Autism Flashcards
(55 cards)
Broad category of symptoms for ASD no.1- using communication for social interaction- social-emotional reciprocity
Social- emotional reciprocity- refers to back and forth communication- includes exchanges of emotion, gestures and verbal communication w/ others- Reciprocity usually expected in conversation is lacking in those with ASD- often don’t use communication to share interests- usually interaction is one sided- when someone with ASD does attempt to interact- may be innapropriate
Broad category of symptoms for ASD no.1- using communication for social interaction- nonverbal communication
- facial expressions/ body posture= crucial in maintaining social interactions- but someone with ASD- uses eye contact and ‘social smiling’ very little- facial expressions = generally limited or sometimes exaggerated-gestures eg pointing and nodding= used inappropriately- usually issues w/ body posture eg not facing person in conversation- nonverbal signals don’t communicate emotions accurately- may be a poor match between emotion apparently being shown and tone of voice
Broad category of symptoms for ASD no.1- using communication for social interaction- Problems developing and maintaining relationships
People with ASD are said to lack a theory of mind- don’t understand other people have minds- so have trouble seeing world from other people’s perspective- hard for them to change their own behaviour to suit social context as they are unaware of the ‘rules’ or conventions that apply in social situations- so may express emotions inappropriately- eg laughing at the wrong time - or may fail to pick up on nonverbal signals that other people use to indicate discomfort- people with ASD- difficulty making friends- don’t initiate friendships or play cooperatively with other children
Broad category of symptoms for ASD no.2- Repetitive behaviours- repetitive behaviour patterns
People with ASD may use language unusually- may repeat what they’ve just heard- from individual words to longer passages of speech (echolalia)- language can sometimes be bizarrely formal- extremely pedantic (has been called little professor syndrome in past)- movements can be highly repetitive from hand gestures (flicking) to whole body motions (spinning)- objects used in the same way over and over again (lining up toys)
Broad category of symptoms for ASD no.1- repetitive behaviours- Routines, rituals and resistance to change
people with ASD stick inflexibly to routines- carrying out a behaviour eg lining up toys -in step by step sequence-no variation- may engage in verbal rituals- eg demanding others use words in a ‘set’ way- may overreact to changes in routines- rigid thinking patterns of ASD also reveal themselves in distinct preference for ‘literal forms of speech’ eg failing to detect flexible uses of language (irony, sarcasm) or other ‘rule breaking’ forms of behaviour
Broad category of symptoms for ASD no.1- repetitive behaviours- restricted fixated interests
Common feature of ASD is an extremely intense preoccupation with a very narrow interest- eg particular toy or object to the total exclusion of others, or with a topic
Broad category of symptoms for ASD no.1- repetitive behaviours- Unusual reactions to sensory input
Many people with ASD are preoccupied w/ touch, usually aversively eg children who intensely dislike having hair brushed- also may have obsessive interest in movement of objects eg spinning- first response to an object or some cases a person may be to lick/ sniff it- may look very closely at objects for long periods of time but for no apparent reason- will become distressed by some stimuli they’re not used to (eg sounds) yet appear completely indifferent to pain (own and others)
Structure and function in the amygdala
Amygdala is mainly responsible for emotional experience- it is where we identify and react to things that cause us to feel certain emotions eg facial expressions- greatly influences social behaviour- due to this- has been suggested amygdala dysfunction is responsible for many social difficulties of ASD eg abnormal eye contact, difficulties associated with face processing and lack of mental understanding/ empathy
Amygdala development in ASD
From age 2- larger than normal growth in amygdala’s volume in children w/ ASD about 6-9% Children w/out ASD- amygdala volume increases w/age but not until they’re older- late adolescence- no difference in amygdala volume between people w/ASD and w/out key difference is that growth in volume occurs earlier in children w/ASD- unusual pattern may result in less neurons later in life- damaging its functioning- larger amygdala growth= more social and communication impairments
Amygdala dysfunction theory
Brothers (last name) called amygdala the ‘social brain’ in humans because of its central role in influencing social behaviour - Baron-Cohen carried out ‘the eyes task’- investigate the links between this impairment and amygdala dysfunction- ppts w/ASD performed significantly worse than the controls - fMRI scans showed that during this task- left amygdala wasn’t activated in ASD ppts at all- but was strongly activated in the controls- suggests amygdala is involved when we infer other’s emotional states from facial expressions-function= impaired w/ those w/ASD
Amygdala eval - supporting evidence
Baron-Cohen- eye test- individuals cannot detect facial expressions when shown in eye area only- fMRI scanner- left amygdala not activated at all in ASD but was for controls- supports fact that ASD individuals have a dysfunctional amygdala- particuarly left- left amygdala- detects other’s emotional states from facial expressions- impaired in ASD- therefore supporting the amygdala dysfunction theory
