autism Flashcards

1
Q

Kanner

A
  • first published a description of children that he believed suffered from “autistic disturbances of affective contact”
    – Observations based on 11 (also see 1971 follow up)
  • Treated people like objects
  • Showed characteristic patterns of speech and language use
  • Displayed immediate and delayed echolalia
    – Reversal of pronoun use (you for I)
  • repetition of what you have just heard
  • Obsessive insistence on sameness
  • Lack of spontaneity and imagination
  • Excellent rote memory
  • ability to memorize things
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2
Q

Kanner’s infantile autism

A
  • no dysmorphic signs, thought to be ‘normally intelligent’
  • unusual parental personality traits (but no cause-effect relationship drawn)
    – “Aloneness from the beginning of life makes it difficult to attribute the whole picture to the manner of early parent child relationship”
  • noticed that children were in their own world from a very early age; likely that parent is not responsible for that
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3
Q

Hans Asperger: The autism spectrum

A
  • One year after Kanner’s publication Hans Asperger (a physician from Vienna) published his paper on “autistic psycopathy”
  • Observations
    – Circumscribed interests
    – Motor delays
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4
Q

Early theory: Refrigerator mothers

A
  • Leo Kanner suspected a lack of parental warmth and attachment to their autistic children
  • Bruno Bettleheim (The Empty Fortress: Infantile Autism and the Birth of the Self)
    – Mothers were causing autism in their child because of their cold and rejecting parenting likened it to being in “a concentration camp”
  • mothers causing autism was widely accepted bc Bettleheim would go on tv and promote this view
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5
Q

Bernard Rimland
refrigerator mothers

A

a psychologist with a son with autism (Infantile Autism: The Syndrome and its Implications for a Neural Theory of Behavior), attacked the “Refrigerator Mother” hypothesis and suggested that there was a biological basis for the condition

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6
Q

Epidemiology

A
  • Occurs in approximately 1 out of every 40 births (US CDC, November, 2018 )
  • More common than CP, cystic fibrosis and Down syndrome
    – Approximately 50,000 children (under the age of 20) in Canada has an ASD
    – 4 males for every female
  • Recent meta-analysis suggest it’s more like a 3:1 ratio
  • fewer girls detected bc seen as a male dominated disorder
  • No association with socio-economic class, ethnic origin
  • No evidence of variation between countries
  • No evidence of actual increase in prevalence
  • No evidence that due to vaccines or any other medical intervention
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7
Q

Familial-hereditary genetic

A
  • May be expressed differently in boys and girls
  • There may be different genetic contributions that lead to different forms of autism (polygenic)
  • Environmental factors affect the expression of autism
  • Autism 2-4% and ASD 10-20% risk in sibling of children with autism–50 times the population base risk
  • Concordance rates MZ-92% and DZ 10%
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8
Q

prevalence

A
  • Apparent increase in prevalence due to:
    – Improved awareness of the whole spectrum
    – Improved diagnostic systems
    – Motivation to diagnose -linked to funding and services
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9
Q

Age of onset in ASD

A
  • Parents’ retrospective reports
    – 30-50% by 12 months
    –About 80% by 24 months
    – <10% after 36 months
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10
Q

Diagnosis

A
  • Autism first included in the Diagnostic and Statistical Manual of Mental Disorders in 1980 DSM-III
  • Several revisions later DSM-5 it is now considered a spectrum disorder –ASD
    – Encompasses previous subtypes of autism, Asperger’s syndrome and pervasive developmental disorder
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11
Q

DSM-5 Criteria for ASD

A
  • Impairments in social-communication
  • pragmatic of language- know how to use language to get certain things
  • Restricted, repetitive and stereotyped
    patterns of behaviour and interest
  • like predictability; can often have motor movements
  • Onset during the developmental period
  • has to happen within childhood period; can be diagnosed in adulthood but won’t suddenly develop in adulthood
  • Symptoms must be present in the early developmental period but may manifest later
  • Symptoms cause clinically significant impairment in social occupational or other important aspect of current functioning
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12
Q

Persistent deficits in social communication and interaction

A

– Deficits in nonverbal communicative behaviours used for social interaction
– Deficits in developing, maintaining and understanding relationships
– Deficits in social-emotional reciprocity
- picking up on social emotional cues
- actually taking in what people are saying

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13
Q

Restrictive, repetitive patterns of behaviour, interests or activities

A

– Stereotyped, repetitive motor movements (use of objects or speech)

– Highly restricted interests that are abnormal in intensity or focus
- spend so much time on those interests that there’s no time for anything else

