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  • 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
    ISSN: 1432-0533
    Keywords: Colchicine ; Myopathy ; Tubulin ; Microtuubules ; Familial mediterranean fever
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Severe colchicine myopathy occurred in a 24-year-old patient treated with colchicine because of familial mediterranean fever complicated by renal amyloidosis. In addition to prominent autophagic vacuoles containing heterogeneous osmiophilic material and pleomorphous bodies, cytoplasmic deposits of finely granular material were detected that have not been noted in previous cases of colchicine myopathy. This granular material was immunoreactive for antibodies to tubulin, α-tubulin, and β-tubulin. These observations substantiate the suggestion that alterations of the microtubular network represent the initial step in the pathogenesis of colchicine myopathy.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1106
    Keywords: Triethyldodecylammoniumbromide ; Local anesthetics ; Neurotoxins ; Conduction block ; Wallerian degeneration ; Blood-nerve barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The blocking effect of triethyldodecylammoniumbromide (TEA-C12), applied locally to the sciatic nerve, was studied in 28 adult BDF1 mice. Clinical parameters, electrophysiological recordings of muscle action potentials evoked by stimulation at the sciatic notch, and morphological aspects are presented. Our results show that both the minimal blocking concentration and half the minimal blocking concentration induce flaccid paresis of the treated hind-limb. There was a complete, long-lasting nerve conduction block due to Wallerian degeneration of the myelinated nerve fibers. In contrast, pain sensation was abolished only on day 4 after application of the minimal blocking concentration, but was preserved during the rest of the time that nerve conduction block was observed. This corresponded to the electron microscopic finding of preservation of unmyelinated nerve fibers. Recovery of nerve conduction was characterized electrophysiologically by occurrence of minute polyphasic regeneration potentials between day 18 and 21, clinically by advanced restitution of muscle force on day 64, and morphologically by nerve regeneration. TEA-C12 also induced a disturbance of the blood-nerve barrier, demonstrated using an intraperitoneally administered biotinylated IgG tracer in the endoneurial space. The morphological features of the acute axonal changes of the myelinated nerve fibers including the degeneration of the axonal mitochondria suggest that the neurotoxic effect of TEA-C12 is possibly mediated by interference with the axonal energy supply. The selective affection of myelinated nerve fibers separates TEA-C12 from other neurotoxins that induce changes of the axonal microorganelles or complete Wallerian degeneration of myelinated and unmyelinated nerve fibers. The selectivity for myelinated nerve fibers and the supposed pathogenetic mechanism exhibit some similarities with the human polyneuropathy caused by acute arsenic acid intoxication.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1106
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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