Cerebral Physiology Research Articles

A neonatal neuroNICU collaborative approach to neuromonitoring of posthemorrhagic ventricular dilation in preterm infants.

Morbidity and mortality in prematurely born infants have significantly improved due to advancement in perinatal care, development of NeuroNICU collaborative multidisciplinary approaches, and evidence-based management protocols that have resulted from a better understanding of perinatal risk factors and neuroprotective treatments. In premature infants with intraventricular hemorrhage (IVH), the detrimental secondary effect of posthemorrhagic ventricular dilation (PHVD) on the neurodevelopmental outcome can be mitigated by surgical intervention, though management varies considerably across institutions. Any benefit derived from the use of neuromonitoring to optimize surgical timing and technique stands to improve neurodevelopmental outcome. In this review, we summarize (1) the approaches to surgical management of PHVD in preterm infants and outcome data; (2) neuromonitoring modalities and the effect of neurosurgical intervention on this data; (3) our resultant protocol for the monitoring and management of PHVD. In particular, our protocol incorporates cerebral near-infrared spectroscopy (NIRS) and transcranial doppler ultrasound (TCD) to better understand cerebral physiology and to enable the hypothesis-driven study of the management of PHVD. IMPACT: Review of the published literature concerning the use of near-infrared spectroscopy (NIRS) and a cerebral Doppler ultrasound to study the effect of cerebrospinal fluid drainage on infants with posthemorrhagic ventricular dilation. Presentation of our institution's evidence-based protocol for the use of NIRS and cerebral Doppler ultrasound to study the optimal neurosurgical treatment of posthemorrhagic ventricular dilation, an as yet inadequately studied area.

Measuring 129 Xe transfer across the blood-brain barrier using MR spectroscopy.

PurposeThis study develops a tracer kinetic model of xenon uptake in the human brain to determine the transfer rate of inhaled hyperpolarized 129Xe from cerebral blood to gray matter that accounts for the effects of cerebral physiology, perfusion and magnetization dynamics. The 129Xe transfer rate is expressed using a tracer transfer coefficient, which estimates the quantity of hyperpolarized 129Xe dissolved in cerebral blood under exchange with depolarized 129Xe dissolved in gray matter under equilibrium of concentration.Theory and MethodsTime‐resolved MR spectra of hyperpolarized 129Xe dissolved in the human brain were acquired from three healthy volunteers. Acquired spectra were numerically fitted with five Lorentzian peaks in accordance with known 129Xe brain spectral peaks. The signal dynamics of spectral peaks for gray matter and red blood cells were quantified, and correction for the 129Xe T 1 dependence upon blood oxygenation was applied. 129Xe transfer dynamics determined from the ratio of the peaks for gray matter and red blood cells was numerically fitted with the developed tracer kinetic model.ResultsFor all the acquired NMR spectra, the developed tracer kinetic model fitted the data with tracer transfer coefficients between 0.1 and 0.14.ConclusionIn this study, a tracer kinetic model was developed and validated that estimates the transfer rate of HP 129Xe from cerebral blood to gray matter in the human brain.

Optimal Hemodynamic Parameters for Brain-injured Patients in the Clinical Setting: A Narrative Review of the Evidence

Defining optimal hemodynamic targets for brain-injured patients is a challenging undertaking. The physiological interference observed in various intracranial pathologies can have varying effects on cerebral physiology at different time points. This narrative review provides an overview of cerebral autoregulatory physiology and common misconceptions, and examines the physiological considerations and clinical evidence for determining optimal hemodynamic parameters in acutely brain-injured patients with relevance to modern neuroanesthesia and neurocritical care practice.

