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Cardiac arrest survivors suffer the repercussions of anoxic brain injury, a critical factor influencing long-term prognosis. This injury is characterised by profound and enduring metabolic impairment. Ketone bodies, an alternative energetic resource in physiological states such as exercise, fasting, and extended starvation, are avidly taken up and used by the brain. Both the ketogenic diet and exogenous ketone supplementation have been associated with neuroprotective effects across a spectrum of conditions. These include refractory epilepsy, neurodegenerative disorders, cognitive impairment, focal cerebral ischemia, and traumatic brain injuries. Beyond this, ketone bodies possess a plethora of attributes that appear to be particularly favourable after cardiac arrest. These encompass anti-inflammatory effects, the attenuation of oxidative stress, the improvement of mitochondrial function, a glucose-sparing effect, and the enhancement of cardiac function. The aim of this manuscript is to appraise pertinent scientific literature on the topic through a narrative review. We aim to encapsulate the existing evidence and underscore the potential therapeutic value of ketone bodies in the context of cardiac arrest to provide a rationale for their use in forthcoming translational research efforts. [ABSTRACT FROM AUTHOR]

Drowning is a leading cause of brain injury in children. Long-term outcome data for drowning survivors are sparse. This study reports neurocognitive outcomes for 154 children hospitalized following drowning. A survey for parent caregivers was distributed online. Likert scale items assessed 10 outcome variables in four domains: motor (three), perception (three), language (three), and social/emotional (one). Cluster analysis, outcome relative risk, and descriptive statistics were applied. Of 208 surveys received, 154 met inclusion criteria. Coma was the most common admission status (n = 137). Cluster analysis identified three outcome groups: Mild (n = 39), Moderate (n = 75), and Severe (n = 40). Motor impairment with cognitive and perceptual sparing (deefferentation) was present in Moderate (P < 1 × 10−26) and Severe (P < 1 × 10−12) but absent in Mild. Locked-in state was endorsed in both Moderate (83%) and Severe (70%). The strongest predictor of good outcome (Mild) was hospitalization with no medical intervention (relative risk [RR] = 6.7). Responsivity on admission (RR = 4.2) or discharge (RR = 12.22) also predicted good outcome. In-hospital prognostication and counseling predicted outcome weakly (RR = 1.3) or not at all. Long-term outcomes in pediatric drowning ranged widely. Overall, motor impairments exceeded perceptual or cognitive (P < 1 × 10−18), with "locked-in state" endorsed in most (93 of 154). The strongest predictors of good outcome were the lack of necessity for interventions and responsivity on admission or discharge. The eponym "Conrad syndrome" is proposed for locked-in state following nonfatal drowning in children. [ABSTRACT FROM AUTHOR]

Cardiac arrest survivors suffer the repercussions of anoxic brain injury, a critical factor influencing long-term prognosis. This injury is characterised by profound and enduring metabolic impairment. Ketone bodies, an alternative energetic resource in physiological states such as exercise, fasting, and extended starvation, are avidly taken up and used by the brain. Both the ketogenic diet and exogenous ketone supplementation have been associated with neuroprotective effects across a spectrum of conditions. These include refractory epilepsy, neurodegenerative disorders, cognitive impairment, focal cerebral ischemia, and traumatic brain injuries. Beyond this, ketone bodies possess a plethora of attributes that appear to be particularly favourable after cardiac arrest. These encompass anti-inflammatory effects, the attenuation of oxidative stress, the improvement of mitochondrial function, a glucose-sparing effect, and the enhancement of cardiac function. The aim of this manuscript is to appraise pertinent scientific literature on the topic through a narrative review. We aim to encapsulate the existing evidence and underscore the potential therapeutic value of ketone bodies in the context of cardiac arrest to provide a rationale for their use in forthcoming translational research efforts.

