2: ASD Flashcards
In ASD there was the triad of impairments and now there is a dyad of impairments (social communication and interaction, rigidity, obsessions and unusual sensory responses). There was a change the DSM-5 which resulted in
In ASD there was the triad of impairments and now there is a dyad of impairments (social communication and interaction, rigidity, obsessions and unusual sensory responses). There was a change the DSM-5 which resulted in the lose all of the subtypes (Retts syndrome, Asperger syndrome etc.) because research had not given validity of the different subcategories (e.g. a child with Aspergers syndrome, this child is expected to develop language in a normal way. Whereas a child that meet diagnosis for Autistic disorder, they are not using language at 13 months). This is the main difference between AS and HFA in the DSM-IV. One of the things that people found (in relation to the issue of child resources), is when you look at those two children when they are 10 years old they are not looking that different. High functioning children with language delay at 10 years of age talk as much and by adulthood its almost impossible to tell the difference between somebody that received a diagnosis of AS and HFA. Therefore we shouldn’t be giving this diagnosis because it’s not justified by the research. There was also a move from the triad of impairment into the dyad of impairment, because it was mainly very difficult to measure and distinguish communication and socialisation. They are so overlapping so finding tests that do those two things separately was really problematic. Therefore, these were the kind of reasons why they made these reasons to change. One problem may be a cultural problem in that people with AS have Aspi’s United etc. that work together (community) and do really good stuff and they may be bothered by losing this identity. For research purposes we aren’t supposed to use the term AS.
The way that we will diagnose ASD, these are the two Royals Royce measurements:
Kathy Lord, Mike Rutter etc
The way that we will diagnose ASD, these are the two Royals Royce measurements: The autism diagnostic interview (ADI), there are tests like this but this one is the most widely used cross culturally with the most data attached to it. This was developed by Kathy Lord, Mike Rutter etc. In this assessment, the parents are interviewed (can take up to 3 hours) which starts taking about when the infant was really young, mile stones, motor mile stones, making eye contact, responding to social gestures from other people. It will go through all of the phases of a child’s life. This has quite good tricks, you start by talking to the parent about certain points within their child’s life (what was your child doing at 6 years old? Child would have at MA of 4) to do good recall to create a bench mark against it.
The other test is the autism diagnostic observation scale
The other test is the autism diagnostic observation scale which is administered by a highly trained clinician an whats more is after the training, they have to be administering them all the time to stay really good at it due to the quickness needed to administer it especially with a toddler woes running all over the place when your trying to assess eye movement etc. But then there are measures from your observations, interactions and history. By bringing all of this information together, there is a good overview of the child. Therefore, your not just dependant on how the child is doing on that day, there is also indications of whats going on in general.
Some research has implicated maternal prenatal vitamins, air pollution etc.,
Lyall et al., 2014
Hallmayer et al, 2011; Frazier et al, 2014
Some research has implicated maternal prenatal vitamins, air pollution etc., in the emergence of ASD (e.g. Lyall et al., 2014). Some researchers have reported that there significant influences of shared environmental effects in twin studies (Hallmayer et al, 2011; Frazier et al, 2014). This is important for clinicians to be aware of the evidence before and against, as parents really do believe that pollutants cause NDD’s. The problem is that quite often, there are methodological problems within these studies, which makes it really difficult to know how to interpret these kinds of findings.
The prevalence for Autism is 1% in the general population (e.g. Baxter et al., 2015).
Simon Baron-Cohen
Williams et al., 2005
The prevalence for Autism is 1% in the general population (e.g. Baxter et al., 2015). This 1% will be based on Autism Diagnostic Interview (ADI) and Autism Diagnostic Observation Scale (ADOS), these are very good tests that are very stringent, very well developed. But we can use something like the Children Autism Spectrum Test which instead will give 5.8% of the population that will then meet criterion. The Autism Quotient (AQ) is a test developed by Simon Baron-Cohen from Cambridge. This test measures ASD traits in people who don’t have ASD (definitely would not meet criterion on ADI) but can have a lot of ASD traits. Simon Baron-Cohen has done a lot of work showing that engineers, mathematicians that have higher levels of ASD traits etc. This is a similar story, only 1 out of 6 of these children will meet criteria for an ASD diagnosis (Williams et al., 2005). Therefore, if we test them with the Children Autism Spectrum Test we are going to get greater prevalence but they won’t meet criterion on the ADOS or ADI. Therefore if you think about studies its going to make a big difference in whether you include the Strict Criteria 1% or Loose Criterion 5% group.
