ABSTRACT
Diabetic distal symmetric sensorimotor polyneuropathy (DPN), the most com mon peripheral neuropathy in developed countries (1-3), affects up to 6070% of diabetic patients (4) and is the leading cause of foot amputation (5). The typical slowing of nerve conduction and the advancing distal symmetrical sensorimotor deficits are thought to reflect an underlying slowly progressive distal axonopathy of the dying-back type primarily affecting sensory nerve fibers (6). Improved blood glucose control substantially reduces the risk of developing DPN in insulin-dependent (type 1) diabetes (7,8), thereby strongly implicating hyperglycemia as a causative factor.
