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速率依赖性 Hoffmann 反射抑制:在痛性糖尿病周围神经病中的实际应用。

Rate-Dependent Depression of the Hoffmann Reflex: Practical Applications in Painful Diabetic Neuropathy.

机构信息

Department of Neurology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Department of Pathology, University of California San Diego, La Jolla, CA, USA.

出版信息

Diabetes Metab J. 2024 Nov;48(6):1029-1046. doi: 10.4093/dmj.2024.0614. Epub 2024 Nov 21.

DOI:10.4093/dmj.2024.0614
PMID:39610132
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11621664/
Abstract

Measurement of the rate-dependent depression (RDD) of the Hoffmann (H) reflex, a technique developed over half a century ago, is founded on repeated stimulation of the H-reflex with tracking of sequentially evoked H-wave amplitudes in the resulting electromyogram. RDD offers insight into the integrity of spinal reflex pathways and spinal inhibitory regulation. Initially, RDD was predominantly utilized in the mechanistic exploration and evaluation of movement disorders characterized by spasticity symptoms, as may occur following spinal cord injury. However, there is increasing recognition that sensory input from the periphery is modified at the spinal level before ascending to the higher central nervous system and that some pain states can arise from, or be exaggerated by, disruption of spinal processing via a mechanism termed spinal disinhibition. This, along with the urgent clinical need to identify biological markers of pain generator and/or amplifier sites to facilitate targeted pain therapies, has prompted interest in RDD as a biomarker for the contribution of spinal disinhibition to neuropathic pain states. Current research in animals and humans with diabetes has revealed specific disorders of spinal GABAergic function associated with impaired RDD. Future investigations on RDD aim to further elucidate its underlying pathways and enhance its clinical applications.

摘要

测量 Hoffmann(H)反射的速率依赖性抑制(RDD),这是一项半个多世纪前发展起来的技术,其基础是用重复刺激 H 反射,并在随后产生的肌电图中跟踪顺序激发的 H 波幅度。RDD 可以深入了解脊髓反射通路和脊髓抑制调节的完整性。最初,RDD 主要用于以痉挛症状为特征的运动障碍的机制探索和评估,这些运动障碍可能发生在脊髓损伤之后。然而,人们越来越认识到,外周感觉输入在上升到更高的中枢神经系统之前,在脊髓水平就已经被修饰了,并且一些疼痛状态可能是由于或通过一种称为脊髓去抑制的机制而被放大的,这种机制会干扰脊髓处理。这种情况,以及迫切需要识别疼痛发生器和/或放大器部位的生物标志物,以促进靶向疼痛治疗,这促使人们对 RDD 作为脊髓去抑制对神经病理性疼痛状态的贡献的生物标志物产生了兴趣。目前对糖尿病动物和人类的研究揭示了与 RDD 受损相关的特定脊髓 GABA 能功能障碍。未来对 RDD 的研究旨在进一步阐明其潜在途径并增强其临床应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/6a5cf2a6b28b/dmj-2024-0614f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/b0eaf4eea972/dmj-2024-0614f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/f5f428e8a111/dmj-2024-0614f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/bdeff818f6c4/dmj-2024-0614f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/431e2498df16/dmj-2024-0614f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/5390daa9d682/dmj-2024-0614f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/6a5cf2a6b28b/dmj-2024-0614f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/b0eaf4eea972/dmj-2024-0614f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/f5f428e8a111/dmj-2024-0614f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/bdeff818f6c4/dmj-2024-0614f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/431e2498df16/dmj-2024-0614f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/5390daa9d682/dmj-2024-0614f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df0/11621664/6a5cf2a6b28b/dmj-2024-0614f6.jpg

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BDNF in Neuropathic Pain; the Culprit that Cannot be Apprehended.神经营养因子在神经病理性疼痛中的作用:一个难以捉摸的罪魁祸首。
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