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Amygdala dysfunction AO1
The amygdala is found at the base of the limbic system, and there are two amygdalae – one in each hemisphere. These are the centre of the emotion processing system of the brain, primarily involved in both recognising and experiencing emotion.
It is thought that in autistic individuals, there is rapid and intense growth of the amygdala between 6-12 months old (Dager, 2022 - MRI)
This results in an overgrowth of non-functioning nerve tissue that interferes with the typical functioning of the amygdala, affecting how well it can connect to other areas of the social brain e.g. thalamus and prefrontal cortex
The thalamus has a role in processing sensory information, and the prefrontal cortex with emotion and inhibition of behaviour. Therefore, in individuals with autism, their sensitivities and social brain functioning can becomes affected - leading to difficulties in social situations
Supporting AO3
Nordahl (2012) the amygdala of children with ASD is 6-9% larger from 2 years of age than children without ASD. By late adolescence there is no difference in volume between ASD and non-ASD individuals. Overgrowth disrupts the normal functioning of the brain
Baron-Cohen (1999) used the ‘eye test’ with ASD and non-ASD individuals and found that those with ASD found it hard to choose the correct description of each expression just looking at the eyes. FMRI scans showed that relative to controls, those with ASD had underactive left amygdala functioning (Shows that amygdala is involved in the social brain)
Dager (2022) found that the faster the growth of the amygdala in infancy, the more social impairments in adulthood
Conflicting AO3
Findings about the role of the amygdala are inconsistent. Martha Herbert et al (2003) reported smaller amygdala volumes in children with ASD compared to controls. Casts some doubt on the validity of the amygdala dysfunction theory
Oversimplification of neural factors and the impact of other areas of the brain. Paul et al (2010) studied two women with lesions that were limited only to their left and right amygdalae – an whilst they showed some signs of impaired social behaviour, this was not to the extent found in ASD. Suggests that amygdala dysfunction on its own is not enough to fully account for the features of ASD
Opposing AO3
The theory of mind hypothesis is a cognitive explanation of autism
existence suggests that the biological explanation is too reductionist or incomplete by itself
Usefulness AO3
Offers a potential target for treatment and more research into identifying biochemical differences associated with amygdala dysfunction. There could be the potential for drug-based treatments to impact amygdala misfunctioning.
If amygdala dysfunction is reliably linked to ASD, then this is objective and easy to test, meaning that at the very least it could lead to earlier diagnosis – shortening the ‘diagnostic journey’, which can be drawn out and highly stressful. Allows earlier support to be provided for the individual
Testability
Theory is testable due to objective and scientific brain scans that can gather data upon the structure and the function of the amygdala
However, brain scans (particularly MRI, as used by Dager) can be exceptionally distressing and overwhelming for autistic individuals - might not be a useful option
Conclusion
Research into ASD is socially sensitive – some people with ASD take against the idea that the disorder needs to be ‘treated’ - a biological explanation may lead to biological treatments such as drugs, which imply a ‘cure’. Social control of behaviour vs providing support
ASD as a spectrum disorder with such a broad range of features and behaviours that broad and holistic explanation must be used
development of research research in 2022 suggests that it is particularly overactivity and growth in the right amygdala rather than the left