Predicting Intracranial Pressure and Brain Tissue Oxygen Crises in Patients With Severe Traumatic Brain Injury

Myers, Risa B.; Lazaridis, C.; Jermaine, Christopher; Robertson, Claudia S.; Rusin, Craig G.

doi:10.1097/ccm.0000000000001838

Cited by 47 publications

(63 citation statements)

References 17 publications

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“…Primary injury is characterized by immediate bleeding and loss of brain tissue when a blunt or sharp object impacts the head. Secondary injury involves complicated cellular and biochemical cascade reactions, including oxidative stress, excitotoxicity, neuroinflammation, free radical-induced injury, and calcium-mediated damage, which lead to blood-brain barrier (BBB) damage, elevated intracranial pressure, cerebral hypoxia, brain edema, and neuronal apoptosis (3–8). Mitochondrial dysfunction has been demonstrated to be a key participant in the pathological processes of secondary brain injury (9, 10).…”

Section: Introductionmentioning

confidence: 99%

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

Shen

Yang

et al. 2019

Front. Neurol.

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Objective: To investigate whether methylene blue (MB) treatment can reverse neuronal mitochondrial dysfunction caused by oxygen glucose deprivation/reoxygenation (OGD) injury and then investigate whether MB treatment can reduce neuronal apoptosis and improve blood-brain barrier (BBB) integrity in traumatic brain injury (TBI) animals.Methods: Reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) were used to evaluate mitochondrial function. The terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL) assay was used to assess neuronal apoptosis in vitro. TUNEL and immunofluorescence staining for neuronal nuclei (NeuN) were combined to assess neuronal apoptosis in vivo. An Evans blue (EB) permeability assay and brain water content (BWC) were used to measure BBB permeability in vivo. The Morris water maze (MWM), rotarod test, and modified Neurological Severity Score (mNSS) test were employed to assess the prognosis of TBI mice.Results: MB treatment significantly reversed neuronal mitochondrial dysfunction caused by OGD injury. Both in vitro and in vivo, MB treatment reduced neuronal apoptosis and improved BBB integrity. In TBI animals, treatment with MB not only improved cognitive and motor function caused by TBI but also significantly improved overall neurological function.Conclusions: Our findings suggest that MB is a potential candidate for the treatment of TBI. Future research should focus on other therapeutic effects and mechanisms of MB in secondary brain injury.

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Section: Introductionmentioning

confidence: 99%

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

Shen

Yang

et al. 2019

Front. Neurol.

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“…Prec@75Rec Prec@90Rec AUPRC Optimal 0.377 ± 0.001 0.303 ± 0.001 0.517 ± 0.003 BL1: Hu et al [20] 0.331 ± 0.001 0.274 ± 0.001 0.473 ± 0.003 BL2: Myers et al [21] 0.338 ± 0.002 0.259 ± 0.001 0.484 ± 0.003…”

Section: Modelsmentioning

confidence: 99%

Forecasting intracranial hypertension using multi-scale waveform metrics

et al. 2020

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Objective: Acute intracranial hypertension is an important risk factor of secondary brain damage after traumatic brain injury. Hypertensive episodes are often diagnosed reactively, leading to late detection and lost time for intervention planning. A pro-active approach that predicts critical events several hours ahead of time could assist in directing attention to patients at risk. Approach: We developed a prediction framework that forecasts onsets of acute intracranial hypertension in the next 8 hours. It jointly uses cerebral auto-regulation indices, spectral energies and morphological pulse metrics to describe the neurological state of the patient. One-minute base windows were compressed by computing signal metrics, and then stored in a multi-scale history, from which physiological features were derived. Main results: Our model predicted events up to 8 hours in advance with alarm recall rates of 90% at a precision of 30.3% in the MIMIC-III waveform database, improving upon two baselines from the literature. We found that features derived from high-frequency waveforms substantially improved the prediction performance over simple statistical summaries of low-frequency time series, and each of the three feature classes contributed to the performance gain. The inclusion of long-term history up to 8 hours was especially important. Significance: Our results highlight the importance of information contained in high-frequency waveforms in the neurological intensive care unit. They could motivate future studies on pre-hypertensive patterns and the design of new alarm algorithms for critical events in the injured brain.

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“…This requires exploration of high-quality large multivariate datasets comprised of continuous, real time physiologic data, and clinical/imaging characteristics to identify phenotypes of injury and patient-specific pathophysiological trajectories. Machine learning methodologies have been emerging with high accuracy in predicting episodes of IHT or brain tissue hypoxia; they do though require prospective validation [29][30][31]. In this overall direction, hugely important are ongoing collaborative projects such as Transforming Research and Clinical Knowledge in TBI (TRACK TBI), and CENTER-TBI.…”

Section: Concluding Thoughts On Future Directionsmentioning

confidence: 99%

Intracranial Pressure Threshold Heuristics in Traumatic Brain Injury: One, None, Many!

et al. 2020

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Critical care of the patient with severe traumatic brain injury (TBI) revolves around strategies to address intracranial hypertension (IHT), and optimizing cerebral perfusion. Strong evidence associates IHT (especially refractory IHT) with mortality, and unfavorable clinical outcomes. However, this association may merely indicate that IHT is a surrogate for severity of injury and not necessarily a modifiable, outcome-altering, treatment target, i.e., some patients die with IHT, not from IHT. Another reason for intracranial pressure (ICP), and derived cerebral perfusion pressure (CPP), to be central tenets of bedside management is the fact that are relatively easily monitored as opposed to other secondary brain injury (SBI) mechanisms such as metabolic and energy crisis, cortical spreading ischemia, diffusion microvascular hypoxia, and mitochondrial failure. Consequently, we may be misled targeting what we can measure, not necessarily what matters. A further concern is that by solely focusing on one pathophysiological aspect we may ignore complex multidimensional cascades leading to SBI, and our treatment interventions run the risk of being counterproductive and harmful. Despite limitations, it is unlikely that ICP-guided management should or will entirely go away in the near future. One telling indication is the concerns, and responses, generated by the Benchmark Evidence from South American Trials: Treatment of Intracranial Pressure (BEST TRIP) trial [1]. This is the only level-1 evidence-producing randomized clinical trial (RCT) on the topic, finding no primary outcome

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Predicting Intracranial Pressure and Brain Tissue Oxygen Crises in Patients With Severe Traumatic Brain Injury

Cited by 47 publications

References 17 publications

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

Forecasting intracranial hypertension using multi-scale waveform metrics

Intracranial Pressure Threshold Heuristics in Traumatic Brain Injury: One, None, Many!

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