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  • Peripheral neuropathy  (3)
  • 1990-1994  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 83 (1992), S. 120-133 
    ISSN: 1432-0533
    Keywords: Sural nerve ; Schmidt-Lanterman incisures ; Myelinated nerve fibers ; Peripheral neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fine structural alterations of Schmidt-Lanterman incisures (SLI) were investigated in a series of 242 unselected sural nerve biopsies that had been examined for diagnostic purposes. The series included cases with Friedreich's ataxia, HSAN I, HMSN I-III, HMSN VI, tomaculous neuropathy, metachromatic leukodystrophy, ceroidlipofuscinosis, dysproteinemic neuropathies, and myotonic dystrophy, in addition to several neuropathies less-specifically classified as either of a predominantly demyelinating, axonal, or neuronal type. The following classification of SLI alterations is proposed: (A) abnormal inclusions: (B) changes in shape and dimension; and (C) modes of disintegration. Abnormal inclusions comprised membranous whorls, uniform and pleomorphous lysosome-like bodies, and accumulation of granular substances at the site of the major dense line, or granular deposits at the site of the intraperiod line of the myelin sheath. Variations of incisural shape and dimension included folding, dilatation, and pocket formation (compartmentalization). Disintegration at incisures comprised a fine, vesicular and a gross, vacuolar type. Various combinations of these changes were observed. The most frequent change consisted of membranous whorls, detected in SLI of 89 biopsies. They were most prominent in chloroquine neuropathy where they occurred in SLI as well as in the adaxonal and abaxonal cytoplasm of Schwann cells. Compartmentalization of the myelin sheath at incisures associated with formation of myelin loops was a frequent feature in myotonic dystrophy. It is concluded, that changes of incisural ultrastructure are sensitive indicators of human neuropathies offering clues to the type of the underlying pathomechanism.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 81 (1991), S. 680-685 
    ISSN: 1432-0533
    Keywords: Endoneurial fibroblasts ; Peripheral neuropathy ; Connective tissue disease ; Vasculitis ; Cell necrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 42 human sural nerve biopsies degeneration of endoneurial cells was evaluated semiquantitatively at the electronmicroscopic level. These cells were of non-Schwannian origin since they were not surrounded by a basement membrane. Most of the degenerating cells resembled endoneurial fibroblasts: their remaining cytoplasmic processes were quite extensive, not finger-like as in macrophages, and their cytoplasm did not contain conspicuous lysosomes or phagolysosomes that would identify them as degenerating macrophages. Criteria for regarding these cells as degenerating were defects of the cytoplasmic surface membrane with extracellularly situated organelles. The ratio between normal and degenerating endoneurial cells in five different groups of peripheral neuropathies was compared to a group of normal controls. No degenerating endoncurial cells were found in the latter. The largest proportion of degenerating endoneurial cells was noted in patients with panarteritis nodosa (30% of the endoneurial cells evaluated). Between 9% and 18% of the evaluated endoneurial cells were seen degenerating in hereditary motor and sensory neuropathies, in neuropathies associated with IgG or IgM gammopathy, and in chronic demyelinating inflammatory polyradiculoneuropathy. These findings suggest that degeneration of endoneurial cells is a nonspecific sign of peripheral neuropathy occurring in various types of neuropathy, although vasculitis represents the most frequent cause. Thus, degeneration of endoneurial cells can be added to the growing list of changes that possibly indicate an inflammatory disorder, even during the intervening stage when apparent inflammatory cell infiltrates are lacking.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Mitochondrial myopathies ; Peripheral neuropathy ; Hereditary motor and sensory neuropathy ; Schwann cells ; Arterioles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fifteen cases of mitochondrial myopathy, three cases of hereditary motor and sensory neuropathy (HMSN) VI, and 280 cases of neuropathies of different etiologies were examined by electron microscopy for the presence of mitochondrial abnormalities in the sural nerve. Altered mitochondria were found in most cases of mitochondrial myopathy, in all cases of HMSN VI, and in 25 cases out of the series of unselected neuropathies. The mitochondrial changes comprised enlargement with an amorphous matrix and distorted cristae, with hexagonal paracrystalline inclusions, and with prominent cristae containing oblique striations, and a variety of rare changes. Most mitochondrial abnormalities were found in Schwann cells. An increase of the number of mitochondria was noted in smooth muscle and endothelial cells of epineurial arterioles of two cases with mitochondrial encephalomyopathy. Neuropathy was present in all cases of mitochondrial myopathy according to morphometrical analysis. Whether neuropathy is caused directly by mitochondrial dysfunction or by other pathogenetic mechanisms remains to be determined.
    Type of Medium: Electronic Resource
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