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Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports
We report on patients with post-traumatic fatigue and hypersomnia who showed injury of the lower portion of the ascending reticular activating system (ARAS) between the pontine reticular formation (RF) and the intralaminar thalamic nucleus (ILN) following mild traumatic brain injury (TBI), using dif...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Wolters Kluwer Health
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753878/ https://www.ncbi.nlm.nih.gov/pubmed/26871783 http://dx.doi.org/10.1097/MD.0000000000002628 |
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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 | We report on patients with post-traumatic fatigue and hypersomnia who showed injury of the lower portion of the ascending reticular activating system (ARAS) between the pontine reticular formation (RF) and the intralaminar thalamic nucleus (ILN) following mild traumatic brain injury (TBI), using diffusion tensor tractography (DTT). Two patients with mild TBI resulting from a car accident were enrolled in this study. Patient 1 was a 51-year-old woman showed abnormalities as 6.9 (cut off: 3.7 points) and 18 (cut off: 10) on the Fatigue Severity Scale and the Epworth Sleepiness Scale at 11 months after onset. Patient 2 was a 64-year-old woman who revealed abnormalities on the Fatigue Severity Scale and the Epworth Sleepiness Scale with 6.8 and 19 at 3 months after onset. In both patients, the upper ARAS in which the neural connectivity of the ILN to the cerebral cortex did not show significant abnormalities. However, we observed the narrowing of the left dorsal lower ARAS between the pontine RF and the ILN in both patients and the tearing (patient 1) and narrowing (patient 2) of the left ventral lower ARAS between the pontine RF and the hypothalamus. Injuries of the dorsal and ventral lower ARAS were demonstrated in patients with fatigue and hypersomnia following mild TBI. We believe that these injuries of the ARAS might be a pathogenetic mechanism of fatigue and hypersomnia in patients with TBI. |
format | Online Article Text |
id | pubmed-4753878 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Wolters Kluwer Health |
record_format | MEDLINE/PubMed |
spelling | pubmed-47538782016-02-26 Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports Jang, Sung Ho Kwon, Hyeok Gyu Medicine (Baltimore) 5300 We report on patients with post-traumatic fatigue and hypersomnia who showed injury of the lower portion of the ascending reticular activating system (ARAS) between the pontine reticular formation (RF) and the intralaminar thalamic nucleus (ILN) following mild traumatic brain injury (TBI), using diffusion tensor tractography (DTT). Two patients with mild TBI resulting from a car accident were enrolled in this study. Patient 1 was a 51-year-old woman showed abnormalities as 6.9 (cut off: 3.7 points) and 18 (cut off: 10) on the Fatigue Severity Scale and the Epworth Sleepiness Scale at 11 months after onset. Patient 2 was a 64-year-old woman who revealed abnormalities on the Fatigue Severity Scale and the Epworth Sleepiness Scale with 6.8 and 19 at 3 months after onset. In both patients, the upper ARAS in which the neural connectivity of the ILN to the cerebral cortex did not show significant abnormalities. However, we observed the narrowing of the left dorsal lower ARAS between the pontine RF and the ILN in both patients and the tearing (patient 1) and narrowing (patient 2) of the left ventral lower ARAS between the pontine RF and the hypothalamus. Injuries of the dorsal and ventral lower ARAS were demonstrated in patients with fatigue and hypersomnia following mild TBI. We believe that these injuries of the ARAS might be a pathogenetic mechanism of fatigue and hypersomnia in patients with TBI. Wolters Kluwer Health 2016-02-12 /pmc/articles/PMC4753878/ /pubmed/26871783 http://dx.doi.org/10.1097/MD.0000000000002628 Text en Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. http://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0, where it is permissible to download, share and reproduce the work in any medium, provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0 |
spellingShingle | 5300 Jang, Sung Ho Kwon, Hyeok Gyu Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports |
title | Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports |
title_full | Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports |
title_fullStr | Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports |
title_full_unstemmed | Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports |
title_short | Injury of the Ascending Reticular Activating System in Patients With Fatigue and Hypersomnia Following Mild Traumatic Brain Injury: Two Case Reports |
title_sort | injury of the ascending reticular activating system in patients with fatigue and hypersomnia following mild traumatic brain injury: two case reports |
topic | 5300 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753878/ https://www.ncbi.nlm.nih.gov/pubmed/26871783 http://dx.doi.org/10.1097/MD.0000000000002628 |
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