The Ritual Play and Altered States of Consciousness: the psychophysical processes in actor creation work

ABSTRACT This article discusses the psychophysical processes of the actor from a laboratory practice developed with the Arkhétypos Group. The exposition presented is the result of the meeting of two researchers, one from the Performing Arts area and the other from Physiology, generating an interdisciplinary discussion about the Ritual Theater. This article analyzes two creative processes experienced by the authors and proposes an approximation with the theory of transient hypofrontality. The methodological approach is based on the anecdotal evidence and a rigorous bibliographic study. The partial results of the research help us understand what happens to the cerebral physiology of the actor who enters the ritual play.

Anesthesia for neurosurgery (Part II)

The central nervous system (CNS) deserves special consideration in the perioperative setting for several reasons for an anesthetist. An understanding of neuroanatomy is essential because neuro anesthesia continues to develop and evolution of neurosurgical practice is accompanied by new challenges for the anesthetist. Basic knowledge and expertise of the neuro-anesthetist can directly influence patient outcome. With the recent advancement in functional and minimally invasive procedures, there is an increased emphasis on the provision of optimal operative conditions, preservation of neurocognitive function, minimizing interference with electrophysiological monitoring, and a rapid, high-quality recovery. So, during neuro anesthesia, anesthesiologist needs to know physiology of CNS including cerebral metabolism and cerebral blood flow. Neuro anesthesia can be challenging, because sometimes apparently contradictory demands must be managed, for example, achieving optimal conditions for neurophysiological monitoring while maintaining sufficient anesthetic depth, or maintaining oxygen delivery to neuronal tissue and simultaneously preventing high blood pressures that might induce local bleeding. One of the peculiarities of neuro anesthesia has always been that as much importance is attached to wakening the patient as sending them to sleep. We have included the anesthesia for neurosurgery in two parts. In the first part, we had discussed cerebral anatomy, physiology and intracranial pressure, in the second part we have included anesthesia considerations for surgery for brain tumor, aneurysmal surgery, temporal lobe surgery, trans sphenoidal surgery and traumatic brain injury. Keywords: Anesthesia, Neurosurgery.

Chapter 5 - Neurovascular physiology and neurocritical care

The neurological intensive care unit plays an integral role in the management of cerebrovascular disease in the acute and perioperative period. Understanding the use of intracranial pressure (ICP) monitoring and how to apply the appropriate intervention for ICP elevation to ensure adequate cerebral perfusion is the foundation of neurocritical care. Careful management of the interplay between cerebral and systemic physiology, particularly in disorders of cerebral autoregulation, is critical in preventing secondary brain injury. Finally, understanding the cerebral pathophysiology of the underlying injured brain in acute stroke, subarachnoid hemorrhage, and arterial stenosis can help to guide the optimal use of interventional endovascular procedures in these disease states.

Real-Time Monitoring of Neurocritical Patients with Diffuse Optical Spectroscopies.

Neurophysiological monitoring is an important goal in the treatment of neurocritical patients, as it may prevent secondary damage and directly impact morbidity and mortality rates. However, there is currently a lack of suitable non-invasive, real-time technologies for continuous monitoring of cerebral physiology at the bedside. Diffuse optical techniques have been proposed as a potential tool for bedside measurements of cerebral blood flow and cerebral oxygenation in case of neurocritical patients. Diffuse optical spectroscopies have been previously explored to monitor patients in several clinical scenarios ranging from neonatal monitoring to cerebrovascular interventions in adults. However, the feasibility of the technique to aid clinicians by providing real-time information at the bedside remains largely unaddressed. Here, we report the translation of a diffuse optical system for continuous real-time monitoring of cerebral blood flow, cerebral oxygenation, and cerebral oxygen metabolism during intensive care. The real-time feature of the instrument could enable treatment strategies based on patient-specific cerebral physiology rather than relying on surrogate metrics, such as arterial blood pressure. By providing real-time information on the cerebral circulation at different time scales with relatively cheap and portable instrumentation, this approach may be especially useful in low-budget hospitals, in remote areas and formonitoring in open fields (e.g., defense and sports).

The impact of hypertonic saline on cerebrovascular reactivity and compensatory reserve in traumatic brain injury: an exploratory analysis.

