Combining neurophysiology and biomechanics to delineate post-stroke gait impairments
结合神经生理学和生物力学来描述中风后步态障碍
基本信息
- 批准号:10599625
- 负责人:
- 金额:$ 38.82万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2020
- 资助国家:美国
- 起止时间:2020-08-01 至 2025-07-31
- 项目状态:未结题
- 来源:
- 关键词:Abnormal coordinationAddressAffectAgeBehaviorBeliefBiomechanicsComplexComputing MethodologiesCouplesCouplingDataDevelopmentEducational InterventionExhibitsFinancial compensationGaitGoalsH-ReflexHip region structureHomosynaptic DepressionHumanHyperactivityHyperreflexiaImpairmentIndividualIntelligenceInternetInterventionKneeKnowledgeLeadLinkMethodsModelingMotionMotor NeuronsMuscleMuscle WeaknessMusculoskeletalNervous System TraumaNeurologicNeuronal PlasticityNeurotransmittersOrthotic DevicesPathologicPatternPelvisPeripheral Nerve StimulationPersonsPhasePhysical therapyPlant RootsProceduresProtocols documentationReflex actionResearchRoboticsRoleSelf-Help DevicesSoleus MuscleSpinalStimulusStrokeTechniquesTestingWalkingWorkabnormal reflexbaseclinically significantconditioningconventional therapyexoskeletonexperienceexperimental studyfemoral nervefootimprovedinnovationkinematicsmultidisciplinarymultimodalityneuromuscularneurophysiologyneuroregulationnovelnovel strategiespost strokepresynapticpreventquadriceps musclerectus femorisrelating to nervous systemresponseside effectspinal reflexstemstretch reflextargeted treatmenttreatment planningworking group
项目摘要
PROJECT SUMMARY
Following stroke, numerous impairments develop that affect walking ability. We lack a clear understanding of
what characterizes these impairments and their relation to impaired walking ability. For example, we applied
exoskeletal knee flexion to assist those with reduced knee flexion post-stroke. The assistance improved knee
flexion but surprisingly worsened compensatory motions such as hip abduction. Preliminary analysis indicated
that the assistance elicited hyperexcitable quadriceps reflex activity. Additionally, the quadriceps response was
abnormally coordinated with hip abductor muscles only in post-stroke individuals. These results question
traditional beliefs regarding which motions are compensatory and which are due to neural impairment. Thus,
the critical gap to restoring functional gait post-stroke is characterizing the interconnection between
biomechanical issues and neural impairments. Our novel approach is to combine state-of-the-art methods in
biomechanics and neurophysiology to develop cause-and-effect models of the interconnection between gait
kinematics, hyperexcitable reflex activity and abnormal coordination. The clinical significance is the
groundwork for targeted interventions such as reflex modulation and neurally intelligent exoskeletons that
interact with the impaired spinal circuitry. It will be shown in our preliminary work that we have years of
experience characterizing post-stroke gait impairments using reflex stimulation, robotics and computational
methods that uniquely qualify our group for this project.
The objective of this proposal is to establish the biomechanical and neurophysiological mechanisms
underlying pathological gait post-stroke. In Aim 1, we determine whether hip abduction is a compensation for
reduced knee flexion by comparing people with stroke to induced similar walking patterns in healthy
individuals. Muscle activation patterns and intralimb coordination will provide evidence towards fundamental
differences in neural control after stroke. In Aim 2, we use reflex neurophysiological methods to probe post-
stroke individuals’ reflex coordination patterns. We expect to find that hyperactive quadriceps reflexes are
associated with impaired knee flexion. We additionally expect to show the interrelation between reflex activity
in the quadriceps and the abductors as predicted by our models representing abnormal coordination. In Aim 3,
we use reflex conditioning protocols during gait based on sophisticated paired peripheral nerve stimulation
techniques. These methods will provide evidence of the spinal mechanisms at the root of abnormal reflex
behavior that likely underlie impaired gait post-stroke. Together this comprehensive testing procedure
incorporates biomechanics and neurophysiology to reveal new knowledge of post-stroke gait impairment.
These results will have broad impact on our understanding of neuromuscular impairments and enable the
development of targeted therapies for treatment.
项目概要
中风后会出现许多影响步行能力的损伤,我们对此缺乏清晰的认识。
这些损伤的特征及其与步行能力受损的关系例如,我们应用了这些损伤的特征。
外骨骼膝关节屈曲可帮助中风后膝关节屈曲减少的患者改善膝关节。
初步分析表明,屈曲但代偿性运动(例如髋部外展)令人惊讶地恶化。
援助引起了股四头肌反射活动的过度兴奋。
仅在中风后个体中与髋关节外展肌的协调异常。这些结果存在疑问。
传统观念认为哪些运动是代偿性的,哪些运动是由于神经损伤造成的。
中风后恢复功能性步态的关键差距是表征之间的相互联系
我们的新颖方法是将最先进的方法结合起来。
生物力学和神经生理学开发步态之间相互联系的因果模型
运动学、过度兴奋的反射活动和异常的协调性具有临床意义。
为反射调节和神经智能外骨骼等有针对性的干预措施奠定基础
与受损的脊髓回路相互作用,我们的初步工作将表明我们有多年的经验。
使用反射刺激、机器人技术和计算来表征中风后步态障碍的经验
使我们团队有资格参与该项目的独特方法。
该提案的目的是建立生物力学和神经生理学机制
在目标 1 中,我们确定髋部外展是否是中风后的一种代偿。
通过比较中风患者来减少膝关节弯曲,以诱导健康人相似的步行模式
肌肉激活模式和肢体内协调将为基础提供证据。
在目标 2 中,我们使用反射神经生理学方法来探讨中风后神经控制的差异。
我们期望发现中风个体的反射协调模式是过度活跃的股四头肌反射。
我们还希望显示反射活动之间的相互关系。
正如我们的模型所预测的,在目标 3 中,股四头肌和外展肌中存在异常协调。
我们在步态期间使用基于复杂的配对周围神经刺激的反射调节方案
这些方法将为异常反射根源的脊柱机制提供证据。
综合测试程序可能会导致中风后步态受损。
结合生物力学和神经生理学,揭示中风后步态障碍的新知识。
这些结果将对我们对神经肌肉损伤的理解产生广泛的影响,并使
开发针对治疗的靶向疗法。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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{{ truncateString('James Sulzer', 18)}}的其他基金
Combining neurophysiology and biomechanics to delineate post-stroke gait impairments
结合神经生理学和生物力学来描述中风后步态障碍
- 批准号:
10222742 - 财政年份:2020
- 资助金额:
$ 38.82万 - 项目类别:
Combining neurophysiology and biomechanics to delineate post-stroke gait impairments
结合神经生理学和生物力学来描述中风后步态障碍
- 批准号:
10052892 - 财政年份:2020
- 资助金额:
$ 38.82万 - 项目类别:
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