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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mixed types of sensory and motor peripheral neuropathy and dementia occurred as neurological complications in patients with established type IV and type V hyperlipoproteinemia. These complications were remedial by control of the hyperlipoproteinemia with diet and/or clofibrate resulting in symptomatic improvement as well as restitution of nerve conduction velocities toward normal. Diabetes mellitus as well as systemic metabolic and toxic disorders which commonly produce neurological complications were excluded. Segmental demyelination with disorganization of myelin lamellae were striking morphological features found on sural nerve biopsy. Fluctuations in memory performance correlated inversely with plasma lipid levels and appear to be a characteristic feature of hyperlipidemic dementia. Hyperlipidemic neuropathy and dementia, although rare, are remediable neurological disorders which should be considered in patients with neuropathy and/or dementia of unknown origin.
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PMID:Hyperlipidemic neuropathy and dementia. 18 Dec 57

Electrophysiological, biochemical, and morphometric observations were made on the peripheral nerves of rats after galactose feeding. Motor nerve conduction velocity was found to be reduced. This was associated with an accumulation of galactitol in the peripheral nerves and a diminution in their myoinositol content. An increased water content and fascicular area, taken in conjunction with a probable increase in the area of the endoneurial spaces, indicated overhydration of the peripheral nerves. Morphometric observations on the myelinated fibre population in the tibial nerve showed no loss of fibres and although both the maximal and the average diameter of the myelinated fibres was slightly less than in age-matched controls, this was insufficient to explain the reduction in conduction velocity. Segmental demyelination was not detected and the relationship between myelin thickness and axon circumference was not altered. Electron microscope observations revealed no ultrastructural changes in the myelinated fibres and, in particular, no abnormalities at the nodes of Ranvier or indication of abnormal hydration of the Schwann cells. The relevance of these findings to the peripheral nerve changes in human and experimental diabetes is discussed.
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PMID:Peripheral nerve abnormalities related to galactose administration in rats. 18 26

This is a clinicopathologic report on three patients with sensory polyneuropathies of different origin. Sensory loss involved all four limbs reaching the upper third of the thighs and the elbow level or higher, in all three patients. In addition to the limbs the central region of the anterior aspect of the trunk, from lower abdomen up to level T2, and on the top of the scalp were involved. There was minimal weakness. This pattern of sensory deficit can best be explained by a length dependent degeneration of fibers. Familial amyloidosis, Portugese type, was responsible for the neuropathy in the first patient, diabetes mellitus in the second and alcoholism in the third one. On teased nerve fiber study, single regenerating fibers were isolated on sural nerve biopsy specimens from patients 1 and 2. Segmental demyelination and/or remyelination occurred in 11 per cent of the fibres in patient 1, in 36 per cent in patient 2 and in 4 of the 19 fibres isolated in patient 3. On cross sections of nerve specimens embedded in Epon there was a striking loss of myelinated fibres which was less important and predominated on smaller fibres in patients 1 and 2. On electron microscopic examination loss of unmyelinated fibres was conspicuous in all three patients. On single fiber studies as well as on sections of embedded specimens, myelinated fibres occasionally showed demyelination in contact to amyloid deposits. The present study demonstrates that in this pattern of neuropathy degeneration of myelinated fibers begins in the distal part of longest axons and may be associated with axonal sprouting in more proximal parts of degenerating axons. As the neuropathy progresses axons of shorter and shorter length become involved.
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PMID:[Progressive centripetal degeneration in polyneuropathies (author's transl)]. 627 81

Peripheral neuropathy is a common complication associated with diabetes mellitus. Segmental demyelination and other pathological changes frequently accompany loss of sensory amd motor nerve function. Morphological changes seen in diabetic nerve myelin may be a result of altered Schwann cell metabolism under hyperglycemic conditions. Using both alloxan and streptozotocin - induced diabetic rats of 2, 4 and 8 months duration of diabetes, metabolic changes in isolated sciatic nerve myelin were assessed using a double-label in vitro incubation system. Incorporation of 3H-fucose and 1-14C-leucine into myelin was determined per microgram protein. Specific activities of incorporated protein precursors were compared as a ratio of fucose to leucine. Using the Newman-Kuels test for multiple comparisons, statistically significant increases were found in the incorporation ratios of diabetic rats at 2 and 4 months of diabetes when tested against age-matched controls.
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PMID:The effect of diabetes on leucine and fucose incorporation into PNS myelin proteins. 726 34