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Characterizing the impact of type-2 diabetes on cortical sensorimotor pathways in chronic stroke : a multimodal neuroimaging study

University of British Columbia

Individuals with type-2 diabetes have an increased incidence of ischemic stroke, and experience higher rates of disability after stroke than non-diabetics. Recent research suggests that type-2 diabetes has adverse effects on neuronal integrity and function, however, to date very little work has examined the interactions of diabetes with chronic stroke recovery. The goal of the present thesis is to address this gap in the literature by employing multimodal magnetic resonance imaging (MRI) techniques to examine the impact of type-2 diabetes on the integrity of surviving sensorimotor neural tissue in individuals with chronic hemiparesis as a result of ischemic stroke. We employ volumetric MRI, diffusion tractography, and magnetic resonance spectroscopy (MRS) to explore the structure of motor and sensory cortex grey matter and white matter projections. We found individuals with chronic stroke and diabetes had lower regional cortical thickness in primary somatosensory cortex, and primary and secondary motor cortices. Contralesional primary and secondary motor cortex thicknesses were negatively related to motor outcomes of the paretic upper-limb in the diabetes group. MRS revealed stroke survivors with diabetes had bilaterally reduced creatine levels in sensorimotor cortex. Diabetes status did not impact gross cortical volumes, white matter volumes, or white matter microstructure in projections from the primary motor and sensory cortex. These results suggest that type-2 diabetes alters cerebral metabolic function, which may result in thinning to sensorimotor grey matter. This work provides preliminary evidence for differential profiles of cerebral recovery from stroke in individuals with diabetes. Given the worldwide increase in the prevalence of diabetes it is critical that we examine the mechanisms of increased post-stroke disability in type-2 diabetes to inform targeted therapies for this population.

Text

2016-04-13

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/57561

Neuroscience

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/