BackgroundIntravenous hypertonic saline is utilized commonly in critical care for treatment of acute or refractory elevations of intracranial pressure (ICP) in traumatic brain injury (TBI) patients. Though there is a clear understanding of the general physiological effects of a hypertonic saline solution over long periods of time, smaller epoch effects of hypertonic saline (HTS) have not been thoroughly analyzed. The aim of this study was to perform a direct evaluation of the high-frequency response of HTS on the cerebrovascular physiological responses in TBI.MethodsWe retrospectively reviewed our prospectively maintained adult TBI database for those with archived high-frequency cerebral physiology and available HTS treatment information. We evaluated different epochs of physiology around HTS bolus dosing, comparing pre- with post-HTS. We assessed for changes in slow fluctuations in ICP, pulse amplitude of ICP (AMP), cerebral perfusion pressure (CPP), mean arterial pressure (MAP), cerebrovascular reactivity (as measured through pressure reactivity index (PRx)), and cerebral compensatory reserve (correlation (R) between AMP (A) and ICP (P)). Comparisons of mean measures and percentage time above clinically relevant thresholds for the physiological parameters were compared pre- and post-HTS using descriptive statistics and Mann-Whitney U testing. We assessed for subgroups of physiological responses using latent profile analysis (LPA).ResultsFifteen patients underwent 69 distinct bolus infusions of hypertonic saline. Apart from the well-documented decrease in ICP, there was also a reduction in AMP. The analysis of cerebrovascular reactivity response to HTS solution had two main effects. For patients with grossly impaired cerebrovascular reactivity pre-HTS (PRx > + 0.30), HTS bolus led to improved reactivity. However, for those with intact cerebrovascular reactivity pre-HTS (PRx < 0), HTS bolus demonstrated a trend towards more impaired reactivity. This indicates that HTS has different impacts, dependent on pre-bolus cerebrovascular status. There was no significant change in metrics of cerebral compensatory reserve. LPA failed to demonstrate any subgroups of physiological responses to HTS administration.ConclusionsThe direct decrease in ICP and AMP confirms that a bolus dose of a HTS solution is an effective therapeutic agent for intracranial hypertension. However, in patients with intact autoregulation, hypertonic saline may impair cerebral hemodynamics. These findings regarding cerebrovascular reactivity remain preliminary and require further investigation.Electronic supplementary materialThe online version of this article (10.1007/s00701-020-04579-0) contains supplementary material, which is available to authorized users.

Prehospital Whole Blood Resuscitation Reduces Fluid Requirement While Maintaining Critical Physiology in a Model of Penetrating Traumatic Brain Injury and Hemorrhage: Implications on Resource-Limited Combat Casualty Care.

Prehospital resuscitation using whole blood (WB) is the standard of care for hemorrhagic shock (HS) but there is no consensus recommendation for resuscitation in the presence of traumatic brain injury (TBI) due to a lack of sufficient evidence. In order to evaluate the optimal resuscitation strategies for TBI+HS, Sprague-Dawley rats were randomized into four groups based on resuscitation fluid and prehospital mean arterial pressure (MAP) threshold (n = 9-10/group): Lactated Ringer's (LR)-60 mm Hg (LR60), LR-70 mm Hg (LR70), WB-60 mm Hg (WB60), WB-70 mm Hg (WB70). All groups received a frontal penetrating ballistic-like brain injury followed by a 35-min period of HS. During the prehospital phase, rats received an initial bolus of resuscitation fluid (WB or LR) followed by LR as needed to maintain MAP above the designated threshold for 90 min. During the in-hospital phase, rats received definitive resuscitation with shed WB. Physiological parameters were recorded continuously and cerebral edema was measured at 3 and 24 h postinjury. The WB60 group demonstrated a significantly lower prehospital fluid requirement compared WB70, LR60, and LR70 (P < 0.05). Compared to the respective LR groups, both the WB60 and WB70 groups also demonstrated improved MAP, cerebral perfusion pressure, brain tissue oxygen tension, and cerebral edema. The edema benefits were observed at 3 h, but not 24 h postinjury, and were localized to the injury site. Together, these results provide evidence that prehospital WB resuscitation and lower MAP resuscitation thresholds can reduce the prehospital fluid requirement while still maintaining critical cerebral physiology in a model of HS and concomitant TBI.

