1
Q
How did Sukharvea make of ASD 1924?
A
- Flattened affective life
- Lack of facial expression and expressive movements
- Keeping apart from peers
- talking in stereotypic ways
- Strong interest pursued exclusively
- Sensitivities to specific noises or smells
2
Q
How did Kanner make of ASD 1943?
A
- Early infantile autism
- Lack of affective contact with others
- inborn autistic disturbances of affective contact
- Intense resistance to change in routines
- Fascination manipulating particular objects (not correctly used)
- Muteness or abnormalities of language
- Superior rote memory and visuo-spatial skills
3
Q
How did Asperger make of ASD 1944?
A
- Childhood autistic psychopathy
- Impair social interaction shown in odd, inappropriate behavior rather than aloofness and indifference
- narrow interest
- repetitive routines on self and others
- Good grammar and vocabulary but inappropriate use of speech
- monologue about special interest
- Limited or inappropriate non verbal communication
- motor clumsiness and mischievous behavior
4
Q
What are Creaks Nine points?
A
- Gross and sustained impairment of emotional relationships
- Serious retardation, with islets of normal or exceptional intellectual function
- Apparent unawareness of personal identity
- Pathological preoccupation with particular objects
- Sustained resistance to change
- Abnormal response to perceptual stimuli
- Acute and illogical anxiety
Speech absent or underdeveloped - Distorted motility patterns
5
Q
What are the ASD implication for DSM-1?
A
- Children with autistic like symptoms were classified as childhood schizophrenic
6
Q
What are the ASD implication for DSM-11?
A
- Consistent with DSM-1
- Diagnostic behaviors of autistic, atypical, and withdrawn behavior
7
Q
What are the ASD implication for DSM-111?
A
- 3:1 predominance of males to females
- Pervasive development disorders =
- Infantile autism
- Childhood onset PDD less than 3yo
- Residual COPDD
- Atypical PDD
8
Q
What is the historical background of autism in the 1970s?
A
- Rutter-psychiatrist = no single cause
- Impaired social relationships (no parent comfort, deficit eye contact, withdrawal, deficit co-op play and empathy)
- Deficit in language (lack of imitation, deficit in gestural communication-pointing, deficit in functional and pretend play, language deficit-speech vs communic. echolia
- Insistence on sameness (stereotypical and repetitive behavior and routine, unusual preoccupation)
9
Q
What is the historical background in late 1980s?
A
- Beginning of “Chinese menu”
- Pervasive developmental disorder = PDD-NOS (AD, late onset, atypical)
- Separated: in qualitative impairment in reciprocal social interaction, qualitative impairment in verbal and nonverbal communication and in imaginative activity, markedly restricted repertoire of activities and interests
10
Q
What are the ASD implications for DSM-IV?
A
- Autistic disorder
- PDD-NOS
- Asperger’s disorder
- Childhood disintegrative disorder, Retts disorder
- Age of onset less than 3yo
- No differentiation between clinical and research
11
Q
What are the implications for ISD-10?
A
- Childhood autism
- Atypical autism, PDD, Asperger’s syndrome, Childhood disintegrative disorder, Rett syndrome
PDD - Differentiation between clinical and research
12
Q
What are the components of the DSM-IV-TR criteria for PDD?
A
- Qualitative impairment in social interaction
- Qualitative impairments in communication
- Restricted repetitive and stereotyped patterns of behavior, interests and activities
- Delays or abnormal functioning in at least one of the following: social interaction, language as used in social communication, symbolic or imaginative play
- The disturbances is not better accounted for by Retts disorder or childhood disintegrative disorder
13
Q
What are the critiques of the “Chinese food menu” definition?
A
- Which symptoms, behaviors, criteria are most important in such a complex and continuum disorder?
- some behaviors are central while other peripheral and identifiable through research
14
Q
What are the components of the DSM-V for ASD?
A
- Triad is reduced to dyad: went from triad (social communication, communication and restricted repetitive stereotyped patterns of behavior) to a dyad (social interaction & communication, and restricted repetitive stereotyped patterns of behavior and/or sensorial issues)
- causes impairment in current functioning and symptoms exist in early childhood
- Dimensionality (level 1, level 2, level 3)
15
Q
What are the specifiers of ASD in DSM-V?
A
- W/Wo intellectual impairement
- W/Wo language impairment
- Associated with a medical, genetic or environmental factor
- Associated with a comorbid neurodevelopmental, mental or behavioral disorder
- With catatonia
- Onset (regression or other atypicality is described)
16
Q
What are the components of Asperger’s syndrome?
A
- Speech normal but possibly included
- Impaired non verbal communication
- Impaired understanding of social conventions
- Repetitive actions, resistance to change, intense attachment
- Motor deficits
- Splinter skills
- Eccentricity
17
Q
What was Lorna Wings components of Aspergers?
A
- Speech not fully normal
- No intrinsic drive for communication by infants/toddlers
- Deficits in sharing pleasure
- Deficits in imaginative play
18
Q
What had to be added in ICD-10 and DSM-IV to be diagnosed with Aspergers?
