Department of Physical Medicine and Rehabilitation, Northwestern University, 355 E. Erie Street, Floor 21, Chicago, IL, 60611, USA.
Single Motor Unit Lab, Shirley Ryan AbilityLab, 355 E. Erie Street, Floor 21, Chicago, IL, 60611, USA.
J Neuroeng Rehabil. 2019 Dec 5;16(1):154. doi: 10.1186/s12984-019-0623-8.
Spasticity, characterized by hyperreflexia, is a motor impairment that can arise following a hemispheric stroke. While the neural mechanisms underlying spasticity in chronic stroke survivors are unknown, one probable cause of hyperreflexia is increased motoneuron (MN) excitability. Potential sources of increased spinal MN excitability after a stroke include increased vestibulospinal (VS) and/or reticulospinal (RS) drive. Spasticity, as clinically assessed in stroke survivors, is highly lateralized, thus RS contributions to stroke-induced spasticity are more difficult to reconcile, as RS nuclei routinely project bilaterally to the spinal cord. Yet studies in stroke survivors suggest that there may also be changes in neuromodulation at the spinal level, indicative of RS tract influence. We hypothesize that after hemispheric stroke, alterations in the excitability of the RS nuclei affect both sides of the spinal cord, and thereby contribute to increased MN excitability on both paretic/spastic and contralateral sides of stroke survivors, as compared to neurologically intact subjects.
We estimated stretch reflex thresholds of the biceps brachii (BB) muscle using a position-feedback controlled linear motor to progressively indent the BB distal tendon in both spastic and contralateral limbs of hemispheric stroke survivors and in age-matched intact subjects.
Our previously reported results show a significant difference between reflex thresholds of spastic and contralateral limbs of stroke survivors recorded from BB-medial (p < 0.005) and BB-lateral (p < 0.001). For this study, we report that there is also a significant difference between the reflex thresholds in the contralateral limb of stroke subjects and the dominant arm of intact subjects, again measured from both BB-medial (p < 0.05) and BB-lateral (p < 0.05).
The reduction in stretch reflex thresholds in the contralateral limb of stroke survivors, based here on comparisons with thresholds of intact subjects, suggests an increased MN excitability on contralateral sides of stroke survivors as compared to intact subjects. This in turn supports our contention that RS tract activation, which has bilateral descending influences, is at least partially responsible for increased stretch reflex excitability, post-stroke, as both contralateral and affected sides show increased MN excitability as compared to intact subjects. Still, spasticity, presently diagnosed only on the affected side, with increased MN excitability on the affected side as compared to the contralateral side (our previous study), may be due to a different strongly lateralized pathway, such as the VS tract, which has not been directly tested here. Currently available clinical methods of spasticity assessment, such as the Modified Ashworth Scale, lack the resolution to quantify this phenomenon of a bilateral increase in MN excitability.
痉挛是一种运动障碍，表现为反射亢进，可发生在半球性中风后。虽然慢性中风幸存者痉挛的神经机制尚不清楚，但运动神经元（MN）兴奋性增加是反射亢进的一个可能原因。中风后脊髓 MN 兴奋性增加的潜在来源包括前庭脊髓（VS）和/或网状脊髓（RS）驱动增加。在中风幸存者中进行临床评估的痉挛具有高度的偏侧性，因此 RS 对中风引起的痉挛的贡献更难协调，因为 RS 核通常双侧投射到脊髓。然而，中风幸存者的研究表明，脊髓水平的神经调节也可能发生变化，表明 RS 束的影响。我们假设，在半球性中风后，RS 核的兴奋性改变会影响脊髓的两侧，从而导致中风幸存者的 MN 兴奋性在瘫痪/痉挛侧和对侧都增加，与神经完整的受试者相比。
我们使用位置反馈控制线性电机逐渐缩进肱二头肌（BB）远端肌腱，在偏瘫中风幸存者的痉挛侧和对侧肢体以及年龄匹配的完整受试者的 BB 中测量 BB 肌的伸反射阈值。
我们之前的报告结果显示，从 BB 内侧（p < 0.005）和 BB 外侧（p < 0.001）记录的中风幸存者痉挛侧和对侧肢体的反射阈值之间存在显著差异。对于这项研究，我们报告说，在中风受试者对侧肢体和完整受试者优势手臂之间的反射阈值之间也存在显著差异，同样是从 BB 内侧（p < 0.05）和 BB 外侧（p < 0.05）测量。
根据与完整受试者阈值的比较，中风幸存者对侧肢体伸反射阈值的降低表明，与完整受试者相比，中风幸存者对侧 MN 兴奋性增加。这反过来又支持了我们的论点，即 RS 束的激活具有双侧下行影响，至少部分负责中风后伸反射兴奋性的增加，因为双侧和受累侧都显示出比完整受试者更高的 MN 兴奋性。尽管如此，痉挛目前仅在受累侧诊断，与对侧相比受累侧 MN 兴奋性增加（我们之前的研究）可能是由于不同的强烈偏侧化途径，例如尚未在此直接测试的 VS 束。目前用于痉挛评估的临床方法，如改良 Ashworth 量表，缺乏量化 MN 兴奋性这种双侧增加的分辨率。
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