Alterations of Norepinephrine Levels in Plasma and CSF of Patients After Traumatic Brain Injury in Relation to Disruption of the Blood-Brain Barrier

Mautes, A.; Müller, Markus; Cortbus, F.; Schwerdtfeger, Karsten; Maier, Bernd Oliver; Holanda, M.; Nacimiento, A. C.; Marzi, Ingo; Steudel, Wolf-Ingo

doi:10.1007/s007010170138

Cited by 35 publications

(20 citation statements)

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“…Low dose ethanol inhibition of N-methyl-D-aspartate (NMDA) receptors could be neuroprotective as potassium and calcium influx through NMDA receptor channels following TBI leads to neuronal excitotoxicity [9][10][11][12][13]. The systemic catecholamine surge following TBI which is associated with worse outcomes has been shown to be moderated by ethanol [14][15][16]. Aquaporin-4, implicated in the development of cerebral oedema following TBI, has also been shown to be suppressed by ethanol [17].…”

Section: Introductionmentioning

confidence: 95%

Ethanol and isolated traumatic brain injury

Brennan

Bernard

Cameron

et al. 2015

Journal of Clinical Neuroscience

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Section: Introductionmentioning

confidence: 95%

Ethanol and isolated traumatic brain injury

Brennan

Bernard

Cameron

et al. 2015

Journal of Clinical Neuroscience

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“…The largest group of papers have looked at catecholamines without consideration of a diagnosis of PSH at all. (15)(16)(17)(18)(19)(20)(21) A similar situation occurs in literature on the effect of TBI on adrenocorticotropic hormone (ACTH)/cortisol levels which have been reported without reference to the occurrence of PSH. (19,(22)(23)(24) Only three single case studies have evaluated catecholamines in the context of PSH.…”

Section: Introductionmentioning

confidence: 70%

“…Following the provision of informed consent (from the patient or their legal representative), consecutive admissions >14 years of age admitted to ICU following severe TBI (21) were assessed over an 18 month period. Subjects were excluded if they were receiving any of the following: 1) NE infusion at doses >0.5 micrograms/kg/min and/or dopamine (D) at doses of >5 micrograms/kg/min; 2) systemic glucocorticoids before or during the ICU admission; 3) thyroid replacement or inhibitor drugs.…”

Section: Data Collectionmentioning

confidence: 99%

Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

Fernandez-OrtegaJuan¹,

BaguleyIan

GatesThomas

et al. 2017

Journal of Neurotrauma

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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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“…One study in cats found spikes in NE following TBI (Rosner et al, 1984) as depicted in Figure 2. Clinically, TBI survivors often receive NE therapy for its vasopressive effects and one study found that NE levels in the CSF and plasma were elevated in TBI survivors treated with NE as well as some individuals who did not receive therapeutic NE; interestingly, the spike in plasma levels was independent of whether or not the blood-brain-barrier remained intact (Mautes et al, 2001). In this study, no evidence of toxicity from NE therapy was reported, nor were there correlations between GCS and NE levels.…”

Section: Norepinephrinementioning

confidence: 99%

Catecholaminergic based therapies for functional recovery after TBI

Osier

Dixon

2016

Brain Research

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Among the many pathophysiologic consequences of traumatic brain injury are changes in catecholamines, including dopamine, epinephrine, and norepinephrine. In the context of TBI, dopamine is the one most extensively studied, though some research exploring epinephrine and norepinephrine have also been published. The purpose of this review is to summarize the evidence surrounding use of drugs that target the catecholaminergic system on pathophysiological and functional outcomes of TBI using published evidence from pre-clinical and clinical brain injury studies. Evidence of the effects of specific drugs that target catecholamines as agonists or antagonists will be discussed. Taken together, available evidence suggests that therapies targeting the catecholaminergic system may attenuate functional deficits after TBI. Notably, it is fairly common for TBI patients to be treated with catecholamine agonists for either physiological symptoms of TBI (e.g. altered cerebral perfusion pressures) or a co-occuring condition (e.g. shock), or cognitive symptoms (e.g. attentional and arousal deficits). Previous clinical trials are limited by methodological limitations, failure to replicate findings, challenges translating therapies to clinical practice, the complexity or lack of specificity of catecholamine receptors, as well as potentially counfounding effects of personal and genetic factors. Overall, there is a need for additional research evidence, along with a need for systematic dissemination of important study details and results as outlined in the common data elements published by the National Institute of Neurological Diseases and Stroke. Ultimately, a better understanding of catecholamines in the context of TBI may lead to therapeutic advancements.

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Alterations of Norepinephrine Levels in Plasma and CSF of Patients After Traumatic Brain Injury in Relation to Disruption of the Blood-Brain Barrier

Abstract: Exogenous administration of NE seems to increase NE levels in plasma and CSF. However, in this group of patients with severe TBI there was no clinical evidence that exogenous administration of NE was detrimental to the traumatized patients.

Cited by 35 publications

References 0 publications

Ethanol and isolated traumatic brain injury

Ethanol and isolated traumatic brain injury

Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

Catecholaminergic based therapies for functional recovery after TBI

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