Descriptive analysis of low versus elevated intracranial pressure on cerebral physiology in adult traumatic brain injury: a CENTER-TBI exploratory study

BackgroundTo date, the cerebral physiologic consequences of persistently elevated intracranial pressure (ICP) have been based on either low-resolution physiologic data or retrospective high-frequency data from single centers. The goal of this study was to provide a descriptive multi-center analysis of the cerebral physiologic consequences of ICP, comparing those with normal ICP to those with elevated ICP.MethodsThe Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) High-Resolution Intensive Care Unit (HR-ICU) sub-study cohort was utilized. The first 3 days of physiologic recording were analyzed, evaluating and comparing those patients with mean ICP < 15 mmHg versus those with mean ICP > 20 mmHg. Various cerebral physiologic parameters were derived and evaluated, including ICP, brain tissue oxygen (PbtO2), cerebral perfusion pressure (CPP), pulse amplitude of ICP (AMP), cerebrovascular reactivity, and cerebral compensatory reserve. The percentage time and dose above/below thresholds were also assessed. Basic descriptive statistics were employed in comparing the two cohorts.Results185 patients were included, with 157 displaying a mean ICP below 15 mmHg and 28 having a mean ICP above 20 mmHg. For admission demographics, only admission Marshall and Rotterdam CT scores were statistically different between groups (p = 0.017 and p = 0.030, respectively). The high ICP group displayed statistically worse CPP, PbtO2, cerebrovascular reactivity, and compensatory reserve. The high ICP group displayed worse 6-month mortality (p < 0.0001) and poor outcome (p = 0.014), based on the Extended Glasgow Outcome Score.ConclusionsLow versus high ICP during the first 72 h after moderate/severe TBI is associated with significant disparities in CPP, AMP, cerebrovascular reactivity, cerebral compensatory reserve, and brain tissue oxygenation metrics. Such ICP extremes appear to be strongly related to 6-month patient outcomes, in keeping with previous literature. This work provides multi-center validation for previously described single-center retrospective results.

Comparison of propofol and sevoflurane on cerebral oxygenation using juglar venous oximetery (SjVo2) in patients undergoing surgery for traumatic brain injury

Background:Traumatic brain injury (TBI) induces major insult to the normal cerebral physiology. The anesthetic agents may infrequently produce deleterious effects and further aggravate damage to the injured brain. This study was conducted to evaluate the effects of propofol and sevoflurane on cerebral oxygenation, brain relaxation, systemic hemodynamic parameters and levels of interleukin-6 (IL-6) in patients with severe TBI undergoing decompressive craniectomy.Methods:A prospective randomized comparative study was conducted on 42 patients undergoing surgery for severe TBI. Patients were randomized into two groups, Group P received propofol and Group S received sevoflurane for maintenance of anesthesia. All patients were induced with fentanyl, propofol, and vecuronium. The effect of these agents on cerebral oxygenation was assessed by jugular venous oxygen saturation (SjVO2). Hemodynamic changes and quality of intraoperative brain relaxation were also assessed. The serum levels of IL-6 were quantitated using enzyme-linked immunosorbent assay technique.Results:SjVO2 values were comparable and mean arterial pressure (MAP) was found to be significantly lower in Group P as compared to those in Group S (P < 0.05). Brain relaxation scores were comparable between the groups. The level of IL-6 decreased significantly at the end of surgery compared to baseline in patients receiving sevoflurane (P = 0.040).Conclusions:Cerebral oxygenation measured by SjVO2 was comparable when anesthesia was maintained with propofol or sevoflurane. However, significant reduction in MAP by propofol needs attention in patients with severe TBI. The decrease in IL-6 level reflects anti-inflammatory effect and probable neuroprotective potential of propofol and sevoflurane.

