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The principal factors deemed to influence NCV are: the integrity and degree of myelination of the largest diameter fibres; the mean axonal cross-sectional diameter; the representative internodal distance, and the distribution of nodal ion channels. Although demyelination can produce a profound deficit in NCV, it has been proposed to play only a minor role in slowing of NCV in diabetic peripheral neuropathy (DPN) (30). It has been suggested that the initial structural deficit responsible for NCV slowing is likely a diminished "length constant" of large diameter axons because of axonal atrophy. However, in a recent study of 57 patients with diabetes an amplitude-independent slowing of NCV supported the occurrence of demyelination (31). Furthermore, our recent study in patients with diabetes with early neuropathy demonstrated significant paran-odal demyelination and remyelination with no evidence of axonal atrophy (32).

To establish a perspective on the expected rate of decline in NCV and the factors which might influence it, it is important to analyze in detail the results from several published studies. In the Diabetic Control and Complications Trial (type 1 diabetes) the sural and peroneal nerve velocities in the conventionally treated group diminished by 0.56 and 0.54 m per second per year, respectively, for 5 years (33). In a prospective 8 year study of 45 type 1 diabetic patients a 1% rise in HbAlc was associated with a

1.3 m per second decrease in maximal nerve conduction velocity (34). In patients with type 2 diabetes a lower rate of decline was observed in a 10-year natural history study of 133 patients with newly diagnosed type 2 diabetes in which NCV deteriorated by 0.39 m per second per year in the sural and 0.3 m per second per year in the peroneal nerves (35). Recently, some composite scores of nerve conduction and selected individual attributes of nerve conduction have been shown to be superior to symptoms or quantitative sensation when assessing a worsening of early neuropathy (36). A part of the alteration in NCV might well depend on nodal ion channel function as opposed to frank structural alterations such as demyelination and axonal atrophy. Recently, the relatively new technique of threshold tracking which measures nodal ion channel function has shown that reduced nodal/paranodal potassium currents are related to glycemic control (37). This technique might well be used in the future together with standard NCV assessment to define therapeutic responses.


Peak amplitude of either the sensory response sensory nerve action potential (SNAP) or the compound muscle action potential (CMAP) reflects the number of responding fibres and the synchrony of their activity. A strong correlation (r = 0.74; p < 0.001) between myelinated fibre density and whole nerve sural amplitude in DPN (38) has been previously demonstrated. Others have shown that a change of 1 ^V in sural nerve SNAP is associated with a decrease of approximately 150 fibers/mm2 and a loss of 200 fibres/mm2 is associated with an approximate 1 mV reduction in the mean amplitude of the ulnar, peroneal, and tibial nerves CMAP (39). In a longitudinal study of patients with type 2 diabetes an approximate 5% per year loss of SNAP has been demonstrated (35).


F-Waves detect any abnormality in the antidromic conduction of the compound neural volley to the ventral spinal cord, the activation of a subpopulation of spinal motor neurons, the orthodromic conduction of the newly established volley, and the postsynaptic activation of muscle fibres in the innervated muscle. The "long-loop" nature, of this measure increases the sensitivity to detect factors that alter the speed of conduction, which might be widely distributed along a nerve. Thus, a subtle change affecting each node might not be detected in measures focused on an isolated distal segment, but might accumulate and become evident in the long latency F-wave response. F-wave latency has been shown to be the most reproducible measure in nerve conduction studies of diabetic polyneuropathy (40). Although minimal latency is the most frequent measures of F-wave activity, the addition of chronodispersion, duration, persistence, and amplitude might add sensitivity to detect an abnormality in slower conducting axons (41).

Distribution of Velocities

The fusion of a collision technique with an analysis of the distribution of conduction velocities has proven to be valuable in exploring the effects of DPN on slower fibres (42). Using a computer-assisted collision procedure with an assessment of velocities in slower conducting fibres, subclinical neuropathy was detected in 58% of subjects compared with only 11% of subjects using standard electrophysiology (42).

Table 4

Frequency of Detection and Sensitivity and Specificity for Detection of Diabetic Polyneuropathy

Table 4

Frequency of Detection and Sensitivity and Specificity for Detection of Diabetic Polyneuropathy

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