There is a fundamental gap in our understanding of how long-latency stretch reflexes (LLSRs) contribute to the control of multijoint posture and movement in the human arm. This is an important problem because many neurological disorders impair stretch reflexes, resulting in well-documented motor dysfunction. Attempts to enhance motor function through a modification of reflex behavior have been largely equivocal, however, due at least in part to the unknown relationships between specific reflex subtypes and motor abilities. Our central theme is that much of the gap can be filled by considering the pathways that contribute to LLSRs and their specific, context-dependent contributions to motor function. LLSRs contain at least two key behavioral compo- nents: stabilizing reflexes, contributing to posture regulation, and triggered reactions for the rapid release of planned actions. We have shown that these behaviors are mediated by separate pathways and that their relative importance depends on the task performed. Our recent work focused on the stabilizing component of the LLSR. Here we propose to investigate triggered reactions. Our central hypothesis is that triggered reactions can act independently from stabilizing reflexes, based on our preliminary data demonstrating that stabilizing LLSRs are lost following stroke but that triggered reactions are spared. Importantly, our data also suggest that appropriately triggered reactions increase speed and coordination in stroke subjects, potentially forming the basis for effective rehabilitation. First, however, we must clarify the LLSR role in controlling unimpaired posture and movement, and its integrity and function following stroke.
Our Specific Aims are: 1) to determine if stabilizing reflexes and triggered reactions are controlled independently; 2) to determine how uncertainty affects the planning, execution and efficacy of triggered reactions; and 3) to determine how brain injury due to stroke im- pairs stabilizing stretch reflexes and triggered reactions. The first two aims focus on the behavioral relevance of triggered reactions, and will be completed in unimpaired subjects using a 3D robotic manipulator to charac- terize LLSRs during the key transition from maintaining arm posture to initiating a reach.
Our third aim will be completed in stroke subjects and age-matched controls. It parallels the first two aims, but also will use diffusion tensor imaging (DTI) to quantify lesions in the descending pathways thought to regulate the stabilizing and triggered components of the LLSR. The contributions of this research will be a clear description of the role of triggered reactions in the control of movement, how that role is integrated with posture-stabilizing components of the LLSR, and how the LLSR is impaired following stroke in relation to the neural pathways contributing to it. With this refined understanding, we hope to lay the groundwork for using triggered reactions in rehabilitation training paradigms aimed at enhancing the ability to voluntarily initiate appropriate motor patterns at appropri- ate latencies in stroke survivors.
We propose to investigate the planning, execution and efficacy of long-latency stretch reflexes in the coordination of multijoint posture and movement, and to link the specific behaviors that can be attributed to this important motor response to correspondingly specific neural structures. This work is relevant to public health because many neural disorders such as stroke, spinal cord injury, Parkinson's disease and cerebral palsy result in impaired stretch reflexes that have been associated with motor disability. Our work will provide a mechanistic basis for understanding these impairments and may lead to enhanced, subject-specific paradigms for enhancing movement initiation and coordination in this population.
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