In a good meta-analysis of twin studies at the IOP, looking at concordance twin pairs in ASD (Tick, Bolton, Happe, Rutter, & Rijsdijk, 2015).
In a good meta-analysis of twin studies at the IOP, looking at concordance twin pairs in ASD (Tick, Bolton, Happe, Rutter, & Rijsdijk, 2015). For monozygot (MZ) there is .98 (massive genetic influence) and in DZ, it changes depending on what criteria is used. If the strict criteria is used (ADI, ADOS) and these children meet criteria for ASD, then it’s 67%, at this point the environmental effects are not significant. However, if the loss criterion is used of 5%, there are greater environmental effects witnessed. Therefore, it is important to think about methodology in the study. The evidence of a genetic effect is obviously massive.
There are genetic mechanisms involved in ASD are complex and include
Jeste & Geschwind, 2014
There are genetic mechanisms involved in ASD are complex and include rare chromosomal anomalies, several individual genes of major effect and numerous common variants of small effect (Jeste & Geschwind, 2014).
In WS, there a bunch of genes that are very clearly identified through a blood test to diagnose the children to identify the genetic anomalies in these children. But this can’t be done with ASD as its much more complicated.
Johnson (2011)
In WS, there a bunch of genes that are very clearly identified through a blood test to diagnose the children to identify the genetic anomalies in these children. But this can’t be done with ASD as its much more complicated. In a way this is why researchers have worked so hard to develop such stringent diagnostic tests because ASD can only be diagnosed on the basis on behaviours. Therefore there is a different approach to dealing with ASD. Johnson (2011) suggests that symptoms of ASD is are likely to emerge from a complex interaction between pre-existing vulnerabilities, and the child’s environment. Initial genetic and environmental risk factors interact to alter the development of brain structure and function, compromising the child’s ability to learn from their environment.
We know that ASD is highly heritable, so if we look at the the younger siblings within a family with a child who has had a diagnosis and map their development to see whats happening to those children to paint a picture.
Jones, Gligaa, Bedford, Charman & Johnson, 2013
Ozonoff et al., 2011
Messinger et al., 2013
We know that ASD is highly heritable, so if we look at the the younger siblings within a family with a child who has had a diagnosis and map their development to see whats happening to those children to paint a picture. In the DSM-IV people gave a diagnosis of ASD at 30 months, at the point were language delay was apparent. Cannot diagnosis a 3month infant with ASD, however you can know that this infant has a sibling with ASD so its more likely to develop ASD. What this paper does is a meta-analysis (Jones, Gligaa, Bedford, Charman & Johnson, 2013) of prospective studies looking at at-risk infants (0 – 2/3years) with high familial risk for ASD (with older sibling with a diagnosis). 20% of these children will meet diagnosis by 3 years old (Ozonoff et al., 2011) but there are also other kinds of problems in 10 – 20% develop sub-clinical ASD traits or other developmental difficulties (Messinger et al., 2013) e.g. difficulties with language, etc. they are not typical developmentally but are severely impaired enough to meet criteria for ASD.
When thinking about atypical development, its really worth thinking about what atypical children do because its the benchmark of comparison.
Mark Johnson
When thinking about atypical development, its really worth thinking about what atypical children do because its the benchmark of comparison. A TD baby, will give out signals and perform actions that elicits a response from a caregiver. Human beings are the most important information source at this point, especially parents and siblings. Babies use mutual gaze, they use facial expression, posture, gesture etc. to regulate social interactions. Mark Johnson suggests that infants do things that impacts on brain development. In ASD, infants have a problem with eye gaze, problems with understanding other people gestures, getting people to engage with them. So its irrational to look at these types of behaviours in these at risk siblings.
In TD infants, research has shown that infants show an early preference for faces over shapes, they like their own mothers face best.
In TD infants, research has shown that infants show an early preference for faces over shapes, they like their own mothers face best. They become increasingly sensitive to changes in eye-gaze and gesture (will follow caregivers eye gaze). Then there is a move toward preferential smiling (an infant at 8-9 months infants don’t just smile at anyone anymore, they smile preferentially at caregivers), these social learning, they become increasingly sensitive to other people’s emotion cues Imitation (important for early social and cog dev). The clinical literature suggest that children of depressed mothers cry more. If you show angry faces to infants get very upset early on. Imitation can also be seen which is very important for social learning.
