Controversial Issues Concerning Norepinephrine and Intensive Care Following Severe Traumatic Brain Injury

Stover, John; Steiger, Peter; Stocker, Reto

doi:10.1007/s00068-006-0004-4

Cited by 5 publications

(6 citation statements)

References 227 publications

(255 reference statements)

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“…Although a number of pharmacological agents have failed to demonstrate prevention of CSRSs in clinical trials, there is preclinical evidence that epileptogenesis may be modulated pharmacologically using the α2‐adrenergic antagonist atipamezole . This class of drugs, however, may further elevate intracranial pressure in severe head injury patients with impaired cerebrovascular autoregulation . In addition, atipamezole is proepileptic, and may exacerbate acute seizures after head injury.…”

Section: Discussionmentioning

confidence: 99%

“…36 This class of drugs, however, may further elevate intracranial pressure in severe head injury patients with impaired cerebrovascular autoregulation. 37 In addition, atipamezole is proepileptic, 36 and may exacerbate acute seizures after head injury. Therefore, this class of drugs needs scrutiny before use in head injury patients.…”

Section: Properties Of Csrs Prophylaxis By Mild Focal Coolingmentioning

confidence: 99%

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Mild passive focal cooling prevents epileptic seizures after head injury in rats

D’Ambrosio

Eastman

Darvas

et al. 2012

Annals of Neurology

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Objective Posttraumatic epilepsy is prevalent, often difficult to manage, and currently cannot be prevented. While cooling is broadly neuroprotective, cooling-induced prevention of chronic spontaneous recurrent seizures has never been demonstrated. We examined the effect of mild passive focal cooling of the perilesional neocortex on the development of neocortical epileptic seizures after head injury in the rat. Methods Rostral parasagittal fluid percussion injury in rats reliably induces a perilesional, neocortical epileptic focus within weeks after injury. Epileptic seizures were assessed by 5-electrode video-electrocorticography (ECoG) 2–16 weeks post-injury. Focal cooling was induced with ECoG headsets engineered for calibrated passive heat dissipation. Pathophysiology was assessed by GFAP immunostaining, cortical sclerosis, gene expression of inflammatory cytokines IL-1α and IL-1β, and ECoG spectral analysis. All animals were formally randomized to treatment groups and data were analyzed blind. Results Cooling by 0.5–2°C inhibited the onset of epileptic seizures in a dose dependent fashion. The treatment induced no additional pathology or inflammation, and normalized the power spectrum of stage N2 sleep. Cooling by 2°C for 5.5 weeks beginning 3 days after injury virtually abolished ictal activity. This effect persisted through the end of the study, over ten weeks after cessation of cooling. Rare remaining seizures were shorter than in controls. Interpretation These findings demonstrate potent and persistent prevention and modification of epileptic seizures after head injury with a cooling protocol that is neuroprotective, compatible with the care of head-injury patients, and conveniently implemented. The required cooling can be delivered passively without Peltier cells or electrical power.

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Section: Discussionmentioning

confidence: 99%

Section: Properties Of Csrs Prophylaxis By Mild Focal Coolingmentioning

confidence: 99%

Mild passive focal cooling prevents epileptic seizures after head injury in rats

D’Ambrosio

Eastman

Darvas

et al. 2012

Annals of Neurology

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“…the Osc+ condition decreased blood flow while the Osc-condition increased it. As noradrenaline modulates vasoconstriction (Stover et al, 2006), these changes in blood flow could result from intervention-induced changes in noradrenaline released in the LC-innervated-regions hippocampal ROI.…”

Section: Limitations and Alternative Mechanismsmentioning

confidence: 99%

Daily biofeedback to modulate heart rate oscillations affects structural volume in hippocampal subregions targeted by the locus coeruleus in older adults but not younger adults

