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  • Electron Microscopy  (5)
  • Chronic inflammatory demyelinating polyneuropathy  (3)
  • Experimental diabetes  (2)
  • 1
    ISSN: 1432-0533
    Keywords: Peripheral nerve ; Experimental diabetes ; Intramembranous particles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Freeze-fracture studies have been made on the sciatic nerve of rats with chronic streptozotocin-induced diabetes mellitus. The density of intramembranous particles was reduced in both the P and E faces of the axolemma of myelinated and unmyelinated axons, in myelin and in the perineurial cells. This may reflect a general reduction in protein synthesis, or excessive protein degradation, related to the diabetic state. The perineurial cells also showed gap junctions which are not normally present in adult rat peripheral nerve. These may represent a reaction to changes in perineurial activity consequent to alterations in the endoneurial tissue fluid.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 53 (1981), S. 257-265 
    ISSN: 1432-0533
    Keywords: Experimental diabetes ; Skeletal growth ; Nerve fibre maturation ; Diabetic neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Observations were made between the ages of 2 and 12 months on rats made diabetic with streptozotocin at the age of 1 month, and compared with the findings in age-matched controls. Tibial length and body weight in the control animals increased progressively over the period examined, the growth rate being more rapid in the initial stages. Both of these parameters were consistently less in the diabetic animals over the whole of the observation period. Myelinated fibre numbers and diameters were measured in the tibial and plantar nerves. In the tibial nerve, fibre diameter did not differ between the diabetic and control animals up until 4 months of age; thereafter it changed little in the diabetic animals, but continued to increase in the controls. The findings in the medial plantar nerve were more difficult to analyse but showed comparable although less pronounced changes; fibre diameter may be have diminished in the diabetic nerves after 6 months. Teased fibre studies demonstrated few abnormalities in the tibial nerve, either in the control or the diabetic rats. In the lateral plantar nerves, there was a significant excess of axonal degeneration and regeneration in the diabetic nerves. It was concluded that diabetes impairs growth in nerve fibre diameter, but only after 4 months of age. Before then, no growth retardation is obvious, despite the fact that tibial length and body weight are less. This suggests that the peripheral nervous system may be protected against growth retardation during the early part of the postnatal growth period. The significance of the axonal degeneration in the plantar nerves is uncertain, but it may represent either an increased vulnerability of diabetic nerve to compression injury or, less probably, a distal axonopathy related to the diabetic state.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Isolated Nerve Fibres ; Electron Microscopy ; Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird eine Technik zur Isolierung peripherer Nervenfasern durch Auffasern und nachfolgende licht-undd elektronenmikroskopische Untersuchung beschrieben. Diese Technik wurde zum Studium ungewöhnlich geschwollener Fasern angewandt, die proximal der Läsion bei durchschnittenen Nerven von Ratten beobachtet wurden. Diese Fasern wurden als das Ergebnis der Demyelinisation bereits remyelinisierter Segmente dargestellt.
    Notes: Summary A technique is described for isolating peripheral nerve fibres by teasing and subsequently examining them by light and electron microscopy. The technique was applied to the study of unusual swollen fibres observed central to the lesion in transected nerves in rats. These were shown to be the result of the demyelination of already remyelinated segments of the fibre.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 18 (1971), S. 150-159 
    ISSN: 1432-0533
    Keywords: Electron Microscopy ; Nerve Regeneration ; Unmyelinated Axons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Eine elektronenmikroskopische Untersuchung über die Regeneration von marklosen Axonen wurde am N. vagus des Kaninchens durchgeführt. Als Folge einer lokalisierten Quetschverletzung des N. vagus am Hals in Höhe der Cartilago thyreoidea wurden die regenerierenden marklosen Axone in den laryngealen Recurrens-Ast abgelenkt, der normalerweise beinahe vollständig aus myelinreichen Fasern aufgebaut ist. Die regenerierenden marklosen Axone kommen um die regenerierenden myelinreichen Axone zu liegen, sind aber mit getrennten Schwannschen Zellen verbunden. Eine mögliche Erklärung für diese aberrierende Regeneration der myelinfreien Axone wird diskutiert, ebenso ihre Bedeutung für die Human-Neuropathologie.
