Short Answers Flashcards
Research into neurodevelopmental disorders poses special challenges: Discuss
Role of IQ in diagnosis: Intellectual impairment is common in developmental disorders (DS, WS). Around half of child with ASD have intellectual impairment. There are more than 1000 genetic causes have been implicated in intellectual impairment (Moser, 1992) which has probably increased quite a lot. For specific disorders (e.g. dyslexia, specific language impairment), impairments in key skills must be below that expected by IQ. A child of 12 had a reading age of 8, if an IQ test suggests the child had learning difficulties, because their poor reading reflects their verbal IQ, its a function of their intellectual level. With dyslexia there must be a discrepancy, the child’s reading is very poor given their intelligence (same in SLI). A specific disorder is not affecting intelligence globally, its really impacting on one aspect of intelligence behaviour.
Comparison of a group of children with ASD who have savant skills (very good at maths, music, art) with a group of children with ASD without savant skills. The non savant ASD children have a much more even profile. The lowest score as always in ASD is comprehension is 80%. working memory index and digit span, savants have an exceptionally high scores. It’s very difficult to control match these kinds of children. Potentially getting two control groups based on VIQ and NVIQ. WS group and a vocal mental age VMA group (that were 2-3 years younger). Judged on language and they have developmental delay. They found that the children with WS knew a lot more about animals etc. resulting in people making claims about their language knowledge etc. However someone suggested that they are 3 years older with more life experience and therefore they may know more for this reason. If these children were assessed on phonemes (Fe, Ber, da), then it would be appropriate to match them on MA, it depends completely on the experimental hypothesis. When designing a study, its important to be aware of all these alternate ways of matching.
Matching ADS children who are 10, who have a verbal mental age of 8 because they have developmental delay in language. These children can be matched chronologically to a group of children with MLD, they are the same age and thus controlled for life experience. However, this is problematic because we don’t know what the aetiology of the children with MLD is and often this can be a real confounding variable. There is no perfect solution to this issue.
However, studies within neurodevelopmental research does not have the luxury of looking at SES as we don’t have big enough samples, we get the children we can get with children with developmental disorders. This may be a problem as wealthier families can give more aid to a child. The constraints of neurodevelopmental studies are the rarity of subjects (e.g. WS) leads to small sample sizes as we can’t randomise people to samples. Often there are not very good tests (lack of availability of appropriate tests), although it has got a lot better over the last 10 years.
Studies of at risk infants at risk of developing ASD will be important for our understanding of symptoms in ASD
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 what is happening to those children to paint a picture. In the DSM-IV people gave a diagnosis of ASD at 30 months, cannot diagnosis a 3month infant with ASD, however you can know that this infant has a sibling with ASD so it’s more likely to develop ASD. What this paper does is a meta-analysis (Jones et al, 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), 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.
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. 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.
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.
Critically evaluate the Weak Central Coherence theory of Autism
Cognitive theories have attempted to explaining deficits and Special Skills in ASD
One of the first theories that tried to explain assets was the Weak Central Coherence Theory was was written by Frith who says that we draw together of diverse information in order to construct higher level meaning in context is disrupted in autism. An early finding is the children with ASD have a visuo-spatial local bias supported by the embedded figures task (CEFT) e.g. Shah & Frith, (1983). Therefore, it was reasoned that children with ASD have enhanced local processing and the global processing is damaged. Happe, 1994 did a meta-analysis and found a peak performance in the block design task. Happé (1996) did a study where she gave people visual Illusions (train track). People secumb to all sorts of illusions because of the way that we use gestalt perception. ASD were not succumbing to illusions as much as TD (participants with ASD succumbed to fewer visual illusions than controls). This was seen as support for the weak central coherence theory.
There was early work on Face Processing e.g. Hobson et al (1988) found that people with ASD better than controls at matching inverted, upside down faces (configural v holistic processing). NT people are better at processing faces the right way up but this effects is not seen in children with ASD. A reason for this is that, the feature (and configural) local elements are not as disrupted when they are turned upside down. Whereas the global elements are very disrupted when we turn them upside down.