Results from behavioural studies show that infant who develop ASD do not show marked impairments in orienting to faces and social gestures (e.g. Elsabagh et al., 2013; Young et al., 2009) or in gaze following (Bedford et al., (2012)
Results from behavioural studies show that infant who develop ASD do not show marked impairments in orienting to faces and social gestures (e.g. Elsabagh et al., 2013; Young et al., 2009) or in gaze following (Bedford et al., (2012) during the first year of life. This is all based on behavioural evidence, in neuroimaging evidence there is a slightly different story. One thing you can do with an infant is social smiling, vocalisations (e.g. during “still face” procedure” where the mother will be chatting with the baby and her face will suddenly freeze in which the babies will get quite alarmed and will do all sorts of things to get the mother responding again). 6 month old, ‘at risk’ siblings appear to be relatively typical in this task.
But then we start getting problems in infant siblings. Ozonoff et al., (2010) reported a
Landa et al., 2007
Yoder et al.,(2009)
But then we start getting problems in infant siblings. Ozonoff et al., (2010) reported a decline in social smiling and gaze in 6-24 months and therefore are beginning to show a different trajectory to typically developing children. There is less shared positive affect at 14 months whereas most 14 month infants get into tickling games thus there is a decline in this behaviour at 14 months (Landa et al., 2007). Developmentally children learn to coordinate a lot of things across different modalities (looking, gestures, listening). We see in DS difficulties with these complex behaviours (e.g. looking and pointing) which most toddlers will do. Yoder et al.,(2009) found the ability to combine gaze, gesture, and vocalisations between 15–24 months predicted 36 month diagnosis and levels of social impairment. Behavioural evidence suggests that social orienting mechanisms are functional during the first year of life but then diverge from typical developmental trajectory. Evidence from neuroscience. Therefore it seems for this evidence within the review that things are not terribly abnormal when you look at it behaviourally in the first year its more after that we start seeing differs trajectories for typically developing and children with ASD.
According to Pelphrey & Carter (2008) and other researchers, the Superior Temporal Sulcus (STS), together with other ‘social brain areas’ is impaired in ASD.
Lloyd-Fox et al., 2013
Esabagh et al., (2012
According to Pelphrey & Carter (2008) and other researchers, the Superior Temporal Sulcus (STS), together with other ‘social brain areas’ is impaired in ASD. The STS is sensitive to biological motion, gaze direction and to facial expression which are all impaired in some people with ASD. Neuroimaging work with at-risks infants, they show reduced STS response to social stimuli 5 months (Lloyd-Fox et al., 2013) which is not getting picked up in behavioural tests. These infants aren’t looking like normal children at the neural level. Infants who were diagnosed with ASD at 3 yrs showed atypical neural responses to gaze shifts at 6-9mths (Esabagh et al., (2012). They are not showing that flexibility to learn from social cues as seen TD children.
Jones & Klin (2013) carried out longitudinal naturalistic (video material) study of children with ASD and typically developing children aged 2–24 months.
Leonard et al., 2013
Jones & Klin (2013) carried out longitudinal naturalistic (video material) study of children with ASD and typically developing children aged 2–24 months. They were interested in looking at trajectories distinguishing the children with ASD from TD children. In TD showed increasing tendency to fixate on the eyes whilst eye fixation decreased in ASD. Trajectories in 2–6 month period different for ASD and TD groups. Suggests erosion of initially typical social orienting skills in ASD at this very early stage of development. This is opposite to the meta-analysis suggests that a lot of those studies have shown that there aren’t really any problems. However, its very difficult to measure these things in very young children and they’d probably need to be very markably abnormal before you recognise them. The other probable is, it would need to be considered how severely autism an infant is (all the same children of various severities are being considered as the same at this age group). Dealing with a complex multidimensional disability. Other symptoms that are less systematically studied and thus harder to draw a firm conclusion are play behaviours (early atypical play in ASD repetitive wheel spinning). In ADOS, there are various toys and the therapist will ask the children to make a family group and have a picnic. Children with ASD don’t treat the toys like social entries. Studied behaviours: body related behaviours, exploratory behaviours (find that children do not investigate the toys etc.), executive functions, motor behaviours (some evidence for atypical development (Leonard et al., 2013) and language (suggests variable trajectories, extraordinary variability in diagnosed individuals).
Cognitive models of ASD; Theory of Mind is a cognitive ability that enables us to understand that other people have feelings, think thoughts: “theory-of-mind” or “mentalising”.
