412 ASD Flashcards
1
Q
core features of autism
A
- impairment in communication
- impairment in social interaction
- repetitive patterns of behaviour and interests
2
Q
impairment in communication
A
- about 50% of kids with ASD do not develop useful language
- echolalia, perseverative speech, deficits in pragmatics (not taking into account context)
3
Q
impairment in social interaction
A
- social imitation
- joint attention
- expressive nonverbal behaviour (communicating what you want, how you’re feeling - pointing)
- reciprocity
- social ‘mind’ (not thinking about people as possibilities for interaction, not interpreting the social nature of things or seeing the world as social)
- theory of mind
4
Q
Theory of Mind
A
- knowing that other people have mental states (desires, beliefs, intentions) that guide their behaviour
- ASD have trouble taking others’ perspectives
- assessed via False Belief tasks (Sally/Anne)
- typical children reach this developmental milestone by age 4 (about 20% of kids with autism have reached it by then)
5
Q
repetitive patterns of behaviour and interests
A
- self-stimulation (stereotyped, patterned, repetitive bx usually involving one or more senses)
- intense, narrow interests (could be related to selective attention - filtering out social information in favour of these interests)
- rigid routines (disruptions are even more upsetting that for typical kids)
- preoccupation with parts of objects (only playing with the wheels of a car)
6
Q
self-stim theories
A
- craving for stimulation that excites nervous system = reinforcement
- blocking out/controlling unwanted stimulation from an overstimulating environment = calms down = reinforcement
7
Q
preoccupation with parts of objects
A
- focus on parts of things when attending to social information (watching movies with eye tracking)
- typical kids focus on faces to receive social information, kids with ASD don’t look at faces (only at parts of the faces or in the periphery
- this avoidance of social information compounds over time = less social input = not developing skills to interact with your social world
8
Q
autism as categorical vs. dimensional
A
- once viewed as a classic categorical disorder
- now, it’s a spectrum: range of IQs, severity of symptoms, language abilities
- family members tend to have autistic traits without meeting full criteria
9
Q
DSM-IV autism diagnoses
A
- autistic disorder: social interaction + repetitive/restrictive interests + language deficits
- asperger’s: social interaction + repetitive/restrictive interests
- pervasive developmental delay, not otherwise specified (PDD-NOS): residual category
10
Q
changes in DSM-5 autism diagnosis
A
- combining all previous diagnoses into one spectrum
- criteria for DSM-IV were being applied differently across clinics
- groups weren’t significantly different from each other - they all met criteria for the new ASD
11
Q
Autism Diagnostic Observation Schedule (ADOS)
A
- semi-structured observation for assessment
- tester engaging the person in tasks while rating their behaviour (like capacity for joint attention, reciprocity, etc.)
- looking for unusual behaviours - the more are present, the more likely ASD is
- has version for younger kids, teens, adults
12
Q
Autism Diagnostic Interview (ADI-R)
A
- often paired with ADOS for assessment
- interviews with parents/caregivers
- trying to triangulate behaviour and get a more accurate diagnosis
13
Q
prevalence of autism
A
- 1-1.5%
- prevalence increasing over time (better identification and broader definitions?)
- prevalent cross-culturally and at all income levels but large variation in diagnostic practices
- 4:1 male to female ratio which increases to 10:1 for milder forms of autism
14
Q
course of autism
A
- there could be symptoms before, but not reliably diagnosed before age 2-3
- may be differences starting from birth
- some lose developmental milestones that they previously achieved
- usually lifelong (but variability in trajectories)
- strong predictors of positive prognoses are better language skills and higher IQ (better social, academic, occupational achievement)
15
Q
efforts toward early identification
A
- eye tracking to see what toddlers are looking at (with autism = focus on geometric figures rather than social images)
- brain enlargement (cortical surface expansion between 6-12 months predicts autism diagnosis)
16
Q
ASD comorbidity
A
- 70% also have IDD, 40% are severe-profound
- 25% have splinter skills
- 5% have isolated and remarkable talents (savant syndrome - difference in degree from splinter skills)
- epilepsy
- ADHD, conduct problems, anxiety, depression
17
Q
splinter skills
A
above average for the population and compared to yourself in other areas
18
Q
environmental etiological factors in ASD
A
- toxin hypotheses: exposure of toxins as a causal factor
- birth complications are a strong predictor (anoxia)
- maternal factors like obesity, diabetes moderately associated
- low in vitamin D, heavy metal exposure like mercury and lead (not necessarily causal, just an association)
19
Q
vaccine hypothesis of ASD
A
- anecdotal evidence about kids starting to show autism symptoms around when they get their vaccines (esp. MMR)
- worry about thimerosal and mercury
- Wakefield: normal development + MMR = behavioural and GI problems (caused media outcry which increased rates of measles and mumps, but the paper was retracted and Wakefield fired)
- later research not able to find any links between MMR/thimerosal/any vaccine and autism
20
Q
heritability of autism
A
- 15-20% of siblings of people with autism also have autism
- 70-90% concordance rates in Mz twins
- 83% heritability estimate
21
Q
molecular genetics of autism
A
- many possible areas on different chromosomes
- complex genetic disorder
- expression of ASD genes may depend on environmental factors during fetal brain development (epigenetics, etc.)
