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Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report
BACKGROUND: Delayed post-hypoxic leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by neurological relapse after an initial recovery from hypoxic brain injury. We describe a patient with impaired consciousness following DPHL, concurrent with injury of the ascending reticular activ...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5517815/ https://www.ncbi.nlm.nih.gov/pubmed/28724360 http://dx.doi.org/10.1186/s12883-017-0917-z |
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author | Jang, Sung Ho Kwon, Hyeok Gyu |
author_facet | Jang, Sung Ho Kwon, Hyeok Gyu |
author_sort | Jang, Sung Ho |
collection | PubMed |
description | BACKGROUND: Delayed post-hypoxic leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by neurological relapse after an initial recovery from hypoxic brain injury. We describe a patient with impaired consciousness following DPHL, concurrent with injury of the ascending reticular activating system (ARAS) shown using diffusion tensor tractography (DTT). CASE PRESENTATION: A 50-year-old male patient was in a drowsy mental state after exposure to carbon monoxide (CO) for about ten hours. About a day after the CO exposure, his mental state recovered to an alert condition. However, his consciousness deteriorated to drowsy 24 days after the exposure and worsened to a semi-coma state at 26 days after onset. When he started rehabilitation six weeks after the CO exposure, he had impaired consciousness, with a Glasgow Coma Scale score of 8 and a Coma Recovery Scale-Revised score of 8. On 6-week DTT, decreased neural connectivity of the upper ARAS between the intralaminar thalamic nucleus and the cerebral cortex was observed in both frontal cortices, basal forebrains, basal ganglia and thalami. The lower dorsal ARAS was not reconstructed on the right side, and was thin on the left side. The lower ventral ARAS was not reconstructed on either side. CONCLUSIONS: Using DTT, we demonstrated injury of the ARAS in a patient with impaired consciousness following DPHL. Our result suggests that injury of the ARAS is a plausible pathogenetic mechanism of impaired consciousness in patients with DPHL. |
format | Online Article Text |
id | pubmed-5517815 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-55178152017-08-16 Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report Jang, Sung Ho Kwon, Hyeok Gyu BMC Neurol Case Report BACKGROUND: Delayed post-hypoxic leukoencephalopathy (DPHL) is a demyelinating syndrome characterized by neurological relapse after an initial recovery from hypoxic brain injury. We describe a patient with impaired consciousness following DPHL, concurrent with injury of the ascending reticular activating system (ARAS) shown using diffusion tensor tractography (DTT). CASE PRESENTATION: A 50-year-old male patient was in a drowsy mental state after exposure to carbon monoxide (CO) for about ten hours. About a day after the CO exposure, his mental state recovered to an alert condition. However, his consciousness deteriorated to drowsy 24 days after the exposure and worsened to a semi-coma state at 26 days after onset. When he started rehabilitation six weeks after the CO exposure, he had impaired consciousness, with a Glasgow Coma Scale score of 8 and a Coma Recovery Scale-Revised score of 8. On 6-week DTT, decreased neural connectivity of the upper ARAS between the intralaminar thalamic nucleus and the cerebral cortex was observed in both frontal cortices, basal forebrains, basal ganglia and thalami. The lower dorsal ARAS was not reconstructed on the right side, and was thin on the left side. The lower ventral ARAS was not reconstructed on either side. CONCLUSIONS: Using DTT, we demonstrated injury of the ARAS in a patient with impaired consciousness following DPHL. Our result suggests that injury of the ARAS is a plausible pathogenetic mechanism of impaired consciousness in patients with DPHL. BioMed Central 2017-07-19 /pmc/articles/PMC5517815/ /pubmed/28724360 http://dx.doi.org/10.1186/s12883-017-0917-z Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Case Report Jang, Sung Ho Kwon, Hyeok Gyu Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
title | Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
title_full | Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
title_fullStr | Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
title_full_unstemmed | Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
title_short | Injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
title_sort | injury of ascending reticular activating system associated with delayed post-hypoxic leukoencephalopathy: a case report |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5517815/ https://www.ncbi.nlm.nih.gov/pubmed/28724360 http://dx.doi.org/10.1186/s12883-017-0917-z |
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