Zochodne D W
Department of Clinical Neurosciences, University of Calgary, Alberta, Canada.
J Peripher Nerv Syst. 1996;1(2):119-30.
Investigations into the etiology of diabetic polyneuropathy have largely concentrated on the mixed peripheral nerve trunk. Although a number of workers have suggested that reductions in mixed nerve blood flow account for early diabetic polyneuropathy, experimental results remain controversial and are not fully sustained by human studies. Later disease is unquestionably associated with microangiopathy. Patients with diabetic neuropathy may have exclusive and severe sensory and autonomic involvement without obvious motor disease. The prominent sensory involvement in early diabetic polyneuropathy may suggest that the disease particularly targets dorsal root ganglia. Dorsal root ganglia (DRG) have features that might suggest they would be vulnerable to changes known to occur in diabetes, i.e. microangiopathy, excessive polyol flux and protein glycosylation. Autonomic ganglia may also be targeted early in the disease. The interest in using growth factors to treat diabetic neuropathy is at least partly based on the hypothesis that these agents might provide important trophic support for DRG neurons.
对糖尿病性多发性神经病变病因的研究主要集中在混合性周围神经干。尽管许多研究人员认为混合神经血流量减少是早期糖尿病性多发性神经病变的原因，但实验结果仍存在争议，且未得到人体研究的充分支持。后期疾病无疑与微血管病变有关。糖尿病神经病变患者可能仅有严重的感觉和自主神经受累，而无明显的运动障碍。早期糖尿病性多发性神经病变中突出的感觉受累可能表明该疾病特别靶向背根神经节。背根神经节（DRG）具有一些特征，这可能表明它们易受糖尿病中已知发生的变化影响，即微血管病变、多元醇通量过多和蛋白质糖基化。自主神经节在疾病早期也可能成为靶点。使用生长因子治疗糖尿病神经病变的兴趣至少部分基于这样的假设，即这些药物可能为背根神经节神经元提供重要的营养支持。
