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Radiology:糖尿病多发性神经病变患者的3T MR神经成像

2021-06-08 shaosai MedSci原创

尽管一些临床和血清学危险因素,如高血糖、血脂异常和肾功能下降已经在体内和体外研究中被确定,但糖尿病多发性神经病变(DPN)的确切代谢过程仍不明确。

尽管一些临床和血清学危险因素,如高血糖、血脂异常和肾功能下降已经在体内和体外研究中被确定,但糖尿病多发性神经病变(DPN)的确切代谢过程仍不明确。疼痛性神经病变症状在很大程度上影响患者的生活质量,然而为何25%-50%的DPN患者会经历疼痛性DPN仍未得到验证。

人们普遍认为,DPN患者的神经性疼痛源于遗传易感性、离子通道表达失调、细胞蛋白糖基化、有毒代谢物积累和中枢对疼痛的敏感性。大多数研究DPN的研究认为周围神经损伤的过程起源于下肢远端C纤维,并在近端运动时逐渐加重。最近使用MR神经造影的体内成像研究显示,大腿是DPN患者可见神经病变的主要部位,不同类型的微结构神经改变与血清学危险因素(高血糖和血脂异常)相关。但是据我们所知,先前的研究只探讨了DPN患者的近端神经损伤,然而近端神经损伤对疼痛症状演变的影响尚不明确。

近日,发表在Radiology杂志的一项研究探讨了DPN患者的神经结构、神经病变负荷及空间分布与疼痛的关系,为临床进一步了解DPN的病理生理提供了参考依据。

本项前瞻性研究于2015年6月至2018年3月期间纳入了自愿参加研究的1型或2型糖尿病患者。参与者均接受了坐骨神经的包括T2脂肪抑制序列的3T MR神经成像,并在此之前进行了临床和电生理测试。对于组间比较,根据数据的高斯或非高斯分布进行方差分析或Kruskal-Wallis检验。计算Spearman相关系数进行相关分析。

本研究共纳入131名参与者(平均年龄62岁±11岁[标准差]),其中82例1型糖尿病患者(n = 45)或2型糖尿病患者(n = 86)被评估为疼痛型(n = 64)、无痛型(n = 37)或无DPN (n = 30)。与无疼痛型DPN(10.4%±1.7,P= .03)或无DPN(8.3%±1.7;P <.001)相比,有疼痛性糖尿病神经病变的受试者在整个神经体积中神经病变的百分比较高(15.2%±1.6)。T2加权高信号神经病变的数量和范围与神经病变失能评分(r = 0.37;95%置信区间[CI]: 0.21, 0.52;r = 0.37;95% CI分别为0.20、0.52)和神经病变症状评分呈正相关(r = 0.41;95% CI: 0.25、0.55;r = 0.34;95%可信区间分别为0.17、0.49)。胫神经传导速度呈负相关(r = -0.23;95% CI: -0.44,-0.01;r = -0.37;95%CI分别为-0.55、-0.15)。神经截面积与神经病变失能评分呈正相关(r = 0.23;95% CI: 0.03, 0.36)。胫神经传导速度呈负相关(r = -0.24;95% CI: -0.45,-0.01)。

表1 疼痛型DPN、非疼痛型DPN和无DPN患者的MR神经造影成像参数、血清学和电生理数据结果。

 

表2 磁共振神经成像参数与临床、流行病学、电生理和血清学数据的相关性。

本研究是第一个表明糖尿病多神经病变(DPN)的神经病变数量和范围在疼痛型和非疼痛型DPN患者之间存在差异的相关研究。本研究结果表明,DPN患者的疼痛不仅仅由外周痛觉感受器的改变和中枢敏感化引起,而且也由周围神经束的广泛损伤引起。

原文出处:

Johann M E Jende,Jan B Groener,Zoltan Kender,et al.Structural Nerve Remodeling at 3-T MR Neurography Differs between Painful and Painless Diabetic Polyneuropathy in Type 1 or 2 Diabetes.DOI:10.1148/radiol.2019191347

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