Mandy DD Part 2

Question 1

What is the triad of impairment

Answer 1

Social communication, reciprocal social interaction & restricted interest and repetitive behaviours. Recently changed to Dyad (communication and interaction merged) and Asperger and pervasive DD not separate

Question 2

Other diagnosis criteria for ASD

Answer 2

Can be W or wout intellectual, lang impairment. Can be W medical, genetic or environmental conditions. Co occur w neuroDD, mental or behavioural. Describe onset. New social communication disorder-ASD-repetitive behaviour, diffs e communication, learning and written language pragmatics

Question 3

ASD symptoms in babies

Answer 3

Reduced social interest, lack of joyful expressions, emotional interest, response to name and interacting
Atypical language development
Lack of coordination of gaze, facial expression, gesture and sound during interactions

Question 4

Asd prevalence

Answer 4

Increase since 2000, 78 was 0.04%, now around 2.44%uk. May be false as increased awareness, criteria more broad, diagnostic substitution (used to be intellect. Disab. Now asd), may have been inaccurate diagnosis. More common in males 4:1 but girls present diff and diagnosed later on

Question 5

Prevalence linked to environmental causes

Answer 5

more premie and perinatal complication babies surviving, parental age increasing, environmental toxins, maternal immune response to pregnancy (flu, fever attladottir 2012)

Question 6

History of Asd

Answer 6

Until mid 20thc originate from emotional coldness of mother, 60s had neurological underpinning, 80s had cog theories about thought diffs, 90s more neuro developmental and brain structures. Resurgence in maternal coldness (Susan greenfield said caused by overuse of technology)

Question 7

Neurocognitive theories history of asd

Answer 7

Executive function: limited evidence and not specific to asd so could just be a risk factor - johnson 2012
Extreme male brain: lack of evidence and bad as contributes to under diagnosis of autism in females

Question 8

Social deficit theory-theory of mind -premack and woodruff definition and mentalizing

Answer 8

P&w: social cog in chimps, the ability to attribute mental states to oneself and others, others have thoughts diff to you. Frith:mentalizing is an unconscious ability to attribute mental states to yourself

Question 9

SDT-baron Cohen and how relates to impairments

Answer 9

Cohen: root of asd is failure to develop and display shared emotion leads to ToM impairment and social diffs early on. Accounts for triad as lack of pretend play, social difficulties arise as representation needed to understand ppl as agents, can’t represent intentions and utterances to convey thoughts

Question 10

Behavioural measures of ToM- SDT

Answer 10

Sally Anne/false belief:happe:ps matched on mental ability age, normal had 50% pass rate at mental age 4 but asd at 9.2 mental age (supports ToM but delay not deficit and only for a certain age, needs lang &working mem). Implicit mental states task:castelli: shapes moving in meaningful ways, asd describe using geo and spatial but normal attribute emotions. Mind eyes BC: what eyes were feeling, asd adults showed impairment, endophenotpye (genetic linked to behaviour), parents of asd less accurate

Question 11

Conflict to mind eyes task back 2007

Answer 11

10-14 year old asd got higher scores when eyes moving (lack of EV) 11-25 were as good as controls. Ppl are non homogeneous and have diff risk factors

Question 12

Neurobiological evidence for social deficit theory/tom- social brain and deficits BC

Answer 12

Part of social brain (medial pfc, anterior cingulate cortex, amygdala, ifg, inferior parietal sulcus, temp par junction, sts, anterior insular. BC: asd lower activation in frontal lobes, amygdala. Controls more powerful in left amygdala (emotional processing) and asd more in temp lobe-verbal (compensation)

Question 13

Neurobio evidence for SDT/ToM-high/low functioning

Answer 13

High/low functioning can be damaging as reducing to productive levels and may not be accurate. Just: 17high functioning scanned while thinking about social interactions-activation in posterior midline regions for controls, not asd. Mean lack of self involvement. Activity correlated W density of fibres connecting to frontal and W behavioural measures of social processing-less in asd. Areas could id asd 97% accuracy

Question 14

ToM and mirror neurone system components

Answer 14

Includes anterior intraperital cortex, temp junction and sts, active when moving or seeing others moving. Overlap between MNS and social network areas in ToM-mediates understanding of emotions of others so diffs could link to asd

Question 15

Experiment for mns depretto 2006, meadow 99, buccino, fadiga

Answer 15

Ps in mri watched ppl do expression and imitates, asd adults showed similar behaviour but more activity in right visual and left anterior parietal, less in insular and amygdala, none in mns. Meadow: localised mirror neurones in monkeys activate during communication sounds. Buccino:facial gestures activates mns in broca, fadiga: those W phenomes activity linked to tongue manip.

Question 16

S and W of mirror neurone system research

Answer 16

S: asd have problems expected if mms was damaged, some evidence for group diffs in mns. W: asd may have mns but use diff, mns diffs aren’t specific to asd, also in schizo, evidence for diffs has not continued

Question 17

Impaired social perception effects in children

Answer 17

Signs at 12m linked to social perception, used for development of social cognition. Social orienteering theory that reduced social attentional bias leads to diffs in development of social brain and ToM carpendale.

