Length-dependent polyneuropathy has long been recognized as a frequent complication of diabetes. A decade of observational and epidemiologic studies support the concept that intermittent hyperglycemia or insulin resistance associated with prediabetes may be sufficient to damage distal nerves. Features of the metabolic syndrome have been implicated as independent neuropathy risk factors in large population-based studies of diabetic patients. Preferential injury to small unmyelinated nerves is suggested by prominent neuropathic pain, predominant sensory injury, and early autonomic dysfunction. Small uncontrolled trials suggest that diet and exercise may transiently improve distal nerve function and neuropathy symptoms in these patients. Patients with prediabetes neuropathy may permit greater insight into the balance between distal axonal injury and nerve regenerative capacity that determines neuropathy progression, and will be good candidates for evaluation of rational therapy based on known pathophysiology of hyperglycemic neuropathy.