Amygdala eval- Reductionist
Amygdala- part of limbic system- alone not enough to explain social deficits in ASD- Paul et al- studied 2 women (1 was SM)- had damaged both amygdala- damage confined to amygdala- didn’t greatly affect surrounding areas- these women showed signs of impaired social behaviour- but impairment= nowhere near as extensive as found in clinically diagnosed ASD- shows how complex regulation of social behaviour is and role of the brain in ASD= complex- risks= oversimplified by focus on just the amygdala- Nordahl also found those w/ weakest neural connectivity between brain areas have most severe autistic traits- amygdala not working alone
amygdala eval- cause or effect
Dysfunctional amygdala has been linked to many conditions eg anxiety and bipolar disorder- makes it difficult to say how region may uniquely explain autism traits- amygdala= known to play crucial role in regulating fear/ anxiety related behaviour- Ollendick- pointed out anxiety is commonly reported- suggests indirect link between amygdala function/ social behaviour impairments by abnormal processing of anxiety- perhaps abnormal amygdala causes anxiety -causes social difficulties in ASD - suggesting it is a direct cause- this is a more complex explanation than conventional amygdala dysfunction theory needs to be established whether amygdala dysfunction is cause or effect of ASD
amygdala eval- method issues
Objective and scientific explanation - use of brain scans (e.g. Baren-Cohen, 1999 used fMRI scan to carry out ‘the eyes task’). High validity - compare amygdala activity using scientific measurements. Amygdala dysfunction can explain social & communication impairments but is less successful in accounting for non-social features of the disorder - repetitive behaviours & obsessive interests
Bio genetics- twin studies
Bailey et al (1995) conducted ‘The British Twin Study’ and found the following concordance rates: MZ twins: 60% DZ: 0% Wider definition of autism (broader autistic phenotype) found the following concordance rates: MZ: 92% DZ: 10%
Bio genetics- family studies
Considerable evidence suggests clinically diagnosed ASD runs in families. Szatmari (1999) - Calculated ‘overall sibling risk’ i.e. the proportion of siblings of people diagnosed with ASD who also have ASD. FINDINGS: 2.2% risk if you have siblings with ASD 0.11% risk if you have NO siblings with ASD 20 times greater risk of developing ASD if your sibling has it.
bio- simplex and multiplex ASD
Bernier et al (2012) Multiplex ASD/Multiplex families – more than one member has ASD/autistic traits not diagnosed as ASD ASD caused by inherited genetic variations. Simplex ASD/Simplex families – only one member has ASD ASD has ‘de novo’ (a new) genetic causes
Simplex and multiplex p2
Sebat et al (2007) ‘ De Novo’ Genetic mutations occur when sequences of DNA are deleted/duplicated as the ovum is fertilised by the sperm. This mutation is then replicated across all cells during cell division. This affects multiple genes known as copy number variations (CNVs). De Novo CNVs account for 10% of ASD diagnoses. More likely to happen when parents are older – age of parents is a risk for simplex ASD.
Bio exp- supporting evidence
Bailey’s twin studies- describe- not 100% has to be other explanations- also 0% question validity of genetics in development of ASD as DZ twins still share 50%
Genetics- reductionist
Focus on nature- ignores nurture- ASD also linked to environmental factors eg exposure to environmental or prenatal factors (Landigran 2010) Child may have a predisposition to ASD through genes but may only develop it if they experience a trigger (diathesis) Genetic explanation is incomplete in order for a more holistic explanation of ASD- genes should be considered alongside environmental- supporting diathesis stress exp
Genetics- cause or effect
Exp relies on heritability studies- so difficult to establish cause and effect when using non experimental methods- Szatmari’s research showed that if you have sibling with ASD other sibling is 20x more likely to have ASD- but closely related family members are more likely to live with each other- so shared environment rather than genes could be the cause of the high concordance rates - adoption studies need to be considered - separate out nature and nurture
Genetics methodological issues
Positive applications- potential to predict ASD in young children or foetuses by screening for certain gene variants - aim to make earlier diagnosis more reliable - avoid long processes of waiting for ASD diagnosis/ put interventions in place - But very large no.s of candidate genes linked to development in autism- poses practical issues as it’s unlikely genetic tests will be able to screen for so many candidate genes w/ high degree of occurence- tricky to decide which genes to target in potential therapies
Individual exp - Theory of Mind
Baron-Cohen (1995) – ‘TOM & ASD’ People with ASD don’t have a fully functioning ToM. They have ‘mindblindness’ (reduced ability to understand mental states of others). Core deficit of ASD - leads to difficulty understanding people and social difficulties.
Precursors to ToM
We aren’t born knowing that others have beliefs and desires that are unique from our own. There are several precursors (or skills) that infants need to develop their theory of mind. ntentionality – key skill for ToM. People act according to things they want - actions are goal directed E.g. reach for an apple - infer they are hungry. Go back inside the house after walking through the door - infer they have forgotten something