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  • Isoniazid  (3)
  • Sural nerve  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 432 (1998), S. 199-205 
    ISSN: 1432-2307
    Keywords: Key words Nerve biopsy ; Sural nerve ; Peripheral neuropathy ; Skin biopsy ; Fixation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Peripheral nerve biopsy is now an established, valuable investigative procedure, but as it can give rise to significant residual symptoms it should only be undertaken after careful consideration of the indications and with informed consent from the patient. Nerve biopsies should only be processed and evaluated in a laboratory with the relevant particular expertise. It is generally recommended that a sural nerve biopsy be performed in combination with a muscle biopsy but not vice versa (muscle biopsies together with a nerve biopsy). Nerve biopsy is not the only means of sampling peripheral nerve tissue to study the peripheral nervous system. Examination of the innervation of the skin may be informative. The same is likely to be true for motor point muscle biopsy. Nerve biopsy is mainly used for morphology although molecular genetic techniques using fresh or archival nerve biopsies are increasingly available. Chemical analysis is undertaken mainly for research purposes.
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  • 2
    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.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 16 (1970), S. 301-323 
    ISSN: 1432-0533
    Keywords: Peripheral Nerves ; Nerve Degeneration ; Endoplasmic Reticulum ; Edema ; Isoniazid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Außer den bekannten Veränderungen bei der Isoniazid (INH)-Neuropathie ließen sich bestimmte Veränderungen im peripheren Nerven nachweisen, die bisher nicht beschrieben worden sind. Dazu gehören enorme Proliferationen eines glatten endoplasmatischen Reticulums in manchen Schwannzellen und extracellulär in den Büngnerschen Bändern gelegene “Nadeln”, π- and μ-Granula. Darüber hinaus ist bei der INH-Neuropathie gelegentlich eine schwere Störung der Blutnervenschranke mit Erythrodiapedesen feststellbar, die nicht zu dem Bild der einfachen Wallerschen Degeneration gehört. Das gleiche gilt für das frühzeitige Auftreten von umfangreichen elektronendichten Strukturen in histiocytären Zellelementen des Endoneuriums. Die Unterschiede der INH-Neuropathie gegenüber anderen Formen distal akzentuierter Neuropathien vom “neuronalen” oder “dying back”-Typ und gegenüber der Wallerschen Degeneration nach Durchschneidung des Nerven werden diskutiert.
    Notes: Summary Several distinctive alterations were observed in INH-neuropathy which have not been noted so far. These were striking proliferations of an agranular endoplasmic reticulum in some Schwann cells, needle-like structures situated intra- and extracellularly within reinnervated bands of Büngner, π- and μ-granules. Furthermore, a severance of the blood nerve barrier was observed leading to erythrodiapedesis which was not seen in Wallerian degeneration. This holds true also for the very early appearance of large electrondense organelles within histiocytic cells of the endoneurium. The distinguishing features of INH-neuropathy and other distally accentuated neuropathies of the “neuronal” or “dying back” type, and of Wallerian degeneration after nerve section are discussed.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 16 (1970), S. 324-341 
    ISSN: 1432-0533
    Keywords: Spinal Cord ; Spinal Ganglia ; Neuromuscular Spindles ; Mitochondria ; Isoniazid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Entgegen anderslautender Angaben in der Literatur werden bei der INH-Neuropathie auch die sensorischen Nervenendigungen in den Muskelspindeln betroffen. Die Veränderungen bestehen in einem Verlust der synaptischen Vesikel, in Mitochondrienschwellungen und-Verdichtungserscheinungen, in terminalen Axonfragmentationen und Reaktionen der zugehörigen intrafusalen Muskelfasern. Außerdem lassen sich schon in frühesten Stadium der INH-Neuropathie, am 4. Tag nach Beginn der INH-Applikation, Veränderungen in den lumbosacralen Spinalganglien und im Rückenmark nachweisen. Die Veränderungen in den Perikaryen gleichen denen bei der retrograden Zellveränderung weitgehend. Über die Spezifität der Alterationen an den sensorischen Nervenendigungen ist vorest keine sichere Aussage möglich, da vergleichbare Untersuchungen über pathologisch veränderte Muskelspindeln, insbesondere nach der einfachen Durchschneidung des Nerven, bisher fehlen.
    Notes: Summary In INH-neuropathy sensory nerve endings of distal muscle spindles may be severely altered. The changes are characterized by a disappearance of synaptic vesicles, mitochondrial swelling or condensation, fragmentation of axon terminals and reactions of the corresponding intrafusal muscle fibers. Also, occasional alterations in lumbosacral spinal ganglia and spinal cord were seen occurring already in the initial stage of INH-neuropathy at the 4th day after the beginning of INH application. The perikaryal changes resemble those of the retrograde cell reaction. Any specificness of the alterations seen in the sensory endings of muscle spindles cannot be ruled out at the present time since there are no comparable fine structural studies of pathological alterations in muscle spindles after simple nerve section or other nerve lesions.
