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The morphological findings in sural nerve biopsy specimens from 15 diabetic patients with mild neuropathy were compared with control biopsies from eight non-neuropathic, non-diabetic subjects, and correlations were sought with electrophysiological studies and quantitative sensory tests for vibration, thermal, and current perception thresholds. Myelinated fibre density was reduced compared with control biopsies (4042 +/- 2090 (+/- SD) vs 6800 +/- 1100 mm-2; p less than 0.01). A strong correlation existed between myelinated fibre density and sural sensory conduction velocity (r = 0.84, p less than 0.001), sural action potential amplitude (r = 0.74, p less than 0.001), peroneal motor conduction velocity (r = 0.58, p less than 0.02), and median sensory amplitude (r = 0.64, p less than 0.01) but there was no correlation between myelinated fibre density and any quantitative sensory test. We conclude that conventional electrophysiological tests in the lower limb are reliable surrogate measures for structural abnormalities in early diabetic neuropathy.

The present paper has been written in order to determine the morphological alterations in the sural nerve from patients with chronic arteriosclerotic occlusive disease. Eight patients with Peripheral Vascular Disease (PVD) and six age-matched control subjects were studied. Morphometric data revealed two groups of patients, one of them with mild disease (n = 5), and the other one with severe damage (n = 3), consisting in loss of myelinated fibres and increase in the number of small fibres (p less than 0.05). Teased nerve fibres and electron microscopic studies also showed two types of patients, with respect to the myelin or the axonal alterations. The unmyelinated fibre population was affected equally in both groups. In conclusion, this study supports the idea that ischemia is able to cause structural alterations in the peripheral nerve, and that it can play a role in the development of neuropathy.

Clinical and neurophysiological studies were conducted in 47 patients with chronic obstructive airways disease and compared with 46 age-matched control subjects. Symptomatic neuropathy was reported in 13% and ankle jerks were absent in 45% of hypoxic patients. Peroneal and median nerve conduction velocities and median and sural sensory nerve amplitudes were significantly reduced in hypoxic patients (p less than 0.01). Six hypoxic patients underwent biopsy of the sural nerve, soleus muscle and overlying skin. Nerve glucose, sorbitol, fructose and myo-inositol concentrations were normal. Detailed light and electronmicroscopy revealed both nerve fibre and microvascular pathology. Segmental demyelination (32%) and unmyelinated fibre degeneration were found to be prominent lesions. The sural nerve perineurium was thickened due to an increase in the number of perineurial lamellae and an increase in intraperineurial space. Basement membrane thickening was observed in capillaries of nerve, muscle and skin. Endothelial cell hyperplasia and hypertrophy were observed in nerve and muscle capillaries but not in skin capillaries. In conclusion, this study has provided neurological, neurophysiological and neuropathological evidence of a neuropathy in hypoxic patients with chronic obstructive airways disease. These findings may be of relevance to some aspects of the aetiology of human diabetic neuropathy.

Clinical, electrophysiological and ultrastructural morphometric observations were made in 5 diabetic non-neuropathic patients, 5 diabetic patients with mild neuropathy and 11 diabetic patients with severe neuropathy. Capillary abnormalities were assessed in simultaneous nerve, muscle and skin biopsies and compared with results from 6 age-matched, non-diabetic control subjects. Nerve capillaries demonstrated markedly greater pathology than skin and muscle capillaries. Endoneurial capillary density was significantly reduced in severely neuropathic diabetic patients (p less than 0.01) when compared with control subjects. Capillary basement membrane (p less than 0.002), endothelial cell (p less than 0.003) and total diffusion barrier (endothelial cell, pericyte, basement membrane) (p less than 0.001) thickness were significantly increased, and oxygen diffusing capacity was significantly reduced (p less than 0.001) in the nerves of patients with severe diabetic neuropathy when compared to control subjects. Endothelial cell profile number and luminal perimeter were significantly increased in asymptomatic (p less than 0.01), (p less than 0.05) and severely neuropathic (p less than 0.001), (p less than 0.05) diabetic patients respectively. However, endothelial cell outer perimeter, a measure of capillary size, showed no significant increase in diabetic patients when compared with control subjects. An association was observed between neurophysiological and neuropathological measures of neuropathic severity. There was no significant correlation between the duration of diabetes and HbA1 levels with capillary pathology or with neuropathic severity. Very few abnormalities of muscle and skin correlated with neuropathic severity. However, all measures of nerve capillary pathology correlated significantly with neurophysiological and neuropathological measures of neuropathic severity.