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  • 1
    Electronic Resource
    Electronic Resource
    The morphopathologic substrates of concussion? (1979)
    Springer
    Acta neuropathologica 47 (1979), S. 1-11 
    Details
    ISSN: 1432-0533
    Keywords: Experimental Concussion ; Peroxidase, neuronal uptake ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neuronal inundation with i.v. infused horseradish peroxidase was studied following concussive brain injury by means of both light and electron microscopy. In animals sustaining mechanical brain injury of insufficient intensity as to elicit either microscopic intraparenchymal hemorrhage or other neuropathological change, yet of sufficient intensity as to provoke a physiological concussive response, vascular peroxidase exudation concomitant with neuronal peroxidase inundation occurred throughout the raphe and reticular core. Initially such inundated neurons were totally flooded with the tracer and as such appeared reminiscent of cells visualized in Golgi preparations. However, over the course of a 24-h period these peroxidase flooded neurons apparently organized the peroxidase into vesicles and vacuoles which assumed a perinuclear position from where the peroxidase ultimately reached both the nucleus und nucleolus. It was remarkable that these events occurred without any evidence of subcellular alteration. We interpret such initial inundation with this protein tracer, its ultimate reorganization, and its nuclear and nucleolar uptake as being consistent with some form of subtle and transient neuronal perturbation. We speculate that as such this neuronal perturbation may constitute a morphological correlate of the concussive episode.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00698266
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  • 2
    Electronic Resource
    Electronic Resource
    The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia (1981)
    Springer
    Acta neuropathologica 55 (1981), S. 205-220 
    Details
    ISSN: 1432-0533
    Keywords: Postischemic recirculation ; Complete cerebral ischemia ; Ischemic neuronal injury ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The neuronal response to complete cerebral ischemia (CCI) of 5–15 min duration was evaluated at the light and electron microscopic level subsequent to postischemic recirculation periods of up to 60 min. Following postischemic reperfusion, the homogeneous neuronal changes characteristic of permanent CCI were modified into a heterogeneous pattern of selectively vulnerable neuronal responses. Four basic types of neuronal injury were represented within this heterogeneous neuronal population. The Type I neuronal response was most numerous and consisted of chromatin clumping, nucleolar condensation and a breakdown of polysomes. This response may represent a reversal of some of the neuronal changes observed after permanent CCI. In addition to the above changes, Type II neurons contained swollen mitochondria and Golgi saccules which appeared as microvacuoles under the light microscope. Type III neurons displayed varying degrees of neuronal shrinkage and numerous swollen mitochondria. Type IV neurons were markedly shrunken and electron-dense with few identifiable subcellular structures. The distribution of Type I neurons was random but the other neuronal responses occurred in “selectively vulnerable” brain regions. The number of Type II, III, and IV neurons increased with extended insult durations but were unaffected by the length of recirculation. Ten minutes of CCI represented the threshold for a significant increase in the number of severely altered neurons. These findings suggest that considerable neuronal injury may be present after 10–15 min of CCI, and the lack of a recirculation period following CCI appears to afford the brain parenchyma an extensive degree of structural protection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691320
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    A scanning electron-microscopic analysis of the intraparenchymal brain vasculature following experimental hypertension (1980)
    Springer
    Acta neuropathologica 51 (1980), S. 203-213 
    Details
    ISSN: 1432-0533
    Keywords: Cerebrovascular ; Acute hypertension ; Peroxidase ; Scanning electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of acute systemic hypertension on the intraparenchymal cerebral vasculature of cats was assessed by morphological means. Intravenous horseradish peroxidase administration coupled with light microscopy was employed to identify brain sites manifesting hypertension-induced peroxidase extravasation and therein the luminal surface of the intraparenchymal vasculature was examined with scanning electron microscopy (SEM). Comparable SEM studies were also conducted within sites reflecting no altered peroxidase permeability. Via these techniques, hypertension was recognized to evoke significant vascular change throughout the neuraxis. The luminal endothelia of that vasculature contained within the peroxidase extravasation sites demonstrated numerous plasmalemmal pits and the occasional presence of balloon- and crater-like lesions which were localized along the