (3-7%)
- neurofibromatosis (4-8%)

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9
Q

NICE: FUNCTIONAL ISSUES & DISORDERS

A

ADLAM & CORMACK (2022)
- feeding issues incl. restricted diets
- urinary incontinence/enuresis
- constipation
- sleep disturbances
- vision/hearing impairment

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10
Q

NICE: MENTAL/BEHAVIOURAL DIFFICULTIES

A

ADLAM & CORMACK (2022)
- ADHD
- attachment/mood disorders
- anxiety disorders/phobias
- oppositional defiant disorder (ODD)
- conduct disorder
- OCD
- psychosis
- self-injurious behaviour
- selective mutism

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11
Q

MEDICAL & PSYCHIATRIC CONDITIONS

A

CROEN (2014)
MEDICAL
- gastro-intestinal disorders (24%^)
- hyper-tension (42%^)
- diabetes (50%^)
- obesity (69%^)
- sleep disorders (90%^)
PSYCHIATRIC
- anxiety (117%^)
- depression (123%^)
- suicide attempts (433%^)

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12
Q

NICE: CONSIDERATIONS I

A

CURTIS (2022)
- prevalence/impact of co-morbidities over lifespan
- newly evolving challenges field faced w/aging/menopause/dementia issues; question of how they present alongside autism
- co-morbid diagnosis = challenging due to atypical presentations
- co-morbid conditions mask underlying autism esp. if it doesn’t fit “tradition”
- other conditions not investigated as blinded by autism diagnosis aka. autism over-shadowing

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13
Q

NICE: CONSIDERATIONS II

A
  • harder to see help/communicate other condition needs
  • very little accessible as interventions oft based on neurotypical models (ie. eating disorder support in sensory differences context; talking therapies in communication difs context)
  • vulnerable to therapy/health inequalities
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13
Q

NICE: CONSIDERATIONS II

A
  • harder to see help/communicate other condition needs
  • very little accessible as interventions oft based on neurotypical models (ie. eating disorder support in sensory differences context; talking therapies in communication difs context)
  • vulnerable to therapy/health inequalities
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14
Q

DSM-5: AUTISM SPECTRUM DISORDER

A
  • combines social communication/reciprocal social interaction impairments into 1 dimension (NOT incl. social imagination)
  • includes sensory impairments in criteria for restrictive/repetitive beh patterns
  • drops sub-types (ie. Asperger Syndrome/childhood disintegrative disorder (CDD) /PDD-NOS)
  • adds new Social Communication Disorder (SCD; impaired social interaction/communication w/o restricted interests) separate from autism
  • defines severity according to support needs
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15
Q

DSM-5: CRITICISMS

A
  • not everyone will have all components as varying skill lvls across areas
  • doesn’t address needs in females
  • doesn’t address signs to allow infancy diagnosis
  • doesn’t consider diagnosis in adulthood where learnt adaptations might “mask”/no longer be helpful during key life stages
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16
Q

ICD

A
  • produced by UN global health agency
  • free/open resource for public health benefit
  • for countries/front line service providers
  • global/multidisciplinary multilingual development
  • approved by World Health Assembly
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17
Q

DSM

A
  • produced by American Psychiatric Association
  • intellectual property of APA
  • primarily for psychiatrists/psychologists
  • dominated by US aka. Anglophone perspective
  • approved by APA Board of Trustees/Assembly
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18
Q

DIAGNOSTIC GUIDELINES VS CRITERIA

A
  • diagnostic guidelines = intended to provide clinicians w/guidance on making diagnosis
  • focus on condition’s essential features (ie. those required for diagnosis/differentiating it)
  • disorder definitions DON’T HAVE CRITERIA but guidelines summarised as bullet points resembling brief required diagnosis elements
  • dif by avoiding algorithmic psuedo-precise requirements (ie. symptom counts/precise durations to dif disorder from “normality”)
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19
Q

ICD-11: ASD CLASSIFICATIONS

A

LEAST-HIGHEST SEVERITY
- ASD w/o intellectual development disorder; w/mild/no functional language impairment
- ASD w/intellectual development disorder; w/mild/no functional language impairment
- ASD w/o intellectual development disorder; w/impaired functional language
- ASD w/intellectual development disorder; w/impaired functional language
- ASD w/intellectual development disorder; w/functional language absence

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20
Q

COGNITIVE ASSESSMENT ROLE

A
  • SIGN/NICE guidelines agree that:
    1. suspected ASC assessment should include not only attempt to establish accurate diagnosis but also to provide accurate assessment of individual’s profile/needs
    2. cognitive profile aids interpretation of ASC history/observations
    3. cognitive profile informs supports/environmental adaptations required
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21
Q

NEUROPSYCHOLOGY

A
  • profile of cognitive strengths/weaknesses (expect unevenness)
  • developmental needs
  • specific cognitive deficits (relative-normative data) incl:
    1. limited TOM
    2. weak central coherence
    3. narrow focus
    4. difficulty redirecting attention
    5. executive function difficulties of various kinds
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22
Q

! SUMMARY: PART I !

