Whole nerve electrophysiologic procedures afford a battery of measures that can provide a noninvasive and objective index of the onset and progression of diabetic polyneuropathy (DPN). Advances in physiologic procedures, digital hardware, and mathematical models have allowed assessment of activity in slower conducting fibers, as well as measures that reflect changes in refractory periods and threshold excitability. These expanded options can augment standard measures of maximal conduction velocity and compound amplitude and greatly enhance the sensitivity of whole nerve measures to both structural (e.g., demyelination) and "nonstructural" (e.g., redistribution of ion channels) deficits associated with DPN. The mechanisms underlying the physiologic events in DPN are multifactorial and their sequence is complex, with different mechanisms contributing to change at overlapping, but distinct points in the progression. Factors influencing early change in velocity may differ from those contributing to chronic deficits and these mechanisms may also differ in their response to various putative therapies. This review attempts to summarize the pattern of whole nerve electrophysiologic change associated with DPN, outlines the strengths and limitations of the various measures that are feasible, and discusses the specific impact of known pathophysiologic mechanisms on these end points.