H 反射作为疼痛性糖尿病周围神经病中脊髓抑制丧失的生物标志物。
The H-Reflex as a Biomarker for Spinal Disinhibition in Painful Diabetic Neuropathy.
机构信息
The Salk Institute for Biological Sciences, La Jolla, CA, USA.
Faculty of Medical and Human Sciences, Institute of Cardiovascular Sciences, University of Manchester and National Institute for Healthy Research/Wellcome Trust Clinical Research Facility, Manchester, UK.
出版信息
Curr Diab Rep. 2018 Jan 23;18(1):1. doi: 10.1007/s11892-018-0969-5.
PURPOSE OF REVIEW
Neuropathic pain may arise from multiple mechanisms and locations. Efficacy of current treatments for painful diabetic neuropathy is limited to an unpredictable subset of patients, possibly reflecting diversity of pain generator mechanisms, and there is a lack of targeted treatments for individual patients. This review summarizes preclinical evidence supporting a role for spinal disinhibition in painful diabetic neuropathy, the physiology and pharmacology of rate-dependent depression (RDD) of the spinal H-reflex and the translational potential of using RDD as a biomarker of spinally mediated pain.
RECENT FINDINGS
Impaired RDD occurs in animal models of diabetes and was also detected in diabetic patients with painful vs painless neuropathy. RDD status can be determined using standard neurophysiological equipment. Loss of RDD may provide a clinical biomarker of spinal disinhibition, thereby enabling a personalized medicine approach to selection of current treatment options and enrichment of future clinical trial populations.
目的综述
神经病理性疼痛可能由多种机制和部位引起。目前治疗糖尿病性神经痛的疗效仅限于不可预测的一部分患者，这可能反映了疼痛发生器机制的多样性，并且缺乏针对个体患者的靶向治疗。本综述总结了支持脊髓去抑制在糖尿病性神经痛中的作用的临床前证据，脊髓 H 反射的速率依赖性抑制（RDD）的生理学和药理学，以及将 RDD 用作脊髓介导疼痛的生物标志物的转化潜力。
最近的发现
在糖尿病动物模型中存在 RDD 受损，在伴有疼痛和无痛性神经病变的糖尿病患者中也检测到了 RDD 受损。可以使用标准神经生理学设备来确定 RDD 状态。丧失 RDD 可能为脊髓去抑制提供临床生物标志物，从而能够采用个性化医疗方法来选择当前的治疗选择，并丰富未来的临床试验人群。
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