A
  • individuals vary across domains/features in dif contexts/life stages
  • difs between diagnostic criteria VS guidelines further supports individual difs in autistic people
  • autism presents alongside other conditions aka. ^ co-morbidity
  • present in boys/girls; lifelong BUT many women = undiagnosed
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23
Q

! SUMMAY: PART I: CLINICAL PSYCHOLOGISTS !

A
  • clinical psychologists/neuropsychologists = well-placed to:
    1. support individuals/families/schools
    2. support diagnosis
    3. provide evidence based support for experienced issues
    4. champion research into developing therapeutic interventions to address inequality/inaccessibility issues caused by intervention over-use based on neurotypical needs
    5. work collaboratively w/inclusivity/diversity/equality intent
    6. enter therapeutic relationships w/inquisitive mind–the client is the expert
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24
Q

PREVALENCE

A

LYALL ET AL (2017)
- 4.2% school aged kids diagnosed (6.4% = boy; 2% = girls)
- 14% don’t have any Special Educational Needs
- true values likely to be higher due to not having functional difficulties/unrecognised by teachers/waiting times

25
Q

IMPROVING DIAGNOSTIC SERVICES

A

CROEN ET AL (2002)
- pop study; 8 successive birth cohorts in California
- 4.5m births; 5038 w/autism (4.9 p/10k prevalence)
- prevalence ^ 5.8 -> 14.9 p/10k during study period; unrelated to maternal age/race/education/gender changes
- diagnosis of Mental Retardation decreased 28.8 -> 19.5 p/10k at the same time
- CONCL: observed increase = results of detection/diagnosis improvements; likely to improve w/better understanding

26
Q

GENETICS

A

YANG & GILL (2007)
- numerous candidate genes located; suggests marks heterogeneity; most encode proteins involved in neural development/function
- calculated heritability = 80%; 35-45% = chance of 2nd twin being autistic if 1st is
- recurrence rate (in family) = 4% (girl)/7% (boy)
- if 2nd kids = autistic -> 25-35% sibling recurrence

27
Q

HALLMEYER ET AL. (2011)

A
  • 192 twin pairs w/at least 1 autistic twin
  • 1st study to use both ADI-R/ADOS
  • susceptibility to ASD = moderate genetic heritability/substantial shared twin environment component
  • shared environmental factors explain 58% autism variance/moderate genetic heritability (autism = 38%)
28
Q

LUNDSTROM ET AL. (2014)

A
  • all 9Y twins in Sweden born between 1992-2001 (19k); 260 affected probands (individual affected)
  • heritability = 84% BUT…
  • MZ recurrence rate = 39%
  • 11/260 = autism only (pop prevalence = 4.2 p/10k)
  • 50.3% = > 4 coexisting disorders (ADHD/LD/TD/ODD/OCD)
29
Q

LUNDSTROM ET AL. (2014): CONCLUSIONS

A
  • almost all kids w/neurodevelopmental conditions = impaired in multiple areas
  • autism = far from sharply demarcate at genotypic/phenotypic lvl
  • genes implicated in autism also implicated in other neurodevelopmental conditions
  • to understand/support autistic people we MUST look at symptoms > categorical labels
30
Q

ENVIRONMENT & G X E

A

HALLMEYER ET AL. (2011); LYALL ET AL. (2017)
- prematurity
- short inter-birth interval
- parental age
- low birth weight
- multiple births
- maternal infections during pregnancy
- foetal drug & toxin exposure
- preterm exposure to air pollution

31
Q

MANDY & LAI (2016)

A
  • pre-conception risks = advanced parental age/valproate/possible SSRIs/traffic related air pollutants & pesticides/heavy metals/severe obesity/maternal diabetes/steroidal activity/immune activation
  • pre-conception protection = folate
  • peri-natal risks = unclear BUT elevated by events associated w/hypoxia (neonatal anaemia/meconium aspiration/birth trauma/v low birthweight)
  • post-natal risks = severe early deprivation (ONLY w/prodromal features ie. reduced social orientating)
32
Q

