Neuropathy in prediabetes and the metabolic syndrome

Abstract

Distal symmetric polyneuropathy (DSPN) and cardiac autonomic neuropathy (CAN) are major chronic complications of diabetes and are associated with loss of quality-of-life (QOL) [ 1 ] and increased morbidity and mortality [ 2, 3 ]. Diabetes is known to be a major cause of peripheral neuropathy [ 4 ]. Neuropathy was considered a chronic complication only occurring after many years of diabetes, but there is now evidence that symptoms, signs, and objective evidence of neuropathy are found as early as from the time of diagnosis of diabetes [ 5 ]. While there have been suggestions of neuropathy preceding the onset of diabetes [ 6 ], there has been some debate as to the validity of these claims [ 7 ]. Yet despite these doubts, a careful and detailed review of the relationship between glycemic control and evidence for neuropathy suggests that the clock starts ticking before the advent of diabetes by current de fi nition [ 8 ]. Perhaps what led to the controversy is not whether or not there was a neuropathy in prediabetes, but what the de fi nition of neuropathy should be. Indeed, there is now widespread recognition that neuropathy may be small or large fi ber, proximal or distal, acute or ch onic [ 9 ], and that it may occur with symptoms or signs demonstrable only on nerve conduction study (NCS), quantitative sensory testing (QST), quantitative autonomic function test (QAFT), or using modern techniques such as skin biopsy with quanti fi cation of intraepidermal nerve fi ber density (IENF) [ 10 ].