Yoo

Nashiro

Dutt

et al. 2023

Preprint

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Using data from a clinical trial, we tested the hypothesis that daily sessions modulating heart rate oscillations affect older adults’ volume of a region-of-interest (ROI) comprised of adjacent hippocampal subregions with relatively strong locus coeruleus (LC) noradrenergic input. Younger (N=106) and older adults (N=56) completed five weeks of heart rate variability biofeedback. Participants were randomly assigned to one of two daily biofeedback practices: 1) engage in slow-paced breathing (around 10-s per breath or 0.10 Hz) while receiving biofeedback to increase their heart rate oscillations (Osc+); 2) engage in self-selected strategies while receiving biofeedback to decrease their heart rate oscillations (Osc−). Biofeedback did not significantly affect younger adults’ hippocampal volume. Among older adults, the two biofeedback conditions affected volume in the LC-targeted hippocampal ROI differentially with the Osc+ condition showing relatively increased volume and Osc− showing relatively decreased volume. Older adults with greater average spectral power of heart rate at around 0.10 Hz during biofeedback sessions showed greater increases in volume across these regions.

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“…Such adverse effects observed within a healthy cohort include reduced end-organ perfusion, tissue hypoxia (including reducing cerebral oxygenation) and impaired tissue healing, having a potentially important consequences for neuronal recovery in patients with sTBI [6] . Accordingly, the use of norepinephrine for patients with sTBI remains controversial [7] .…”

Section: Introductionmentioning

confidence: 99%

“…The last review of this topic was greater than a decade ago [8] and despite the routine adoption of norepinephrine administration to achieve CPP targets, evidence has emerged that suggests norepinephrine contributes to paradoxical hypoperfusion secondary to vasoconstriction in other end organs, in addition to evidence suggesting norepinephrine may contribute to cerebral vasospasm in patients following subarachnoid hemorrage [6][7][8][9][10] . Furthermore, according to most reviews into this topic, little evidence exists evaluating the effect of norepinephrine on clinical outcomes in sTBI, particularly those with multisystem trauma [8 , 11] .…”

Section: Introductionmentioning

confidence: 99%

In adult patients with severe traumatic brain injury, does the use of norepinephrine for augmenting cerebral perfusion pressure improve neurological outcome? A systematic review

Lloyd-Donald

Spencer

Cheng

et al. 2020

Injury

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Background and objective: Despite multiple interventions, mortality due to severe traumatic brain injury (sTBI) within mature Trauma Systems has remained unchanged over the last decade. During this time, the use of vasoactive infusions (commonly norepinephrine) to achieve a target blood pressure and cerebral perfusion pressure (CPP) has been a mainstay of sTBI management. However, evidence suggests that norepinephrine, whilst raising blood pressure, may reduce cerebral oxygenation. This study aimed to review the available evidence that links norepinephrine augmented CPP to clinical outcomes for these patients. Methods: A systematic review examining the evidence for norepinephrine augmented CPP in TBI patients was undertaken. Strict inclusion and exclusion criteria were developed for a dedicated literature search of multiple scientific databases. Two dedicated reviewers screened articles, whilst a third dedicated reviewer resolved conflicts. Results: The systematic review yielded 4,809 articles, of which 1,197 duplicate articles were removed. After abstract/title screening, 45 articles underwent full text review, resulting in the identification of two articles that investigated the effect of norepinephrine administration on clinical outcomes in patients following TBI when compared to other vasopressors. Neither study found a difference in neurological outcome between the vasopressor groups. No articles measured the effect of norepinephrine compared to no vasopressor use on the clinical outcome of patients with sTBI. Conclusions: Despite being a mainstay of pharmacological management for hypotension in patients following sTBI, there is minimal clinical evidence supporting the use of norepinephrine in targeting a CPP for either improving neurological outcomes or reducing mortality. Outcomes-based clinical trials exploring the role of brain tissue perfusion and oxygenation monitoring are required to validate any benefit.

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Controversial Issues Concerning Norepinephrine and Intensive Care Following Severe Traumatic Brain Injury

Cited by 5 publications

References 227 publications

Mild passive focal cooling prevents epileptic seizures after head injury in rats

Mild passive focal cooling prevents epileptic seizures after head injury in rats

Daily biofeedback to modulate heart rate oscillations affects structural volume in hippocampal subregions targeted by the locus coeruleus in older adults but not younger adults

In adult patients with severe traumatic brain injury, does the use of norepinephrine for augmenting cerebral perfusion pressure improve neurological outcome? A systematic review

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