The formation of anew medical discipline: psychiatry in Austria in the 19thcentury

The first psychiatric chairs and university departments of psychiatry in Austria were founded in Vienna and Graz in 1870: hence they celebrate their 150th anniversary this year 2020. These foundations represent apeak in the development of psychiatry as ascientific medical discipline. It is the aim of this paper to sketch that step by step development in its connection with the development of care institutions of the time and with reference to important personalities in the field. Vienna-as the metropole of the state and the most prominent place in the field-is taken as an example. One can distinguish four developmental periods: (1)The establishment of care institutions (asylums), at first without an own medical staff and unqualified male and female keepers (late 18thcentury up to early 19th). (2)The growing independance of these institutions-in Vienna the 'Tower of Fools'-and the emergence of 'alienists' who began to reflect on their activities and to share their experiences on academic grounds and the publication of afirst Austrian textbook (1st half of 19thcentury). (3)From the 1850s on several alienists habilitated, partly with special emphasis on forensic psychology or cerebral anatomy and physiology, and developed asystematic academic teaching, again with anew 'modern' textbook, in some connection with anew care institution, and the foundation of ascientific association of psychiatry and forensic psychology in 1868. (4)An early activity of that association was to call for the institution of achair and auniversity department of psychiatry within the asylum, both realised in 1870.

Near-Infrared Cerebrovascular Reactivity for Monitoring Cerebral Autoregulation and Predicting Outcomes in Moderate to Severe Traumatic Brain Injury: Proposal for a Pilot Observational Study.

BackgroundImpaired cerebrovascular reactivity after traumatic brain injury (TBI) in adults is emerging as an important prognostic factor, with strong independent association with 6-month outcomes. To date, it is unknown if impaired cerebrovascular reactivity during the acute phase is associated with ongoing impaired continuously measured cerebrovascular reactivity in the long-term, and if such measures are associated with clinical phenotype at those points in time.ObjectiveWe describe a prospective pilot study to assess the use of near-infrared spectroscopy (NIRS) to derive continuous measures of cerebrovascular reactivity during the acute and long-term phases of TBI in adults.MethodsOver 2 years, we will recruit up to 80 adults with moderate/severe TBI admitted to the intensive care unit (ICU) with invasive intracranial pressure (ICP) monitoring. These patients will undergo high-frequency data capture of ICP, arterial blood pressure (ABP), and NIRS for the first 5 days of care. Patients will then have 30 minutes of noninvasive NIRS and ABP monitoring in the clinic at 3, 6, and 12 months post-injury. Outcomes will be assessed via the Glasgow Outcome Scale and Short Form-12 questionnaires. Various relationships between NIRS and ICP-derived cerebrovascular reactivity metrics and associated outcomes will be assessed using biomedical signal processing techniques and both multivariate and time-series statistical methodologies.ResultsStudy recruitment began at the end of February 2020, with data collection ongoing and three patients enrolled at the time of writing. The expected duration of data collection will be from February 2020 to January 2022, as per our local research ethics board approval (B2018:103). Support for this work has been obtained through the National Institutes of Health (NIH) through the National Institute of Neurological Disorders and Stroke (NINDS) (R03NS114335), funded in January 2020.ConclusionsWith the application of NIRS technology for monitoring of patients with TBI, we expect to be able to outline core relationships between noninvasively measured aspects of cerebral physiology and invasive measures, as well as patient outcomes. Documenting these relationships carries the potential to revolutionize the way we monitor patients with TBI, moving to more noninvasive techniques.International Registered Report Identifier (IRRID)DERR1-10.2196/18740

A Short-Term Western Diet Impairs Cholesterol Homeostasis and Key Players of Beta Amyloid Metabolism in Brain of Middle Aged Rats.