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 15 (1970), S. 156-175 
    ISSN: 1432-0533
    Keywords: Peripheral Nerve ; Nerve Degeneration ; Axon ; Mitochondria ; Isoniazid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Im N. ischiadicus der Ratte kommen etwa doppelt so viele marklose als markhaltige Nervenfasern vor. Das normale zahlenmäßige Verhältnis dieser beiden Fasertypen schwankt in weiten Grenzen. Schon im ungeschädigten Nerven lassen sich bereits an einzelnen marklosen Nervenfasern verschiedenartige regressive Veränderungen wie Strukturverlust und perlschnurförmige Auftreibungen nachweisen; sie sind in der Regel von akuten, toxisch bedingten Veränderungen durch das Fehlen charakteristischer Schwann-Zellreaktionen zu differenzieren. Bei der INH-Neuropathie degenerieren anfangs im Verhältnis zu den markhaltigen nur wenige marklose Nervenfasern. Einige marklose Axone können unregelmäßig konturiert, geschwollen oder geschrumpft erscheinen; dabei lösen sich die Tubuli und Filamente auf; in manchen Fällen verdichtet sich ausch das Axolemm. Die Axonveränderungen werden von Störungen der normalen Axon-Schwann-Zellrelation begleitet. In den Anfangsstadien können manche Schwann-Zellen hochgradig deformiert sein; später verlieren sie ihre Oberflächendifferenzierung und runden sich (auf dem Querschnitt) ab. In der Regel zeigen die marklosen Nervenfasern bei der INH-Neuropathie die gleichen Veränderungen und Störungen der Axon-Schwann-Zellrelation wie bei der Wallerschen Degeneration. Extreme prolapsartige Verformungen von Axonen und Schwann-Zellen sowie mitochondriale Granula haben wir jedoch nur bei der INH-Neuropathie, nicht aber bei der Wallerschen Degeneration beobachtet.
    Notes: Summary In sciatic nerves of rats, there are more than twice as much unmyelinated than myelinated axons. Their ratio varies in a wide range from one area to the other. Some regressive changes are seen already in unmyelinated axons of normal controls (loss of structural components, axonal beading). Usually, these alterations can be distinguished from early experimental lesions by the lack of characteristic Schwann cell reactions. In the beginning of INH-neuropathy, fewer unmyelinated than myelinated nerve fibers are degenerating. Some of the unmyelinated axons may become irregularily folded, swollen, or shrunken while there is a progressive loss of tubules, filaments, normal mitochondria, and sometimes an increase in the thickness of the axolemma. The axonal changes are accompanied by a disturbance of the normal axon-Schwann cell relation. Initially, some Schwann cells may become extremely irregular; later they lose their surface differentiation while their cross sectional contour becomes rather rounded. In general, unmyelinated axons in INH-neuropathy show similar alterations and disturbances of the axon-Schwann cell relation as seen in Wallerian degeneration. Yet extremely deformed unmyelinated nerve fibers, axons as well as Schwann cells, and mitochondrial granules were only observed in INH-neuropathy.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 273 (1993), S. 499-509 
    ISSN: 1432-0878
    Keywords: Ranvier's node ; Development ; Sural nerve ; Axon ; Myelin sheath ; Paranodal junctions ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Developmental alterations of paranodal fiber segments have not been investigated systematically in human nerve fibers at the light- and electron-microscopic level. We have therefore analyzed developmental changes in the fine structure of the paranode in 43 human sural nerves during the axonal growth period up to 5 years of age, and during the subsequent myelin development up to 20 years and thereafter. The nodal, internodal, and paranodal axon diameters reach their adult values at 4–5 years of age. The ratio between internodal and paranodal axon diameters remains constant at 1.8–2.0. Despite a considerable increase in myelin sheath thickness, the length of the paranodal myelin sheath attachment zone at the axon does not increase correspondingly, because of attenuation, separation from the axolemma, and piling up of myelin loops in the paranode. Separation of variable numbers of terminal myelin loops from the underlying axolemma results in the formation of bracelets of Nageotte, whereas the transverse bands of these loops disappear. The adaptation of the paranodal myelin sheath to axonal expansion during development probably occurs by uneven gliding of the paranodal myelin loops simultaneously with internodal slippage of myelin lamellae. Since mechanically stabilizing structures (tight junctions and desmosomes between adjacent paranodal myelin processes; transverse bands between myelin loops and paranodal axolemma) are unevenly arranged, especially during rapid axonal growth, paranodal axonal growth with simultaneous adaptation of the myelin sheath is probably discontinuous with time.
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