A
- Social interaction deficit and RRB are same for ASD and ASP
- Aspergers DSM-IV: no significant language delay, no significant cognitive delays, no deficit in self help skills an adaptive behaviors, no impoverished curiosity about world
- Aspergers ICD-10: single word by age 2, communicative phrase by age 3
- Normal cognitive development during first 3 years
- may be delayed motor milestone and clumsiness, isolated splinter skills
19
Q
What are the impairment for social, emotional and communicative challenges?
A
- Impaired mind reading
- Impaired emotion processing (experience and identifying emotion of others, complex emotions, emotion contagion, cognitive empathy, sympathy)
- Communication impairments: language (spoken, written, signed), non verbal language (facial expression, posture, movements, gestures, vocalizations-laugh &cry), rules of communication (inappropriate topic initiation, not responding to question, poor conversation rapport, repetitiveness)
20
Q
What are the different restricted, repetitive and sensory-perceptual anomalies?
A
- Repetitive sensory motor stereotypes: movement, objects, speech, self injurious behavior (SIB)
- Sensory perceptual anomalies: hearing, vision, tactile, taste, olfactory, pain, hyper focus
- Repetitive sensory motor stereotypes: sensory soothing, sensory seeking
21
Q
What are the social-emotional development and play?
A
- 3-6 month period-sharing emotions: face-face sharing and regulation of mutual attention and affective expression
- 5-6 months: less attention to caregivers and more on objects and nearby events
- 6-18 months: shared attentional focus on objects and events with social partners coordinated joint attention
- 9-24 months: initiate joint attention
- 11 months: functional play
- 24-36 months symbolic play
22
Q
What are additional shared characteristics for development and play?
A
- Imagination and creativity: pretend play = functional and symbolic
- Imagining the impossible: counterfactual thinking
- generativity: verbal fluency, design fluency, ideational fluency
- Islets of ability - splinter skills
- attachment vs impairments in social interaction
- Proto-imperatives -instrumental or demand
- cognitive abilities: rote memory, assembly tasks, mechanical reading
- Savants
23
Q
What are the motor skills?
A
- Body schema: hypo-tonia and hyper-tonia, dyspraxia and apraxia (impairments of voluntary movements, gross and fine motor
- Impaired sense of self: personal identity: physical attributed, social being, interpersonal self
24
Q
What is the difference between incidence and prevalence?
A
- Incidence: new cases in a period of time (date of onset, Dx process can take time, what age)
- Prevalence: number of cases In total for a specified context (i.e., existing cases at a point in time of ASD in 2-10yo in Montreal), used to calculate how common is ASD
25
How to check if there is an epidemic?
- Case ascertainment (large enough base population, designate epidemiological pop., systematically screen-administrative record review, questionnaire, standardized instruments)
- Case confirmations (clinical examinations, expert record review)
26
Why is there an increase in ASD (1 in 80 to 1 in 100)?
- Better case ascertainment (Nypical schools, general hospitals, GD and Pediatric screening)
- Changes in Dx criteria (DSM changes, broader range of communication deficits as well as restricted repetitive behaviors)
- Comorbidity with other neurodev disorders that were given precedence (26% of cases that were DI now are ASD)
- Age of identification (downward shift in age diagnosis contributes to recent rise in cohorts, major component)
- Awareness (better screening, physicians are less reluctant to refer for follow up ad give tentative Dx, awareness through media, social contagion)
- Admin decisions
- Services
27
What are the different distribution differences for ASD?
- gender: LFA not big disparity, symptoms are milder or different, compensation strategies = culture impact, sex differences, diagnostic bias
- Geographical
- Racial and social class: black children 2x more likely, higher social class,
- Other: foreign citizenship/immigration status
28
What are the different age onsets for ASD?
- Idiopathic-spontaneous and regressive
- early onset is less than 18mo socio-emotional communicative impaired or absent
- late onset or regressive is when the child is normal until around 18 mo and then a decline
- plateau is when child is normal until around 18mo and then slows or stops
- Continuum: no particular age onset
- acquired autism after disease
29
What are the different trajectories for people with ASD that is positive?
- Resistance to change-certain characteristics or attributes: ASD may be residual symptom, cognitive functioning, linguistic potential
- Positive changes with maturation and intervention (HFA): instrumentality decrease, empathy increase, social initiation, sharing enjoyment, RB decrease, behavioral inflexibility decrease, intense interest becomes preferred, challenging behavior decrease
- Positive changes with maturation and intervention (LFA): stereotypies may remain or increase, SIB remain or increase, inflexibility may remain or increase
30
What are the different trajectories for people with ASD that is negative?
- Adolescence-double hit disorder: transient or permanent anxiety, depression, HFA may improve but transient issues may arise
- environmental factors: change of schools, change of living conditions, loss of a loved one
- Cyclic changes: menstrual, seasons, weather
31
What is the development for adult outcomes for finishing school?