Do individuals with Williams syndrome show preserved language skills?
Early accounts of WS proposed that language is preserved (Bellugi et al, 1988, 1997). People believed the WS had a completely preserved language module, although they are really damaged globally intellectually. There was a study which asked WS to describe animals/creatures and the children were coming up with very obscure animals which resulted in people believing they had wide verbal categories etc. Once tested in larger groups with proper standardised language testing they found that its not the case at all. In a standardised language test of hundreds of children, 85% of TD 5 year olds will know this word. Therefore, we are using these measures that are really well developed. Later research revealed there is a delayed development of vocabulary and comprehension, a delayed & atypical grammatical skills (use of past tense and irregular verbs), atypical development of categorisation and delayed development of phonological segmentation (being able to segment words quite well is a real building block of development of language).
DS and WS show atypical perceptual processing, executive functions & language.
In WS, their spatial processing is so impaired, they can’t even make a square with the four blocks. The DS have made the global shape of the square but they have been very insensitive to the internal features. In the Navon task (D made of lots of little Y’s), a child with WS is good at doing the y’s/the local features but there are really bad at doing the global features. However id DS, there is only global features. Therefore, there is a really different pattern of perceptual processing here. Is the featural processing bias like what is seen n ASD? A child with ASD can do the block design test and its been hypothesised that its because they are local processers. But to get a score on WASI block design, they have to make it and do it in time, ASD always get the blocks back together again in time. Therefore, it can be argued that they do well because they have a local bias but they don’t have any problems putting it back together again because if they did they wouldn’t get a good score on this test. Thus they display a global ability? The local bias in WS compared to DS is qualitatively quite different.
Multifactorial Explanation for what causes these difficulties in WS. Farran & Jarrold, (2005) found that 11–33 yr old individuals with WS are poor at encoding spatial relations between local elements (they may have the local elements but working out how they are put together is very difficult). People with WS, do not use typical mental rotation strategies (Farran et al, 2001), this has implications for the block design task as it has different sides with different patterns. Instead, they rely on manual manipulation of blocks resulting in slow performance.
DS and WS show impairments in emotion recognition and ToM and engage in increased social approach, possibly linked with poor response inhibition
Porter et al (2007) investigated different explanations for atypical social approach in DS and WS. Indiscriminate approach seen in DS and WS is also seen in people with acquired amygdala damage and acquired frontal lobe impairments. Hypothesis 1: Atypical social approach in WS & DS may be due to poor emotion recognition reflecting abnormal amygdala functioning. Hypothesis 2: Atypical social approach in WS & DS may reflect poor control of behaviour reflecting a frontal lobe abnormality. Hypothesis 3: Atypical social approach in WS & DS may a heightened salience for social stimuli. In this particular study, there are 20 participants with WS CA: 5.33 – 43.67: MA: 3.58 – 6.41 (general cognitive ability). There are 20 participants with DS CA: 5.75 – 40.75: MA: 4.00 – 6.16 and 40 TD controls matched on gender, CA and MA to DW and WS participants (at least they have some older people in their study too). They looked at emotion recognition abilities and the relationship with social approach. They found that William syndrome abilities, were the same as the MA matched controls, so they had developmental delay. Looked at emotion recognition abilities and their relationship with social approach: WS abilities commensurate (corresponding in size or degree) with MA, DS below mental age (e.g. VMA came out at 4, they were worse than an average 4 year olds). They also showed a tendency to report negative emotions as positive. DS particularly marked difficulties recognising sad emotions in general and were significantly poorer than WS participants in recognising sad paralanguage. Domain general problem with those negative emotions.
