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LC LIFESPAN PSYCHOLOGY A > Understanding Autism > Flashcards

Understanding Autism Flashcards

1
Q

how did kanner and asperger (1944) observe early infantile autism?

A

as a childhood condition where children failed to integrate into social interactions, and had atypical communication with others

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2
Q

triad of impairments

A
  1. social interaction difficulties
  2. communication difficulties
  3. restricted, repetitive behaviours and interests
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3
Q

social interaction difficulties

A

unresponsive behaviour and not sharing interests

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4
Q

communication difficulties

A

repetitive and impoverished language, and not engaging in pretend play

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5
Q

restricted, repetitive behaviours and interests

A

fascination with objects and routines, seen in stimming behavioue

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6
Q

DSM 2013 compressed autism into…

A
  1. persistent deficits in social communication and social interaction
  2. restricted, repetitive behaviours, activities, or interests
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7
Q

what percent of the population are autistic?

A

1%

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8
Q

what does the increase in autism diagnosis suggest?

A

a greater understanding and broadening of symptoms, along with higher use of screening tools

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9
Q

prevalence of autism in males than females

A

3:1, and women tend to gain a later diagnosis

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10
Q

when is the prevalence of autism highest?

A

in 6-12 year-olds, as behaviour is more likely to be picked up on

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11
Q

when is the biggest increase in diagnosis?

A

between 13-18 years-old

recognition of previously missed cases

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12
Q

why might classic childhood symptoms not be the best marker for ASD in adults?

A

as adults have learnt how to engage in neurotypical social interaction

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13
Q

how can late diagnosis be explained?

A

camouflaging behaviour

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14
Q

camouflaging behaviour

A
  1. compensation
  2. masking
  3. assimiation
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15
Q

compensation

A

improving behavioural symptoms makes it unlikely to score in the range of autism at a diagnostic manual

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16
Q

masking

A

presenting a known or less autistic persona

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17
Q

assimilation

A

used to fit into social situations

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18
Q

evidence of genetic factors in the aetiology of autism

A

folstein and rutter (1977) found 36% of MZ and 0% of DZ twins are concordant for autism diagnosis

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19
Q

what did plomin (1994) find?

A

higher concordance for autism in MZ twins over other conditions

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20
Q

what does a median estimate of 76% for MZ concordance reflect?

A

a broadening of autistic symptoms between 1977-2011 and increased use of screening tools

21
Q

tick et al (2016) found __% of the variance in autism is explained by inherited genetic factors

A

93%

22
Q

what does heritability of autism not specify?

A

which genes or SNPs are involved

genome wide association studies should be used to find contributing SNPs to risk of autism

23
Q

evidence of autism having a polygenic cause

A

49% of variance in ASD was explained by common variants

24
Q

what has the potential to confer risk for later ASD?

A

prenatal exposures, which can impact foetus development and cause genetic changes

25
Q

environmental risk factors- advancing paternal age

A

offspring of men over 40 years-old were 5.75x more likely to be autistic

advancing paternal age caused a higher likelihood of passing on greater gene mutations

26
Q

kinney et al (2008) found a dose response relationship between…

A

exposure to severe storms during pregnancy and risk for developing autism after birth

27
Q

how does mind-blindness explain social characteristics of autism?

A

through an inability to read others mind and understand behaviour in terms of belief-desire reasoning

28
Q

baron-cohen (1985) observed __% of children with ASD failed the false-belief task

A

80%

29
Q

what did autistic children struggle with the concept of?

A

theory of mind

30
Q

examples of deficits in TOM

A
  • joint attention
  • false-belief
  • deception
  • emotional understanding
31
Q

how did baron-cohen attempt to explain the cause of autism?

A

damage to innate domain-specific TOM modules

32
Q

which brain abnormalities led to failures in mindreading, along with later social difficulties?

A

abnormalities in the superior temporal sulcus (STS) and medial prefrontal cortex (mPFC)

33
Q

evidence against mind-blindess

A

20% of autistic children passed false-belief tasks, and TOM is not heritable in neurotypical children

challenges the belief of an innate module

34
Q

what does mind-blindness fail to explain?

A

non-social symptoms of autism, and TOM may not be linked to social impairments

35
Q

how does executive dysfunction explain autiusm?

A

domain-general cognitive dysfunction of autism, through the conscious control of thought and action

36
Q

what tasks are used to measure mental flexibility?

A

pre-potent responses task and shfting task

37
Q

how did autistic children perform in mental flexibility tasks?

A

performed poorer than controls across all executive function measures

38
Q

abnormal brain activity in ______ _____ in adults with ASD

A

frontal lobe

39
Q

what did russel et al (1991) find?

A

executive function and TOM correlated in ASD, but this correlation decreases in adolescence

40
Q

what does the executive function account fail to explain?

A

islets of ability

41
Q

how does weak central coherence explain autism?

A

explains islets of ability, through the tendency to draw together diverse information to construct higher meaning in context

42
Q

what did happe (2006) hypothesise?

A

autistic individuals will have difficulty with global processing and prefer featural and local information

43
Q

where did autistic children show superior performance?

A

in the embedded figures task (1983)

44
Q

where did autistic children make more errors?

A

in the homographs test (1997) as they struggled to take in sentence context to understand the word

45
Q

what does longitudinal research show for weak central coherence?

A

it predicts TOM, but not social communication, executive function, or RRBI

46
Q

where did the fractionable triad hypothesis originate from?

A

happe questioned whether autism is a single disorder with a single cause, due to the weak correlations between the fractionable triad in the general population

47
Q

what might core symptoms have?

A

distinct causes at the genetic, neural, and cognitive level

48
Q

why is it difficult to identify a single gene for autism

A

as core symptoms are independently heritable, and have different causes and behavioural presentations

LC LIFESPAN PSYCHOLOGY A (10 decks)

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