Secondary thalamic lesions after ligation of the middle cerebral artery: an ultrastructural study
(1995) In Acta Neuropathologica 91(1). p.61-66- Abstract
- Earlier light microscopic, immunocytochemical and morphometric investigations indicate that noxious substances transported with the vasogenic edema from hemispheric infarcts influence the character, timing and extent of the secondary thalamic lesions. The object of the present study was to analyze the ultrastructure of the secondary damage and the cytolytic nerve cell change which ensues in the thalamus within a week after the infarction. Adult spontaneously hypertensive rats (SHR) were studied either 7 days after permanent ligation of the right middle cerebral artery (MCA) (n = 4) or 7 days after a 2-h temporary occlusion of the MCA (n = 4). Light microscopy revealed damage in the ipsilateral thalamic nuclei and the electron microscopic... (More)
- Earlier light microscopic, immunocytochemical and morphometric investigations indicate that noxious substances transported with the vasogenic edema from hemispheric infarcts influence the character, timing and extent of the secondary thalamic lesions. The object of the present study was to analyze the ultrastructure of the secondary damage and the cytolytic nerve cell change which ensues in the thalamus within a week after the infarction. Adult spontaneously hypertensive rats (SHR) were studied either 7 days after permanent ligation of the right middle cerebral artery (MCA) (n = 4) or 7 days after a 2-h temporary occlusion of the MCA (n = 4). Light microscopy revealed damage in the ipsilateral thalamic nuclei and the electron microscopic analysis showed that the cytolytic nerve cell degeneration was somatodendritic. Central chromatolysis was not observed. Somatodendritic nerve cell degeneration, as found in the secondary thalamic lesions in the present study, has been described in excitotoxic brain damage as well as in chronic, edematous lesions in stroke-prone spontaneously hypertensive rats. The possibility that the cytolytic thalamic nerve cell lesion is influenced by excitatory, noxious substances spreading with the edema fluid from the infarct has, thus, to be considered. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1110518
- author
- Nordborg, C and Johansson, Barbro LU
- organization
- publishing date
- 1995
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Brain infarct, Temporary arterial occlusion, Permanent arterial occlusion, Vasogenic edema, Thalamus
- in
- Acta Neuropathologica
- volume
- 91
- issue
- 1
- pages
- 61 - 66
- publisher
- Springer
- external identifiers
-
- pmid:8773147
- scopus:0029655560
- ISSN
- 1432-0533
- DOI
- 10.1007/s004010050392
- language
- English
- LU publication?
- yes
- id
- dac5515c-0fd6-4870-8b9e-a117ab11f463 (old id 1110518)
- date added to LUP
- 2016-04-01 15:48:05
- date last changed
- 2021-04-18 05:47:23
@article{dac5515c-0fd6-4870-8b9e-a117ab11f463,
abstract = {{Earlier light microscopic, immunocytochemical and morphometric investigations indicate that noxious substances transported with the vasogenic edema from hemispheric infarcts influence the character, timing and extent of the secondary thalamic lesions. The object of the present study was to analyze the ultrastructure of the secondary damage and the cytolytic nerve cell change which ensues in the thalamus within a week after the infarction. Adult spontaneously hypertensive rats (SHR) were studied either 7 days after permanent ligation of the right middle cerebral artery (MCA) (n = 4) or 7 days after a 2-h temporary occlusion of the MCA (n = 4). Light microscopy revealed damage in the ipsilateral thalamic nuclei and the electron microscopic analysis showed that the cytolytic nerve cell degeneration was somatodendritic. Central chromatolysis was not observed. Somatodendritic nerve cell degeneration, as found in the secondary thalamic lesions in the present study, has been described in excitotoxic brain damage as well as in chronic, edematous lesions in stroke-prone spontaneously hypertensive rats. The possibility that the cytolytic thalamic nerve cell lesion is influenced by excitatory, noxious substances spreading with the edema fluid from the infarct has, thus, to be considered.}},
author = {{Nordborg, C and Johansson, Barbro}},
issn = {{1432-0533}},
keywords = {{Brain infarct; Temporary arterial occlusion; Permanent arterial occlusion; Vasogenic edema; Thalamus}},
language = {{eng}},
number = {{1}},
pages = {{61--66}},
publisher = {{Springer}},
series = {{Acta Neuropathologica}},
title = {{Secondary thalamic lesions after ligation of the middle cerebral artery: an ultrastructural study}},
url = {{http://dx.doi.org/10.1007/s004010050392}},
doi = {{10.1007/s004010050392}},
volume = {{91}},
year = {{1995}},
}