Although animal and human physiological studies have informed potential mechanisms of diabetic neuropathy (1), the real‐world variability in clinical presentation and complexities in measurement have severely hindered a clear understanding of its epidemiology, its impact on the population with type 1 diabetes, and the development of therapies. The most common form—and therefore the one usually referred to simply as “diabetic neuropathy”—is the diffuse, symmetrical, slowly progressive, length‐dependent damage to the peripheral and autonomic nervous system classified technically by the term “diabetic distal symmetrical polyneuropathy” (1). It remains asymptomatic for years, may first present with abnormal sensation symmetrically at the tips of the toes, and may over time spread to the stocking‐and‐glove distribution. It involves injury to different anatomical nerve types that show variable clinical manifestations between individuals. Nerves can be classified as small, thinly myelinated or unmyelinated fibers that make up the autonomic as well as the pain and temperature sensory fibers, while large, myelinated fibers are responsible for other sensory and skeletal muscle functions. Some people have a large fiber–predominant pattern and experience numbness, tingling, or imbalance, while others have small fiber–predominance with burning and stabbing pain, impairment in sensing heat and cold, or a propensity toward clinical autonomic abnormalities like lightheadedness or gastroparesis (1). Some people experience a combination, and regardless of the pattern, people can be asymptomatic for extended periods even though their physical examination or specialized testing reveals marked impairments in nerve structure and function. With progression to foot muscle weakness or clinical autonomic manifestations like dry feet from limited sweat production, the subsequent risk of ulcer, infection, and amputation intensify. Complications like these are feared by people with diabetes more than death itself (2), and of great concern is the recent evidence of a resurgence in amputations (3–5).

中文翻译：

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重新思考1型糖尿病的神经病变：我们是否最了解最重要的是什么？

尽管动物和人类生理学研究已经揭示了糖尿病性神经病的潜在机制（1），但现实世界中临床表现的变化和测量的复杂性严重阻碍了对其流行病学，其对1型糖尿病人群的影响以及对糖尿病的认识。疗法的发展。最常见的形式（因此通常简称为“糖尿病性神经病”）是对周围和自主神经系统的弥漫性，对称性，缓慢进行性，长度依赖性的损伤，从技术上讲，其分类为“糖尿病性远端对称性多发性神经病” （1）。它多年来一直无症状，可能首先对称地出现在脚趾尖处，并随着时间的流逝传播到袜子和手套上。它涉及不同解剖神经类型的损伤，这些损伤在个体之间表现出不同的临床表现。神经可分为构成自主神经以及疼痛和温度感觉纤维的细，有髓或无髓小纤维，而有髓的大纤维负责其他感觉和骨骼肌功能。有些人的纤维主要是大纤维，麻木，刺痛或不平衡，而另一些人的纤维特别小，有烧灼和刺痛，感冒和感冒的障碍，或倾向于临床上的自主神经异常，如头昏眼花或胃轻瘫（ 1）。有些人会经历一种结合，而不论其模式如何，即使他们的身体检查或专门检查显示神经结构和功能明显受损，他们也可能长时间无症状。随着脚部肌肉无力的发展或临床自主性表现（如汗液产生受限导致脚干），随后发生溃疡，感染和截肢的危险加剧。糖尿病患者比死亡本身更担心此类并发症（2），而最近截肢术复发的证据（3-5）令人极为关注。