In this study we aim to explore the underlying mechanisms behind the loss of independent joint control after stroke. Despite the debilitating nature of this impairment, a complete explanation for its development remains incomplete. Our hypothesis is that after ischemic damage to the corticospinal tract, contralesional motor cortex and bulbospinal pathways become more heavily relied upon. Here we aim to test this hypothesis using a powerful combination of neuroimaging techniques and robotic devices. We first aim to test the connection between structural losses in ipsilesional corticospinal tract and altered functional connectivity between contralesional motor cortex and brainstem regions. We then aim to connect losses of independent joint control to both corticospinal tract morphology and altered functional connectivity. A confirmation of this relationship would lend support to the hypothesis that damaged corticofugal pathways provide inadequate drive to the paretic limb during increased shoulder abduction, thus explaining the need to utilize contralesional cortex to access bulbospinal pathways. Increased reliance on these bulbospinal pathways can explain the loss of independent joint control. Understanding the mechanisms underlying loss of independent joint control lays the foundation for designing more specific therapeutic interventions for individuals with acute stroke that will reduce the use of the contralesional cortex and thus preserve functional movements such as reaching
|Effective start/end date||1/1/15 → 12/31/16|
- American Heart Association Midwest Affiliate (15PRE22680003)
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