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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 14 (1978), S. 113-119 
    ISSN: 1432-0428
    Keywords: Streptozotocin diabetes ; diabetic neuropathy ; peripheral nerves ; ultrastructure ; Schwann cells ; endoneurium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the present study was to examine whether the nerve water content and the Schwann cell cytoplasm are increased in early experimental diabetes, as suggested in the sorbitol theory. The sciatic nerves of streptozotocin diabetic rats were found to have an increased wet weight. The amount of Schwann cell cytoplasm was reduced by 30%. The increased wet weight was paralleled by enlargement of the cross sectional area of the nerve which was explained by an expansion of the endoneurial space. The findings indicate the existence of endoneurial oedema and are in part in conflict with the sorbitol theory. Extension of the space surrounding the nerve fibres may explain the increased resistance to ischaemia in diabetic patients.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 19 (1980), S. 222-228 
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; axonal transport ; Streptozotocin diabetes ; nerve crush ; nerve regeneration ; insulin treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The axonal transport of proteins in crushed nerves of streptozotocin (40 mg/kg) diabetic rats was investigated 4 weeks after induction of diabetes. 35S-methionine was used as a marker for protein and 3H-fucose as a marker for glycoprotein. The precursors were injected into the fifth lumbar spinal ganglion and the accumulation of TCA-insoluble activity proximal and distal to a sciatic nerve ligature was measured at different time intervals after application of a crush. The start of accumulation distal to the ligature was delayed by 1 hour for proteins as well as for glycoproteins. Furthermore, the total amount of accumulated protein after 19 h was decreased by 18% while the decrease was 21% for glycoprotein. By insulin treatment the differences could both be prevented and reversed after 3 days of normoglycaemia. These findings demonstrate an impaired response to a nerve crush and might be the explanation for the regenerative abnormalities of peripheral nerves in diabetes.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 19 (1980), S. 229-233 
    ISSN: 1432-0428
    Keywords: Galactose-feeding ; axonal transport ; diabetic neuropathies ; nerve crush
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Axonal transport was studied in galactosefed rats. Precursors for proteins and glycoproteins were injected into the fifth lumbar spinal ganglion and retrograde axonal transport as well as slow axonal transport were estimated at different time intervals during the following 4 weeks. Galactose-feeding was found to produce a progressive reduction of the retrograde axonal transport of glycoproteins in intact nerve (2.9±0.2 (arbitrary units) after five days of galactose-feeding as compared to 1.9±0.7 after 28 days, 2p=0.025). The slow axonal transport velocity of structural proteins was reduced from 0.97 ±0.09 mm/day to 0.84±0.04 mm/day, 2p=0.0030. The present findings as well as structural and electrophysiological abnormalities of the nerves of galactose-fed rats are similar to the changes found in diabetic rats. The similarities point to a decisive role for glucose or its metabolites in the development of diabetic neuropathy.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 38 (1995), S. 1191-1196 
    ISSN: 1432-0428
    Keywords: Key words Magnetic stimulation ; diabetic neuropathy ; motor pathway ; paired magnetic stimulation ; diabetic encephalopathy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Central motor pathways were studied in 17 normoalbuminuric insulin-dependent diabetic (IDDM) patients who had been diabetic for more than 20 years, and compared with findings in 17 age-, sex-, and height-matched control subjects. The central motor conduction time was calculated from recordings of the compound muscle action potentials of the abductor pollicis brevis muscle after single transcranial and spinal root magnetic stimulation. The central motor conduction time from motor cortex to cervical spinal roots was 9.8 ± 1.65 ms in diabetic patients and 10.1 ± 1.48 ms in control subjects. In diabetic patients with neuropathy the central motor conduction time was 9.5 ± 1.76 ms vs 10.1 ± 1.56 ms in patients without neuropathy. The excitability of the motor pathways was studied by paired transcranial magnetic stimulation at interstimulation intervals of 30–1000 ms. In normal control subjects, an early facilitation of the amplitude of the compound muscle action potential at an interstimulation interval of 30 ms was found, while no facilitation was present in diabetic patients. In addition the compound muscle action potential latencies were prolonged at interstimulation intervals of 30–50 ms in diabetic patients. The changes of excitability did not correlate with the presence of peripheral neuropathy, metabolic control or diabetes duration. It is concluded that long-term normoalbuminuric IDDM patients have impaired excitability but normal central conduction time of the motor pathways. [Diabetologia (1995) 38: 1191–1196]
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 38 (1995), S. 1191-1196 
    ISSN: 1432-0428