    Notes: Summary An electron microscope investigation has been made into the regeneration of unmyelinated axons in the vagus nerve of the rabbit. Following a localized crush injury of the vagus nerve in the neck at the level of the thyroid cartilage, the regenerating unmyelinated axons become diverted into the recurrent laryngeal branch, which is normally composed almost entirely of myelinated fibres. Here the regenerating unmyelinated axons become arrayed around the regenerating myelinated axons, but are associated with separate Schwann cells. The possible explanation for this aberrant regeneration of the unmyelinated axons is discussed, as is its significance for human neuropathology.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 14 (1969), S. 237-249 
    ISSN: 1432-0533
    Keywords: Electron Microscopy ; Wallerian Degeneration ; Nodal Changes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird über ultrastrukturelle Veränderungen in den Ranvierschen Knoten des N.suralis der Ratte im Laufe der Wallerschen Degeneration berichtet. Die Untersuchungen erfolgten 12 und 120 Std nach einer örtlichen Quetschungsverletzung. Die ersten bemerkbaren Veränderungen finden sich im Axon. Nodale und paranodale Anhäufungen von Mitochondrien, multivesikulären und lamellären Körpern, wie auch kleinen blasen- und röhrenartigen Bildungen sind teilweise in den Knoten sichtbar und am deutlichsten nach 24–36 Std erkennbar. Gleichzeitig erfolgt eine Aufsplitterung der Neurofilamente und Neurotubuli, die ihre Liniengestaltung verlieren und sich zusammenballen. Die Zone der erhöhten Dichte gerade unterhalb des nodalen Axolemmas bleibt erhalten. Veränderungen im Myelin beginnen etwas später und bestehen in einem vesikulären Verfall der Endomyelinlamellen und einer Trennung der Endomyelinschlaufen vom Axolemma durch Schwannzellenfortsätze. Dieser Vorgang schien mit einem Zurückziehen des Myelins vom Knoten im Zusammenhang zu stehen. Schwannzellenfortsätze erstrecken sich auch so weit, daß sie das nodale Axon bedecken, wobei sie die nodalen Schwannzellenfortsätze vom Axolemma trennen. Das Endstadium ist die Unterbrechung des nodalen Axons und die Verschmelzung der Myelinenden als Teil der Ovoidbildung.
    Notes: Summary Observations are reported on the ultrastructural alterations at the nodes of Ranvier in the rat sural nerve during the course of Wallerian degeneration. These were examined between 12 and 120 hours after a localized crush injury. The earliest detectable changes are in the axon. Nodal and paranodal accumulations of mitochondria, multivesicular bodies, lamellar bodies and small vesicular and tubular profiles are seen at a proportion of the nodes and are most evident at 24–36 hours. Concomitantly with this, the neurofilaments and neurotubulus fragment, lose their alignment and clump together. The zone of increased density just beneath the nodal axolemma is preserved. Changes in the myelin begin slightly later and consist of vesicular breakdown of the terminal myelin lamellae, and separation of the terminal myelin loops from the axolemma by Schwann cell processes. The latter event appeared to be associated with retraction of the myelin from the node. Schwann cell processes also extend to cover the nodal axon, separating the Schwann cell nodal processes from the axolemma. The final stage is the interruption of the nodal axon and the fusion of the ends of the myelin as part of ovoid formation.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 26 (1973), S. 317-327 
    ISSN: 1432-0533
    Keywords: Peripheral Neuropathy ; Tangier Disease ; Schwann Cells ; Electron Microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nerve biopsy findings are recorded for two previously reported patients with Tangier disease (hereditary high density lipoprotein deficiency). Both cases showed unusual clinical manifestations in comparison with other reported cases. The neurological disorder, symptoms from which began in the third decade, gave rise to a lower motor neuron deficit of unique distribution, which was accompanied by progressive sensory impairment limited for many years to loss of pain and temperature sensibility, ultimately involving all sensory modalities. Both biopsy specimens displayed similar features, with a gross loss of unmyelinated and myelinated axons, an extensive accumulation of lipid within Schwann cells, and excessive endoneurial collagenization. The axonal loss appeared to represent a primary axonal degeneration, there being no evidence of a demyelinating process. It is suggested that the accumulation of cholesterol within Schwann cells may be the result of a failure of cholesterol removal mechanisms or of intracellular lipid transport.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 11 (1968), S. 93-102 
    ISSN: 1432-0533
    Keywords: Diabetic Neuropathy ; Hypertrophic Changes ; Nerve Biopsy ; Electron Microscopy ; Segmental Demyelination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Beobachtungen an Nervenbiopsien bei 10 aufeinanderfolgenden Patienten mit diabetischer Neuropathie wurden unternommen. 1 Patient wies die für eine hypertrophische Neuropathie typischen licht-und elektronenmikroskopischen Veränderungen auf. 5 zeigten typische hypertrophische Veränderungen, die aber nur bei elektronenmikroskopischer Untersuchung sichtbar waren; bei weiteren wurden ähnliche geringe Veränderungen entdeckt. Es wird angenommen, daß diese Veränderungen durch segmentale Demyelinisation verursacht wurden.
