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Brain, Vol 120, Issue 7 1131-1138, Copyright © 1997 by Oxford University Press


ARTICLES

Local human sural nerve blood flow in diabetic and other polyneuropathies

M Theriault, J Dort, G Sutherland and DW Zochodne
Neurosciences Research Group, University of Calgary, Alberta, Canada.

Microangiopathy is considered relevant to the pathogenesis of several forms of peripheral nerve disease, particularly diabetic polyneuropathy. In diabetes, however, it is uncertain whether reductions in mixed nerve trunk blood flow account for early features of polyneuropathy in contrast to later disease, where microvascular changes have been described. To address this issue, we measured local sural nerve blood flow in patients with mild diabetic polyneuropathy who were enrolled in a clinical trial (n = 26), patients with other polyneuropathies being studied by diagnostic sural nerve biopsy (n = 17), patients with vasculitic polyneuropathy (n = 3) and one patient with rapidly progressive severe diabetic polyneuropathy and lumbosacral plexopathies. Standardized measurements were made at 10 sites along the sural nerve of each patient prior to sural nerve resection for biopsy. We used a laser Doppler flowmetry probe sensitive to red blood cell flux to measure sural nerve blood flow. This was slightly higher in patients with mild diabetes compared with those with other polyneuropathies, but was reduced in patients with vasculitis. In patients with mild diabetes, there was no relationship between sural nerve blood flow and prebiopsy sural nerve action-potential amplitude, sural myelinated fibre density, haemoglobin A1C, duration of diabetes or age of the patient. Ten diabetic patients entered in the clinical trial had sural nerve blood flow recorded in one sural nerve, followed 1 year later by a second sural nerve blood flow measurement prior to biopsy of the contralateral sural nerve. Despite a mild trend toward decline in fibre density between the nerves over this period of time, sural nerve blood flow was similar. The patient with severe diabetic polyneuropathy and lumbosacral plexopathies had reduced sural nerve blood flow. Our findings do not provide evidence that reductions in sural nerve blood flow are associated with early peripheral neuropathy in diabetes, unlike vasculitis. The early trend toward slight rises in sural nerve blood flow may be a result of early functional microangiopathy that accompanies nerve dysfunction but does not cause it.
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