ZELAZO et al (1996) tested TOM in adults with Down Syndrome (mean mental age: 5.1 yrs) and non-handicapped MA matched pre-school children. DS participants showed poorer performance on several standard TOM tasks. He also looked at whether or not they were showing corresponding deficits on an EF task: colour-shape card-sorting task (EF) in which subjects were required to switch between two incompatible sets of rules. There appeared to be a kind of ink between difficulties on these EF task that seemed to be related to difficulties in ToM. Intuitively social behaviour feels very different to other types of cognitive behaviour but this is suggesting that they are very linked.
How do children with Williams and Down syndromes differ? Illustrate your answer by referring to experimental studies directly comparing the two groups.
D’Souza et al., (2015) Studied infants with WS (28m), DS (30m) and TD (14m) (all with MA 14m – Bayley scale of infant development which looks at many different aspects of development). Infants were familiarized with a schematic (cartoon) face, after which they saw a novel face in which either the features (eye shape) or the configuration of the features were changed. Even by this stage of development, the TD infants sensitive to featural and configural change (specialised face processing here), WS only sensitive to featural change (visual spatial problems seemed to be impacting at this stage) and the DS infants looked at both types of stimuli at levels that didn’t differ from chance (the experimental paradigm could not elicit anything from the DS because they were not showing any kind of patten that a could be measured). This suggests syndrome specific differences in early face processing between TD and WS and TD and DS and DS and WS.
Annaz et al., (2009) (look at this paper because she uses a different kind of methodology) talks about modularisation, in that, its a developmental process to become modularised. In this study they used cross-sectional trajectory analyses to test part-whole face perception in groups of children (around 8 years) with WS, DS, HFA, LFA & TD. Assessed changes in part-whole face perception that relate to age, mental age, face face recognition ability etc within different diagnostic groups. All children completed tests of receptive vocabulary, pattern construction and facial recognition. When a TD child has got these skills on face perception and pattern construction this is what their face processing is going to be like. Therefore, you can look across these different tests to see if there is something quite strange going on in terms of the links between cogntiive mechanisms.
The Experimental Paradigm (Annaz et al., 2009). There is a Whole-face condition and a Part-face condition. There are upright, 90”orientation and inverted trials that can upside down. The question asks, Which of the lower stimuli matches the upper (target) face? The decision is made on the basis of the features or the global configuration. This is the Benton face recognition task with frontal and different orientations yet the WS performed as well as TD controls (the study from when they are two in which they are showing abnormal facial processing, by 8 there are showing normal facial recognition as TD), HFA, LFA & DS performed more poorly than TD controls, HFA performed at higher levels than LFA (SS) and DS and the DS and LFA did not differ. The experimental results of the HFA group (on some trials they need to make a judgement on just the eye or the whole face and the face were in different rotations and were inverted), therefore, its the pattern of performance across these different conditions thats going to be important. The HFA group did not have a problem when the faces were turned upside down as do TD, and that they are much more interested in features, weak central coherence and enhanced perceptual functioning theories. Normal part/whole effect but performance did not reliably decrease on inverted stimuli conditions Results across tasks suggested that good levels of face recognition (on the Benton test) could be delivered by a system that is insensitive to the orientation of faces (on the part–whole task). If the object recognition system has greater feature-based sensitivity in ASD than In TD, it may be able to support an adequate level of the within-category discrimination that is required for face recognition. Therefore, they are using different mechanisms, this is true for language in ASD where the trajectory is qualitatively quite different. In WS performing as well as TD children on Benton test face recognition and are looking normal. But they showed really different underlying processes: WS group did not show an emerging inversion effect for whole faces although they did show an emerging inversion effect for part-face discrimination. Therefore the WS group are relying on different components of the faces in be able to achieve the task, in the same with that the ASD people are although they are not compensating as well as people with WS. The DS group performed as poorly as LFA on face recognition task (Benton) and they differed from TD and other groups in discriminating features better when they were presented in whole faces than when they were presented in isolation (drawing of a house was all outline/ navon figure was a large letter/ global). Therefore the pattern is the sam in processing faces as has been found when processing non-social stimuli in DS. Results suggested poor featural processing in DS. Global style may reflect poor processing of local elements.
