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SUMMARY Clinical, electrophysiological, and electron microscopical data are presented on 10 diabetic patients with severe progressive neuropathy, predominantly motor in type, in the presence of good blood glucose control, and for one patient with painful neuropathy and third cranial nerve palsy. Endothelial cell hyperplasia was seen in small vessels in all cases, and seven patients showed plugging of the vascular lumen by degenerate cellular material and electron dense protein. It is suggested that these cells desquamate and occlude smaller peripheral vessels at a point of narrowing. In one case the lumen of a vessel was occluded by thrombus. Electron microscopical examination showed a vessel occluded by degranulated platelets.Electrophysiological studies showed a pattern of denervation that was asymmetrical and distally predominant in some patients, suggesting that the neuropathy, at least in part, relates to multiple small infarcts.Peripheral nerves in diabetes sustain widespread damage consisting of segmental demyelination' and axonal degeneration.2 Various clinical syndromes occur as a result, and it is now customary to refer to "diabetic neuropathies" rather than to the single entity of diabetic neuropathy. The aetiology of diabetic neuropathy is still under question, and the relative importance of metabolic and vascular factors is uncertain.Many of the syndromes of diabetic neuropathies manifest diffuse sensory or motor features, suggesting a metabolic effect; it is possible, however, that diffuse small vessel disease could also result in symmetrical abnormalities of nerve function. In 1959 Fagerberg described "vascular lesions in peripheral nerve in the form of hyalinisation, caliber reduction and thickening of the wall which were more common in patients with diabetic neuropathy than in other groups."3 He attributed such change to progressive degenerative disease and assumed that they were responsible for the structural damage to the myelin sheath in diabetic patients. Timperley et al described plugging of small blood vessels with fibrin or thrombus, and also focal areas of necrosis and loss of nerve fibre.4 Similarly, Williams et al, in an electron microscopical study, described thrombi and hyperplasia of vascular endothelial cells sufficient to occlude the lumen of small vessels.5 They suggested Accepted for publication 15 May 1985 that hyperplasia of endothelial cells could result in profound alterations of local blood flow and might account for a symmetrical form of neuropathy. Material and methodsWe studied 11 patients with diabetes ( Table 1). Nine of these had type II diabetes and two type I. The age range of the patients was 31-77 (mean 58.2) years with a duration of diabetes of one to 25 (mean 6.2) years. The duration of the neuropathic syndrome was relatively short at two to 24 (mean 12) months. All but one patient had a range of random blood glucose concentrations consistently below 9 mmol/l (162 mg/100 ml). The glycosylated haemoglobin values in the patients were near to the normal range (m...

We present the results of an electron microscopical study of a further series of sural nerve biopsies from patients with diabetic neuropathy and attempt to clarify some of the mechanisms by which abnormali-

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