BACKGROUND 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. METHODS 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. RESULTS 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). CONCLUSION 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.

中文翻译：

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脑卒中幸存者对侧肢体的伸展反射兴奋性高于对照组。

背景技术以反射亢进为特征的痉挛是在半球性卒中后可能引起的运动障碍。虽然慢性中风幸存者痉挛的神经机制尚不清楚，但反射亢进的可能原因之一是运动神经元（MN）兴奋性增加。脑卒中后脊髓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。如在中风幸存者中临床评估的那样，痉挛高度偏侧化，因此，RS对中风诱发的痉挛的贡献更难以调和，因为RS核通常向两侧向脊髓突出。然而，对卒中幸存者的研究表明，脊髓水平的神经调节也可能发生变化，这表明RS束的影响。我们假设在发生半球性卒中后，与神经学上完整的受试者相比，RS核兴奋性的改变会影响脊髓的两侧，从而有助于增加卒中幸存者的束缚/痉挛和对侧的MN兴奋性。方法我们使用位置反馈控制的线性马达估算半球卒中幸存者的痉挛和对侧肢体以及年龄匹配的完整受试者的BB远端肌腱，从而估计肱二头肌（BB）肌肉的拉伸反射阈值。结果我们先前报道的结果显示，从BB内侧（p <0.005）和BB外侧（p <0.001）记录的中风幸存者痉挛和对侧肢体的反射阈值之间存在显着差异。对于这项研究，我们报道，卒中患者对侧肢体的反射阈值与完整受试者的优势臂之间的反射阈值之间也存在显着差异，再次从BB内侧（p <0.05）和BB外侧（p <0.05）进行测量。结论中风幸存者对侧肢体拉伸反射阈值的降低（基于与完整受试者阈值的比较）表明，与完整受试者相比，中风幸存者对侧的MN兴奋性增加。这反过来支持了我们的论点，即具有双侧下降影响的RS束激活至少部分负责中风后伸展反射兴奋性的增加，因为与完整对象相比，对侧和患侧均表现出增加的MN兴奋性。不过，痉挛 目前仅在患侧被诊断出，与对侧相比，患侧的MN兴奋性增加（我们先前的研究），可能是由于不同的强侧化途径，例如VS道，尚未经过直接测试这里。目前可用的痉挛性评估临床方法，例如改良的Ashworth量表，缺乏量化这种MN兴奋性双侧增加现象的解决方案。