marginal lines. In sites demonstrating no peroxidase exudation, these plasmalemmal pits were infrequent; yet, the balloon and crater-like lesions, again localized along the marginal lines, were now conspicuous and regular endothelial features. Within the peroxidase extravasation sites, plasmalemmal pits could be identified within minutes of the onset of the hypertensive event, while in all loci endothelial balloons were observed prior to the appearance of craters. These results demonstrate that numerous plasmalemmal pits, the SEM correlates of vesicles observed with transmission electron microscopy, appear to be temporally and spatially linked to the peroxidase extravasation and as such this may suggest that these phenomena are causally linked. The significance of endothelial balloons and craters, which are most prevalent in sites not manifesting peroxidase extravasation, is unclear; however, based on a parallel study conducted in the pial vasculature, the suggestion is advanced that their appearance may be linked to the loss of microvascular autoregulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687387
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  • 4
    Electronic Resource
    Electronic Resource
    Acute ultrastructural response of hypoxic hypoxia with relative ischemia in the isolated brain (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 637-648 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral hypoxia ; Cerebral ischemia ; Ultrastructure ; Neocortex ; Brain isolation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The acute cortical response to surgical brain isolation and subsequent extracorporal normoxic or 30 min hypoxic (PaO2=20 mm Hg) perfusions (hypoxic hypoxia with relative ischemia) was evaluated. Cerebral blood flow, arterial pH and CO2 were maintained constant during both perfusions; only the arterial oxygen content was changed. The isolated brain model used in this and previous investigations produces no qualitative ultrastructural changes in the neocortex following brain isolation and normoxic perfusion. However, the acute cortical structural response to 30 min of hypoxic hypoxia with relative ischemia demonstrated a number of important observations. Hypoxic hypoxia produced ultrastructural responses common to cerebral ischemia such as nuclear chromatin clumping, nucleolar condensation and cytoskeletal breakdown. Although neuronal abnormalities seen after 30 min of hypoxic hypoxia were similar to those acute neuronal changes observed following complete cerebral ischemia without recirculation, they differed three ways: (a) mitochondrial swelling and microvacuolation were observed in many cortical pyramidal neurons. (b) Glycogen particles within astroglial processes were observed even after a 30-min period of hypoxic hypoxia. (c) Perivascular astroglial swelling was minimal despite considerable perineuronal swelling. In contrast, incomplete cerebral ischemia produces mitochondrial changes similar to those in hypoxic hypoxia but also causes the depletion of tissue glycogen and perivascular glial swelling. Thus, hypoxic hypoxia with relative ischemia produces a unique acute ultrastructural response compared to either complete or incomplete cerebral ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691291
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Moderate hypothermia reduces blood-brain barrier disruption following traumatic brain injury in the rat (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 495-500 
    Details
    ISSN: 1432-0533
    Keywords: Traumatic brain injury ; Hypothermia ; Blood-brain barrier ; Hypertension ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of moderate hypothermia on blood-brain barrier (BBB) permeability and the acute hypertensive response after moderate traumatic brain injury (TBI) in rats were examined. TBI produced increased vascular permeability to endogenous serum albumin (IgG) in normothermic rats (37.5°C) throughout the dorsal cortical gray and white matter as well as in the underlying hippocampi as visualized by immunocytochemical techniques. Vascular permeability was greatly reduced in hypothermic rats cooled to 30°C (brain temperature) prior to injury. In hypothermic rats, albumin immunoreactivity was confined to the gray-white interface between cortex and hippocampi with no involvement of the overlying cortices and greatly reduced involvement of the underlying hippocampi. The acute hypertensive response in normothermic rats peaked at 10 s after TBI (187.3 mm Hg) and returned to baseline within 50 s. In contrast, the peak acute hypertensive response was significantly (P〈0.05) reduced in hypothermic rats (154.8 mm Hg, 10 s after TBI) and returned to baseline at 30 s after injury. These results demonstrate that moderate hypothermia greatly reduces endogenous vascular protein-tracer passage into and perhaps through the brain. This reduction may, in part, be related to hypothermia-induced modulation of the systemic blood pressure response to TBI.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00304468
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    Paper (German National Licenses)
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