    Notes: Summary Observations have been made on 10 consecutive nerve biopsies from patients with diabetic neuropathy. 1 patient showed the typical appearances of hypertrophic neuropathy on light and electron microscopy. 5 displayed typical hypertrophic changes visible only on electron microscopy and minor abnormalities of a similar nature were seen in 2 others. It was considered that they were likely to have resulted from recurrent segmental demyelination.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 239 (1992), S. 361-362 
    ISSN: 1432-1459
    Keywords: Guillain-Barré syndrome ; Chronic inflammatory demyelinating polyneuropathy ; Demyelination ; Axonopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute inflammatory demyelinating polyneuropathy or the Guillain-Barré syndrome (GBS) has come to be accepted as a clinical entity, although the boundary between it and chronic inflammatory demyelinating polyneuropathy has given rise to discussion. Recent observations have suggested that the GBS may represent the consequence of more than one pathogenetic mechanism. In most cases the salient pathological change is demyelination. In some this may be mediated predominantly by lymphocytes; in others, where the demyelination is produced primarily by macrophages, the process may be antibody-mediated. Both electrophysiological and pathological evidence indicates that occasional patients with the GBS show extensive axonal degeneration. Although this could represent a “bystander effect” secondary to inflammatory infiltration, at times it may reflect a direct attack on axons. Elucidation of the nature of the pathogenetic mechanisms is essential before rational therapy can be devised.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1459
    Keywords: Chronic inflammatory demyelinating polyneuropathy ; Cranial nerve lesions ; Magnetic resonance imaging ; Nerve biopsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Five cases of chronic inflammatory demyelinating polyneuropathy are described in which cranial nerve involvement accompanied a more generalized neuropathy. Clinical, electrophysiological, radiological and nerve biopsy findings are presented. Cranial nerve lesions in this form of polyneuropathy may be related to lesions of the peripheral nerves or of the central nervous system, when they may be accompanied by MRI evidence of more widespread CNS demyelinating lesions. In cases of early onset, the occurrence of focal cranial nerve lesions may serve to distinguish chronic inflammatory from inherited demyelinating polyneuropathies.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1459
    Keywords: Peripheral neuropathy ; Paraproteinaemia ; Chronic inflammatory demyelinating polyneuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Observations have been made on a consecutive series of 62 patients with peripheral neuropathy associated with benign monoclonal paraproteinaemia. The paraprotein class was IgM in 46 cases, IgG in 11 and IgA in 5. Although showing variations between patients, the clinical picture was similar for those with either IgM or IgG paraproteins, usually consisting of a late-onset, slowly progressive, distal sensorimotor demyelinating polyneuropathy, often with tremor and ataxia as prominent features. Tremor was slightly more common in patients with IgM paraproteins, in whom there was a male preponderance. The patients with both paraprotein classes were indistinguishable clinically and electrophysiologically from chronic idiopathic demyelinating polyneuropathy. In the 5 patients with an IgA paraprotein, there was a distal sensorimotor neuropathy in 4 which was demyelinating in 1. In 1 there was proximal demyelinating motor neuropathy. Immunoglobulin deposition on myelin was observed only in the patients with IgM paraproteinaemia, more commonly with a kappa light chain. No deposition of immunoglobulin in the endoneurium was seen. IgM deposits on the perineurium are a feature of normal nerve and were present in all cases. Widely spaced myelin was confined to cases with IgM paraproteins in which immunoglobulin deposition was detected on myelin. The response to treatment could not be assessed systematically but, in general, the patients with IgG and IgA paraproteins responded more satisfactorily (to corticosteroids, cytotoxic drugs, or plasma exchange) than did those with an IgM paraprotein.
    Type of Medium: Electronic Resource
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