Abstract
Bimanual coordination requires a delicate interplay of excitation and inhibition between the cerebral hemispheres. At the centre of this interhemispheric communication is the Corpus Callosum (CC), a large band of white matter connecting the two hemispheres. The present thesis focused on one aspect of bimanual coordination, an effect known as bimanual cost which is borne out of bilateral inhibition between the primary motor cortices. When one hand moves, the excitation of the primary motor cortex responsible for movement coincides with transcallosally-mediated inhibition of the adjacent primary motor cortex. If both hands move then both primary motor cortices are inhibited by each other, leading to slower hand movement. We demonstrated this effect by showing that participants responding to a stimulus with two hands were significantly slower than if responding with only one hand.
Autistic Spectrum Disorder (ASD), a pervasive neurodevelopmental disorder associated with a deficit in the white matter connecting brain regions such as the motor cortices was also investigated. Our main hypothesis in study one was that participants with ASD would have a smaller time difference between one-handed and two-handed reaction times compared to controls due to a deficit in the white matter of the CC, impairing interhemispheric communication. Contradictory to this hypothesis, we found that bimanual cost was significantly higher in those with ASD compared to controls. These findings led us to the formation of the Competition and Dominance Model (CDM) which stipulates that the primary motor cortices can dynamically exert dominance by transcallosally activating inhibitory networks in the opposing cortical regions. Upstream of the primary motor cortices we also implicated the subcortical thalamus as a mediator that can bilaterally propagate varying levels of activation to support movement onset.
Our behavioural findings and new model explaining bimanual cost then led to the formulation of hypotheses accounting for neuroanatomical differences in the ASD brain. In study two we investigated these differences using Diffusion Tensor Imaging (DTI) to assess white matter and Voxel Based Morphometry (VBM) to assess Grey Matter Density (GMD) of those with ASD. Primarily we hypothesised a deficit in the grey matter of the primary motor cortices in those with ASD compared to matched-controls, and a deficit in the associated white matter connecting the motor cortices via the CC. We also hypothesised that there may be differences in the level of asymmetry between the primary motor cortices, namely that those with ASD have a larger difference in mean GMD compared to matched-controls. Even though the grey matter of the primary motor cortices was significantly different between the two groups, there was no indication that the white matter was significantly disrupted in the group with ASD. In terms of the proposed CDM, we infer that participants with ASD had over developed excitatory networks leading to over inhibition of the adjacent primary motor cortex during bimanual movement. Our results complemented a slowly growing body of literature supporting intact white matter and specific regional differences in the GMD of people with ASD.