Autism Spectrum Disorder (Final) Flashcards

1
Q

Impairment in Communication

A

About 50% of children with autism do not develop any useful language. Echolalia: repeating things that you heard before (parroting things back to someone). Perseverative speech: Getting stuck on a specific topic. Impairment in pragmatics: “Can you look at me?” “Yes.” Answering the literal question.

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2
Q

Impairment in Social Interaction

A

Qualitative impairment in social interaction: Social imitation (difficulties learning from others), joint attention, expressive nonverbal behaviour (hard to get the attention of others onto shared objects), reciprocity, social “mind” (less of a tendency to view others as social partners).

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3
Q

Impairment on Social Interaction: Difficulty with Theory of Mind (ToM)

A

Knowing that others have mental states (desires, beliefs, intentions) that state guides their behaviour. Helps us gain perspective. Often assessed via False belief tasks: assess that people can hold incorrect beliefs, and even though you know that these beliefs are false, they still guide their behaviour. Other people can have different knowledge than I do, and that can cause them to behave in different ways.

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4
Q

Repetitive Patterns of Behaviours & Interests: Self-stimulation

A

Different theories of how self-stimulation can help: 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. Intense, narrow interests. Rigid routines. Preoccupation with parts of objects.

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5
Q

Focus on Parts

A

We spend a lot of time looking at faces and parts of faces that help to communicate and facilitate social interaction. People with ASD spend less time looking at social communicating features of the face (e.g. eyes).

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6
Q

Autism as a Spectrum

A

Has gone through a lot of change in how it’s been considered in the DSM over the years. Current research emphasizes that it’s a spectrum. Evidence of dimensional spectrum: within diagnosis, severity of symptoms vary. Within diagnosis, language ability varies. Within diagnosis, any level of IQ is possible. Presence of traits in close relatives.

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7
Q

Autism: DSM-5 Definition

A

3 disorders from DSM-IV collapsed in DSM-5 to make ASD. Because of the overlapping criteria for those three disorders (Autistic disorder, Asperger’s disorder, Pervasive Developmental Delay not otherwise specified) they were being applied inconsistently, and distinction between groups was becoming less meaningful.

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8
Q

Autism Spectrum Disorder Criteria A

A

Persistent deficits in social communication and interaction, as manifested by: Deficits in social-emotional reciprocity. Deficits in non-verbal communicative behaviours used for social interaction. Deficits in developing, maintaining, and understanding relationships.

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9
Q

Autism Spectrum Disorder Criteria B

A

Restricted, repetitive patterns of behaviour, interests, or activities, as manifested by at least two of the following:
1. Stereotyped or repetitive motor movements, use of objects, or speech.
2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or non-verbal behaviour.
3. Highly restrictive, fixated interests that are abnormal in intensity and focus.
4. Hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of environment (e.g., indifference to pain/temperature, excessive smelling).

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10
Q

Autism Spectrum Disorder Criteria C

A

Symptoms must be present during early developmental period.

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11
Q

Autism Spectrum Disorder D

A

Symptoms cause clinically significant impairment.

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12
Q

For both criteria A and B, severity is rated on:

A

1) If you need support
2) Need substantial support
3) Need very substantial support

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13
Q

Social Communication Disorder

A

Defined by difficulties in social communication:
1) Deficits in communication for social purposes.
2) Impairment of ability to change contexts to needs of listener (e.g. speaking differently to a child rather than an adult).
3) Difficulties following rules for conversation and storytelling, such as taking turns in conversation, rephrasing when misunderstood, knowing how to use verbal/non-verbal signals to regulate interaction.
Restricted, repetitive patterns of interest have never been present.

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14
Q

Assessment: Autism Diagnostic Observation Schedule (ADOS)

A

ADOS is the gold standard. Semi-structured observation. Sit with kid and take them through different tasks. Presses: You’re pushing them in different tasks to try and elicit a certain social response. A certain pattern of behaviour is likely to appear. We know that children with autism are likely to b have a certain way (E.g., unstructured presentation of toys).

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15
Q

Assessment: ADI-R – Autism Diagnostic Interview
(revised)

A

Paired with ADOS. Interview with parents/caregivers of child suspected of having ASD.

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16
Q

Prevalence of Autism

A

Prevalence is 1 to 1.5%. Prevalence has increased over time: Actual increase in number of children who have autism vs. Better identification and broader definitions? Cultural and contextual differences. Gender differences: 4:1 male to female ratio. 10:1 male to female ration in less severe ASD.

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17
Q

Development Course of Autism

A

Most often identified by parents in the months preceding child’s 2nd birthday. Diagnoses made around 2 to 3 years are generally stable. Some children display symptoms since birth. Some children seem to lose easy developmental milestones. Usually lifelong. Variability in trajectories of children with ASD. Strongest predictors of adult outcomes: Language and IQ.

18
Q

Development Course of Autism: Efforts to create very early identification tests

A

Examples:
1. Using eye tracking to see what toddlers are looking at. Todders 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.

19
Q

Comorbidity

A

A lot of overlap between ASD and IDD. 70% of youth with autism meet criteria for IDD. 40% meet criteria for severe or profound IDD. 25% have “splinter skills”. 5% display isolated and remarkable talents (can grow out of these skills).

20
Q

Comorbidity - Differentiation 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 behaviours appropriate for their mental age.