Cholesterol homeostasis is crucial for brain functioning. Unhealthy nutrition can influence cerebral physiology, but the effect of western diets on brain cholesterol homeostasis, particularly at middle age, is unknown. Given the link between brain cholesterol alteration and beta amyloid production, the aim is to evaluate whether a diet rich in fat and fructose affects the protein network implicated in cholesterol synthesis and shuttling between glial cells and neurons, as well as crucial markers of beta amyloid metabolism. Middle aged rats are fed a high fat-high fructose (HFF) or a control diet for 4 weeks. Inflammatory markers and cholesterol levels significantly increase in hippocampus of HFF rats. A higher activation of 3-hydroxy 3-methylglutaryl coenzyme-A reductase, coupled with lower levels of apolipoprotein E, LXR-beta, and lipoproteins receptors is measured in hippocampus from HFF rats. The alteration of critical players of cholesterol homeostasis is associated with increased level of amyloid precursor protein, presenilin 1, and nicastrin, and decreased level of insulin degrading enzyme. Overall these data show that a western diet is associated with perturbation of cholesterol homeostasis in middle aged rats, mostly in hippocampus. This might trigger molecular events involved in the onset of neurodegenerative diseases.

Brain Tissue Oxygen and Cerebrovascular Reactivity in Traumatic Brain Injury: A Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Exploratory Analysis of Insult Burden.

Pressure reactivity index (PRx) and brain tissue oxygen (PbtO2) are associated with outcome in traumatic brain injury (TBI). This study explores the relationship between PRx and PbtO2 in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution intensive care unit (ICU) sub-study cohort, we evaluated those patients with archived high-frequency digital intraparenchymal intracranial pressure (ICP) and PbtO2 monitoring data of, a minimum of 6 h in duration, and the presence of a 6 month Glasgow Outcome Scale -Extended (GOSE) score. Digital physiological signals were processed for ICP, PbtO2, and PRx, with the % time above/below defined thresholds determined. The duration of ICP, PbtO2, and PRx derangements was characterized. Associations with dichotomized 6-month GOSE (alive/dead, and favorable/unfavorable outcome; ≤ 4 = unfavorable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevated ICP and low PbtO2 episodes. However, most of the acute ICU physiological derangements were impaired cerebrovascular reactivity, not ICP elevations or low PbtO2 episodes. Low PbtO2 without PRx impairment was rarely seen. % time spent above PRx threshold was associated with mortality at 6 months for thresholds of 0 (area under the curve [AUC] 0.734, p = 0.003), > +0.25 (AUC 0.747, p = 0.002) and > +0.35 (AUC 0.745, p = 0.002). Similar relationships were not seen for % time with ICP >20 mm Hg, and PbtO2 < 20 mm Hg in this cohort. Extreme impairment in cerebrovascular reactivity is seen during concurrent episodes of elevated ICP and low PbtO2. However, the majority of the deranged cerebral physiology seen during the acute ICU phase is impairment in cerebrovascular reactivity, with most impairment occurring in the presence of normal PbtO2 levels. Measures of cerebrovascular reactivity appear to display the most consistent associations with global outcome in TBI, compared with ICP and PbtO2.

The CAnadian High-Resolution Traumatic Brain Injury (CAHR-TBI) Research Collaborative.

In traumatic brain injury (TBI), future integration of multimodal monitoring of cerebral physiology and high-frequency signal processing techniques, with advanced neuroimaging, proteomic and genomic analysis, provides an opportunity to explore the molecular pathways involved in various aspects of cerebral physiologic dysfunction invivo. The main issue with early and rapid discovery in this field of personalized medicine is the expertise and complexity of data involved. This brief communication highlights the CAnadian High-Resolution Traumatic Brain Injury (CAHR-TBI) Research Collaborative, which has been formed from centers with specific expertise in the area of high-frequency physiologic monitoring/processing, and outlines its objectives.

