Autism Spectrum Disorder Flashcards

1
Q

Core features of Autism (3)

A
  • Impairment in communication (quite common along the spectrum)
  • Impairment in social interaction
  • Repetitive/Restrictive patterns of behaviors and interests
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2
Q

About …% of children with autism do NOT develop any useful language

A

50%

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3
Q

Language Impairments (qualitative) examples (3)

A

(1) Echolalia: repeating things you heard (parroting back)
(2) Preservative speech: Getting stuck on a specific topic
(3) Impairment in pragmatics: Answer question correctly (but very literal sense)
-> The context isn’t taken into account in the same way: leads to miscommunication

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4
Q

Echolalia in ASD

A
  • Important step in language development in kids with ASD
  • Help with speech production and comprehension
  • Not everyone with ASD has echolalia when they’re younger but it helps
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5
Q

Qualitative impairment in social interaction, examples (5)

A

(1) Social imitation: Learning from others - social learning impaired (e.g. bobo doll)
(2) Joint attention: Ability to coordinate your attention/focus on a social partner/object of mutual interest
(3) Expressive nonverbal behavior: Hard to get the attention of others onto shared object
=> Hard to engage in nonverbal behavior in a way that people are understanding you
(3) Reciprocity: Doing things for others & getting things back
(4) Social “mind”: Less of a tendency to view others as social partners
(5) Difficulty with Theory of Mind (ToM)

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6
Q

Joint attention in ASD

A

Non-verbal process when you’re connecting with someone else & then redirecting to another thing
-> Help share your enjoyment of an object → way of social communication that’s impaired

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7
Q

Theory of Mind (ToM) in ASD

A

Knowing that others have mental states (desires, beliefs, intentions) that state guides their behavior
=> Often assessed via False belief tasks

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8
Q

Development of theory of mind in neurotypical vs ASD kids (age)

A

4yo!
~100% of neurotypical kids developed ToM
~85% of kids with Down syndrome
~20% of kids with ASD

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9
Q

Repetitive Patterns of Behaviors & Interests, examples: (4)

A

(1) Self-stimulation (e.g. hand flapping, sniffing…)
(2) Intense, narrow interests
(3) Rigid routines
-> Kids with ASD rly benefit from routines
-> Can become dyregulated if routines are disrupted
(4) Preoccupation with parts of objects
E.g. door of the car - not using it as a car

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10
Q

What function does Self-stimulation occupies in ASD? (3)

A

3 Theories
- A craving for stimulation to excite their nervous system
- A way of blocking out and controlling unwanted stimulation from environment that is too stimulating
- Maintained by sensory reinforcement it provides

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11
Q

Historical perspectives in ASD

A
  • Once viewed as classic, categorical disorder
  • Current research emphasizes autism spectrum
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12
Q

ASD: Categorical or Dimensional? (4)

A

Dimensional
- Within diagnosis, severity of symptoms vary
- Within diagnosis, language ability varies
- Within diagnosis, ANY level of IQ possible
- Presence of traits in close relatives

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13
Q

DSM-IV vs DSM-5: ASD

A
  • DSM-IV
    • Autistic disorder: social interaction; restrictive/repetitive interests, language deficits
    • Asperger’s disorder: social interaction; restrictive/repetitive interests
    • Pervasive Developmental Delay not otherwise specified (PDD-NOS)
  • DSM-5 = Autism spectrum disorder
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14
Q

Why all diagnosis into one spectrum in DSM-5? (4)

A
  • Research indicated that these criteria were being applied inconsistently across clinics
  • Distinctions between the groups NOT meaningful
  • Everyone diagnosed with one of those disorders should meet criteria for ASD
  • Biggest study on this issue found that 91% of children who had DSM-IV Pervasive Dev Delay diagnoses met criteria for ASD
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15
Q

Story behind the term “Asperger’s”

A

-> Hans Asperger, the psychiatrist for whom the disorder was named, was associated with/sympathetic to the ideals of the Nazi party:

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16
Q

Assessment: Autism Diagnostic Observation Schedule (ADOS) – what does it look like?

A
  • Semi-structured observation (observational tasks)
  • Presses: A certain pattern of behavior is likely to appear, e.g., unstructured presentation of toys
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17
Q

Prevalence of autism has … over time

A

Increased (~3% in the last 25 years)
=> Actual increase in number of children who have autism vs. Better identification and broader definitions?

