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Open AccessJournal ArticleDOI

Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group

Jens P. Dreier, +93 more
- 01 May 2017 - 
- Vol. 37, Iss: 5, pp 1595-1625
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TLDR
Consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions are provided, which offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.
Abstract
Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.

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Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research

Andrew I R Maas, +342 more
- 01 Dec 2017 - 
TL;DR: The InTBIR Participants and Investigators have provided informed consent for the study to take place in Poland.
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Functional vascular contributions to cognitive impairment and dementia: mechanisms and consequences of cerebral autoregulatory dysfunction, endothelial impairment, and neurovascular uncoupling in aging

TL;DR: Increasing evidence from epidemiological, clinical and experimental studies indicate that age-related cerebromicrovascular dysfunction and microcirculatory damage play critical roles in the pathoge as discussed by the authors.
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Commonalities in epileptogenic processes from different acute brain insults: Do they translate?

TL;DR: The identification of impending epilepsy biomarkers to allow better patient selection, together with better alignment with multisite preclinical trials in animal models, should guide the clinical testing of new hypotheses for epileptogenesis and its prevention.
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Spreading depolarization is not an epiphenomenon but the principal mechanism of the cytotoxic edema in various gray matter structures of the brain during stroke.

TL;DR: It is summarized that spreading depolarization is the electrophysiological correlate of the cytotoxic edema in various gray matter structures of the brain and vasogenic edema is the other major type of cerebral edema with relevance to ischemic stroke.
References
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Journal ArticleDOI

Penumbral tissues salvaged by reperfusion following middle cerebral artery occlusion in rats.

TL;DR: A time window for salvage of penumbral tissues by reperfusion in a model of transient focal ischemia that gives infarction of both the caudoputamen and the neocortex is demonstrated.
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Sympathetic activation triggers systemic interleukin-10 release in immunodepression induced by brain injury.

TL;DR: It is found that in a rat model of acute brain injury, the βreceptor antagonist propranolol prevented the increase of interleukin-10 plasma levels and this may represent a common pathway for immunodepression induced by stress and injury.
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Which EEG patterns warrant treatment in the critically ill? Reviewing the evidence for treatment of periodic epileptiform discharges and related patterns.

TL;DR: A review of the literature was conducted to understand the nature of periodic discharges and the strength of the data on which management recommendations have been based, and a modification to current criteria for the diagnosis of nonconvulsive seizures is suggested.
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Cortical spreading depression causes and coincides with tissue hypoxia

TL;DR: The results indicate that tissue hypoxia associated with CSD is caused by a transient increase in O2 demand exceeding vascular O2 supply and increasing O2 availability shortens the duration of CSD and improves local redox state.
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