PATHOLOGY OF ACUTE AND CHRONIC ISCHEMIC NEUROPATHY IN ATHEROSCLEROTICPERIPHERAL VASCULAR-DISEASE

Citation
H. Nukada et al., PATHOLOGY OF ACUTE AND CHRONIC ISCHEMIC NEUROPATHY IN ATHEROSCLEROTICPERIPHERAL VASCULAR-DISEASE, Brain, 119, 1996, pp. 1449-1460
Citations number
81
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
119
Year of publication
1996
Part
5
Pages
1449 - 1460
Database
ISI
SICI code
0006-8950(1996)119:<1449:POAACI>2.0.ZU;2-Q
Abstract
The peripheral nerve pathology in ischaemic limbs with atherosclerotic peripheral vascular diseases (PVD) is difficult to ascertain because of the limited number of reports. In addition, it has been debated whe ther chronic ischaemia per se could cause morphological abnormalities in peripheral nerves. In this prospective study, we examined pathologi cal findings in the sural, saphenous, deep peroneal, superficial peron eal and tibial nerves, taken from seven acutely and nine chronically i schaemic amputated legs in which ischaemia was due to non-diabetic sev ere PVD. For morphological comparison, nerves were also taken from amp utated legs without ischaemic disease and those in which PVD was assoc iated with diabetes. In acutely ischaemic nerves pathological changes were dependent upon the duration of ischaemia. Axonal degeneration of both myelinated and unmyelinated nerve fibres (MFs and UMFs) with occl uded vessels was prominent, if acute ischaemia was present for >24 h. Focal lesions, a hallmark of acute ischaemic neuropathy, were seen in both acute and chronic PVD nerves. Chronic PVD nerves also revealed co nsiderable variations in the density of MFs between the fascicles of i ndividual nerves and between the nerves of individual subjects; demyel ination and remyelination, endoneurial oedema particularly at the subp erineurial region, swollen endothelial cells, various but infrequent a xonal changes, and relative preservation of UMFs were also seen. All p athological changes found lit acute and chronic PVD nerves except for a high rate of demyelinated and remyelinated nerve fibres, have been d escribed in experimental models of acute ischaemic/reperfusion injury Demyelination could be induced by chronic ischaemia. Thus, pathologica l alterations in chronic ischaemic neuropathy may be due to the combin ed effects of acute ischaemia/reperfusion and chronic hypoxia.