Emerging science continues to establish the detrimental effects of malnutrition in acute neurological diseases such as traumatic brain injury, stroke, status epilepticus and anoxic brain injury. The primary pathological pathways responsible for secondary brain injury include neuroinflammation, catabolism, immune suppression and metabolic failure, and these are exacerbated by malnutrition. Given this, there is growing interest in novel nutritional interventions to promote neurological recovery after acute brain injury. In this review, we will describe how malnutrition impacts the biomolecular mechanisms of secondary brain injury in acute neurological disorders, and how nutritional status can be optimized in both pediatric and adult populations. We will further highlight emerging therapeutic approaches, including specialized diets that aim to resolve neuroinflammation, immunodeficiency and metabolic crisis, by providing pre-clinical and clinical evidence that their use promotes neurologic recovery. Using nutrition as a targeted treatment is appealing for several reasons that will be discussed. Given the high mortality and both short- and long-term morbidity associated with acute brain injuries, novel translational and clinical approaches are needed. [ABSTRACT FROM AUTHOR]

Diffuse cortical diffusion changes on magnetic resonance imaging (MRI) are characteristically ascribed to global cerebral anoxia, typically after cardiac arrest. Far from being pathognomonic, however, this neuroimaging finding is relatively nonspecific, and can manifest in a myriad of disease states including hypoxia, metabolic derangements, infections, seizure, toxic exposures, and neuroinflammation. While these various conditions can all produce a neuroimaging pattern of widespread cortical diffusion restriction, many of these underlying causes do have subtly unique imaging features that are appreciable on MRI and can be of clinical and diagnostic utility. Specific populations of neurons are variably sensitive to certain types of injury, whether due to differences in perfusion, receptor type density, or the unique tropisms of infectious organisms. In this narrative review, we discuss a number of distinct etiologies of diffuse cortical diffusion restriction on MRI, the unique pathophysiologies responsible for tissue injury, and the resulting neuroimaging characteristics that can be of assistance in differentiating them. As widespread cortical injury from any cause often presents with altered mental status or coma, the differential diagnosis can be enhanced with rapid acquisition of MRI when clinical history or detailed physical examination is limited. In such settings, the distinct imaging features discussed in this article are of interest to both the clinician and the radiologist. [ABSTRACT FROM AUTHOR]

Emerging science continues to establish the detrimental effects of malnutrition in acute neurological diseases such as traumatic brain injury, stroke, status epilepticus and anoxic brain injury. The primary pathological pathways responsible for secondary brain injury include neuroinflammation, catabolism, immune suppression and metabolic failure, and these are exacerbated by malnutrition. Given this, there is growing interest in novel nutritional interventions to promote neurological recovery after acute brain injury. In this review, we will describe how malnutrition impacts the biomolecular mechanisms of secondary brain injury in acute neurological disorders, and how nutritional status can be optimized in both pediatric and adult populations. We will further highlight emerging therapeutic approaches, including specialized diets that aim to resolve neuroinflammation, immunodeficiency and metabolic crisis, by providing pre-clinical and clinical evidence that their use promotes neurologic recovery. Using nutrition as a targeted treatment is appealing for several reasons that will be discussed. Given the high mortality and both short- and long-term morbidity associated with acute brain injuries, novel translational and clinical approaches are needed.

Palliative care (PC) teams commonly encounter patients with disorders of consciousness (DOC) following anoxic or traumatic brain injury (TBI). Primary teams may consult PC to help surrogates in making treatment choices for these patients. PC clinicians must understand the complexity of predicting neurologic outcomes, address clinical nihilism, and appropriately guide surrogates in making decisions that are concordant with patients' goals. The purpose of this article was to provide PC providers with a better understanding of caring for patients with DOC, specifically following anoxic or TBI. Many of the tips acknowledge the uncertainty of DOC and provide strategies to help tackle this dilemma. [ABSTRACT FROM AUTHOR]

