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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    International journal of legal medicine 105 (1993), S. 243-245 
    ISSN: 1437-1596
    Keywords: Intraventricular haemorrhage ; Head injury ; Traumatic subarachnoid haemorrhage ; Intraventrikuläre Blutung ; Kopftrauma ; Traumatische Subarachnoidalblutung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Law
    Description / Table of Contents: Zusammenfassung Der Fall eines 26 Jahre alten Mannes wird beschrieben, welcher nach einer Episode von Traumen eine tödliche intraventrikuläre Hirnblutung erlitt. Bei der Obduktion wurde nach dem ersten Eindruck eine traumatische Subarachnoidalblutung vermutet, und die anfängliche Untersuchung war daher auf die Strukturen des Halses und auf die Vertebralarterien gerichtet, jedoch mit negativen Resultaten. Die Sektion des fixierten Gehirns zeigte eine massive intraventrikuläre Blutung mit sekundärer Beteiligung des Subarachnoidalraums und Ausbreitung in das Hirnparenchym. Keine Blutungsquellen oder natürliche Erkrankungen der Hirngefäße konnten gefunden werden. Die praktischen Aspekte der Diagnose und der vorsichtige Ansatz, welcher notwendig ist, um Subarachnoidalblutungen zu interpretieren, werden betont. Die Bedeutung der intraventrikulären Blutung nach Trauma ist mit der Einführung der Computertomographie offensichtlicher geworden. Die Implikationen dieses und ähnlicher Fälle werden bedacht.
    Notes: Summary A case of a 26-year-old man who suffered a fatal intraventricular cerebral haemorrhage following an episode of trauma is described. The initial appearance at necropsy suggested a traumatic subarachnoid haemorrhage and initial investigation was directed towards the anterior neck structures and the vertebral arteries with negative results. Dissection of the fixed brain showed a massive intraventricular bleed with secondary involvement of the subarachnoid space and dissection into the cerebral parenchyma. No bleeding points or natural disease of the cerebral vessels could be identified. The practical aspects of diagnosis and the cautious approach necessary in interpreting subarachnoid bleeding is emphasised. The significance of intraventricular haemorrhage following trauma has become more apparent with the advent of computed tomographic scanning. The implications for this and similar cases are considered.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1463
    Keywords: Aging ; amyotrophic lateral sclerosis ; synaptophysin ; brain aging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Aged-related spinal cord changes such as neuronal loss have been related to the degree of clinical severity of amyotrophic lateral sclerosis (ALS); morphological data on synapses are, however, wanting. Variations in synaptophysin (Sph) expression in aging and ALS were thus studied at the level of lower motor neurons in 40 controls with non-neurological diseases and 11 cases of ALS. Control sections of formalin fixed paraffin embedded cervical (C7/8), thoracic (T10) and lumbar spinal cord (L5) and C6, C7, C8 and L5 of ALS cases were stained with haematoxylin and eosin, luxol fast blue (LFB), and immunostained with a mouse monoclonal antibody against Sph. The neuropil of the anterior horn (AH) in all control cases demonstrated Sph positivity. A dot-like pattern of positivity of presynaptic terminals on soma of motor neurons and fine immunoreactivity along neuronal processes were observed. A significant reduction of Sph immunostaining was observed in the neuropil with increasing age and 3 different somatic patterns were seen: a-well preserved Sph reactivity around the soma and the proximal dendrites of histologically normal neurons; b-few chromatolytic neurons showing large numbers of dot-like presynaptic terminals around the cell body and in a “fused” pattern; c-intense, diffuse, and homogeneous reactivity of some neurons. Attenuation of Sph reactivity in the AH neuropil, to its complete loss, was observed in all ALS cases. In addition to patterns a-c, two additional microscopic findings were noted in ALS: d-chromatolytic neurons showing complete absence of Sph reactivity; e-absence of Sph reactivity around the soma and the proximal dendrites of histologically normal surviving neurons. Our findings demonstrate that there is a decrease in Sph immunostaining with aging, thus suggesting an alteration in dendritic networks of the AH with aging. Changes in the pattern of Sph immunoreactivity in cell bodies may represent synaptic plasticity and/or degeneration. Reinnervation may also be a possible mechanism as a response to neuronal loss in oldest control cases. Sph reactivity results may thus lend support to the presence of superimposed aging components in ALS cases which may give an insight into explaining the increasing severity of the disease which is encountered with advancing age.
    Type of Medium: Electronic Resource
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