Evidence shows that disrupted abilities are often down-stream effects of unique syndrome specific developmental trajectories IMPORTANT TAKE HOME MESSAGE
In a study by Bertrand et al. (1997) who compared children in study 1 with WS (9-10yrs) to chronological aged (CA) matched and mental ages (MA) matched controls on object drawing task. In a second study, they compared TD children of 4yrs, 5yrs, 6ys, 7yrs on an object drawing task. They were looking at the development of TD children of being able to draw objects. In the first study they found that children WS produced fewer recognisable drawings the CA and MA age matched children. WS included fewer major parts of each object in their drawings than CA and MA matched, WS drawings were more disorganised than CA matched but not significantly different to MA matched. Therefore WS are not developing completely normally on these components but on this component they are looking like children that have the same level of language or have the same MA. They also found that typical 4-yr-olds produced fewer recognisable drawings, with fewer major parts and higher levels of disorganisation than older age groups. This is suggesting that what is seen in WS is quite characteristic of what is seen in younger children. Typically developing children go through the local processing before global processing. If children are compared with MA controls and they are performing in a similar way, then these children are ‘developmentally delayed’ if they are much worse than MA matched children then they have a deficit. There needs to be a distinction between delays and deficits. In study 2: Children with WS show similarities to TD 4 yr olds thus a DEVELOPMENTAL DELAY, but children with WS show more serious disorganisation of drawings than TD 4 yr olds thus a ATYPICAL TRAJECTORY (deficit in global processing abnormalities in WS).
Its important to think about trajectories in NDD. Couzens et al., (2011) Block Design performance in DS is qualitatively different to that of TD people. DS showed a rapid improvement from 4 to about 8 yrs then gradually increases until around 30 yrs. TD performance declines in early adulthood. Gibson et al., (1988) suggested rapid decline in BD performance during 4th decade in DS but not in Intellectual Disability. In ASD trajectory, there seems to be a decline in memory for words in ASD in older people, the control group was carefully matched on a 1-1 basis with the ASD people which worked because they were HFA and had easy profiles. She found that in the TD group memory increased in comparison to the sharp decline of the ASD group.
We do know that studies comparing groups with DS and WS all show that figure copying is superior in DS who are nothing like as impaired as children with WS.
Executive Functions: In a study by Constanzo (2013) who matched compared WS and DS with TD children on Executive Function Tasks. They compared 15 participants with WS (CA = 10–35), 15 participants with DS (CA 8–21) and 15 TD children (CA = 7.4). As there are very few people with WS they take any age. Furthermore, they are also matched on mental age. They looked at attention, memory, planning, categorization, shifting and inhibition. When a person is participating in the Wilcokson Card task for example, they have to change ‘set shift’ quickly. People with executive problems will continue sorting by previous rule for quite a while before they can re-update the rule. Costanzo (2013) found that both groups showed impairments in auditory sustained attention, visual selective attention, visual categorization (visual fixation, poorly modulated eye gaze) and working memory. They found that DS were poor in shifting and verbal aspects of memory (they are not good at set-shifting and they have problems with language). The WS were specifically poor in planning. WS were stronger than DS in visual sustained attention, verbal categorization and verbal inhibition. There WS do well on things, it often has a verbal component, which is a relative strength for them in comparison to their visual spatial ability. This is not see in DS.
