Functional connectivity associated with motor recovery after internal capsule lesions

与内囊损伤后运动恢复相关的功能连接

基本信息

批准号：
10612393
负责人：
Shashank Amit Anand
金额：
$ 4.77万
依托单位：
WASHINGTON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-05-01 至 2024-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10612393
关键词：
Acute Address Adult Affect Animals Area Behavioral Bilateral Biology Blood Blood Vessels Brain Cause of Death Chronic Chronic Phase Clinical Collection Corticospinal Tracts Coupled Defect Devices Diffusion Electrodes Endothelin-1 Face Feedback Fiber Functional Magnetic Resonance Imaging Generations Goals Health Human Image Implant Industry Infarction Injury Internal Capsule Intervention Learning Lesion Limb structure Macaca Macaca mulatta Measurement Measures Mediating Medical Modeling Motor Motor Cortex Orthotic Devices Outcome Oxygen Paresis Patients Performance Phase Physiology Primates Quality of life Recommendation Recovery Recovery of Function Rehabilitation device Rehabilitation therapy Residual state Rest Scanning Signal Transduction Stroke Survivors System Technology Testing arm blood oxygen level dependent brain computer interface brain remodeling chronic stroke clinical predictors clinically relevant clinically significant disability efficacy validation functional outcomes graph theory gray matter haptic feedback improved injured insight motor function improvement motor function recovery motor impairment motor recovery nonhuman primate novel post stroke rehabilitation strategy response restoration robotic device stroke recovery stroke rehabilitation stroke survivor stroke therapy tool white matter

项目摘要

Project Summary Stroke survivors face significant long-term health consequences, with rehabilitation being essential to improve their recovery and quality of life. Currently, patients who do not restore motor function after 3-6 months are unlikely to show further recovery. Lesions with white matter tract involvement typically correlate with worse outcomes. For example, corticospinal tract lesions (CST) lesions produce worse motor deficiencies and portend poor functional recovery. Brain-computer interface mediated stroke rehabilitation (BCI-SR) can be a powerful rehabilitation tool. In BCI-SR, a patient learns to modulate localized brain activity that is recorded by electrodes. This can be used to control an orthosis to move the paretic limb. Most BCI systems utilize signals from affected hemisphere, attempting to drive plasticity in injured cortex. However, residual brain function after stroke limits BCI-SR efficacy, making ipsilesional BCI difficult to use in patients with the worst injuries. In humans, contralesional BCI-SR devices have used the uninjured hemisphere to drive further rehabilitation after the traditional plateau in motor function recovery. Clinical predictions of functional outcome after stroke are imprecise. Resting state functional connectivity (rsFC) measures the correlation of blood oxygen level-depending (BOLD) fluctuations at rest across the brain, providing a powerful tool to study brain network remodeling after stroke. However, human studies investigating brain remodeling after a stroke typically include patients with diverse lesions and do not have access to baseline measurements that allow rsFC comparison pre- and post-stroke. Animal studies could address both issues by enabling the generation of replicable, homogenous, and specific infarcts and by allowing collection of baseline measurements prior to infarct generation. There is also an absence of adequate animal studies characterizing rsFC changes associated with BCI rehabilitation strategies. Our project goal is to further characterize rsFC changes associated with CST lesions and test a BCI-mediated rehabilitation strategy after motor recovery plateaus. We will generate uniform lesions in the CST of six Rhesus macaques and after three months of natural recovery, drive contralesional BCI-SR. In each primate, we will collect resting-state functional MRI at baseline before lesioning, after CST lesioning, and during contralesional BCI-SR. We will then identify acute and chronic changes in rsFC that correspond with CST lesioning, innate recovery, and brain-computer-interface mediated rehabilitation. Through these approaches, we seek to validate the efficacy of a novel stroke rehabilitation strategy while providing insight into recovery-associated changes in rsFC.