IN previous communications Chopra and Hurwitz (1968, 1969) have reported that nerve conduction was abnormal in diabetics with and without neuropathy while normal in non-diabetics with occlusive peripheral vascular disease. Chopra (1969) has also shown that electromyography in diabetics was of neurogenic type and in keeping with a peripheral nerve rather than an anterior horn cell lesion. These studies, as well as those of several other authors, are in accord with the finding that segmental demyelination is the main pathological change in the nerves of patients with diabetic neuropathy (Thomas and Lascelles, 1965, 1966). Also, the observation by the latter authors that segmental demyelination predominates over combined axon and myelin destruction (Wallerian type degeneration) means that the peripheral nerve lesion arises independently and is not secondary to neuronal degeneration involving anterior horn cells or dorsal root ganglia. However, if slowed conduction in diabetics without neuropathy was also associated with pathological changes in the peripheral nerves then this would be confirmation that structural damage had indeed occurred in these patients as well as in those with objective neuropathy. Correction or amendment of the abnormal diabetic state at as early a stage as possible in patients might then be expected to prevent the cumulative and perhaps irreversible effects of age, ischaemia, environmental and metabolic damage on the peripheral nerves in diabetics.

In this paper a description is given of sural nerve changes in diabetic patients both with and without neuropathy. To try to assess the relative roles of a metabolic abnormality and ischaemia on the function of the diabetic nerve, the present findings are compared with those reported by Chopra and Hurwitz (1967) in the sural nerves of non-diabetic patients with chronic occlusive vascular disease.