Abstract
Introduction: There is growing appreciation for the extent of bidirectional plasticity between the brain and body in response to behavioural and pathologic physiological activity. In individuals with a history of traumatic anterior cruciate ligament rupture (ACL), we recently demonstrated lateralized homotopic alterations in sensorimotor cortical thickness and white matter microstructural connectivity that corresponded to skeletomotor functional deficits1. Our findings suggest corticomotor involvement in loss of function after injury.
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