LOCAL HUMAN SURAL NERVE BLOOD-FLOW IN DIABETIC AND OTHER POLYNEUROPATHIES

Citation
M. Theriault et al., LOCAL HUMAN SURAL NERVE BLOOD-FLOW IN DIABETIC AND OTHER POLYNEUROPATHIES, Brain, 120, 1997, pp. 1131-1138
Citations number
51
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
120
Year of publication
1997
Part
7
Pages
1131 - 1138
Database
ISI
SICI code
0006-8950(1997)120:<1131:LHSNBI>2.0.ZU;2-E
Abstract
Microangiopathy is considered relevant to the pathogenesis of several forms of peripheral nerve disease, particularly diabetic polyneuropath y. In diabetes, however it is uncertain whether reductions in mixed ne rve trunk blood flow account for early features of polyneuropathy in c ontrast to later disease, where microvascular changes have been descri bed. To address this issue, we measured local sural nerve blood pow in patients with mild diabetic polyneuropathy who were enrolled in a cli nical trial (n = 26), patients with other polyneuropathies being studi ed by diagnostic sural nerve biopsy (n = 17), patients with vasculitic polyneuropathy (n = 3) and one patient with rapidly progressive sever e diabetic polyneuropathy and lumbosacral plexopathies. Standardized m easurements were made at 10 sites along the sural nerve of each patien t prior to sural nerve resection for biopsy. We used a laser Doppler f lowmetry probe sensitive to red blood cell flux to measure sural nerve blood flow. This was slightly higher in patients with mild diabetes c ompared with those with other polyneuropathies, but was reduced in pat ients with vasculitis. In patients with mild diabetes, there was no re lationship between sural nerve blood flow and prebiopsy sural nerve ac tion-potential amplitude, sural myelinated fibre density haemoglobin A (1C) 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 p ow measurement prior to biopsy of the contralateral sural nerve. Despi te a mild trend toward decline in fibre density between the nerves ove r this period of time, sural nerve blood flow was similar The patient with severe diabetic polyneuropathy and lumbosacral plexopathies had r educed sural nerve blood flow. Our findings do not provide evidence th at reductions in sural nerve blood pow are associated with early perip heral neuropathy in diabetes, unlike vasculitis. The early trend towar d slight rises in sural nerve blood flow may be a result of early func tional microangiopathy that accompanies nerve dysfunction but does not cause it.