Background: Some patients resuscitated from out-of-hospital cardiac arrest (OHCA) progress to death by neurological criteria (DNC). We hypothesized that initial brain imaging, electroencephalography (EEG), and arrest characteristics predict progression to DNC.Methods: We identified comatose OHCA patients from January 2010 to February 2020 treated at a single quaternary care facility in Western Pennsylvania. We abstracted demographics and arrest characteristics; Pittsburgh Cardiac Arrest Category, initial motor exam and pupillary light reflex; initial brain computed tomography (CT) grey-to-white ratio (GWR), sulcal or basal cistern effacement; initial EEG background and suppression ratio. We used two modeling approaches: fast and frugal tree (FFT) analysis to create an interpretable clinical risk stratification tool and ridge regression for comparison. We used bootstrapping to randomly partition cases into 80% training and 20% test sets and evaluated test set sensitivity and specificity.Results: We included 1,569 patients, of whom 147 (9%) had diagnosed DNC. Across bootstrap samples, >99% of FFTs included three predictors: sulcal effacement, and in cases without sulcal effacement, the combination of EEG background suppression and GWR ≤ 1.23. This tree had mean sensitivity and specificity of 87% and 81%. Ridge regression with all available predictors had mean sensitivity 91 % and mean specificity 83%. Subjects falsely predicted as likely to progress to DNC generally died of rearrest or withdrawal of life sustaining therapies due to poor neurological prognosis. Two of these cases awakened from coma during the index hospitalization.Conclusions: Sulcal effacement on presenting brain CT or EEG suppression with GWR ≤ 1.23 predict progression to DNC after OHCA. [ABSTRACT FROM AUTHOR]

Background: Patients resuscitated from cardiac arrest who have severe neurological or functional disability at discharge require high-intensity long-term support. However, few data describe the long-term survival and health-care utilization for these patients.Methods: We identified a cohort of cardiac arrest survivors ≥ 18 years of age, treated at a single center in Western Pennsylvania from January 2010 to December 2019, with a modified Rankin scale (mRS) of 5 at hospital discharge. We recorded demographics, cardiac arrest characteristics, and neurological exam at hospital discharge. We characterized long term survival and mortality through December 31, 2020 through National Death Index query. We described survival time overall and in subgroups using Kaplan-Meier curves and compared using log-rank tests.We linked cases with administrative data to determine 30, 90 day, and one-year hospital readmission rate. For subjects unable to follow commands at discharge, we reviewed records from index hospitalization to the present to describe improvement in neurological status and return home.Results: We screened 2,687 patients of which 975 survived to discharge. We identified 190 subjects with mRS of 5 at hospital discharge who were sent to non-hospice settings. Of these, 43 (23%) did not follow commands at discharge. One-year mortality was 38% (n = 71) with a median survival time of 4.2 years (IQR 0.3-10.9). Duration of survival was shorter in older subjects but did not differ based on, sex, or ability to follow commands at hospital discharge. Within the first year of discharge, 58% (n = 111) of subjects had at least one hospitalization with a median length of stay of 8 days [IQR 3-19]. Of subjects who did not follow commands at hospital discharge, 5/43 (11%) followed commands and 9 (21%) were reportedly living at home on subsequent encounters.Conclusions: Of survivors treated over a decade at our institution, 20% (n = 190) were discharged from the hospital with severe functional disability. One-year mortality was 38%, and hospital readmissions were frequent. Few patients discharged unable to follow commands regained the ability over the period of observation, but many did return to living at home. These data can help inform decision maker expectations for patient trajectory and life expectancy. [ABSTRACT FROM AUTHOR]

Abstract This article highlights the possibility of positive outcomes associated with prolonged CPR and anoxic brain injury contesting the idea that such patients will invariably end up in a persistent vegetative state.

Few data characterize the role of brain computed tomography (CT) after resuscitation from in-hospital cardiac arrest (IHCA). We hypothesized that identifying a neurological etiology of arrest or cerebral edema on brain CT are less common after IHCA than after resuscitation from out-of-hospital cardiac arrest (OHCA). We included all patients comatose after resuscitation from IHCA or OHCA in this retrospective cohort analysis. We abstracted patient and arrest clinical characteristics, as well as pH and lactate, to estimate systemic illness severity. Brain CT characteristics included quantitative measurement of the grey-to-white ratio (GWR) at the level of the basal ganglia and qualitative assessment of sulcal and cisternal effacement. We compared GWR distribution by stratum (no edema ≥1.30, mild-to-moderate <1.30 and >1.20, severe ≤1.20) and newly identified neurological arrest etiology between IHCA and OHCA groups. We included 2,306 subjects, of whom 420 (18.2%) suffered IHCA. Fewer IHCA subjects underwent post-arrest brain CT versus OHCA subjects (149 (35.5%) vs 1,555 (82.4%), p < 0.001). Cerebral edema for IHCA versus OHCA was more often absent (60.1% vs. 47.5%) or mild-to-moderate (34.3% vs. 27.9%) and less often severe (5.6% vs. 24.6%). A neurological etiology of arrest was identified on brain CT in 0.5% of IHCA versus 3.2% of OHCA. Although severe edema was less frequent in IHCA relative to OHCA, mild-to-moderate or severe edema occurred in one in three patients after IHCA. Unsuspected neurological etiologies of arrest were rarely discovered by CT scan in IHCA patients. [ABSTRACT FROM AUTHOR]