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18
Q

Gender diff in ASD

A

4:1 male to female ratio
-> 10:1 male to female ratio in LESS severe ASD

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19
Q

Course of autism

A

Most often identified by parents in the months preceding child’s 2nd birthday
- Neurotypically developing children are developing rapidly at this age but kids with ASD might be delayed
- Some children display symptoms since birth
- Some children seem to LOSE early developmental milestones — can be for other reasons tho (e.g. malnutrition, injuries… but red flag for ASD)

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20
Q

Diagnoses made around … years are generally stable

A

2 to 3 years

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21
Q

Efforts to create very early identification tests for ASD (under 2yo). Examples: (2)

A

(1) Using eye tracking to see what toddlers are looking at
=> Toddlers with autism focus on geometric rather than social images
(2) Brain enlargement (cortical surface) - brain grows faster (synaptic pruning on neurons not used)
=> If growing quicker, bigger pruning (implicated in milestones)
=> Recent data indicate that rate of cortical surface expansion between 6 and 12 months predicts diagnosis of autism at 24 months

22
Q

Is ASD a transient diagnosis?

A

Usually lifelong
- Challenges might look diff at diff ages, but mostly lifelong condition
- Less than 50% are as independent as a neurotypical kid
- Variability in trajectories of children with ASD

23
Q

Strongest predictors of adult outcomes in ASD

A
  • Language
  • IQ: More positive outcomes if IQ above 70 vs below
24
Q

Some kids with ASD have ‘savant syndrome’ and others not. What factors might play?

A

Unique cognitive/behavior profile in autistic adults with savant syndrome
=> Heightened sensory sensitivity, obsessional behaviours, technical/spatial abilities, and systemising (=drive to identify patterns/relationships/rules about how things happen) define savant syndrome