Rather than having a group with a massive age range and comparing them with a group of little children, Carney, Brown & Henry (2013) used regression techniques rather than relying on MA (much younger) matched control group. They looked at EF and focussing on areas that we know are particular problematic both disorders: Visuospatial (WS weakness) and verbal (DS weakness) tasks used to probe executive- loaded working memory (ELWM), inhibition, fluency and set-shifting. They saw executive functioning deficits (compared to TD participants) were observed in both groups but they say a level of syndrome specificity. Children with neurodevelopmental disorders do not show the same patterns on test of executive functions. There were WS-visuo spatial difficulties, on tests of Executive loaded working memory and fluency, thus we can see where its impacting. In DS, there were relative verbal difficulties in the domain of set-shifting (delayed language processing system will affect card sorting etc.). But results also suggested that its not incredibly clear how it pans out with executive functions, there is not a constant manifestation of visual-spatial processing across executive functions task and equally the same for DS.
Language acquisition in the early in TD children
Expressive Language (spoken) and Receptive Language (comprehension) is acquired automatically in typical development. Early non-verbal social/communication skills are incredibly important in the development of language (joint attention). This will slow up language accusation if we do not see the normal onset of joint attention. Problems in auditory perception and phonological processing and/or problem in short-term auditory memory which will impact on the ability to learn long words. Interactive Specialisation Model Interaction of a number of brain regions to produce specialised responses to particular kinds of stimuli (Johnson, 2011). Atypical skills in Neurodevelopmental Disorders reflect constraints on cognitive and linguistic development which predicts a different kind of trajectory thats not necessarily a deficit or an area of spared function but a different developmental pathway to acquire a skill.
Discussed modular and neuro-constructivist accounts of development in context of language: Pam argues we should think in this way.
Karmiloff-Smith (1998); Different trajectories “Development itself is the key to understanding developmental disorders”. These disorders are very dynamic in the way it changes over time. Bellugi et al (2000) WS ‘the general cognitive impairment seen in adolescents and adults with Williams syndrome stands in stark contrast to their relative strength in language, their facility and ease in using sentences with complex syntax, not generally characteristic of other mentally retarded groups’. When people first described WS, there was this idea that WS children had a low IQ very similar to DS yet they have these amazing vocabularies and and really good syntax. This was being taken as evidence for modularity of function. Pam’s spokes person: Karmiloff- Smith “It is theoretically misleading and empirically inaccurate to claim that grammar is spared in WS”. Rather than thinking about it in modular terms (unimpaired syntax module). Karmiloff- Smith all aspects of language are the end product of development rather than its starting point. One thing builds on top of each other. Neuroconstructivist account, higher level specialisations such as morphology, syntax, the lexicon and pragmatics are likely to be the emergent product of development rather than its starting state (Karmiloff- Smith, 1992). Methodological issues in WS research Absolute versus Relative Strengths Compared to Visual Spatial skills language is good in WS:
Discussed different language constraints on language development in DS, WS & ASD as there are really quite different
DS: Sticky ear. Phonological memory: There are additional verbal short-term memory problems that cannot be explained by hearing loss or speech production problems. Impairments on non-word repetition task (tam/pennel/doppelate) that are associated with poorer comprehension, reduced MLU and reading problems. Small oral cavity, large tongue, high-arched palate, facial nerves and muscles implicated in DS thus poor speech intelligibility. There is less skilled at speech motor functions and coordinated speech movements involving the lips, tongue. Expressive skills generally more impaired than receptive skills, children understand more than they can say.
Children with WS speak before they point by several months which is extremely unusual. Talking is linked to pointing, infant point and looks at an object and shares attention with someone else. Delays in early language development in WS: Delayed expressive language (Mervis et al., (2003). Comprehension and production of referential pointing gestures and engagement in triadic joint attention does not precede the onset of referential expressive in WS. Onset of referential language precedes the onset of pointing by several months (Mervis & Bertrand, 1997).