NEUROBIOLOGY

A
  • virtually every brain structure = implicated in autism:
    1. cerebral cortex
    2. amygdala
    3. hippocampus
    4. basal ganglia
    5. brain stem
    6. cerebellum
    7. corpus callosum
33
Q

NEUROBIOLOGY: STRUCTURE VS FUNCTION

A
  • brain weight/volume & head circumference = greater w/autism
  • cellular/molecular bases of pathological early overgrowth = unknown
  • unknown if overgrown neural systems cause autism characteristics
34
Q

NEUROLOGY: CAUSAL HYPOTHESES

A
  1. neuron excess causing local over-connectivity in key brain regions
  2. disturbed neuronal migration during early gestation
  3. unbalanced excitatory-inhibitory networks
  4. abnormal synapse/dendritic spine formation
35
Q

! SUMMARY: PART II !

A
  • strong genetic origin BUT issues w/research (ie. low stat power/sample heterogeneity/need to consider epigenetic factors across lifespan)
  • appears to result from developmental factors affecting many/all functional brain systems
  • neuroanatomical studies/teratogen (compounds/environmental factors interfering w/normal in utero dev) association strongly suggest autism’s mechanism = brain dev alteration soon post conception
  • starts event cascade in brain (local overgrowth w/under-connectivity) sig influenced by environmental factors
36
Q

TOM: SALLY-ANNE TEST

A

BARON-COHEN ET AL. (1985)
- typically dev 4 year olds answer correctly (aka. Sally looks for ball in her basket)
- 80% autism answered Sally would look in Anne’s box -> implicated poor TOM
- BUT maybe unable to get involved in story requiring suspended belief? Sally = doll w/o mind so meaningless q?

37
Q

MINDBLINDNESS THEORY

A

BARON-COHEN (1995)
- proposes there are empathising deficits in autism relative to mental age
- empathising includes:
1. attributing mental states to oneself/others to explain beh (TOM)
2. having appropriately emotional reactions to others’ mental states (ie. affective reactions aka. sympathy)

38
Q

TOM: DEVELOPMENT

A
  • likely that shared attention = early branch in TOM/empathy development through maturity
  • possible that early imitation skills predict later empathy skills
39
Q

UNDERSTANDING INTENTIONS: ANOTHER ROLE FOR MIRROR NEURONS (?)

A
  • same neural structures involved in processing/controlling executed actions/felt sensations/emotions also active when same actions/sensations/emotions detected in others
  • understanding intentions depends on recognition of own states in others
40
Q

SOCIAL INTEREST: SOCIAL COGNITION IMPACT

A
  • babies = very social aka. orient to mother’s voice in utero/born w/interest in faces; social frame sets scene for language/learning
41
Q

SOCIAL INTEREST: SOCIAL FRAME

A
  • WITH:
    1. take lead from looking at others (ie. what are they looking at/feeling/doing?)
    2. good at multi-tasking as have to integrate visual/auditory inputs w/context
    3. become quickly adept in social world; play constantly
  • WITHOUT:
    1. everything matters (no filter)
    2. seek consistency/stability
    3. difficulties w/multi-tasking
    4. meaning comes from environment NOT others
42
Q

EXECUTIVE FUNCTION = PRIMARY DEFICIT (?)

A
  • behs associated w/autism = caused by difs in flexibility/planning/other executive dysfunctions
  • tends to be seen as model which works well w/repetitive/restricted interest BUT less well for social cognition
  • EF model = less popular today BUT maybe all theories imply EF issues
43
Q

FAHIE & SYMONS (2003)

A
  • sig correlations (r = .68) between composite EF/TOM measure in 5-9Ys
  • executive function may underlie both TOM/social issues
44
Q

PRIMARY DEFICIT MODELS

A
  • shifted from competing explanations -> potentially overlapping models
  • describe social cognition continua
  • stimulate research into social cognition development
  • contribute to understanding of metacognition > generally
  • less successful in knowing what causes social cognition difs/differentiating between causal factors & dif social cognition outcomes
45
Q

CENTRAL COHERENCE (CC)

A
  • normal tendency to integrate info in context for meaning oft at surface form expense
  • autistic people process details well at global configuration/meaning expense
    FRITH (1989)
  • this detail focus = “weak coherence”
  • weak coherence = style NOT deficit; -> assets/issues; bias can be overcome
46
Q

CC: COGNITIVE STYLE

A
  • weak (ie. good proof reading) - CC (ie. good gist recall) - strong
  • both extremes could have costs/benefits/sex difs
47
Q

HAPPE ET AL. (2001)

A
  • designed to invite local completion at odds w/global coherence of sentence
  • ie. “in the sea there are fish and (chips/other sea life) -> chips = weak coherence; sea life = strong
  • “chips” = locally coherent w/final 2 words in isolation BUT incongruent in sentence context
48
Q

CC: TYPICAL DEVELOPMENT

A

BOOTH & HAPPE (2010)
- no sig between male/female BUT…
- males made fewer local completions w/age
- no relationship w/IQ
- BUT is this weak central coherence/impaired inhibitory control?

