Biological explanations of autism Flashcards
when does the amygdala develop?
Growth % in ASD?
difference in teen years?
what may the growth lead to?
from 2 years to late childhood.
Nordahl - 6-9% faster in ASD.
No difference in teen years.
lead to abnormalities between neurone in amygdala which may damage functioning in ASD.
what did the Leslie brothers say?
what did baron Cohen stated the amygdala has?
what could abnormal development influence?
the amygdala was part of the social brain.
amygdala has many neural connections with frontal lobe. Any abnormal development in amygdala could influence processes in frontal lobe and lead to social and behavioural deficits like social perception, social behaviour and processing of social information.
when processing social information those with ASD have a limited ability at what?
What task did baron Cohen do?
Processing social information – limited ability of those with ASD to understand facial expressions in others.
‘eyes task’. Photographs of others eyes, all in fMRI scanner. ASD worse. Scan showed left amygdala did not activate at all but strongly activated in control group.
what supporting research is there for amygdala dysfunction?
damage to amygdala but not yet diagnosed with ASD.
Kennedy et al – SM, ‘woman who knew no fear’. Lost function in amygdala due to rare genetic condition. Personal space twice as close. Suggest amygdala crucial role in managing social behaviour so we don’t appear odd or Strange to others.
Animal studies of primates – Brothers, Ring and Kling, Emery et al – cant really generalise to humans. Impossible to communicate with animals. Remove amygdala through psychosurgery.
what contradictory research is there for amygdala dysfunction?
Howard et al – increased size of amygdala in ASD patients, other studies – Pierce et al - show decreased size in ASD patients. Suggests it lacks external reliability – inconsistent.
why is amygdala dysfunction only a partial explanation?
Deficits in communication may not be a direct cause of the amygdala but a 3rd intervening factor. Amygdala dysfunction can’t process fear and anxiety normally. Argued that fearlessness affects social functioning. Too simplistic. Amygdala may alter fear responses which indirectly affect social behaviour.
No evidence to say the amygdala is any more dysfunctional in those with ASD than other brain regions like hippocampus. Too simplistic to focus on one brain structure.
what is a gene made up of?
what evidence is there that ASD runs in families?
DNA that stores information on biological features.
Peter Szatmari - at least partially genetic cause. General population with no family with ASD – 0.11% chance of ASD.
Brother/sister already diagnosed – 2.2%, 20x greater risk of developing ASD.
How much DNA do twins share?
whats the concordance rate?
Monozygotic twins – 100% DNA
DIzygotic twins – 50% DNA
Anthony Bailey et al – Concordance rate for MZ twins 60% for autism (before change to single ASD diagnosis under DSM-5) but 0% for DZ twins.
how does reproduction work?what can occur?
50% from mother and 50% from father. This DNA from each is fused to form a cell – reproduce further to fully from. Random genetic mutations (De Novo) can occur.
what mutation links to autism?
Bernier et al – CHD8 – mutation in this gene have strong likelihood they have autism, gastrointestinal disorders, larger head, wide set eyes. Examined 3,730 children – 15 independent mutations in CDH8 gene. No abnormalities in 8,792, including 2,289 siblings.
whats Fragile X?
symptoms?
cause? %?
ASD can be non-syndromic or syndromic.
Co occur in Syndromic with ASD is Fragile X. symptoms include intellectual disabilities, unusually long face, protruding ears.
FXS is caused by a mutation in the FMRI 1 gene on x chromosome. Around 60% with FXS also have criteria for ASD. FMRI 1 key factor in developing ASD.
what supporting research is there for genetic predisposition?
Colvert et al – 6,423 twin pairs aged 8+ using questionnaires, observations and interviews. Concordance rate for MZ twins – 77-99%. DZ twins – 22-65%. Multiple research methods – triangulation, increase validity. MZ twins higher CR which is expected if genes were cause of ASD.
what contradictory research is there for genetic predisposition?
Hallmayer et al – 192 twin pairs. Results challenged high heritability model of autism estimating to be 55%. Remaining 45% to be environmental.
why is genetic predisposition only a partial explanation?
Cause of ASD cannot be entirely genetic otherwise expect CR to be 100% for MZ. Diathesis stress model? - Landrigan – ASD pre-natal influences. Toxic chemicals and viruses that mother is exposed to when carrying the baby.
what methodological issues does genetic predisposition have?
high CR caused by shared environmental factors. Joseph – differences in CR between MZ and DZ nothing more than environmental differences.
