Week 10: Autism course Flashcards

1
Q

Prevalence of Autism

A

Prevalence of autism is 1 to 1.5%

Prevalence has increased over time

Could be an actual increase in number of children who have autism vs.

Or a better identification and broader definitions

Cultural and contextual differences

Present cross-culturally and cross-nationally

Found at all income levels

Gender differences

4: 1 male to female ratio
10: 1 male to female ratio in “high functioning” ASD

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2
Q

Development Course of Autism

A

Most often identified by parents in the months preceding child’s second
birthday

Diagnoses may around 2 to 3 years are generally stable

Some children display symptoms since birth

Some children seem to lose early developmental milestones

Efforts to create very early ID tests because early treatment yeilds better results

For example:
(1) using eye tracking to see what toddlers are looking at
-Toddlers with autism focus on geometric rather than social images
(2) Brain enlargement
-Recent data indicate that rate of cortical surface expansion between 6 and
12 months predicts diagnosis of autism at 24 months (Hazlett et al. 2017)

Usually lifelong

Variability in trajectories of children with ASD

Strongest predictors of adult outcomes

  • Language
  • IQ
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3
Q

Comorbidity

A

Intellectual disability

  • 70% of youth with autism meet criteria for ID
  • 40% meet criteria for severe or profound ID

25% have “splinter skills” - special talents above that which you would expect given the child’s usual abilities or what you would expect from the general population

5% display isolated and remarkable talents - really exceptional

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4
Q

Differentiating autism from ID

A

Children with ID have

  • No specific deficit in joint attention
  • No specific deficit in theory of mind
  • No specific deficit in pretend play
  • Social behaviors appropriate for their mental age (even if lower than their chronological age)

Other comorbid conditions

  • Epilepsy
  • ADHD, conduct problems, anxiety disorders, depression
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5
Q

Etiology of Autism

A
  • Environmental factors
  • Genetic factors
  • Brain development
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6
Q

Etiology of Autism: Environmental Factors

A

Toxin hypotheses

Gluten-based diet (cereal)

Casein-based diet (milk)

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7
Q

Increase in number of vaccinations children receive

A

1900 – 1 – Small pox

1960 – 5 – Add diphtheria, tetanus, pertussis, polio

1980 – 8 – no small pox, add MMR (measles, mumps, rubella)

2000 – 11 – includes hepatitis, meningitis

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8
Q

Current vaccination schedule in Quebec

A

14 separate shots by 6 years of age

Includes pneumonia, flu, rotavirus, chickenpox

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9
Q

Vaccinations and autism

A

Thimerosal
-Preservative in vaccines
-Removed from nearly all vaccines in 2001 (e.g., some flu vaccines, not given
to children)
-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 (although in California and Denmark, increase in
autism happened well after the introduction of the MMR vaccine)
-Reasonable biological explanation

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10
Q

Wakefield the asshat and the MMR

A

Wakefield et al. 1998
-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
-Note that the authors were careful to point out that this study did not
prove a link between behavioral problems and vaccination
-Also noted that only a subset of autistic cases linked to vaccine

After publication, MMR vaccine rates dropped
In UK
-1996 – 92%
-2006 – 85% (compared to 94% for other vaccines)

2006 incidence rates for measles and mumps were 13 and 37x times higher than in 1997

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)
-Compared children who had received MMR vaccine (440,655) and children who
had not received MMR vaccine (96, 648)
-Children in the vaccinated group did not have greater risk of developing autism
compared to the unvaccinated group
-There was also no association between age of vaccination and autism
-6 studies have found no evidence of a link between thimerosal and autism
-3 studies have found no evidence that thimerosal is associated with more
minor neurological difficulties

De Stefano et al. 2013, Journal of Pediatrics
-Examined association between level of immunological stimulation in
first two years of life and development of autism
-Found no association
-Greater number of vaccines not associated with autism

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11
Q

Anti-vaccination group funded a study involving randomly assigning
monkeys to receive different types of vaccines

A

Not ethical to assign babies to a 1990s vaccine schedule

Gadad et al. (2015) in Proceedings of the National Academy of Sciences

  • 79 rhesus macaques randomly assigned to receive:
  • 1990s pediatric vaccination schedule
  • 1990s pediatric vaccination schedule but four times faster (because monkeys develop faster)
  • 2008 expanded pediatric vaccination schedule
  • Only thimerosal containing vaccines
  • Only the MMR vaccine
  • Control - saline

Gadad et al. (2015)
-Vaccinations were not associated with any behavioral changes
-E.g., stereotyped behavior, fear-disturbed behavior, positive social
behaviors, non-social exploring behaviors
-Vaccinations not associated with any neuropathological changes in the cerebellum, hippocampus, and amygdala

Its all balls

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12
Q

Scientific inference and Vaccine Skepticism

A

Null hypothesis: Assume no relationship
-Using probability theory, determine how likely the observed relationship is if there is really no relationship
-Could we expect to observe this association by chance?
-P < .05 means that there is less than a 5% chance that we would observe an association this big if, in reality, there was really no
relationship
-It does not mean that there is a 5% chance that there is no relationship

We do not quantify the likelihood of no relationship
-We cannot “prove” the null hypothesis

This leads to people interpreting this as unproven

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13
Q

Lancet retracted the paper

A

In January 2011, reported in the British Medical Journal that the data reported were in fact fraudulent

Wakefield lost his medical license in the United Kingdom

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14
Q

Etiology of Autism: Heritability

A

15-20% of siblings of individuals with ASD have the disorder

  • Concordance rates
  • 70-90% in identical twins
  • Heritability of an underlying liability for ASD is 90%
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15
Q

Etiology of Autism: Molecular

Genetics

A

-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

What happens in utero affects this

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16
Q

Etiology of Autism: Brain

Development

A

-Evidence of differences in brain structure and functioning in children
with autism but not clear if causal
-Differences in structure
-Many areas (frontal lobe, cerebellum, medial temporal, limbic)
-Differences in function

-Very high rates of epilepsy and seizures
-Decreased activation of emotion processing regions
-Structural and functional differences in the amygdala
-Decreased activation of “mirror neurons”
(Neurons that are activated when you do an action and also when you see
someone else do it)
-Altered activation of facial recognition area
-Children as young as 6 months show different brain activity when they see their
mother versus a stranger
-Children with autism don’t show this

17
Q

Summary

A
  • Prevalence of autism is 1 to 1.5% and has increased due to better identification and broader definitions
  • Autism is highly comorbid with intellectual disability
  • Vaccines do not cause autism
  • Autism is highly heritable and associated with marked differences in brain structure and function