49
Q

EMPATHISING-SYSTEMISING (E-S) THEORY

A

LAWSON ET AL. (2004)
- systemising = drive to analyse/build systems ie:
1. technical (ie. machines)
2. natural (ie. biological/geographical phenomena)
3. abstract (ie. maths)
4. social (ie. football league tables)
- fascination w/underlying rules/regularities
- E-S theory holds that autism = empathising deficits + intact/superior systemising

50
Q

INTENSE WORLD HYPOTHESIS

A

MARKRAM & MARKRAM (2001)
- autistic people perceive world as overwhelmingly multisensory stimulation aka. sensory over-responsivity
- social situations = esp. complex/intense
- social experiences -> withdrawal/self-soothing behs (aka. less opportunity to experience social interaction)
- NOT fixed; varies depending on tiredness/body cues; no conscious perception

51
Q

BAYESIAN DECISION THEORY

A

PELLICANO ET AL. (2012)
- relatively recent model
- perception = unconscious inference
- sensory perception = similar in autism BUT sensory input interpretation to yield perceptions DOESN’T use prior knowledge
- prior beliefs generating top-down predictions = somehow compromised -> increased reliance on bottom-up sensory evidence (aka. hypo-priors)

52
Q

BAYESIAN DECISION THEORY: PERCEPTION RELIABILITY

A

PELLICANO ET AL. (2012)
- produces ^ accurate BUT less reliable/interpretable perceptions
- eg. shadows help interpret object via shape/size/orientation/slant; if all you perceive are lines/curves/colours they may not draw inferences about what it is/intentions

53
Q

BAYESIAN DECISION THEORY: EXPECTATIONS

A
  • priors support interpretation BUT also expectation/prediction ability
  • may shed light on intense desire for sameness; may not be issue w/change but prediction
  • fewer/weaker priors (hypo-priors) could result in reduced generalisation; oft seen as issue for autistic people; could constrain motor plans to already known (hence stimming)
54
Q

BAYESIAN DECISION THEORY: STIMULI EXPOSURE

A
  • becoming comfortable w/new situations may require more exposure to stimulus/context
  • self-generated repetitive behs (aka. individual = full control) might be means of reducing environmental uncertainty (self-intervention)
  • sensory inputs from others = less tolerated < similar sensory inputs created by autistic person
55
Q

AUTISM = PREDICTION DISORDER

A

SINHA ET AL. (2014)
- bottom-up info processing explanation
- autistic brain relies on sensory systems at expense of ^ integrative processing requiring awareness of contextual subtleties necessary for prediction
- prediction processes may be critical to adaptive cognitive/beh/social function

56
Q

AUTISM = PREDICTION DISORDER: EXPERIENCES

A
  • inability to approximate relevant future -> stressful reactions/overstimulation
  • only remedy = complex social situation avoidance/focus on highly predictable routines
  • compromised prediction skills -> “magical” world where events occur unexpectedly/w/o cause
  • immersion in this capricious environment = overwhelming/compromising of interaction
57
Q

DOUBLE EMPATHY PROBLEM

A

MILTON (2012)
- successful social interaction requires participation of minimum 2 people
- where interactions between people w/w/o autism = unsatisfactory -> both parties take responsibility
- BUT neurotypical people oft have little empathy for autistic people; manifests in failure to create autism-enabling environments/adapting own beh (ie. insisting on societal eye contact norms)

58
Q

CORE DEFICITS = CORE STRENGTHS

A
  • autistic people have unique view of world:
    1. Silicon valley
    2. research
    3. problem solving
    4. areas requiring creativity
59
Q

! SUMMARY: PART III !

A
  • autism presents in many dif ways; few models can explain variability
  • most suggest bottom-up perceptual processes = favoured
  • cognition can appear unaffected BUT context = missed -> generalisation/prediction affected
  • produces “empathy disorder”
  • causal paths from early neurogenesis to social cognitive outcome = still uncertain
60
Q

FUTURE RESEARCH IMPLICATIONS

A
  • studying cognitive style in autism might:
    1. provide evidence to support neurodiversity movement
    2. raise awareness of positive autism aspects
    3. inform educational approaches working to strengths

Psychopathology & Development (12 decks)

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