TY - JOUR
T1 - Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage
AU - Gao, Billy
AU - Pollock, Jeffrey A.
AU - Hinson, Holly E.
N1 - Funding Information:
The project described was supported by Award Number 5K12HL108974-03 from the National Heart, Lung, and Blood Institute. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. This publication was supported by Oregon Clinical and Translational Research Institute (OCTRI), grant number (UL1TR000128) from the National Center for Advancing Translational Sciences (NCATS) at the National Institutes of Health (NIH). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Publisher Copyright:
© 2014 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.
PY - 2014/3
Y1 - 2014/3
N2 - 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.
AB - 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.
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U2 - 10.1002/acn3.44
DO - 10.1002/acn3.44
M3 - Article
AN - SCOPUS:85026922052
SN - 2328-9503
VL - 1
SP - 215
EP - 219
JO - Annals of Clinical and Translational Neurology
JF - Annals of Clinical and Translational Neurology
IS - 3
ER -