• Solomon Tesfaye, Dinesh Selvarajah, Rajiv Gandhi, Marni Greig, Pallai Shillo, Fang Fang, and Iain D Wilkinson.
• Diabetes Research Unit, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, United Kingdom Department of Human Metabolism Unit, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, United Kingdom Academic Unit of Radiology, Faculty of Medicine, Dentistry and Health, University of Sheffield, Sheffield, United Kingdom.
• Pain. 2016 Feb 1; 157 Suppl 1: S72-S80.

AbstractDiabetic peripheral neuropathy (DPN) affects up to 50% of patients with diabetes and is a major cause of morbidity and increased mortality. Its clinical manifestations include distressing painful neuropathic symptoms and insensitivity to trauma that result in foot ulcerations and amputations. Several recent studies have implicated poor glycemic control, duration of diabetes, hyperlipidemia (particularly hypertryglyceridaemia), elevated albumin excretion rates, and obesity as risk factors for the development of DPN. However, similar data are not available for painful DPN. Moreover, although there is now strong evidence for the importance of peripheral nerve microvascular disease in the pathogenesis of DPN, peripheral structural biomarkers of painful DPN are lacking. However, there is now emerging evidence for the involvement of the central nervous system in both painful and painless DPN afforded by magnetic resonance imaging. This review will focus on this emerging evidence for central changes in DPN, hitherto considered a peripheral nerve disease only.

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