Mechanisms Impairing Finger Extension Following Stroke

描述(由申请人提供)：本研究的目标是研究中风后手指伸展的特征。许多潜在的机制与手的慢性损伤有关。然而，这些不同的机制对损害的相对影响还没有完全阐明，因为对健康的手的理解仍然不完整。特别令人感兴趣的是，与屈曲相比，手指伸展的损害相对更大，因为这种不对称可能有助于我们更好地了解中风后发生的变化。据此，提出了以下目标： 1.检查关节姿势对伸展神经力学的影响。手指伸展是一个复杂的过程，来自5个不同肌肉的肌腱合并形成伸肌罩，伸肌罩是连接到手指指骨背侧的腱。特定肌肉的激活(或丧失)效果很难预测，尤其是当手指姿势发生变化时。在这项研究中，将建立伸缩罩的有限元模型，以量化向手指传递的力。手指姿势对伸展生物力学的影响将与其对肌肉内电极记录的神经激活模式的影响进行比较。开发的模型将用于评估AIMS 2和3.2中测量的变化的影响。2.比较卒中后周围机械组织的变化。观察到手指扭矩产生的疲软可能归因于肌肉和软组织的变化。关节阻抗的增加或不对称性肌肉萎缩可能会使手指伸展相对更困难。在这项研究中，将使用系统识别技术评估中风幸存者的被动关节阻抗。萎缩将使用磁共振成像(MRI)和超声波技术进行测量。 3.研究中风后的神经激活模式。延伸性缺陷可能另一种或另外的神经起源。手指屈肌过度协同激活和/或主动激活手指伸肌的能力降低可能会导致手指伸展功能受损。虽然中风后手指屈肌过度协同激活，特别是在其他肢体肌肉激活的过程中，但这种增加是否由皮质调节尚不确定。在这项研究中，功能磁共振将被用来检查手指、手臂和腿部伸展/屈曲时的皮质活动。自主激活肌肉的能力将通过肌电图仪进行评估。自主激活信号将与通过电刺激神经获得的信号进行比较。手指伸展的慢性损伤是大脑半球中风后最常见的缺陷，对功能、就业和生活质量造成严重影响。然而，它的起源仍然不完全清楚，因为一些机制，潜在的相互冲突的治疗，可能起到作用。从这项研究中获得的知识将有助于通过针对特定区域进行治疗来促进手的康复。

DESCRIPTION (provided by applicant): The objective of this study is to characterize finger extension following stroke. A number of potential mechanisms have been implicated in chronic impairment of the hand. The relative impact of these various mechanisms on impairment, however, has not been fully elucidated, as understanding of even the healthy hand remains incomplete. Of special interest is the relatively greater impairment of finger extension as compared to flexion as this asymmetry may help us to better understand the changes occurring after stroke. Accordingly, the following aims are proposed: 1. Examine Effect of Joint Posture on Extension Neuromechanics. Finger extension is a complex process with tendons from 5 different muscles merging to form the extensor hood, an aponeurosis connected to the dorsal side of the finger phalanges. The effect of activation (or loss) of a given muscle is difficult to predict, especially as the finger posture changes. For this study, a finite element model of the extensor hood will be created to quantify force transmission to the finger. The effects of finger posture on extension biomechanics will be compared with its effects on neural activation patterns, recorded with intramuscular electrodes. The developed model will be used to estimate the impact of changes measured in Aims 2 and 3. 2. Compare Mechanical Tissue Changes in Periphery Following Stroke. Observed weakness in finger torque production may be attributable to changes in muscle and soft tissue. Increases in joint impedance or asymmetrical muscle atrophy could make finger extension relatively more difficult. For this study, passive joint impedance will be assessed using system identification techniques on stroke survivors. Atrophy will be measured using magnetic resonance imaging (MRI) and ultrasound techniques. 3. Examine Neural Activation Patterns Following Stroke. Extension deficits may alternatively or additionally have neurological origins. Excessive coactivation of the finger flexors and/or reduced ability to voluntarily activate the finger extensors may contribute to impaired finger extension. While excessive finger flexor coactivation has been shown following stroke, especially during activation of muscles in other limbs, it has not been determined whether this increase is cortically mediated. For this study, functional MRI will be used to examine cortical activity during finger, arm, and leg extension/flexion. The ability to voluntary activate muscles will be assessed through electromyography. Voluntary activation signals will be compared with those obtained from electrical stimulation of the innervating nerve.Chronic impairment of finger extension is the most common deficit following hemispheric stroke, with profound consequences on function, employment, and quality of life. Its origins, however, remain incompletely understood, as a number of mechanisms, with potentially conflicting treatments, may contribute. The knowledge gained from this study will facilitate hand rehabilitation by targeting specific areas for treatment.