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Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage
Patients with poor-grade aneurysmal subarachnoid hemorrhage (SAH) are likely to die due to irreversible acute-stage primary brain damage. However, the mechanism(s) and pathology responsible for their high mortality rate remain unclear. We report our findings on the brains of individuals who died in...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Japan Neurosurgical Society
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5221775/ https://www.ncbi.nlm.nih.gov/pubmed/27357086 http://dx.doi.org/10.2176/nmc.oa.2016-0061 |
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author | SATOMI, Junichiro HADEISHI, Hiromu YOSHIDA, Yasuji SUZUKI, Akifumi NAGAHIRO, Shinji |
author_facet | SATOMI, Junichiro HADEISHI, Hiromu YOSHIDA, Yasuji SUZUKI, Akifumi NAGAHIRO, Shinji |
author_sort | SATOMI, Junichiro |
collection | PubMed |
description | Patients with poor-grade aneurysmal subarachnoid hemorrhage (SAH) are likely to die due to irreversible acute-stage primary brain damage. However, the mechanism(s) and pathology responsible for their high mortality rate remain unclear. We report our findings on the brains of individuals who died in the acute stage of SAH. An autopsy was performed on the brains of 11 SAH patients (World Federation of Neurosurgical Societies grade 5) who died within 3 days of admission and who did not receive respiratory assistance. All brains were free of intracranial hematoma and hydrocephalus; all harbored ruptured aneurysms. In all brains, multiple infarcts with perifocal edema were scattered throughout the cortex and subcortical white matter of the whole brain. Infarcts with a patchy – were more often seen than infarcts with a wedge-shaped pattern. Microscopic examination revealed multiple areas with cytotoxic edema and neuronal death indicative of acute ischemic changes. Edema and congestion were more obvious in areas where the subarachnoid clot tightly adhered to the pia mater. Pathologically, the brains of deceased patients with acute poor-grade SAH were characterized by edema and multifocal infarcts spread throughout the whole brain; they were thought to be attributable to venous ischemia. Diffuse disturbance in venous drainage attributable to an abrupt increase in the intracranial pressure and focal disturbances due to tight adhesion of the subarachnoid clot to the pia mater, may contribute strongly to irreversible brain damage in the acute stage of SAH. |
format | Online Article Text |
id | pubmed-5221775 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Japan Neurosurgical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-52217752017-01-17 Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage SATOMI, Junichiro HADEISHI, Hiromu YOSHIDA, Yasuji SUZUKI, Akifumi NAGAHIRO, Shinji Neurol Med Chir (Tokyo) Original Article Patients with poor-grade aneurysmal subarachnoid hemorrhage (SAH) are likely to die due to irreversible acute-stage primary brain damage. However, the mechanism(s) and pathology responsible for their high mortality rate remain unclear. We report our findings on the brains of individuals who died in the acute stage of SAH. An autopsy was performed on the brains of 11 SAH patients (World Federation of Neurosurgical Societies grade 5) who died within 3 days of admission and who did not receive respiratory assistance. All brains were free of intracranial hematoma and hydrocephalus; all harbored ruptured aneurysms. In all brains, multiple infarcts with perifocal edema were scattered throughout the cortex and subcortical white matter of the whole brain. Infarcts with a patchy – were more often seen than infarcts with a wedge-shaped pattern. Microscopic examination revealed multiple areas with cytotoxic edema and neuronal death indicative of acute ischemic changes. Edema and congestion were more obvious in areas where the subarachnoid clot tightly adhered to the pia mater. Pathologically, the brains of deceased patients with acute poor-grade SAH were characterized by edema and multifocal infarcts spread throughout the whole brain; they were thought to be attributable to venous ischemia. Diffuse disturbance in venous drainage attributable to an abrupt increase in the intracranial pressure and focal disturbances due to tight adhesion of the subarachnoid clot to the pia mater, may contribute strongly to irreversible brain damage in the acute stage of SAH. The Japan Neurosurgical Society 2016-12 2016-06-30 /pmc/articles/PMC5221775/ /pubmed/27357086 http://dx.doi.org/10.2176/nmc.oa.2016-0061 Text en © 2016 The Japan Neurosurgical Society This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/ |
spellingShingle | Original Article SATOMI, Junichiro HADEISHI, Hiromu YOSHIDA, Yasuji SUZUKI, Akifumi NAGAHIRO, Shinji Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage |
title | Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage |
title_full | Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage |
title_fullStr | Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage |
title_full_unstemmed | Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage |
title_short | Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage |
title_sort | histopathological findings in brains of patients who died in the acute stage of poor-grade subarachnoid hemorrhage |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5221775/ https://www.ncbi.nlm.nih.gov/pubmed/27357086 http://dx.doi.org/10.2176/nmc.oa.2016-0061 |
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