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Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage
INTRODUCTION: Paroxysmal sympathetic hyperactivity (PSH) is a hyperadrenergic syndrome that may follow acute brain injury characterized by episodic, hyperadrenergic alterations in vital signs. Identifying commonality in lesion localization in patients with PSH is challenging, but intraparenchymal he...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BlackWell Publishing Ltd
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043289/ https://www.ncbi.nlm.nih.gov/pubmed/24904923 http://dx.doi.org/10.1002/acn3.44 |
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author | Gao, Billy Pollock, Jeffrey A Hinson, Holly E |
author_facet | Gao, Billy Pollock, Jeffrey A Hinson, Holly E |
author_sort | Gao, Billy |
collection | PubMed |
description | INTRODUCTION: Paroxysmal sympathetic hyperactivity (PSH) is a hyperadrenergic syndrome that may follow acute brain injury characterized by episodic, hyperadrenergic alterations in vital signs. Identifying commonality in lesion localization in patients with PSH is challenging, but intraparenchymal hemorrhage (IPH) represents a focal injury that might provide insight. We describe a series of patients with IPH that developed PSH, and review the literature. METHODS: Patients with IPH who developed PSH were identified from OHSU hospital records. A literature review was conducted to identify similar cases through PUBMED, OVID, and Google Scholar. RESULTS: Three cases meeting criteria for PSH were identified. Hemorrhage volume ranged from 70 to 128 mL, and intracranial hemorrhage score ranged from 2 to 3. The laterality of the hemorrhage and significant volume of hemorrhage was similar in each of the patients, specifically all hemorrhages were large, subcortical, and right-sided. A literature search identified six additional cases, half of whom reported a right hemisphere hemorrhage and the majority also had subcortical localization. CONCLUSIONS: Our literature review identified six cases of IPH associated with PSH with five cases having subcortical lesion locations, echoing the areas of disruption in our three cases. On the basis of these observations, we hypothesize that injuries along the pathway from the insular cortex to downstream sympathetic centers may remove tonic inhibition leading to unchecked sympathetic outflow. Prospective investigations of lesion location in patients with IPH and PSH are warranted to test this hypothesis, especially with advanced neuroimaging techniques. |
format | Online Article Text |
id | pubmed-4043289 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BlackWell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-40432892014-06-03 Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage Gao, Billy Pollock, Jeffrey A Hinson, Holly E Ann Clin Transl Neurol Case Study INTRODUCTION: Paroxysmal sympathetic hyperactivity (PSH) is a hyperadrenergic syndrome that may follow acute brain injury characterized by episodic, hyperadrenergic alterations in vital signs. Identifying commonality in lesion localization in patients with PSH is challenging, but intraparenchymal hemorrhage (IPH) represents a focal injury that might provide insight. We describe a series of patients with IPH that developed PSH, and review the literature. METHODS: Patients with IPH who developed PSH were identified from OHSU hospital records. A literature review was conducted to identify similar cases through PUBMED, OVID, and Google Scholar. RESULTS: Three cases meeting criteria for PSH were identified. Hemorrhage volume ranged from 70 to 128 mL, and intracranial hemorrhage score ranged from 2 to 3. The laterality of the hemorrhage and significant volume of hemorrhage was similar in each of the patients, specifically all hemorrhages were large, subcortical, and right-sided. A literature search identified six additional cases, half of whom reported a right hemisphere hemorrhage and the majority also had subcortical localization. CONCLUSIONS: Our literature review identified six cases of IPH associated with PSH with five cases having subcortical lesion locations, echoing the areas of disruption in our three cases. On the basis of these observations, we hypothesize that injuries along the pathway from the insular cortex to downstream sympathetic centers may remove tonic inhibition leading to unchecked sympathetic outflow. Prospective investigations of lesion location in patients with IPH and PSH are warranted to test this hypothesis, especially with advanced neuroimaging techniques. BlackWell Publishing Ltd 2014-03 2014-02-25 /pmc/articles/PMC4043289/ /pubmed/24904923 http://dx.doi.org/10.1002/acn3.44 Text en © 2014 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Case Study Gao, Billy Pollock, Jeffrey A Hinson, Holly E Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
title | Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
title_full | Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
title_fullStr | Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
title_full_unstemmed | Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
title_short | Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
title_sort | paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage |
topic | Case Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043289/ https://www.ncbi.nlm.nih.gov/pubmed/24904923 http://dx.doi.org/10.1002/acn3.44 |
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