21
Q

Etiology of Autism - Vaccinations

A

Some vaccines used to have a preservative called Thimerosal. Was removed from nearly all vaccines in 2001. 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.

22
Q

Etiology of Autism - Vaccinations (Wakefield et al. 1998)

A

12 Children. Normal development followed by onset of behavioural difficulties and gastrointestinal problems. For 8 children, onset was linked to MMR vaccine by parents or physician. Not that the authors point out that this study did not prove a link between behavioural problems and vaccination. After publication, MMR vaccine rates dropped. Paper was retracted and data was reported fraudulent.

23
Q

Etiology of Autism - Vaccinations (subsequent research evidence after Wakefield et al.)

A

12 epidemiological studies have found no link between the MMR vaccine and autism. Largest: All children born in Denmark between January 1991 and December 1998 found no association between age of vaccination and autism.

24
Q

Etiology of Autism: Toxin hypotheses (Modabbernia et al., 2017)

A

Found that vaccines were unrelated to ASD. But things like birth complications were strongly associated with ASD (low vitamin D, heavy metal exposure, lack of oxygen). But the reason why these mechanisms lead to ASD are not very well known.

25
Q

Etiology of Autism: Heritability

A

15-20% of siblings of individuals with ASD have the disorder. Concordance rates: 70-90% of identical twins. Huge study done in Sweden produced a heritability rate of around 83%. Strong genetic contribution to ASD.

26
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.

27
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: 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 vs a stranger. Children with autism don’t show this.

28
Q

“Biomedical” Treatments

A

Vitamins and diet: Vitamin supplements (C, B6, magnesium). Diet: Gluten-free, Secretin.

29
Q

“Biomedical” Treatments: Secretin

A

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 were noted. Since that time, several studies showed no effect.

29
Q

Psychotropic Medications

A

Currently used primarily to treat other psychiatric symptoms that may be present, rather than core features of autism. SSRIs for anxiety/obsessive-compulsive behaviour. Stimulants for ADHD symptoms. Antipsychotics for aggression and agitation.

30
Q

Treatments for Autism: Oxytocin?

A

Oxytocin is a neuropeptide hormone implicated in social bonding and social behaviours: “happiness hormone”. Rational: If we increase oxytocin in kids with ASD, we will help promote increased and better social functioning. A lot of RCts done on this have demonstrated small improvements. Increasing oxytocin, even if it shown to work, is not going to eliminate all impairments or differences in people with ASD vs without.

31
Q

Goals of Treatment for Children with Autism

A

Minimize core challenges. Maximize independence and quality of life.

32
Q

Treatment Strategies: Applied Behaviour Analysis (ABA)

A

1) Discrete Trial Training: Structured behavioural approach. Therapist begins with a prompt that should elicit the desired skill/behavior. Prompt the behaviour. Positively reinforce the desired behaviour. Shaping.
2) Reinforcing natural occurring behaviours: Reinforcing spontaneous social interactions with attention, responsiveness etc. This will hopefully lead to more of these interactions.

33
Q

Treatment Strategies: Developmental Social Pragmatic Models (DSP)

A

Core feature of ASD is difficulty engaging in activities jointly with another person. Aim to promote social communication and interaction by being responsive to the child. Caregivers can improve children’s development of social communication through the ways they respond when they’re interacting with kids. Build on the child’s communication.

34
Q

Evidence Base for Treatments with Autism

A

Journal of Clinical Child and Adolescent Psychology commissions reviews in which experts review the evidence base for different treatment approaches. 2015 review of treatments for autism identified two well-established treatments. Individual, Comprehensive ABA. Teacher-Implemented, Focused ABA + DSP.

35
Q

Individual Comprehensive ABA

A

Intensive and long lasting interventions. Start prior to age 5. Communication, social skills, cognition, behaviour. management, pre-academic skills. Shown to be associated with improvements in IQ and adaptive behaviour.

36
Q

Teacher-Implemented, Focused ABA + DSP

A

Delivered in a classroom. Less intensive than comprehensive interventions. Combines ABA and DSP techniques. Research has found that this approach is associated with greater joint engagement in play activities with caregivers and teachers.

37
Q

Recent ABA meta-analyses: Yu et al. (2020)

A

Any ABA treatment or treatment derived from/similar to ABA. Wide range of dosage and duration. No significant effects for the outcomes of general symptoms of ASD, receptive language, adaptive behaviour, daily living skills, IQ, verbal IQ, nonverbal IQ, restricted and repetitive behaviour, motor and cognition. However, significant effects were shown on socialization, communication and expressive language.

38
Q

Recent ABA meta-analyses: Eckes et al. (2023)

A

Only studied ‘comprehensive’ ABA-based interventions. Found a medium effect of comprehensive ABA-based interventions vs treatment as usual on intellectual function and better adaptive behaviour, but no improvements in language.

39
Q

Controversy around ABA

A

Many advocates in the autism community do not think ABA should be used with children with autism. Common complaints:
1) Historical use of harsh punishment to reduce unwanted stimming behaviours (e.g. handflapping).
–> Neurodiversity argument is that these behaviours may be ‘atypical’ but are largely harmless and should be accepted.
2) Dosage of intervention way too much: up to 40 hours a week in some cases historically.
3) People in the Autism community not being sufficiently consult around implementation of ABA
–> are treatment goals aligned with what people want for themselves?