Bradley, Jane Louise; (1995) Quantitative aspects of blood vessels and perineurium in diabetic neuropathy. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

The cause of diabetic polyneuropathy is at present unknown. Abnormalities of the vasa nervorum are well documented, but a causal relationship between their occurrence and that of diabetic polyneuropathy remains equivocal. Recent studies have reported findings that support this hypothesis, in particular the claim that the number of "closed" endoneurial capillaries is greater in diabetic neuropathy than in control subjects, this being positively correlated with the severity of neuropathy. As these studies were undertaken on elderly diabetic patients (mean age > 50 years), accompanying vascular disease would not be unexpected. Perineurial basal laminal thickening has also been observed in patients with diabetic neuropathy, but its relationship to concomitant microangiopathy has not so far been documented. I have examined sural nerve biopsies from a series of 27 younger diabetic patients with symmetric distal sensory and autonomic neuropathy (mean age 39.8 years). Morphometric observations on endoneurial capillaries and perineurial cells were compared with results from age-matched organ donor control cases and patients with type I hereditary motor and sensory neuropathy (HMSN I). Perineurial basal lamina thickness was significantly greater in the diabetic cases than in the organ donor control group. Capillary luminal area did not differ between the 3 groups and the presence of "closed" capillaries in the diabetic cases was not confirmed. Capillary density was also comparable between the diabetic and organ donor cases, but was reduced in patients with HMSN I, this being related to hypertrophic changes and a resultant increase in fascicular area. The finding that transverse capillary endothelial cell area, and nuclear and pericapillary basal laminal area were all increased both in patients with diabetes and HMSN I make it difficult to present these abnormalities as evidence in favour of a vascular basis for the neuropathy as HMSN I is a condition in which a vascular basis can be discounted.

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