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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 88 (1994), S. 426-432 
    ISSN: 1432-0533
    Keywords: Diabetic neuropathy ; Perineurium Basal lamina ; Endoneurial capillaries
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Measurements were made of the thickness of the basal lamina of perineurial cells in the sural nerve in a series of patients with diabetic neuropathy and compared with a group of patients with type I hereditary motor and sensory neuropathy (HMSN) and with organ donor control cases. The thickness was significantly greater in the diabetic patients as compared both with the HMSN cases and the organ donor controls. This was most obvious for the intermediate layers of the perineurium. Perineurial basal laminal thickness was only slightly greater in the HMSN cases than in the organ donor controls and the difference was not statistically significant. The thickening of the perineurial cell basal laminae was compared with the thickening of the basal laminal zone around the endoneurial microvessels. No significant correlation was found either for the diabetic neuropathy or HMSN cases or for the organ donor controls. As had been observed previously, the basal laminal zone around the endoneurial capillaries was of increased thickness both in the diabetic neuropathy and the HMSN cases and, although it was greater for the diabetic neuropathy patients, the difference was not statistically significant. Taken together, these findings indicate that the thickening of the basal lamina of the perineurial cells in a more characteristic feature of diabetic neuropathy than is thickening of the basal laminal zone around the endoneurial capillaries. The results suggest that the causative mechanisms are likely to differ, a conclusion supported by the morphological appearances: the basal laminal thickening around the perineurial cells is uniform, whereas that around the capillaries consists of basal laminal reduplication. Atrophy and necrosis of perineurial cells were observed in patients with diabetic neuropathy but rarely in the cases with HMSN and not in the organ donor cases. This may be similar to the degeneration of endoneurial fibroblasts that has been described as a non-specific finding in neuropathies.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; hereditary motor and sensory neuropathy ; sural nerve ; endoneurial capillaries ; basal lamina
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nerve biopsies were obtained from 27 patients with diabetic neuropathy. All had a symmetric distal sensory and autonomic neuropathy or a purely sensory neuropathy. Mean age was 39.8 years (range 23–57 years). Two patients had Type 2 (non-insulin-dependent) diabetes mellitus and the remainder Type 1 (insulin-dependent) diabetes. Morphometric observations on endoneurial capillaries were compared with results from organ donor control cases and from patients with type 1 hereditary motor and sensory neuropathy. The area of the lumen of the capillaries did not differ between the three groups. The area occupied by the capillary endothelial cells in transverse section and the number of endothelial cell nuclei were increased both in the patients with diabetic neuropathy and hereditary motor and sensory neuropathy, as was the thickness of the surrounding basal laminal zone. ‘Closure’ of endoneurial capillaries in diabetic neuropathy, reported in another study, was not confirmed. Capillary density and nearest-neighbour distances were similar in the diabetic and organ donor control cases. Capillary density was reduced in the patients with hereditary motor and sensory neuropathy, this being related to increased fascicular area consequent upon the presence of hypertrophic changes. The presence of thickening of the pericapillary basal laminal zone and endothelial cell hyperplasia both in diabetic and hereditary motor and sensory neuropathy, the latter being a neuropathy in which a vascular basis can be discounted, makes it difficult to use such changes as an argument favouring a vascular cause for diabetic neuropathy. There were differences in the basal laminal zone between the diabetic and hereditary motor and sensory neuropathy cases suggesting that the reduplicated basal lamina was more persistent in the diabetic patients.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 239 (1992), S. 361-362 
    ISSN: 1432-1459
    Keywords: Guillain-Barré syndrome ; Chronic inflammatory demyelinating polyneuropathy ; Demyelination ; Axonopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute inflammatory demyelinating polyneuropathy or the Guillain-Barré syndrome (GBS) has come to be accepted as a clinical entity, although the boundary between it and chronic inflammatory demyelinating polyneuropathy has given rise to discussion. Recent observations have suggested that the GBS may represent the consequence of more than one pathogenetic mechanism. In most cases the salient pathological change is demyelination. In some this may be mediated predominantly by lymphocytes; in others, where the demyelination is produced primarily by macrophages, the process may be antibody-mediated. Both electrophysiological and pathological evidence indicates that occasional patients with the GBS show extensive axonal degeneration. Although this could represent a “bystander effect” secondary to inflammatory infiltration, at times it may reflect a direct attack on axons. Elucidation of the nature of the pathogenetic mechanisms is essential before rational therapy can be devised.
    Type of Medium: Electronic Resource
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