Question 18

ERP/EEG studies of social perception -elsabbagh gaze study

Answer 18

P400 response from direct gaze. Elsabbagh 2012: infants W and without fam risk, measured p400 from direct then away gaze, both controls and risk had more + response in away but at risk showed no diff in response between direct and away

Question 19

Functional near infrared spectroscopy

Answer 19

Measures infrared light to show change in blood o2 levels and vol in cortex. Lloyd 2018: infants W fam risk and not shown social vids and pics and non social, human vocalisation and non vocal sounds. Found later asd reduced activation to social vids, vocal sounds and enhanced to non vocal

Question 20

Social perception- a type of SDT and weaknesses

Answer 20

Diffs due to social perception diffs, impact development of social cog. W: focus on deficits, issues W replication of findings-British asd study found no diffs in looking, doesn’t allow for uneven profiles, orienting deficits may be more subtle (timing)

Question 21

Weak central coherence theory

Answer 21

Frith 94: asd have preference for processing as collection of detail in absence of global meaning whereas normal have bottom up approach. Adults W asd faster at imbedded figures task but not supported in meta analysis. Asd adults don’t use context in homograph task, not consistently replicated and could be due to lang. happe: world in pieces: percents of asd vs parents of dyslexia or nothing. 50%fathers, 33% mothers detail focused

Question 22

Neural basis of wcc

Answer 22

Enhanced sensory in low level cortices, reduced long range connectivity. Manjaly: studies using hidden figures have more parietal and occipital activity in asd and reduced frontal circuits. Asd children 7-1# had reduced frontal parietal but no enhanced occipital so low visual perception.

Question 23

S and W of neural basis of wcc

Answer 23

S: cog theories useful for explaining behaviour and treatment, shift in focus to sensory and perceptual diffs, evidence of brain good for debunking myths. W: replication failures , know little about normal development of coherence, not descriptive (no treatment/outcome)

Question 24

Asd symptoms in adults

Answer 24

Core behavioural symptoms improve over time but some persist, have difficulty living independently, motor coordination, sensory activities, sleeping and eating probs. Intellectual disability in 25-50%. May have hyperlexia (good reading but can’t comprehend)

Question 25

Old forms of asd

Answer 25

Asperger used to be Ford those without sig cog/lang delay. Pervasive is those W symptoms but not enough for diagnosis. Rhett is a part of pervasive but had normal development and spec symptoms but insufficient evidence so became asd.

Question 26

Increase in prevalence, girls symptoms and cost

Answer 26

In use, more diagnosis when special schools introd,,diagnostic substitution as mental retardation has decreased same amount asd increased. Girls have lower iq, cog impair, fewer stereotypes behaviours, qs about universal screening at 12m but not diagnosed till 4-5. Cost for case is 2.7bill 25bill for adults

Question 27

Characteristics of adhd

Answer 27

Has 2 dimensions: inattention and hyperactivity/impulsivity - not all children with adhd are hyperactive
3 subtypes: hyperactive (hyp), inattentive (inatt) or combined

Question 28

Adhd prevalence

Answer 28

5.8-7% 2012 and increasing although polanczyk did 54 studies W strict criteria and found prevalence unchanged. 3:1 m to f, 9:1 referred. Girls more likely to have inattentive and be less disruptive so less diagnosed and less comorbid conditions biederman

Question 29

Diff between test sensitivity and test specificity

Answer 29

Test sensitivity: ability of a test to correctly id those w the disease
Test specificity: ability of test to correctly id those without the disease (true pos and neg rate)

Question 30

Adhd diagnosis

Answer 30

Dsm5, Psych assessment, interviews, observations. Sesnsitity 70-90%. Symptoms casing impairment before 7, can be diagnosed at 4 but most around 6. Impairs occurred in 2 or more settings, clear evidence of sig functional impairment, not accounted for by any other disorder

Question 31

Measurement test for adhd

Answer 31

Connor continuous performance test-children 8+, respond and ignore targets, uses response speed, false alarms and misses and hits. Measures in attentiveness by higher misses, impulsivity by false alarms and anticipatory . Most rviews or questionnaires like connors 3rd edition part/teacher self report scale to look at S and W

Question 32

Weaknesses of adhd tests

Answer 32

subjective criteria (one person difficulty might not be others), many non specific problems that overlap w other disorders (sleep, learning diffs, aggression)

Question 33

EEG for diagnosis

Answer 33

Accessible and cheap, neurone activations of cortex.Jasper: slowing eeg rhythms in frontocentral sensors in behavioural problem children. Barry : increased theta, decreased beta waves, group diffs and sensitivity 90%more than dsm. Offered in private clinics costs £350, calc theta beta ratio, approved in us but not Mai tool as no standardised cut off, reliability checks and research evaluation, done by companies who profit. Replication failures diffs in children and adults, low sensitivity , not just ration only some adhd showed

Question 34

Adhd developmental change

Answer 34

50% childhood adhd resolved by adulthood but some not diagnosed into adult. Criteria change like less playing and danger sense at preschool, forgetful and sitractsd and fidgeting in school, inner restlessness and incomplete details at adult. Blais: 247/2232 met criteria for childhood adhd persisting to adulthood (more symptoms, lower iq, conduct and drug use) 122/2232 diagnosed later had less external probs, higher in but similar symptoms (gone or misdiagnosis/masking?)

Question 35

Real vs not

Answer 35

Lancet article questioning, attribute behaviour due to children having no consideration for others, deficit in moral control. Changed from moral to bio but thought to be due to brain damage hohman then dysfunction as not all had lesions. Ken Robinson thought consequence of education system. Johnston due to poor parenting. Social construct theory

Question 36

Schooling link and stigma

Answer 36

Schooling besula 2008, social kofler 2011, behaviour and substance of abuse kofler 2011, mental health, employability and discrimination. Mislabeled as lazy, disruptive as seen they have control over their symptoms