Hickman, Lydia Jane ORCID: 0000-0002-5658-9446 (2024). Movement and cognition in Autism and Parkinson’s Disease: similarities, points of distinction, and underlying biological mechanisms. University of Birmingham. Ph.D.
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Hickman2024PhD.pdf
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Abstract
An increased prevalence of Parkinson’s Disease (PD) diagnosis is apparent in the autistic (ASD) population. However, genetic studies have failed to provide evidence for a strong link between the two conditions, meaning it may not be the case that autistic individuals are genetically more likely to develop PD. Anecdotally, movement differences in ASD have been likened to those exhibited by individuals with PD. Given that PD diagnosis is primarily movement-based, similarities in ASD and PD movement may explain the increased PD diagnosis prevalence in the autistic population: if it is indeed the case that autistic movement appears parkinsonian, this may facilitate autistic individuals meeting diagnostic criteria for PD. This could have serious implications for the specificity of the PD diagnostic process. With a lack of direct comparison studies assessing behavioural and cognitive profiles in ASD and PD, it is unclear whether quantifiable similarities exist between the two conditions. Extant evidence for a potential overlap between the two conditions relies on the comparison of findings from separate research studies, and thus is limited due to variation in participant demographics and tasks used.
In this thesis I conducted the first direct comparison of behavioural and cognitive profiles in ASD and PD, in addition to members of the general population. Chapter 2 demonstrated many similarities in the kinematic features of animations (free movement) produced by the ASD and PD groups, but only the similarity in jerk between ASD and PD was distinct from performance in the general population. All three groups were additionally comparable with respect to movement-based theory of mind ability. Chapter 3 conducted a more sensitive investigation of autistic and parkinsonian movement using a restricted movement task devoid of theory of mind demands. Here, kinematic features were uncovered that differed between the three groups (e.g., speed modulation, sub-movements and reaction time). This Chapter also determined the utility of movement assessments for classifying group membership, demonstrating higher levels of classification accuracy when trait questionnaires were combined with kinematic features in a range of classification models. This highlights that clinical diagnostic processes may be improved through the incorporation of kinematic assessments.
Alongside providing insight into the behavioural and cognitive similarities between ASD and PD, the thesis presented novel findings with respect to ASD and PD separately. For example, Chapters 2 and 3 conducted the first kinematic assessments of older autistic adults, revealing that some, but not all, components of younger autistic movement remain distinct from non-autistic movement in older age. In addition, the first assessment of individuals with PD on the tasks presented in Chapters 2 and 3 revealed novel kinematic features that differed in this population (e.g., speed modulation), and patterns of movement speed differences between the two Chapters were aligned with the motor motivation hypothesis of PD.
Finally, Chapter 4 investigated biological mechanisms underlying movement differences between the three groups, setting out evidence from two pharmacological intervention studies. Specifically, movement differences resulting from PD dopaminergic medication and the dopamine antagonist haloperidol were explored. These studies implicated dopamine in a range of ASD- and PD-relevant kinematic features, strengthening the proposal that movement differences in ASD and PD are the product of dopaminergic mechanisms. Results across the three Chapters are consistent with hyper-dopaminergic functioning in ASD and hypo-dopaminergic functioning in PD. Overall, this thesis provides a greater understanding of the overlap between behavioural and cognitive presentations of ASD and PD, as well as underlying biological mechanisms which may account for this overlap.
Type of Work: | Thesis (Doctorates > Ph.D.) | |||||||||
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Award Type: | Doctorates > Ph.D. | |||||||||
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Licence: | All rights reserved | |||||||||
College/Faculty: | Colleges (2008 onwards) > College of Life & Environmental Sciences | |||||||||
School or Department: | School of Psychology | |||||||||
Funders: | Biotechnology and Biological Sciences Research Council | |||||||||
Subjects: | B Philosophy. Psychology. Religion > BF Psychology | |||||||||
URI: | http://etheses.bham.ac.uk/id/eprint/14572 |
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