25
Differentiating autism from ID (4)
Children with ID have: - No specific deficit in joint attention - No specific deficit in ToM - No specific deficit in pretend play - Social behaviors appropriate for their mental age
26
Etiology of Autism (3)
- Environmental factors - Genetic factors - Brain development
27
Myth about vaccine creating ASD.
- Thimerosal was a preservative in vaccines (now removed) -> Coincided with increased prevalence of ASD - Mercury: Symptoms of autism are noticed right around the time children get their vaccinations, Increased use of MMR vaccine appeared to coincide with increased prevalence of autism - Wakefield's study
28
Wakefield et al. 1998: Study about MMR vaccine
- 12 children: Normal development followed by onset of behavioral difficulties and gastrointestinal problems - For 8 children, onset was linked to MMR vaccine by parents or physician (even though authors mentioned it was NOT causation), Also noted that only a subset of autistic cases linked to vaccine => After publication, MMR vaccine rates dropped in Western world 2006 incidence rates for measles and mumps were 13 and 37x times higher than in 1997
29
Wakefield et al. 1998: Update on paper
- Lancet retracted the paper - In January 2011, reported in the British Medical Journal that the data reported were fraudulent - Wakefield lost his medical license in the United Kingdom - BUT, since then, concern about vaccine and ASD didn’t quite go away
30
MMR vaccine: Subsequent research evidence
- 12 epidemiological studies have found no link between the MMR (measles/mumps/rubella) vaccine and autism - Largest: All children born in Denmark between January 1991 and December 1998 (N = 537, 303): => Children in the vaccinated group did NOT have greater risk of developing autism compared to the unvaccinated group; also NO association between age of vaccination and autism
31
Etiology of Autism: Toxin hypotheses and findings
- Toxin exposure causes ASD? => Found that Thimerosal was unrelated to ASD BUT: - birth complications - advanced parental age - maternal obesity/diabetes - vitamin D deficiency - heavy metals (e.g. mercury/lead), YES
32
Etiology of Autism: Molecular Genetics
Points to particular areas on many different chromosomes as possible locations for genes for ASD => ASD is likely to be a complex genetic disorder => Expression of ASD genes may be influenced by environmental factors occurring primarily during fetal brain development
33
Etiology of Autism: Brain Development (2)
Evidence of differences in brain structure and functioning in children with autism BUT not clear if causal: (1) Differences in structure (e.g. frontal lobe, cerebellum...) (2) Differences in function → can contribute potentially to epilepsy and seizures (2a)-> Decreased activation of emotion processing regions e.g. amygdala (impaired fight/flight, emotional memory...) (2b) -> Decreased activation of “mirror neurons” (2c) -> Altered activation of facial recognition area (Children as young as 6 months show different brain activity when they see their mother versus a stranger BUT NOT ASD children)
34
“Biomedical” Treatments for ASD
Vitamins: e.g., supplements in Vitamin C, B6,magnesium Diet: Gluten-free, more secretin -> don't rly work
35
Secretin def
Hormone produced in the intestinal glands -> Used to treat peptic ulcers -> Three children with autism received it for unrelated conditions and improvement in symptoms of autism noted
36
Secretin: does it work?
Several well-designed studies showing NO effect => Conclusion: NOT effective Other than secretin, limited research
37
Psychotropic Medications and ASD (3)
Currently used primarily to treat other psychiatric symptoms that may be present, rather than core features of autism: (1) SSRIs for anxiety/obsessive-compulsive behavior (2) Stimulants for ADHD symptoms (3) Antipsychotics for aggression and agitation
38
Oxytocin def
Neuropeptide hormone implicated in social bonding and social behaviors -> ‘happiness hormone’
39
Oxytocin & ASD: Does it work?
Rationale: if we increase oxytocin in ASD, help to promote increased social functioning. Many RCTs demonstrated improvements
40
Oxytocin & ASD: Caution
Work with animals suggests may be long-term consequences (irregular mating behaviours) => Not a panacea: not gonna eliminate all impairments in ASD
41
Goals of Treatment for Children with Autism (2)
- Minimize core challenges - Maximize independence and quality of life
42
Overview of things implied in Treatment Strategies (6)
- Engaging children in treatment - Decreasing other disruptive behaviours that might interfere with life - Teaching appropriate social behaviour - Increasing functional, spontaneous communication - Promoting cognitive skills - Teaching adaptive skills to increase responsibility and independence
43
Treatment Strategies (4)
(1) Applied Behavior Analysis (ABA) (2) Individual, Comprehensive ABA (4) Developmental Social Pragmatic Models (DSP) (3) Teacher-Implemented, Focused ABA + DSP
44
Applied Behavior Analysis (ABA), components (2)
Rly rooted in classical and operant conditioning. Use reinforcement to shape new behaviors. (1) Discrete Trial Training - Structured behavioral approach - Therapist begins with a prompt that should elicit the desired skill/behavior - Positively reinforce the desired behavior - Shaping (2) Reinforcing naturally occurring behaviors - Read a story and reinforce use of language
45
Developmental Social Pragmatic Models (DSP)
(1) Core feature of ASD is difficulty engaging in activities jointly with another person => rly focus on that (2) Aim to promote social communication and interaction by being responsive to the child - Caregivers can improve children’s dev of social communication through the ways they respond when they’re interacting with their kids (3) More naturalistic interaction
46
2015 review of treatments for autism identified two well established treatments
(1) Individual, Comprehensive ABA (2) Teacher-Implemented, Focused ABA + DSP
47
Individual Comprehensive ABA (4)
(1) Very Intensive interventions consisting of 20 to 40 hours per week for 2 to 3 years  (2) Start prior to the age of 5 years (3) Communication, social skills, cognition, behavior management, pre-academic skills (4) Limitations: RCTS enrolled a small number of participants => No improvement in IQ and adaptive behavior
48
Teacher-Implemented, Focused ABA + DSP (4)
(1) Less intensive than comprehensive interventions (2) Delivered in a classroom (3) Combines ABA and DSP techniques (4) Associated with greater joint engagement in play activities with caregivers and teachers
49
Highlighting TWO Recent ABA meta-analyses
Overall, mixed research regarding efficacy of ABA => Some support for improvements in certain outcomes, but then other studies don’t find support for improvements in those outcomes…
50
Study: 11 studies, 632 participants, efficacy of ‘comprehensive’ ABA-based interventions. Results?
Lots of results => Initial evidence language abilities as treatment MODERATOR — greater language comprehension and expression at start of treatment = bigger gains in intellectual functioning
51
Controversy around ABA: Common complaints (3)
(1) Historical use of harsh punishment (e.g. electric shock) to reduce unwanted stimming behaviors (e.g., handflapping) (2) Dosage of intervention way too much (up to 40 hours a week) (3) People in the Autism community NOT being sufficiently consulted around implementation of ABA -> Are treatment goals aligned with what people want for themselves? -> Who advocates for children and chooses what behaviors should and shouldn’t be reinforced vs extinguished?