Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

Paroxysmal sympathetic hyperactivity (PSH) affects a significant minority of people in the intensive care unit after severe traumatic brain injury. Systematic research has yet to elucidate or quantify the extent of the role of the catecholamines or adrenocortical and thyroid axis hormonal influences...

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Published inJournal of neurotrauma Vol. 34; no. 1; pp. 109 - 114
Main Authors Fernandez-Ortega, Juan F., Baguley, Ian J., Gates, Thomas A., Garcia-Caballero, Manuel, Quesada-Garcia, Juan G., Prieto-Palomino, Miguel A.
Format Journal Article
LanguageEnglish
Published United States Mary Ann Liebert, Inc 01.01.2017
Subjects
Adrenocorticotropic Hormone - blood
Adult
Autonomic Nervous System Diseases - blood
Autonomic Nervous System Diseases - diagnosis
Autonomic Nervous System Diseases - etiology
Brain Injuries, Traumatic - blood
Brain Injuries, Traumatic - complications
Brain Injuries, Traumatic - diagnosis
Catecholamines - blood
Female
Hormones
Humans
Hydrocortisone - blood
Hyperactivity
Male
Middle Aged
Norepinephrine - blood
Prospective Studies
Thyroid gland
Traumatic brain injury
Young Adult
traumatic brain injury
cortisol
catecholamines
hormonal influences
paroxysmal sympathetic hyperactivity
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Summary:Paroxysmal sympathetic hyperactivity (PSH) affects a significant minority of people in the intensive care unit after severe traumatic brain injury. Systematic research has yet to elucidate or quantify the extent of the role of the catecholamines or adrenocortical and thyroid axis hormonal influences in the condition. Data were prospectively collected on 80 consecutive patients, 18 of whom developed clinical signs of PSH (22.5%). Catecholamine and hormonal data were collected sequentially at 4-h intervals or during and between episodes of PSH. Evaluated variables showed 200-300% increases in catecholamines and, to a lesser extent, adrenocortical hormones during paroxysms. The majority of PSH episodes (72%) were noted to be in response to an observable triggering event. These changes were not observed in subjects without PSH. These data go some way to explain why PSH produces adverse consequences in survivors of TBI with the condition.
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ISSN:0897-7151
1557-9042
1557-9042
DOI:10.1089/neu.2015.4364