Autistic spectrum behaviours Flashcards
Describe the characteristics of Autistic Spectrum Behaviours
- Using communication for social interaction; this concerns the difficulties people with ASD have in using communication.
- Social- emotional reciprocity. Reciprocity refers to the normal back-and-forth of everyday communication. If we start a conversation with someone, we usually expect an appropriate response. But this reciprocation lacks in individuals with ASD, so someone with the disorder doesn’t use communication to share their interests/emotions. They don’t imitate social interactions or respond to others attempts. They can’t maintain the normal flow of a conversation. Interaction= one sided.
- Non-verbal communication. Facial expressions and body posture are usually crucial in maintaining social interactions, but someone with ASD uses eye contact and ‘social smiling’ very little. Their facial expressions generally are limited or sometimes exaggerated. Gestures such as pointing and nodded are used wrong. There may be a poor match between tone of voice and facial expressions.
- Problems developing and maintaining relationships. ‘Lack of mind theory’- don’t understand other people have minds, so they have trouble seeing the world from someone else’s perspective. It is hard for them to change their own behaviour to suit the social context. So they are unaware of the ‘rules’ or conventions that apply in social situations. They may express emotions inappropriately. eg, laughing at the wrong time. - Repetitive behaviours.
-Repetitive behaviour patterns. People with ASD may use language unusually. They might repeat what they have just heard, from individuals words to longer passages of speech. Language can be formal. Movements also highly repetitive. eg, hand gestures.
- Routines, rituals and resistance to change. People withASD stick inflexibly to routines, carrying out a behaviour in a step-to-step sequence with no variation. They may over react in verbal rituals, such as demanding that other people use words in a ‘set’ way.
- Restricted and fixed interests. A common feature of ASD is an intense preoccupation with a very narrow interest or topic.
- Unusual interactions to sensory input. Preoccupied with touch, usually aversively. They may have an obsessive interest in the movement of objects, eg. opening and closing of doors. Their first response to an object may be to lick or sniff it. May also become distressed to stimuli they’re not used to.
What is the biological explanation of ‘Amygdala Dysfunction in Autism?’
- Structure and function of the Amygdala.
- The amygdala is a cluster of 13 nuclei in the medical temporal lobe of hte brain. There are 2 of them. One oin each brain hemisphere. It is one of the brains most highly worked structures, with neural connections to the hypothalamus, the prefrontal cortext, the hippocampus ect.. The functioning of the amygdala has a powerful influence on the activity f the brain as a whole and ultimatley o behaviours, particulary those associated with motivation, emotion ad social interactionm.
- Amggdala development in ASD.
- The amygdala develops in differnt ways in children with and without ASD. from 2 years of age, there is a lrger than normal growth in amygdala volume in children with ASD, by about 6% to 9%. In normal chidren amygdala volume increases with age but only when children are older. Meaning, that by the time they reach late addolesence and adulthood, there is essentially no difference in amygdala volume between people with and withou ASD.
- Amygdala dysfunction theory of ASD.
- The amydgala is part of what Leslie brothers (1990) call the ‘social brain; in humans because of its central role in influencing social behaviour. Simon Baron-Cohen and colleagues (2000) applied this behaviour to ASD. They suggested because the amygdala has many neural connections to the frontal cortext, abnormal development of the amygdala in childhood is a major cause of the main social and behavioural defecits found in ASD. One specific instance of impaired social processing in ASD is the diminsihed ability to understand the expressions of emotions in people.
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Evaluate Amygdala dysfunction as a biological explanation for ASD behaviours
- Support from clinical studies.
- Studys investigating ppl w ASD but have experienced damage to one or both of their amygdala. Daniel kennedy and his co-workers (2009) studied the famous case of the women known as S.M. She lost the functioning of both her amygdala due to a genetic disorder. Researchers found that her preffered ‘personal space’ distance for social interaction was half that for mactyhed control pp. Also rater herself ‘perfectly comftarble’ with very close distances. That were voted by controls as ‘ very uncomftrble’. Which supports the amygdala dysfunction theory.
- Inconsistent findings. Studies into the link between amydala volume and the severity of ASD symptoms providing differing outcomes. In adults, some studies showed an increased volume in ASD pp, but others showed decreased. In children, contrary to the findings of Nordhel et al, Martha Herbet et al (2003) reported smaller amygdla volume in pp with ASD compared to controls. Research findings from different age groups= conflicting. The precise role of the amygdala in ASD is unclear. SO= doubles on the validity of amygdala dysfunction theory.
- -Indirect ratger than direct effects. The amygdala is known to play a crucial role in fear and anxiety related behaviours eg, flight/fight. People w a dysfunctional amygdala cannot process fear and anxiety= influences social functioning. Ollendick et al (2009) pointed out anxiety is a commonly reported feature of ASD. Suggesting an indirect link between amygdala function and social behaviour impairments by abnormal processing of anxiety.
- Danger of oversmiplification,
Apply the biological explanation of ‘Amygdala Dysfunction’ to a method of modifying behaviour, using oxytocin.
Oxytocin is a hormone known to be involved in human social bonding. It appears to increase trust, generosity and intimacy and reduce anxiety. It also has an important role in regulating a behaviour commonly impaired in ASD- eye contact.