Phonological short-term memory: Memory for digits “5,2” “9,2,4,8,3” and Non-word repetition “meb” “teebudieshawlt”. There are higher word and digit span scores in WS than in DS (e.g. Vicari et al., 2004) but severe deficits in phonological ST memory in DS (children with DS have memory problems that are independent of hearing etc.). WS same (or worse) than TD or learning disabled controls matched on overall mental age, nonverbal ability or on receptive vocabulary (e.g. review by Brock et al., 2002). Therefore, a number of studies have found that WS aren’t incredibly impaired in comparison to DS on phonological short term memory. Phonological memory (non-word repetition) significantly associated with vocabulary in WS (Grant et al., 1997). Suggesting that vocabulary is resting on the same skills seen in TD.
According to Udwin & Yule (1990), 37% of a sample of children with WS were hyperverbal, which is an excessive use of stereotyped phrases, over-familiarity, introduction of irrelevant experiences, perseverative responding (keeping on at something past the point when they should). Stojanovik (2006) found that children with WS poorer at providing information or clarification than children with SLI. John et al., (2009) found that hildren with WS weakened tendency to communicate their lack of understanding in conversation. Therefore, there are these breakdowns in communication that can be seen in ASD. You may say something to a child and they may nod indicating they have understood but they won’t tell you that they haven’t understood. Therefore, we are seeing qualitatively atypical language.
For WS, its worth looking at evidence from Neuroscience because its a genetic disorder and there is not the degree of heterogeneity that there is with ASD. In TD children (>9 yrs) and adults, we see different ERPs that show different latency, amplitude and distribution to grammatical function words than to semantic content words. We can see at the level of the brain signature that these are different categories of linguistic information. Adolescents and adults with WS do not show this difference, we are seeing a different pattern of ERP’s to those different categories of linguistic information. Brain activity to language shows normal asymmetries in infancy in WS (it looks as though its developmental as there are no basic problems to start with), but by age 3 – 4 years atypical pattern seen in children and adults is observed (Mills et al., 2003). Therefore, by 3-4 there is already this quite abnormal neural substrate for language. In WS, language system develops along a different trajectory compared to controls. There are one group of very active WS researchers still basically thinking in a very modular kind of way. Pam thinks that the evidence for the neuro-constructivist account, especially this ERP evidence is very strong.
Discussed wide heterogeneity in language and co- morbid language disability in ASD. Exploring subgroups in this group
Older empirical studies of ASD found that 50% of individuals never acquire functional speech, however recent research suggest that around 25% of individuals never acquire speech. There are unbelievably variable language trajectories in ASD, most children with ASD are delayed in reaching early milestones, especially onset of words and phrases. There is some show accelerated language development in 3rd or 4th year. This might be due to the DSM criteria too as a child had to show a really serious language delay at 3 years old, but then sometimes these children began acquiring language really quickly after 3. There would be a child with a diagnosis of Aspergers because they were using 2-3 word phases by 3 and the child with autism that wasn’t using any thus these children looked very different. But a couple of years later there was very little difference in their language because the child was late but showed accelerated language. Thus another reason for looking at different developmental trajectories.
Does not happen that often but can be seen in some children. Some show pattern of regression, they begin to use words at 12–15 months but stop speaking late in the second year (Pickles et al., 2009). Some, but not all, regain language use, but others never speak again. There are potential constraints on language in ASD. Impoverished atypical social interactions because they are not showing these patterns of attention towards other people (e.g. dyadic). Boucher, (2012) called this “self-originating social deprivation” this happens during the period when the foundations of communicative interchange and language are normally established (in the 2nd-3rd year joint attention, using language).
This problem in joint attention affects triadic interactions and ToM. They are really important for enabling us to understand aspects of language understanding cause and effect relationships (e.g. I say something and her face looks sad), metaphorical language, irony, sarcasm etc. all of the kinds of skills developed in the social communication context.