– Insistence on sameness, inflexible adherence to routines

– Hyper or hyporeactivity to sensory input
- too reactive or under reactive

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14
Q

Latest genetic research suggest different types of autisms

A
  • Recent genetic evidence suggest that it has multiple genetic causes and should be called autism spectrum disorders or autisms
    – Research team at U of Toronto lead by Stephen Scherer have identified genetic mutations that have the highest probability of causing autism, and those that do not have a role
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15
Q

Genetic and environmental interactions in autism

A

Definitive etiology underlying ASD have not yet been identified, accumulated evidence has identified various factors, including environment al, genetic, and epigenetic factors

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16
Q

environmental & prenatal factors

A
  • viral infection
  • parental age
  • zinc defficiency
  • abnormal fetal development
  • germ cell mutation
  • fetus brain development dysfunction
17
Q

epigenetic factors

A
  • DNA methylation
  • histone modification
  • micro RNA
18
Q

genetic factors

A
  • copy number variation
  • point mutation
  • translocation
19
Q

A common cause for autism?

A
  • Despite the variability within the spectrum
  • Researchers have focused on the similarities among persons with ASD and searched for a common cause for
    – difficulties in social interaction
    – Difficulties in verbal and non-verbal communication
    – restricted and repetitive interests and activities
20
Q

Theory of mind theory (Simon Baron-Cohen and colleagues)

A

– Ability to attribute independent mental states to self and others in order to predict and explain actions.
- lack understanding that other person is an individual independent of oneself
– Considered a cognitive dysfunction

  • Does not account for repetitive and restricted interests
  • Although theory of mind is delayed it is not absent
21
Q

Theory of autism: The extreme male brain
(Simon Baron-Cohen and colleagues)

A
  • People with autism excel with understanding objects but do poorly with understanding people
  • Systematizers
    – Autism better than typical males
  • figuring out how systems work/how objects function
  • Empathizers
    – Typical females better than typical males
  • understanding what people are feeling
22
Q

Problem with extreme male theory

A
  • Not all people with autism have enhanced perceptual functioning
  • only a small subset have this
  • No conclusive evidence of a connection between superior perception and poor social competence in autistic children
  • doesn’t explain repetitive behaviour
  • not always accurate
  • Cognition alone or ‘pure logic’ does not explain how humans interpret social-emotional cues
  • Does not explain repetitive behaviours and restricted interests
23
Q

Theory of autism: Enhanced Perceptual Functioning (EPF) Laurent Mottron & colleagues

A
  • There are enhanced low level sensory abilities in people with autism
  • Superior visual and auditory processing (e.g., visual spatial and perfect pitch)
  • Attention to detail (local perception)
  • Overfunctioning of brain areas responsible for primary perceptual processing overwhelms higher level cortical areas
24
Q

Theory of autism: Social Motivation Hypothesis (Geraldine Dawson and colleagues)

A
  • “an early and extreme lack of motivation toward social information, leading to the development of a social-specific reward deficit”
  • most children motivated/rewarded by social interaction but autistic children are not
  • Learning from social opportunities are diminished further magnifying the difference
  • Concurrently non-social interests and skill areas are being developed usually in silos
25
Q

Social-motivation theory of autism

A

less time spent attending to faces and other social stimuli in ASD would lead to a developmental cascade resulting in decreased social competence over time

26
Q

Prospective studies of siblings of autistic children

A
  • Prospective studies show us how ASD symptoms emerge over time before there is a diagnosis of ASD
  • Lack of shared eye contact, smiling and communicative babbling not present at 6 months but gradually emerges during the latter part of the first year of life in infants later diagnosed with autism
  • gradual decrease of eye contact, etc.
27
Q

Focused interests (FI) and the brain reward circuitry

A
  • If not faces then what is capturing attention?
    – Objects of FI have high attentional salience
  • girls can be very intensely captivated by people and social interaction
    – Different reward processing in autism, particularly in response to social stimuli
  • decreased activation in the nucleus accumbens in response to monetary rewards but not FIs in autistic adults
    – Over time attention to certain non-social stimuli could be systematically reinforced by an atypical reward system and may lead to the development of RI
28
Q

Summary: Theories of autism

A
  • Thus far, no one theory has satisfactorily accounted for all features of ASD
  • Repetitive and restricted interests have proven to be particularly difficult to reconcile
  • Heterogeneity in ASD makes it difficult to find one cause, likely there are multiple types and causes
29
Q

A developmental account of autism

A
  • Genetic, biological, neurological processes that prime children for learning within their social context in autistic children affects their ability to engage in learning to the same extent as nonautistic

– Developmental perspective
* Lower social competence in these children is a result of
– Different attentional and perceptual attunement and possibly reward circuitry to their environment coupled with a lack of experience/skill development (compounded over time) in a variety of relational contexts
- Parent-child, peer relations, community
- not necessarily a social disorder; brain is learning based on experiences