Baron-Cohen, Leslie & Frith, 1985
Cognitive models of ASD; Theory of Mind is a cognitive ability that enables us to understand that other people have feelings, think thoughts: “theory-of-mind” or “mentalising”. Classic example of false belief test Sally-Anne task (Baron-Cohen, Leslie & Frith, 1985). Doll leaves marble, unknown to the first doll, the other doll moves it. Q: Where will Sally look for her marble? A: Where she thinks it is. In the original study they compare children with ASD, Down syndrome, and typical development at 3-4 years, TD: 85% pass, DS: 86% pass (in later research much less children with DS pass this type of tests) yet only ASD: 20% pass (today the children understand how to do the Sally Ann test). This challenge does not represent what happens in the real social world, as the task is much more complex.
This is called a first order false belief task,
Baron-Cohen review 2001
Peter Hogson
This is called a first order false belief task, actor has false belief about the world ‘Mary does not know the marble has been moved’ there is only one step in our reasoning in a first order false belief task. There are really complicated ones that are much more like what happens in the real world. Second-order false belief tasks: actor has false belief about another person’s belief about the world “Mary doesn’t know that John knows that the marble has moved.” People perform this type of task in micro seconds every day. ToM very widely investigated in Autism (Baron-Cohen review 2001), some individuals with Autism pass ToM tests e.g. 20% of children ASD pass in both Baron-Cohen and Perner task. Peter Hogson wrote about limitations of these very cognitive ways of understanding the social communication impairment (Pam likes-on VLE), he suggested that social cognition is more complex than that.
Klin (2000) tested a group of HFA and AS participants with a mean age of 16 with IQ’s in the normal range.
Klin (2000) tested a group of HFA and AS participants with a mean age of 16 with IQ’s in the normal range. Participants achieved an age equivalent score of 3.9 years on the Vineland Adaptive Behaviour Scales (subdomain of how people interact with each other) and the Interpersonal relationship scale. They could pass TOM tasks pitted at a higher level than 4–6 years. Although we are saying that ToM is measuring social communication disability in ASD, yet on the Vineland Adaptive Behaviour Scales they are showing deficits. Therefore really bringing the paradigm into question. One suggestion Klin (2000) says is the verbal nature of the task, some ToM tasks are very complicated (higher order ToM) in which people need a phenomenal auditory working memory to remember all of the sub clauses.
We know from Astington and Jenkins (1999) early study, that if there are large cohorts of typically developing children, there is a very high correlation between theory of mind performance and language skills.
We know from Astington and Jenkins (1999) early study, that if there are large cohorts of typically developing children, there is a very high correlation between theory of mind performance and language skills. People with good language can hack out a solution to a ToM task. Also the explicit nature of the ToM task is very different to what the Vineland would measure which is more naturalistic (remembering multiple peoples state of mind at once). These tests are not testing anything like that. The dichotomous nature of the task, its rare there are social problem solving situations where there are only two choices, its far too simplistic. The other problem is they either pass or fail the sally ann test, this test over estimates the social skills of people who pass it. This is seen in the Klin study where the adolescents did not have good social skills but they could pass. If they are judged on their ToM performance, it will be concluded they have theory of mind. Those that fail it will have some aspects of ToM, even children that are very socially impaired will occasionally show ToM.
Klin et al., (2000) tested autistic participants on the social attribution geometric shapes task developed by (Heider & Simmel, 1944) who found that 99% of NT made attributions to do with personality and emotions (e.g. that triangle was frightened).
Klin et al., (2000) tested autistic participants on the social attribution geometric shapes task developed by (Heider & Simmel, 1944) who found that 99% of NT made attributions to do with personality and emotions (e.g. that triangle was frightened).
People with Aspergers think that NT are weird when they give emotions and personalities to moving shapes. When Klin did this with a group of HFA and AS adolescents who could pass 2nd order TOM tasks were only sensitive to a quarter of the social elements described by controls. Very insensitive to movement cues and ASD used fewer mental state terms, ASD used mental state terms inappropriately, ASD derived fewer personality features, ASD raised irrelevant points (confusing in social situations). Both groups showed poorer recognition of social than non-social emotions. For both groups the ability to report personal social emotion- experience was significantly associated with the ability to recognise social emotions in others, independent of age and verbal ability. A person with ASD example, the large triangle is oscillating at 90 degrees around the small circle an thus explained it in a very scientific way to how a NT person would do it. Results reported no between-group differences in levels or patterns of performance on the experimental tasks.
