Sung Jia-Ying, Tani Jowy, Chang Tsui-San, Lin Cindy Shin-Yi
Department of Neurology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Department of Neurology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
PLoS One. 2017 Feb 9;12(2):e0171223. doi: 10.1371/journal.pone.0171223. eCollection 2017.
This study investigated sensory and motor nerve excitability properties to elucidate the development of diabetic neuropathy. A total of 109 type 2 diabetes patients were recruited, and 106 were analyzed. According to neuropathy severity, patients were categorized into G0, G1, and G2+3 groups using the total neuropathy score-reduced (TNSr). Patients in the G0 group were asymptomatic and had a TNSr score of 0. Sensory and motor nerve excitability data from diabetic patients were compared with data from 33 healthy controls. Clinical assessment, nerve conduction studies, and sensory and motor nerve excitability testing data were analyzed to determine axonal dysfunction in diabetic neuropathy. In the G0 group, sensory excitability testing revealed increased stimulus for the 50% sensory nerve action potential (P<0.05), shortened strength-duration time constant (P<0.01), increased superexcitability (P<0.01), decreased subexcitability (P<0.05), decreased accommodation to depolarizing current (P<0.01), and a trend of decreased accommodation to hyperpolarizing current in threshold electrotonus. All the changes progressed into G1 (TNSr 1-8) and G2+3 (TNSr 9-24) groups. In contrast, motor excitability only had significantly increased stimulus for the 50% compound motor nerve action potential (P<0.01) in the G0 group. This study revealed that the development of axonal dysfunction in sensory axons occurred prior to and in a different fashion from motor axons. Additionally, sensory nerve excitability tests can detect axonal dysfunction even in asymptomatic patients. These insights further our understanding of diabetic neuropathy and enable the early detection of sensory axonal abnormalities, which may provide a basis for neuroprotective therapeutic approaches.
本研究调查了感觉和运动神经兴奋性特性，以阐明糖尿病性神经病变的发展情况。共招募了109例2型糖尿病患者，其中106例进行了分析。根据神经病变严重程度，使用总神经病变评分降低值（TNSr）将患者分为G0、G1和G2 + 3组。G0组患者无症状，TNSr评分为0。将糖尿病患者的感觉和运动神经兴奋性数据与33名健康对照者的数据进行比较。分析临床评估、神经传导研究以及感觉和运动神经兴奋性测试数据，以确定糖尿病性神经病变中的轴突功能障碍。在G0组中，感觉兴奋性测试显示，50%感觉神经动作电位的刺激增加（P<0.05），强度-时间常数缩短（P<0.01），超兴奋性增加（P<0.01），亚兴奋性降低（P<0.05），对去极化电流的适应性降低（P<0.01），并且在阈下电紧张中对超极化电流的适应性有降低趋势。所有这些变化在G1（TNSr 1 - 8）和G2 + 3（TNSr 9 - 24）组中持续发展。相比之下，G0组中仅50%复合运动神经动作电位的刺激有显著增加（P<0.01）。本研究表明，感觉轴突中轴突功能障碍的发展早于运动轴突，且方式不同。此外，感觉神经兴奋性测试即使在无症状患者中也能检测到轴突功能障碍。这些见解加深了我们对糖尿病性神经病变的理解，并能够早期检测感觉轴突异常，这可能为神经保护治疗方法提供依据。
