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Preceding the joint meeting of the 19th annual Diabetic Neuropathy Study Group of the European Association for the Study of Diabetes (NEURODIAB) and the 8th International Symposium on Diabetic Neuropathy in Toronto, Canada, 13-18 October 2009, expert panels were convened to provide updates on classification, definitions, diagnostic criteria, and treatments of diabetic peripheral neuropathies (DPNs), autonomic neuropathy, painful DPNs, and structural alterations in DPNs.
Diabetes Care 33:2285-2293, 2010
CLASSIFICATION AND DEFINITION OF DIABETIC NEUROPATHIES- The neuropathies developing in patients with diabetes are known to be heterogenous by their symptoms, pattern of neurologic involvement, course, risk covariates, pathologic alterations, and underlying mechanisms (1,2). Thomas (3) and Boulton et al. (4) separated these into generalized and focal/multifocal varieties (e.g., multiple mononeuropathy, lumbosacral, thoracic, and cervical radiculoplexus neuropathies) (3,4). It is known that similar patterns of neuropathy occur in patients without diabetes (2). Moreover, diabetic patients can develop chronic inflammatory demyelinating polyradiculopathy.
The evidence that generalized varieties can be further classified into at least two major subgroups seems compelling (3,4). The typical DPN is a chronic, symmetrical, length-dependent sensorimotor polyneuropathy (DSPN) and is thought to be the most common variety (1). It develops on (or with) a background of longstanding hyperglycemia, associated metabolic derangements (increased polyol flux, accumulation of advanced glycation end products, oxidative stress, and lipid alterations among other metabolic abnormalities) and cardiovascular risk factors (5-7). Alterations of microvessels, similar to those observed in diabetic retinopathy and nephropathy, appear to be associated with the pathologic alterations of nerves (8). Total hyperglycemic exposure is perhaps the most important risk covariate (5,7). This variety has been shown to be stabilized, perhaps even improved, by rigorous glycemic control. This polyneuropathy has been shown to be statistically associated with retinopathy and nephropathy (1,6). Autonomic dysfunction and neuropathic pain may develop over time.
The atypical DPNs are different from DSPN in several important features, i.e., onset, course, manifestations, associations, and perhaps putative mechanisms (3,4,9). They appear to be intercurrent varieties, developing at any time during the course of a patient's diabetes (3,9). Onset of symptoms may be acute, subacute, or chronic, but the course is usually monophasic or fluctuating over time. Pain and autonomic symptoms are typical features (3,9) and altered immunity has been suggested. Studies have suggested that impaired fasting...