Abnormalities in speech perception shown in experimental studies. The enhanced perceptual functioning model and it suggested that people with ASD are incredibly sensitive to perceptual information. When people with ASD are processing language, they are listening to the psychoacoustic qualities if the speech than NT and there is an increased sensitivity to perceptual (pitch) components of speech (Heaton 2008). There can be a paradigm where children can hear two works, one after another, there can be slight changes to the pitch in the two words. In a large shift, a TD child will hear that easily but as the pitch distance gets smaller, TD children do not hear it at all as they are busy working out the word. But a child with ASD will recognise a small as well as a large pitch difference in childhood and adulthood. This could potentially cause disruption. People with ADS have problems in processing speech in noise. When we are listening to speech in an environment that is really noisy, we look at the person very clearly to disambiguate. Therefore, its confounded with not looking at people for information. However, there is evidence in problems processing speech in noise. There are some basic psychoacoustic abnormalities going on in the way that people with ASD are processing pitch information etc.
Heterogeneity in language subgroups/co-morbidity. Kjelgaard et al (2001) tested 89, 4–14 yr old children (80m/9f) who met DSM-1V criteria for Autistic Disorder. The would probably more impaired than some children who have a diagnosis of ASD now, they certainly would have had language delay. They completed the Goldman-Fristoe Test of Articulation and PPVT and EVT. The did receptive and productive vocabulary to see how many words they know and can produce and what their lower level phonological processing and articulation is like. 90% of the sample could do this two tests. Next there was the CELF (massive battery that looks at all different aspect of language) and non-word repetition task (building up phonemes to see how many you can remember). Only 50% of the sample were able to complete this later task. When testing ASD its important to think about what task they are going to be able to complete, because if they cant do the test you can’t get any information on their language skills.
How do children with conduct problems with and without callous-unemotional traits differ in their presentation of cognitive and affective abilities?
Raine et al (1998) adult offenders, those that have committed an offence in an emotional and impulsive way: These people have decreased prefrontal activity and increased sub-cortical activity (including the amygdala). Essentially, they are very emotional, their brains are working in a highly changed way in terms of emotion processing and not down regulating that effectively. (psychopaths) however, showed more normal prefrontal activity. Raine et al (2002) showed that people with antisocial personality disorder had an 11% reduction in volume in the gray matter in the prefrontal cortex. Raine et al (2007) also showed white matter differences in the prefrontal area in pathological liars (which is a different form of antisocial behaviour). Therefore, to is likely that these issues have come from very early on in childhood.
To grow up with impairments relating to vmPFC means that there may be impairments with decision making e.g. risks behaviour (Bechara et al., 1994). Deficits in emotion processing are also associated to impaired decision making, reflected in behaviours such as risk taking and impulsive behaviours (Bechara et al., 2000).
Hostile Attribution bias by Ken Dodge proposed this social-cognitive mechanism for (aggressive behaviour) understanding antisocial behaviour which is essentially if the world has taught a child that people are out to get them, then thats how they should behave. This is quite an adaptive response. Children are looking out for cues in the environment that aren’t friendly. These are the people that ask a person in a bar what they are looking at when in fact they are looking at nothing, they are looking out for danger in the environment. If these children were at home with aggressive parents and they don’t know when the next hit around the head was coming, its in the child interest to look out for it. A Hostile Attribution is characterised by hypervigilent selective attention to hostile cues, hostile attributions to others’ ambiguous behaviour, favourable evaluations of the likely consequences of antisocial behaviour and a tendency to remember aggressive/hostile acts. Longitudinal work suggests that these biases develop partly as a consequence of adverse early life experiences Dodge et al. (1990), Weiss et al., (1992), Hill et al (2008).
The Hostile Attribution becomes a self fulfilling cycle, a person that behave this way will evoke the same response from other people. Hostile Attributions are also associated with impaired peer relationships and reactive aggression. Children who hold hostile attributions are typically poor at social problem-solving and repeated social failures may bring about the development of negative self- perceptions of competence. Predicts a cycle of hostile attribution leading to aggressive behaviours that decrease opportunities for successful social interactions. Evans et al (2002) suggest that hostile attributions may interfere with normal empathy functioning in a different way to psychopathy (the need to show someone who’s boss who has wronged them). Processing other peoples’ emotions. People that are hypervigilent (history of physical abuse). If these children are shown faces, some that are ambiguous, others are very clear in what emotions they are. If these children who have experienced a lot of aggression their lives are more likely to recognise angry faces (Pollak) even in the ambiguous faces. Children with high CU traits are really poor at recognising or processing stress emotions (fear and sadness in particular), this is true for visual stimuli, vocal stimuli and body postures as well. They are not recognising fear in the environment (Blair & Viding, 2008; Munoz, 2009).
