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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 52 (1980), S. 141-145 
    ISSN: 1432-0533
    Keywords: Brain tissue necrosis ; Phagocytic pigments ; Ceroid ; Pigment maturation ; Histochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ceroid pigment of macrophages were subdivided into four different types according to their own color and their ability to stain with luxol fast blue. With reference to this mode a series of more than 200 brain infarcts which had happened 1 day to 56 years before death, was examined systematically. According to the results the ceroid variants do not only succeed one another chronologically but they also represent histochemically successive phases of development which correspond to the progressive auto-oxidation of unsaturated lipids. The occurrence of the different stages is chronologically defined. During this development cortical and subcortical macrophages show different speeds in the ageing process of their pigments. There is no evidence for an essential participation of proteins in the maturation of the ceroid. Not during any phase of development is the reaction pattern identical with that of neuronal and glial lipofuscin.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1437-2320
    Keywords: Brain death ; Malignant brain swelling ; Temporal pattern ; Hirntod ; Maligne verlaufende Hirnschwellung ; Zeitverläufe
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Dynamik der therapeutisch nicht beeinflußbaren Hirnschwellung wurde an 96 autopsierten Fällen analysiert. Sie waren aus einem großen Material von Hirntod-Fällen nach folgenden Gesichtspunkten ausgewählt worden: die Initialläsion wie auch der Eintritt des Hirntodes waren zeitlich genügend scharf bestimmbar, sie hatten weder Entzündungen noch Tumoren oder Hirnoperationen, sie waren nicht Kinder unter 1 Jahr und sie hatten keine sekundären Infarkte oder Rezidivblutungen nach einer Aneurysma-Ruptur. Die Daten zeigen eine ausgeprägte Variation des Zeitintervalles von der Primärläsion bis zum Eintritt des Hirntodes. Sie reicht von 0 Stunden bis zu 11 Tagen mit einem Medianwert von 24 Stunden. Diese Intervalle sind unabhängig von Art und Schwere der Initialläsion (Tab. I) und vom Alter (Tab. II) mit Ausnahme von Kindern unter 10 Jahren, die nach Kürzerer Zeitdauer gestorben waren. Der Schwellungsprozeß zeigt also eine Eigendynamik, die aber wegen der großen Variation nicht durch stetige Progression erklärt werden kann. Die Analyse der Zeitspannen mit Hilfe des Weibull-Wahrscheinlichkeitsnetzes (Abb. 2) zeigt eine bimodale Häufigkeitsverteilung, die aus der Überlagerung von 2 Faktoren zu erklären ist, nämlich: 1. dem Hirnödem und 2. dem finalen Verlust der Autoregulation der Hirngefäße mit irreversibler Schwellung des Gehirns und hochgradiger intrakranieller Druckerhöhung. Im Durchschnitt verläuft die maligne, letal endende Hirnschwellung rascher als das übliche Hirnödem. Sie wird aber bis zu 11 Tagen beobachtet, ohne daß Hinweise auf sekundär entstandene Hirnschäden vorliegen.
    Notes: Summary The dynamics of brain swelling which does not respond to any form of treatment was analysed in 96 autopsy cases. These were selected from many cases of brain death, according to the following criteria: the time of occurrence of the initial lesion, as well as the onset of brain death, could be precisely determined; the patients had no inflammation, tumour of the brain or previous brain operation; there were no children under one year of age and there were no secondary infarctions or recurrences of bleeding after rupture of an aneurysm. The findings show a wide variation in the period of time between the primary lesion and the onset of brain death. This ranges from zero hours to eleven days, with a median of 24 hours. These intervals are independent of the nature and severity of the lesion (Table I) and of the age (Table II) with the exception of children under ten years, who died after a shorter interval. This process of brain swelling appears to show inherent dynamics, which because of the great variation cannot be explained by a steady progression. The analysis of the time intervals on Weibull-probability graph-paper (Figure 2) shows a bimodal frequency distribution, which can be explained by the superimposition of two factors, namely (i) brain oedema and (ii) a final loss of autoregulation of the cerebral vessels with irreversible swelling of the brain and severe intracranial hypertension. On average, this malignant and fatal brain swelling advances more rapidly than the “ordinary” brain oedema, but it can be observed up to eleven days without any signs of secondary damage to the brain.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 52 (1980), S. 147-151 
    ISSN: 1432-0533
    Keywords: Special chromolipids ; Histochemistry ; Fluorescent microscopy ; Hemorrhagic brain tissue necroses
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A serial and comparative histochemical examination of lipopigments in human brain tissue necroses led to a more exact characterization of a chromolipid called “hemoceroid”. It arises only in necroses with hemorrhages and not in anemic necroses nor in subdural hematomas. Its histochemical properties differ from those of all developmental stages of ceroid. An ageing phenomenon is absent. The very intense autofluorescence of the thick, clotted pigment ist striking. Hemoceroid seems to arise extracellularly and is absorbed secondarily by macrophages.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 62 (1983), S. 15-23 
    ISSN: 1432-0533
    Keywords: Brain death ; Ischemic neuronal alterations ; Brain stem ; Meningoencephalitic reaction ; Reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The varying cell picture of the brain in brain death is impressive. Some authors have interpreted this cell picture as a result of intravital autolysis and others as necrosis, at which the maturation time obviously plays an important part. The following time-dependent cerebral changes were established on the basis of an evaluation of 190 brain death cases: (1) neuronal necroses that arise at different rates within the cerebral cortex and the lower brain stem; (2) a hemorrhagic-meningoencephalitic reaction that occurs exclusively at least 4 days after brain death or hemorrhages alone after intervals of at least 48 h; and (3) a washed-out tissue picture. The alterations in the spinal border zone of the total infarction, like in the brain itself, increase rapidly after 48 h. The regular onset of inflammatory alterations after long brain death intervals can only be explained by partial recirculation due to a decline of the high intracranial pressure. The hermorrhages and increasing necroses in some cases with longer intervals therefore are likewise evidence of a not entirely complete cerebral ischemia in spite of an angiographically demonstrable circulatory arrest.
    Type of Medium: Electronic Resource
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