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  • Mitochondria  (5)
  • Demyelination  (3)
  • 1
    ISSN: 1432-0533
    Keywords: Key words Zidovudine ; Myopathy ; Nucleus ; Mitochondria ; AIDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Long-term zidovudine (also termed azidothymidine, AZT) treatment of AIDS patients may cause severe myopathy characterized by conspicuous mitochondrial and nuclear changes. The mitochondrial changes are attributed to an inhibitory effect of AZT on the mitochondrial γ-polymerase in a variety of cells. Inhibition of the nuclear α-polymerase is another well-known side effect of AZT, whereas the (nuclear) β-polymerase appears to be rather insensitive. The nuclear changes seen in AIDS patients are usually considered secondary to the human immunodeficiency virus infection. To eliminate the influence of the virus on the nuclei, we studied the effect of AZT on non-infected, organotypic co-cultures of spinal ganglia, spinal cord, and skeletal muscle from fetal rats. We noted significant changes not only in the mitochondria but also in the nuclei of spinal ganglia, spinal cord, and muscle cells, which depended more on the duration of AZT application (1, 3, 5, and 8 days) than on the concentration (0.1, 1, 10, 100 and 1000 μM). The alterations of the mitochondria consisted mainly of swelling, loss of cristae and, finally, disappearance. The nuclei showed nucleolar segregation, marginal condensation of heterochromatin, formation of interchromatin and perichromatin granules, nuclear protrusions and pseudoinclusions and, finally, disintegration. The changes were not as pleomorphic as those seen in biopsy specimens from AIDS patients who had received long-term treatment with AZT. However, this difference can easily be attributed to the short duration of drug application in tissue culture compared to the long-term medication in patients.
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  • 2
    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.
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  • 3
    ISSN: 1432-0533
    Keywords: Zidovudine ; Myopathy ; Nucleus ; Mitochondria ; AIDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Zidovudine (formerly azidothymidine) is a potent inhibitor of the human immunodeficiency virus (HIV) reverse transcriptase and represents the first approved drug showing clinical efficacy in HIV-associated diseases. However, considerable toxicity causing macrocytic anemia, neutropenia, and myopathy has been reported, with severe mitochondrial alterations as a special feature of this myopathy. The mitochondrial changes are consistent with the fact that zidovudine acts as an inhibitor of the mitochondrial gamma-polymerase. Electron microscopically, we could confirm the presence of severely altered mitochondria in a 32-year-old male, who developed a necrotizing myopathy after daily administration of 1,000 mg zidovudine over a period of 15 months. In addition, there were even more severe nuclear changes that, for the most part, have not been documented electron microscopically in HIV-related myopathy either with or without zidovudine treatment, especially in non-necrotic and non-regenerating fibers. Since various in vitro studies have shown interference of zidovudine with nuclear DNA metabolism even in human cell lines, we assume that the nuclear changes that we observed are at least in part related to zidovudine treatment.
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  • 4
    ISSN: 1432-0533
    Keywords: Muscle spindle ; Denervation ; Reinnervation ; Muscle fiber atrophy ; Mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The fine structure of normal, denervated, and reinnervated muscle spindles in lower lumbrical muscles of rats was studied morphometrically at time intervals ranging from 3–14 months. In control spindles, the mean transverse area of mitochondria was estimated to be more than twice as large in nuclear chain than in typical nuclear bag fibers. Following denervation, there was a severe decrease of the mean number and transverse area of mitochondria, and a moderate, but statistically significant decrease of the mean transverse area of intrafusal muscle fibers (IMFs) despite an increase of the number of IMFs. At 12–14 months of reinnervation, changes of the transverse areas of IMFs were statistically insignificant, but the mean values for the mitochondria were incompletely restored. At 4×3 months, after fourfold repeated crush injuries to the nerve, most of the values estimated (transverse area of mitochondria; number, shape, and transverse area of IMFs and nuclei) tended to approach those in denervated rather than in reinnervated IMFs. The differences of the reactions of intra- and extrafusal muscle fibers following complete motor and sensory denervation appeared to be in accordance with their normal dimensional dissimilarities.
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  • 5
    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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  • 6
    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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  • 7
    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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  • 8
    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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