Using the Victim Suffering paradigm previously used by Pardini et al (2003).
Differences of empathy in children with behavioural problems with and without CU traits, children with ASD and TD children. First addressed was children own feelings of emotions, the children were given a little scenario that was either relating to something disgusting, embarrassing, scary or something that would usually make them feel guilty. The children were asked to report how much of the emotion they would feel in this scenario. The high CU group reported feeling much less scared and guilty in most circumstances. Therefore, not only are they poor at recognising fear, they also report not feeling it much themselves either. They also used the paradigm where they asked children to imagine a situation where there is something happening which is a little frustrating and they behave in an aggressive way to get over it “You are really thirsty and need a drink of water. Another boy is drinking slowly at the water fountain and you are thinking about pushing him out of the way so you can get a drink”. In the first section the children were asked what they thought would happen as a result this, will you get into trouble, will you get what you want, will you make that person feel bad, will you make your self feel bad, will you show them who’s boss. Then they were asked: How much do you care about… getting the tangible ‘reward’ as a result of your behaviour, being punished for your behaviour, making the victim feel bad as a result of your behaviour, making yourself feel bad as a result of your action, gaining a sense of dominance (showing your peer ‘who’s boss’) as a result of their actions. In the findings, the expectation section is similar to ToM and the second stage was more affective. The results found that everyone was able to say/understand that if they hurt someone they would feel bad (no group difference).
For both: How much would you care if you felt bad or someone else felt bad? The high CU group in comparison to the other groups do not really care. Interesting, the CD with CU traits never differ from controls on any type of emotion processing task that we did. The psychopaths know that they don’t care, they are also really good at ToM. In a basic ToM task, the first and second order ToM: theres a boy, he has some chocolate, he puts it in the fridge, his sister knows he put in the fridge, he goes and takes it out and hides it. Where does she think it is? She thinks its in the fridge. But on no, she saw him, so where does he think that she thinks that it is? He thinks, that she’s thinks it’s in the fridge because he doesn’t know that she saw him. This study was done with 11-12 year olds, its expected that the ASD group to do be able to do 1st and 2nd order ToM by this time, these are bright kids and they can usually problem solve around ToM problems by this stage. In fact the ASD group did not do this, nor did the control group. The high CU group who had the lowest IQ of the groups too, scored at absolute ceiling, their ToM is impeccable. They can follow other peoples thought processes, they just don’t care about them.
Conclusions: There is a dissociation between the type of empathy deficit in children with CU and children with ASD. Children with CP/CU+ have difficulties attributing feelings of fear and guilt to themselves, Emotion processing and affective empathy deficits were found to be unique to children with CP/CU+, no deficits were observed for children with CP/ CU-, or children with ASD, Cognitive empathy (ToM) deficits were found to be unique to children with ASD, no deficits were observed for children with CP/CU+ or CP/CU-. The data supports the theory that cognitive and affective empathy are dissociable abilities and that children with CP/CU+ and ASD suffer from distinct forms of empathy deficit (Blair, 2005). These findings were replicated by Schwenck et al (2012, JCPP). Further research in empathy and CU have found negative relationship between PCL-R scores and self-report empathy (Holmqvist, 2008). Negative relationship between ‘Empathic Concern’ subscale and CU traits (Pardini, Lochman & Frick, 2003). However, the relationship between emapthy and CU may be mediated by gender and age (Dadds et al., 2009).
