Mechanisms Impairing Finger Extension Following Stroke

描述（由申请方提供）：本研究的目的是描述卒中后手指伸展的特征。许多潜在的机制已被牵连在慢性损害的手。然而，这些不同机制对损伤的相对影响尚未完全阐明，因为即使对健康手的理解也仍然不完整。特别令人感兴趣的是，与屈曲相比，手指伸展的损伤相对较大，因为这种不对称性可能有助于我们更好地了解中风后发生的变化。因此，提出了以下目标： 1.检查关节疼痛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帽，一个连接到手指指骨背侧的腱膜。给定肌肉的激活（或丧失）的影响很难预测，特别是当手指姿势改变时。对于本研究，将创建伸肌帽的有限元模型，以量化传递至手指的力。手指姿势对伸展生物力学的影响将与肌内电极记录的神经激活模式的影响进行比较。所开发的模型将用于估计目标2和3中衡量的变化的影响。2.比较中风后心脏机械组织的变化。观察到的手指扭矩产生的无力可能归因于肌肉和软组织的变化。关节阻抗增加或不对称肌肉萎缩可能会使手指伸展相对更加困难。对于本研究，将使用系统识别技术对卒中幸存者进行被动关节阻抗评估。将使用磁共振成像（MRI）和超声技术测量萎缩。 3.检查中风后的神经激活模式。伸展缺陷可替代地或另外具有神经起源。手指屈肌的过度共激活和/或主动激活手指伸肌的能力降低可能导致手指伸展受损。虽然过度的手指屈肌共激活已被证明中风后，特别是在其他肢体的肌肉激活，它还没有确定这种增加是否是皮质介导的。对于本研究，将使用功能MRI检查手指、手臂和腿部伸展/屈曲期间的皮质活动。将通过肌电图评估自主激活肌肉的能力。自愿激活信号将与那些从电刺激的支配nerve.Chronic障碍手指伸展是最常见的缺陷半球中风后，功能，就业和生活质量的影响深远。然而，它的起源仍然不完全清楚，因为一些机制可能会导致潜在的相互冲突的治疗。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进行手部康复。

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.