- Finish school: HFA do well, - 10% uni are on spectrum, - struggle with social aspects and self-organization,
- MFA move to supported college programs (continuing ed until 21),
- LFA stop receiving formal education by early to middle high school and learn self care and daily life skills
32
What is the development for adult outcomes for employment?
- HFA may succeed in education and find employment
- Positive traits: reliability, conscientiousness
- Negative traits: low stress tolerance, rigidity, concreteness, paranoia
- MFA minority find work in less socially demanding jobs
- LFA tiny minority find work
33
What is the development for adult outcomes for living arrangements?
- Many continue to live with parents or other family members
- supported living (group homes or larger facilities
- Very small minority live independently
- Incarceration
34
What is the development for adult outcomes for relaitonships?
- Life partnerships: 4% long term relationships but doesn't all last, challenges for financial, emotional, inflexibility and restricted interest, not about not wanting but about social abilities and can lead to inappropriate or criminal behavior, incel
- Friendships: less than 25% enter into self initiated friendship, based on limited interests, online friends, family based friendship, community based activity friendship
35
What is the development for adult outcomes for leisure activities?
- predictable
- solitary
- HFA may have typical hobbies or activities with less social involvement
36
What is the development for adult outcomes for hazards?
- Criminality: slightly higher than non-ASD pop., threats, violence to others or property, arson, HFA offend due to generalizing porn
- Addiction: harder to quit due to excessive rigidity
- Antisocial behavior: spitting, masturbation, SIB
- Accidents and illness: more common than in non-ASD pop (HFA), suicidal ideations and attempts
- Life expectancy: 3x higher death rate, learning abilities leading to accidents and seizures
37
What causes autism?
- Etiology
- Neurobiology
- Psychological processes
- Manifest behavior
38
What are the criteria's for judging the strength of theories?
- Specificity criterion: if theory proposes factor X is necessary and sufficient to cause a particular facet of autism, he factor X must be unique to people with ASD
- Universality criterion: if a theory proposes that critical factor X is necessary cause of one of the defining or additional shared features of autistic behavior, then factor X must be shown to occur universally in all people with ASD
- Primacy criterion: requires that factor X must occur at an earlier developmental stage than the abnormality that factor X is supposed to explain
39
What are the two groups for risk factors for developing ASD?
- genetic and environmental
40
What are other autism risk factors?
- Life events: stress events, hypoxia, breech
- Environmental exposure: maternal smoking, birth location outside N.A. and Europe, maternal use of medication
- Parental age
- Natal factors: jaundice, prematurity, pre-eclampsia
- environmental exposure pre & post natal: valporic acid, SSRI, thalidomide, mercury, automobile fumes, early gestational exposure to certain pesticides, maternal illness
- maternal stress levels
41
What are the ASD risk factors associated with genetics?
- chromosomes, genes, constituents of genes and gene products, DNA between the genes, RNA editing dysregulation
- Genotype: human genome is not blueprint, set of constraints, phenotype
42
What is methylation?
- Process of transferring a single carbon atom and three hydrogen atoms (methyl group) from one substance to another in the body
- Demethylation: maintain physical, mental and emotional health
43
What happens to the grey/white matter of people with ASD?
- atypicality's in density of grey and white matter
| - Grey matter in cerebellum is decreased relative to neurotypical brain
44
What are the implications of the amygdala for people who have ASD?
- enlargement of the amygdala
- greater volume in right amygdala in toddlerhood = poorer social and communication outcomes at age 6
- Increased amygdala size correlated with severity of social and communication deficits
45
What are the implications of the cerebellum for people who have ASD?
- reduced purkinje cells (inhibitory control of neural activity
- Abnormality reported in older children and adults
46
What are the implications of the corpus collosum for people who have ASD?
- Smaller size in children
| - correlated with degree of restricted and repetitive behaviors at 24 months old
47
What are the implications of the gut brain axis for people who have ASD?
- Alterations in macrobiotic composition
| - Influences brain function
48
What are the implications of the serotonin levels for people who have ASD?
- Helps with development of social skills during gestational period and early childhood
- Can be over or under production
- problem with transporter substance
- abnormalities in provision and action of serotoninergic receptor cells
49
What are the implications of oxytocin/vasopresin for people who have ASD?
- Oxytocin receptor gene variation is linked to increase stress reactivity and decreased empathy
- intranasal oxytocin: reduced receptive behaviors, increased recognition of social info and emotion of other, increased social approach and comprehension
50
What are the implications of GLU and GABA for people who have ASD?
- GLU = excitatory neurotransmitter
- GABA = inhibitory neurotransmitter
- EI theory: imbalance of GLU and GABA (reduced levels of GABA confirmed)
51
What are the implications of DA for people who have ASD?
- Malfunction of dopaminergic system= motor abnormalities
- abnormalities of DA production, transmission and receptive have been linked with emotion dysregulation and anomalies of attention, executive dysfunction and repetitive behaviors
52
What are the implications of the circadian rhythms and ASD?
- Children with ASD show sleep problems
| - Issues with melatonin, cortisol and mTOR
Dev. Advanced Issues: Autism
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