22
Q
etiology of ASD: brain development
A
- not clear if causal
- differences in structure (frontal lobe, cerebellum, medial temporal, limbic)
- differences in function (decreased activation of mirror neurons especially in social situations, altered activation of facial recognition area like when viewing mother vs. stranger)
- structural and functional differences in the amygdala
23
Q
fad treatments for autism
A
- vitamin supplements for B6, magnesium, etc,
- gluten-free or secretin diets
- secretin produced in the intestine, used to treat ulcers, but evidence shows it isn’t effective
- anecdotal evidence for anything doesn’t mean it actually works
24
Q
psychotropic meds for ASD
A
- used to treat co-occurring problems, not core features of autism
- SSRIs for anxiety/OCD/depression
- stimulants for ADHD
- antipsychotics for aggression
- work just as well as in typical kids, but be extra careful monitoring them in kids with ASD
25
Q
oxytocin for ASD
A
- neuropeptide hormone involved in social bonding and social behaviours
- studies showed improvements in social interactions for kids taking intranasal oxytocin (ToM, eye contact, social connection)
- small samples so far, but promising
- animal studies warn of potential long-term effects to be cautious of
26
Q
treatment strategies for ASD
A
- decreasing disruptive behaviours
- appropriate social behaviour
- improving functional, spontaneous social communication
- cognitive skills
- adaptive skills to increase responsibility and independence
27
Q
Applied Behaviour Analysis (ABA) for ASD
A
(1) discrete trial training (structured behavioural approach) for behaviours that aren’t already present
- prompt the behaviour + reinforce the desired behaviour
- shaping: reinforce approximations/attempts of desired behaviour (every effort toward the behaviour)
(2) reinforce naturally occurring behaviour
- use of language, initiating conversation = reinforce = more likely to repeat that
28
Q
Developmental Social Pragmatic (DSP) models of treatment for ASD
A
- targeting joint attention to improve social communication and interaction by being responsive to the child
- promoting any type of communication (verbal or nonverbal) that the child initiates
- pragmatic: just trying to communicate any way you can
- building on what the child is doing
29
Q
two best established treatments for ASD
A
- individual, comprehensive ABA
- teacher-implemented, focused ABA + DSP
30
Q
individual comprehensive ABA for ASD
A
- intensive (20-40hrs/week) for 2-3 years
- start prior to 5 yrs
- communication, social skills, behaviour management, pre-academic skills (teaching skills that will help you in school)
- small studies show improvements in IQ and adaptive behaviour
- gains could be achieved with 6-28 hrs/weeks
31
Q
teacher-implemented focused ABA + DSP
A
- delivered in a classroom, less intensive than individual
- reinforcing communication + ABA
- associated with greater joint engagement in play activities with caregivers and teachers
32
Q
Yu et al. meta-analysis
A
- broad: any ABA-type treatment (wide range of duration and dosage)
- no impacts on receptive language, adaptive behaviour, daily living skills, IQ, restricted/repetitive bx, motor, cognition
- saw good effects on socialization, communication, expressive language
- not general improvements, but still positive
33
Q
Eckes et al. meta-analysis
A
- only including comprehensive ABA (early childhood, 20-40hrs/week, personalized, promoting several skills at once, using multiple methods, one-on-one + group activities, requires parents)
- good effects on intellectual functioning and adaptive behaviour
- no improvements in language abilities, symptom severity, parental stress
- language abilities may act as a moderator (greater receptive/expressive language at baseline = bigger intellectual gains)
34
Q
controversy around ABA
A
- historical use of harsh punishment to reduce unwanted behaviours (like self-stim which isn’t harmful to anyone even if it is atypical)
- dosage of intervention is way too intense
- people with autism not being consulted about ABA implementation (is the intervention what is best for them, who advocates for kids and which behaviours should be reinforced or extinguished)