Assessing the Impact of 3% Hypertonic Saline Hyperosmolar Therapy on Intubated Children With Isolated Traumatic Brain Injury by Cerebral Oximetry in a Pediatric Emergency Setting.

BACKGROUND Intubated pediatric patients with isolated traumatic brain injury (TBI) are a diagnostic challenge for early detection of altered cerebral physiology instigated by trauma-induced increased intracranial pressure (ICP) while preventing secondary neuronal damage (secondary insult detection) and assessing the effects of increased ICP therapeutic interventions (3% hypertonic saline [HTS]). Invasive brain tissue oxygen monitoring is guiding new intensive care unit TBI management but is not pediatric emergency department (PED) readily accessible. Objective measurements on pediatric isolated TBI-altered bihemispheric cerebral physiology and treatment effects of 3% HTS are currently lacking. Cerebral oximetry can assess increased ICP-induced abnormal bihemispheric cerebral physiology by measuring regional tissue oxygenation (rcSO2) and cerebral blood volume index (CBVI) and the mechanical cerebrospinal fluid removal effects on the increased ICP-induced abnormal bihemispheric cerebral physiology.In the PED intubated patients with isolated TBI, assessing the 3% HTS therapeutic response is solely by vital signs and limited clinical assessment skills. Objective measurements of the 3% HTS hyperosmolar effects on the PED isolated TBI patients' altered bihemispheric cerebral physiology are lacking. We believe that bihemispheric rcSO2 and CBVI could elucidate similar data on 3% HTS impact and influence in the intubated isolated TBI patients. OBJECTIVE This study aimed to analyze the effects of 3% HTS on bihemispheric rcSO2 and CBVI in intubated patients with isolated TBI. METHODS An observational, retrospective analysis of bihemispheric rcSO2 and CBVI readings in intubated pediatric patients with isolated TBI receiving 3% HTS infusions, was performed. RESULTS From 2010 to 2017, 207 intubated patients with isolated TBI received 3% HTS infusions (median age, 2.9 [1.1-6.9 years]; preintubation Glasgow Coma Scale score, 7 [6-8]). The results were as follows: initial pre-3% HTS, 43% (39.5% to 47.5%; left) and 38% (35% to 42%; right) for rcSO2 80%, and 16.5 (6 to 33, P 80%, and 16.5 (6 to 33, P 10 showed rcSO2 10 and required the greatest number of 3% HTS infusions. For 3% HTS 15% rcSO2 change time effect, all patients achieved positive change with subdural hematomas and hemispheric rcSO2 readings 10 demonstrated the greatest significant positive delta change and required the greatest numbers of 3% HTS infusions. Overall, 3% HTS produced a significant positive 15% change within 2.1 minutes of infusion, whereas heart rate showed no significant change. During trauma neuroresuscitation, especially in intubated isolated TBI patients requiring 3% HTS, cerebral oximetry has shown its functionality as a rapid adjunct neurological, therapeutic assessment tool and should be considered in the initial emergency department pediatric trauma neurological assessment and neuroresuscitation regimen.

Continuous and entirely non-invasive method for cerebrovascular reactivity assessment: technique and implications.