-Bonnie Auyeng et al, 2015. Tested 32 males with ASD. With a control of 34 male pp.
- Researchers used eye-tracking technology to measure eye-movements of pp during a semi-structured interview. PP were randomly selected to receive an intranasal dose of either oxytocin or a placebo.
- Findings confirmed previous studies in showing that pp with ASD looked significantly less often at the interviews eyes and for less time, than the control. However, pp who were given oxytocin, significantly increased the number of eye contacts and time spent making them compared to the placebo.
What is the biological explanation of ‘Genetic Predisposition’ In ASD?’
-Family studies. There is considerable evidence that clinically diagnosed ASD runs in families. Peter Szatman (1999) combined the data from several family studies to calculate the overall sibling risk. Indicating the proportion of siblings of people diagnosed with ASD who also meet the criteria for ASD. In other words, it is the risk of an individual developing ASD if a sibling has it. In this study the risk was 2.2%. No siblings = 0.11% So if you have siblings with ASD you have 20 times greater risk of developing it yourself.
- Twin studies. Antony Bailey et al (1995) analysed data from the British twin society. The researchers selected pairs of twins where 1 individual from each pair of twins met the diagnostic criteria for ASD. The concordance rate for MZ twins was 60% but 0% for DZ twins. The researchers then looked at a wider definition of ‘autism’ to include social and cognitive impairments that would not necessarily be part of a diagnosis of autism. They found a remarkable 92% concordance rate for MZ twins and 10% for DZ.
- Simplex and multiplex ASD. Researchers noticed that families affected by ASD differ in one significant way. In some only 1 family member has ASD. These ‘one of’ cases are known as simplex ASD. On the other hand, in multiplex families more than 1 member of family has a diagnosis ofASD or several members may have autistic traits; not diagnoses as ASD. An important distinction as it is thought that the mechanism of genetic causation differs. In multiplex families, ASD is likely to be caused by genetic variations that are inherited. Genetic causes of simplex ASD = ‘de novo’ - new genetic mutations that occur when others sequences of DNA are deterred or duplicated as an egg is fertilised by a spurm- mutation.
- Syndromic and non-syndromic ASD. Syndromic is where ASD accompanies another condition which is the main disease
Evaluate Genetic Predisposition as a biological explanation for behaviour in Addiction.
- Research support. Colvet et al (2015) selected twins from the ‘Twins Early Development Study (TEDS)’ Which includes all twins born between 1994 and 1996. Several measures of autistic traits to assess 6000+ twins, 8 and over. Includes questionnaires + interviews. Concordance rates for MZ twins = 0.77-0.99. DZ twins = 0.22-0.65. Researchers are able to calculate estimates of heritability of ASD, ranging from 56% to 95% depending on the measure used.
- Incomplete Evaluation./
Twin studies cannot rule out environmental factors as MZ/DZ twins are usually raised in the same families. The Diathesis Stress model proposes that ASD is covered by genetic preopidisons iand early damaging insult to the brain (stress). Handrigan 2010- ‘Environmental trigers’ Highlights many important triggers, eg, the various toxic chemicals that the developing brain may be exposed to in early pregnancy. In conclusion, genes don’t often complete explanation. More useful to focus on envirometal; factors as we can reduce counteract effects.
What is the individual differences explanation of ‘Theory of Mind’ in ASD?
-what is theory of mind?
Theory of mind is that much social interaction and communicative behaviour requires us to e aware that other people have their own ways of representing the world in their minds, By understanding other peoples internal mental states we can interpret and predict their behaviourr. Possessing this =- TOM.
Simon Baden Cohen (1995) argues that this understanding is impaired in ASD. So people with ASD do not have full functioning ToM. They have reduced or delayed ability to recognise and understand the internal mental states of others.
-Preeuroors to a ToM. A ToM emerges out of skills that usually appear early in development,. These include the ability to follow another persons gaze. A key skill= Ability to establish joint attention. Micheal Scaife and Jerome Bruner (1975) found that typically developing children can do this by 14 months. But, it is impaired or delayed in child with ASD.
- Baren Cohen ‘2 foundation of ToM:’.
- Mental vs Physical; a child is told a story including 2 characters 1 is holding a glass of pop (physical). other is thinking about a glass of pop ( mental). Child responds to various questions about what the characters can do (who drinks the pop?). Correctawnser indicates that the child understands the difference. easy no ASD/Diff w ASD.
- Appearance vs Reality. Typically developing children from about 4 years of age can usually understand that object are not all they seem. eg, bath bomb looks like a cake is not a cake. Children w ASD find this overwhelming.
Evaluatet as an Theory of mind’ Individual Differences explanation for behaviour in ASD.
What is the Individual explanation of ‘Weak Coherence theory’ in ASD?
Evaluate Weak Coherence Theory as an individual explanation for behaviour in ASD
What is the Social Psychological explanation of ‘Emphasising-systemisng theory’ in ASD?’
Evaluate ‘Emphasising Systemising theory’ as a social psychological explanation for ASD
What is the Social Psychological Explanataion of ‘The refrigerator mother’ in ASD?
Evaluate the ‘Refrigerator Mother’ as a social psychological explanation for ASD.
What is the method of modifying behaviour ‘Picture Exchange Communication System’ in ASD?
