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  • 1
    ISSN: 1432-0533
    Keywords: Key words Schwann cell inclusions ; Demyelination ; Myelinated nerve fibers ; Morphometry ; Peripheral ; neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the cytoplasm of Schwann cells of a sural nerve biopsy from a 21-year-old female patient with chronic neuropathy we noted numerous unique, usually double membrane-bound, osmiophilic, granular or globular inclusions, approximately 30–600 μm in diameter. Some of these membrane-bound vesicular or tubular structures contained less dense or no osmiophilic inclusions. Morphometry revealed a reduction of the myelin area per endoneural area to approximately 13% (normal value: 20– 30%) and of the density of myelinated nerve fibers to 5,412/mm2 (normal value at this age: 6,000–9,000/mm2). Large myelinated nerve fibers were predominantly reduced in number, and no myelinated nerve fibers with diameters larger than 4.5 μm were seen. Numerous, usually small onion bulb formations indicated a predominantly demyelinating type of neuropathy. This is to the best of our knowledge the first case of a chronic demyelinating neuropathy in which this kind of presumably pathognostic deposits in the cytoplasm of Schwann cells was detected.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Developing peripheral nerves ; Myelination ; Hypomyelination ; Axon ; Conduction velocity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous studies on sural nerves were extended to human femoral, ulnar, facial and trochlear nerves. An asynchronous development of axon diameter and myelin sheath thickness was noted in all nerves studied. Whereas axons reach their maximal diameter by or before 5 years of age, maximal myelin sheath thickness is not attained before 16–17 years of age, i.e., more than 10 years later. The slope of the regression lines for the ratio between axon diameter and myelin thickness is significantly steeper in older than in younger individuals; it also differs if small and large fibers with more or less than 50 myelin lamellae are evaluated separately. The number of Schmidt-Lanterman incisures during later stages of development is related to myelin thickness, but the length of the spiral of the myelin lamella, thought to unrolled, in relation to its width, i.e., internodal length, varies considerably during development. The changes of the relationship between axons and myelin sheath thickness during normal human development have to be taken into account if hypomyelination is considered as a significant pathological phenomenon in peripheral neuropathies, especially in children. The implications of the present findings concerning conduction velocity of peripheral nerve fibers and other electrophysiologic parameters are discussed.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 43 (1978), S. 169-178 
    ISSN: 1432-0533
    Keywords: Peripheral nerve ; Myelin ; Axon ; Development ; Interrelationship
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Axon caliber and myelin sheath thickness of individual nerve fibers were evaluated in the developing human sural nerve using three different methods of measurement: 1. ocular micrometer evaluation of large fibers, 2. photographic enlargements for evaluating large numbers of nerve fibers of all sizes, and 3. electron microscopic enlargements for more precise measurements in selected nerves. the average axonal diameter doubles from 5 months gestation to about 5 years of age. Large fiber group axons increase, during the same period, by a factor of 3–3.5 with a slight decrease thereafter. The myelin thickness increases more slowly, but continuously, between 5 months gestation until the age of 14. This asynchronous development of axons and myelin sheaths results in a statistically significant change of the ratio between axonal caliber and myelin thickness. The slope of the regression line is steeper in older than in younger individuals, and the correlation coefficient increases during development of the nerve.
    Type of Medium: Electronic Resource
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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 14 (1970), S. 261-283 
    ISSN: 1432-0533
    Keywords: Allergic Neuritis ; Electron Microscopy ; Mononuclear Cells ; Demyelination ; Remyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Kaninchen mit einer experimentell-allergischen Neuritis (EAN) wurden 8 Tage bis 4 Monate nach der Injektion einer Emulsion aus heterologem Nervengewebe mit Freundschem Adjuvans phasenkontrast- und elektronenmikroskopisch untersucht. Im akuten Stadium der Demyelinisation ist eine Beteiligung von mononucleären Infiltratzellen am Vorgang der Entmarkung peripherer Nervenfasern in der gleichen Weise nachweisbar, wie es Lampert (1969) bei der EAN von Ratten dargestellt hat. Da die Markscheidenschäden jedoch nicht immer in unmittelbarem Kontakt mit den Infiltratzellen auftreten, sind humorale Faktoren, die möglicherweise von den Infiltratzellen ausgeschieden werden, als Ursache der Markscheidenschäden nicht mit Sicherheit auszuschließen. Der weitere Abbau der geschädigten Markscheiden findet dann sowohl in den zu Makrophagen transformierten Infiltratzellen als auch in den proliferierenden Schwann-Zellen statt. Ausnahmsweise dominieren unter den Infiltratzellen auch bei der einfachen experimentell-allergischen Neuritis neutrophile Leukocyteninfiltrate; sie kommen in Zusammenhang mit anderen Zeichen einer schweren Störung der Gefäßnervenschranke wie Erythrodiapedesen und Fibrinexsudaten im fortgeschrittenen Stadium der Gewebsschädigung vor. Auf Axonläsionen und die im Ausheilungsstadium der EAN vorkommenden Zwiebelschalenformationen sowie die wiederholt beobachteten Gruppen regenerierter, von einer gemeinsamen Basalmembran gebündelter Nervenfasern wird kurz hingewiesen.
    Notes: Summary Rabbits with experimental allergic neuritis (EAN), induced by intradermally injected emulsified heterologous antigen together with Freund's adjuvant, were investigated by phase and electron microscopy 8 days to 4 months after the injection. Early lesions of the myelin sheaths in EAN can be demonstrated to occur in close contact with infiltrated mononuclear cells as has been reported by Lampert (1969) in rats. Yet since myelin lesions are not always restricted to areas of immediate contact with infiltrated mononuclear cells, it cannot be excluded that humoral factors, possibly excreted by the infiltrated cells, may initiate the myelin lesions. Further breakdown of myelin sheaths takes place in proliferating Schwann cells as well as in infiltrated mononuclear cells. Occasionally, neutrophilic leucocytes predominate among the cellular infiltrates. They occur together with erythrodiapedesis, and fibrinous exsudates in areas of severance of the blood-nerve barrier. Axonal lesions, and during remyelination, “onion bulb” formation were also seen as a sequence of the demyelinating lesions. Also, bundles of small regenerated nerve fibers enclosed by a single basement membrane were repeatedly observed in areas with remyelinated nerve fibers.
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  • 6
    ISSN: 1432-1459
    Keywords: Ethylene oxide ; Peripheral neuropathy ; Morphometry ; Electron microscopy ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case is reported of ethylene oxide polyneuropathy after 5 months of exposure. There was symmetrical distal weakness of both lower extremities and transitory reduced nerve conduction velocities with increased latencies. Sural nerve biopsy revealed nerve fibre degeneration of the Wallerian type, associated with reduction of axonal cross-sectional areas and some degree of nerve fibre regeneration that could be confirmed morphometrically. In addition, there was conspicuous paranodal vesicular disintegration of individual myelin lamellae. Unusual cisternae with introverted hemidesmosomes were noted in endoneurial fibroblasts.
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  • 7
    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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