    Keywords: Magnetic stimulation ; diabetic neuropathy ; motor pathway ; paired magnetic stimulation ; diabetic encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Central motor pathways were studied in 17 normoalbuminuric insulin-dependent diabetic (IDDM) patients who had been diabetic for more than 20 years, and compared with findings in 17 age-, sex-, and height-matched control subjects. The central motor conduction time was calculated from recordings of the compound muscle action potentials of the abductor pollicis brevis muscle after single transcranial and spinal root magnetic stimulation. The central motor conduction time from motor cortex to cervical spinal roots was 9.8±1.65 ms in diabetic patients and 10.1±1.48 ms in control subjects. In diabetic patients with neuropathy the central motor conduction time was 9.5±1.76 ms vs 10.1±1.56 ms in patients without neuropathy. The excitability of the motor pathways was studied by paired transcranial magnetic stimulation at interstimulation intervals of 30–1000 ms. In normal control subjects, an early facilitation of the amplitude of the compound muscle action potential at an interstimulation interval of 30 ms was found, while no facilitation was present in diabetic patients. In addition the compound muscle action potential latencies were prolonged at interstimulation intervals of 30–50 ms in diabetic patients. The changes of excitability did not correlate with the presence of peripheral neuropathy, metabolic control or diabetes duration. It is concluded that long-term normoalbuminuric IDDM patients have impaired excitability but normal central conduction time of the motor pathways.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Keywords Muscular atrophy ; diabetic neuropathy ; MR-imaging ; stereology ; motor dysfunction.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic patients with polyneuropathy develop motor dysfunction. To establish whether motor dysfunction is associated with muscular atrophy the ankle dorsal and plantar flexors of the non-dominant leg were evaluated with magnetic resonance imaging in 8 patients with symptomatic neuropathy, in 8 non-neuropathic patients and in 16 individually matched control subjects. In the neuropathic patients the muscle strength of the ankle dorsal and plantar flexors was reduced by 41 % as compared to the non-neuropathic patients (p 〈 0.005). Volume of the ankle dorsal and plantar flexors was estimated with stereological techniques from consecutive cross-sectional images of the lower leg. The neuropathic patients had a 32 % reduction in volume as compared with the non-neuropathic patients (p 〈 0.005). To determine the regional distribution of atrophy cross-sectional magnetic resonance images were performed at predetermined levels of the lower leg in relation to bone landmarks. In the neuropathic patients there was an insignificant increase of 3 % of muscle area at the proximal lower leg level, whereas the atrophy was 43 % (p 〈 0.002) at the mid lower leg level and 65 % (p 〈 0.002) distally. Analysis of individual muscles confirmed that the atrophy predominated distally. We conclude that muscular atrophy underlies motor weakness at the ankle in diabetic patients with polyneuropathy and that the atrophy is most pronounced in distal muscles of the lower leg indicating that a length dependent neuropathic process explains the motor dysfunction. [Diabetologia (1997) 40: 1062–1069]
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 12 (1976), S. 539-546 
    ISSN: 1432-0428
    Keywords: Streptozotocin diabetes ; axons ; myelin sheath ; nerve degeneration ; neural conduction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A diminution of the cross sectional area of myelinated fibres in the common peroneal nerve was observed in rats four weeks after the induction of diabetes with streptozotocin. Small fibres were affected more than larger ones and the axon reduction was twice that of the myelin sheath. The fibre diminution and the decreased axon/myelin ratio may explain the slowing of nerve conduction in experimental diabetes.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 12 (1976), S. 547-553 
    ISSN: 1432-0428
    Keywords: Streptozotocin diabetes ; myelinated nerve fibres ; nerve degeneration ; diabetic neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a morphometric study of isolated fibres of the common peroneal nerve in short-term diabetic rats reduced fibre calibre was observed. No segmental demyelination or remyelination was found, but the nodes of Ranvier were slightly widened and paranodal bulbi were swollen relative to fibre calibre. It is suggested that axonal dwindling is the primary event in experimental diabetes. The reduction of the myelin sheath may be a consequence of the abnormal nerve cell offshoot. The results obtained suggest that streptozotocin diabetes in the rat is a useful model for the elucidation of diabetic neuropathy.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 20 (1981), S. 110-112 
    ISSN: 1432-0428
    Keywords: Axonal transport ; diabetic neuropathies ; streptozotocin diabetes ; nerve crush
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The accumulation of 3H-fucose labelled glycoprotein and 35S-methionine labelled protein carried by the retrograde axonal transport in the sensory fibres of the sciatic nerve was examined on the day after injection of streptozotocin in rats. The accumulation of fucose-label was reduced (2.8 ± 0.4 (SD) versus 2.1 ± 0.5 (arbitrary units), 2p = 0.0044) indicating a decreased retrograde flux of glycoproteins. This early transport abnormality could have a key role in the development of peripheral neuropathy in diabetes.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 56 (1982), S. 157-160 
    ISSN: 1432-0533
    Keywords: Diabetic neuropathy ; Streptozotocin diabetes ; Mast cells ; Peripheral nerves ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mast cell proliferation has been reported in peripheral nerves of streptozotocin diabetic rats. We examined the question by light microscopy using morphometric techniques including estimation of shape and size. After 4 weeks of diabetes the mast cell area in transverse sections was 32.7±7.0 μm2 vs. 22.5±5.4 μm2 in controls (P〈102). Mast cell profiles approximated to ellipses in longitudinal sections, the long diameter being 11.4±1.2 μm vs. 14.0±1.0 μm in controls (P〈104). Correspondingly, the profile number was increased (30 ±6%) in longitudinal sections and decreased in transverse sections (11±16%). The present study does not provide evidence for mast cell proliferation in peripheral nerves in experimental diabetes, and, furthermore, underlines the need of evaluation of dimensions in studies of particle numbers.
    Type of Medium: Electronic Resource
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