Continuous cerebrovascular reactivity assessment in traumatic brain injury (TBI) has been limited by the need for invasive monitoring of either cerebral physiology or arterial blood pressure (ABP). This restricts the application of continuous measures to the acute phase of care, typically in the intensive care unit. It remains unknown if ongoing impairment of cerebrovascular reactivity occurs in the subacute and long-term phase, and if it drives ongoing morbidity in TBI. We describe an entirely non-invasive method for continuous assessment of cerebrovascular reactivity. We describe the technique for entirely non-invasive continuous assessment of cerebrovascular reactivity utilizing near-infrared spectroscopy (NIRS) and robotic transcranial Doppler (rTCD) technology, with details provided for NIRS. Recent advances in continuous high-frequency non-invasive ABP measurement, combined with NIRS or rTCD, can be employed to derive continuous and entirely non-invasive cerebrovascular reactivity metrics. Such non-invasive measures can be obtained during any aspect of patient care post-TBI, and even during outpatient follow-up, avoiding classical intermittent techniques and costly neuroimaging based metrics obtained only at specialized centers. This combination of technology and signal analytic techniques creates avenues for future investigation of the long-term consequences of cerebrovascular reactivity, integrating high-frequency non-invasive cerebral physiology, neuroimaging, proteomics and clinical phenotype at various stages post-injury.

The Effects of Balloon Occlusion of the Aorta on Cerebral Blood Flow, Intracranial Pressure, and Brain Tissue Oxygen Tension in a Rodent Model of Penetrating Ballistic-Like Brain Injury.

Trauma is among the leading causes of death in the United States. Technological advancements have led to the development of resuscitative endovascular balloon occlusion of the aorta (REBOA) which offers a pre-hospital option to non-compressible hemorrhage control. Due to the prevalence of concomitant traumatic brain injury (TBI), an understanding of the effects of REBOA on cerebral physiology is critical. To further this understanding, we employed a rat model of penetrating ballistic-like brain injury (PBBI). PBBI produced an injury pattern within the right frontal cortex and striatum that replicates the pathology from a penetrating ballistic round. Aortic occlusion was initiated 30 min post-PBBI and maintained continuously (cAO) or intermittently (iAO) for 30 min. Continuous measurements of mean arterial pressure (MAP), intracranial pressure (ICP), cerebral blood flow (CBF), and brain tissue oxygen tension (PbtO2) were recorded during, and for 60 min following occlusion. PBBI increased ICP and decreased CBF and PbtO2. The arterial balloon catheter effectively occluded the descending aorta which augmented MAP in the carotid artery. Despite this, CBF levels were not changed by aortic occlusion. iAO caused sustained adverse effects to ICP and PbtO2 while cAO demonstrated no adverse effects on either. Temporary increases in PbtO2 were observed during occlusion, along with restoration of sham levels of ICP for the remainder of the recordings. These results suggest that iAO may lead to prolonged cerebral hypertension following PBBI. Following cAO, ICP, and PbtO2 levels were temporarily improved. This information warrants further investigation using TBI-polytrauma model and provides foundational knowledge surrounding the non-hemorrhage applications of REBOA including neurogenic shock and stroke.

Neurocritical Care for Extracorporeal Membrane Oxygenation Patients.

To review the neurocritical care aspects of patients supported by extracorporeal membrane oxygenation, including cerebral physiology, neurologic monitoring, use of sedatives and anti-seizure medications, and prevalence and management of extracorporeal membrane oxygenation associated brain injury. PubMed database search using relevant search terms related to neurologic complications, neurocritical care management, and brain injury management in patients with extracorporeal membrane oxygenation. Articles included original investigations, review articles, consensus statements and guidelines. A detailed review of publications performed and relevant publications were summarized. We found no practice guidelines or management strategies for the neurocritical care of extracorporeal membrane oxygenation patients. Such patients are at high risk for hypoxic-ischemic brain injury, intracranial hemorrhage, cerebral edema, and brain death. Improving clinical outcomes will depend on better defining the neurologic complications and underlying pathophysiology that are specific to extracorporeal membrane oxygenation. Currently, insufficient understanding of the pathophysiology of neurologic complications prevents us from addressing their etiologies with specific, targeted monitoring techniques and interventions. A large knowledge gap exists in our understanding and treatment of extracorporeal membrane oxygenation-related neurologic complications. A systematic and multidisciplinary approach is needed to reduce the prevalence of these complications and to better manage the neurologic sequelae of extracorporeal membrane oxygenation in a way that will improve patient outcomes.