Altered blood rheology in the pathogenesis of diabetic and other neuropathies

Simpson, L. O.

doi:10.1002/mus.880110709

Cited by 56 publications

(18 citation statements)

References 130 publications

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“…It is proposed that hemorheological abnormalities such as increased blood viscosity and poorly deformable red blood cells may well lead to endoneurial ischemia and hypoxia (Simpson, 1988;Ford et al, 1992;Nukada et al, 1993b;Young et al, 1996;Vigilance and Reid, 2005). Erythrocyte aggregation, fibrinogen, and plasma and corrected whole-blood viscosity were all significantly different in neuropathic diabetic patients compared with control subjects, as were assessments of microvascular flow.…”

Section: Structural Changes Of Microvesselsmentioning

confidence: 99%

Ischemia and diabetic neuropathy

Nukada

2014

Handbook of Clinical Neurology

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Section: Structural Changes Of Microvesselsmentioning

confidence: 99%

Ischemia and diabetic neuropathy

Nukada

2014

Handbook of Clinical Neurology

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“…To summarize, in diabetic nerves, polyol flux, 'pseudohypoxia', true hypoxia, nonenzymatic glycosylation of microvessel proteins, the generation of damaging oxygen free radical species, hyperviscosity, loss of RBC deformability and increased platelet aggregation all likely contribute toward an eventual cascade of microvascular disease and ischemia (23,24,102,112,182,219).…”

Section: (Ii) Clinical Featuresmentioning

confidence: 99%

Diabetic Neuropathies: Features and Mechanisms

Zochodne

1999

Brain Pathology

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Diabetic neuropathies include both focal neuropathies and diffuse polyneuropathy. Polyneuropathy, the most common of the diabetic neuropathies excluding focal entrapment, has not yet been explained by a single disease mechanism despite intensive investigation. A number of abnormalities appear to cascade into a 'vicious cycle' of progressive microvascular disease associated with motor, sensory and autonomic fiber loss. These abnormalities include excessive polyol (sugar alcohol) flux through the aldose reductase pathway, functional and structural alterations of nerve microvessels, nerve and ganglia hypoxia, oxidative stress, nonspecific glycosylation of axon and microvessel proteins, and impairment in the elaboration of trophic factors critical for peripheral nerves and their ganglia. While an initiating role for nerve ischemia in the development of polyneuropathy has been proposed, the evidence for it can be questioned. The role of sensory and autonomic ganglia in the development of polyneuropathy has had relatively less attention despite the possibility that they may be vulnerable to a variety of insults, particularly neurotrophin deficiency. Superimposed on the deficits of polyneuropathy is the failure of diabetic nerves to regenerate as effectively as nondiabetics. Polyneuropathy has not yet yielded to specific forms of treatment but a variety of new trials addressing plausible hypotheses have been initiated. This review will summarize some of the clinical, pathological and experimental work applied toward understanding human diabetic neuropathy and will emphasize ideas on pathogenesis.

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“…Both earlier qualitative and more recent quantitative studies have demonstrated a wide range of abnormalities which include basement membrane thickening, endothelial cell hypertrophy and hyperplasia with vessel closure [3][4][5][6][7][8][9][10]. Such changes, when accompanied by haemorheological abnormalities [11,12], may well result in the endoneurial hypoxia which has been demonstrated in patients with severe human diabetic neuropathy [13]; Hypoxia in turn may result in the development and progression of neuropathy [14,15].…”

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confidence: 99%

Endoneurial localisation of microvascular damage in human diabetic neuropathy

et al. 1993

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Twenty diabetic patients with neuropathy underwent clinical and neurophysiological evaluation together with a detailed morphometric assessment of capillary pathology in endoneurial and epineurial microvascular beds of the sural nerve. Morphological data were compared with ten non-diabetic control subjects. There were no significant differences in control subjects between basement membrane area, endothelial cell area, endothelial cell profile number or luminal area of endoneurial when compared with epineurial capillaries. In contrast, when compared with epineurial capillaries, endoneurial capillaries from diabetic patients demonstrated a significant increase in basement membrane (p < 0.001) and endothelial cell (p < 0.001) area and a significant reduction in luminal area (p < 0.001). There was no significant difference in endothelial cell profile number between endoneurial and epineurial capillaries amongst diabetic patients. Previous studies have demonstrated a good correlation between the degree of microangiopathy and measures of neuropathic severity. In the present study increased endoneurial capillary basement membrane area was significantly related to reduced peroneal nerve conduction velocity (p < 0.001), myelinated fibre density (p < 0.001) and elevated vibration (p < 0.05) and thermal (p < 0.001) perception. Increased endothelial cell area and reduced luminal size were related to a reduced peroneal nerve conduction (p < 0.05, p < 0.01, respectively), reduced myelinated fibre density (p < 0.05, p < 0.01) and elevated thermal perception (p < 0.05, p < 0.001). Epineurial capillary basement membrane, endothelial cell and luminal area failed to relate to measures of neuropathic severity.(ABSTRACT TRUNCATED AT 250 WORDS)

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Altered blood rheology in the pathogenesis of diabetic and other neuropathies

Cited by 56 publications

References 130 publications

Ischemia and diabetic neuropathy

Ischemia and diabetic neuropathy

Diabetic Neuropathies: Features and Mechanisms

Endoneurial localisation of microvascular damage in human diabetic neuropathy

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