Severe acquired brain injury has long-term physical and cognitive effects. Identifying patient variables predictive of recovery in different brain injury populations would generate improved prognostic information and help rehabilitation teams set appropriate therapeutic goals. This cohort study of 447 NHS neurorehabilitation inpatients aimed to identify functional and cognitive predictors of recovery following severe acquired brain injury caused by trauma, stroke and anoxia. Motor and cognitive impairment ratings were collected at admission and discharge using the Functional Independence Measure and Functional Assessment Measure (FIM+FAM), and injury-related and demographic data were collated from medical records. Predictors of physical, cognitive and overall recovery were identified via hierarchical regression analyses. Several key findings emerged. Firstly, on-admission motor skills predicted functional and overall outcomes across groups. Secondly, on-admission social interaction skills predicted cognitive discharge outcomes in stroke and trauma, and overall outcomes for stroke, but did not predict anoxia outcomes. Thirdly, age predicted all forms of recovery for stroke only. Further group-specific factors were also identified as predicting motor and cognitive recovery, indicating that factors key to the rehabilitation trajectory may differ between populations. These variables should be considered in rehabilitation goal planning, although further research is required to explore their contributions to recovery. [ABSTRACT FROM AUTHOR]

Background: Shock is common in patients resuscitated from out-of-hospital-cardiac arrest (OHCA). Shock severity can be classified using the Society for Cardiovascular Angiography and Intervention (SCAI) Shock Classification. We aimed to examine the association of SCAI Shock Stage with in-hospital mortality and neurological outcome in comatose OHCA patients undergoing targeted temperature management (TTM).Methods: This study included 213 comatose adult patients who underwent TTM after OHCA between January 2007 and December 2017. SCAI shock stage (A through E) was assigned using data from the first 24 hours, with shock defined as SCAI shock stage C/D/E. Good neurological outcome was defined as a modified Rankin Scale (mRS) less than 3.Results: In-hospital mortality was higher in the 144 (67.6%) patients with shock (46.5% v. 23.2%, unadjusted OR 2.88, 95% CI 1.51-5.51, p = 0.001). After multivariable adjustment, each SCAI shock stage was incrementally associated with an increased risk of in-hospital mortality (adjusted OR 1.80 per stage, 95% CI 1.20-2.71, p = 0.003). Good neurological outcome was less likely in patients with shock (31.9% vs. 53.6%, unadjusted OR 0.41, 95% CI 0.23-0.73, p = 0.002) and a higher SCAI shock stage was incrementally associated with a lower likelihood of good neurological outcome after multivariable adjustment (adjusted OR 0.67 per stage, 95% CI 0.48-0.93, p = 0.015).Conclusion: Higher shock severity, defined using the SCAI Shock Classification, was associated with increased in-hospital mortality and a lower likelihood of good neurological outcome in OHCA patients treated with TTM. [ABSTRACT FROM AUTHOR]

Introduction: Out-of-hospital cardiac arrest (OHCA) is a major cause of death and disability in the United States. Cardiac arrest centers (CAC) are necessary for the management of these critically ill and complex post arrest patients due to their specialized services and provider expertise. We report the case of a patient with OHCA and the systems of care involved in his resuscitation and recovery. Case Report: Emergency medical services attended a 39-year-old male with ongoing bystander cardiopulmonary resuscitation (CPR) after a witnessed collapse. Despite receiving appropriate advanced cardiac life support, including three defibrillations, he remained in refractory ventricular fibrillation. A prehospital physician identified him as an extracorporeal cardiopulmonary resuscitation (ECPR) candidate due to his age, witnessed arrest, refractory rhythm, and functional status. He was expedited to a CAC but no longer qualified for ECPR due to the time limit. He was resuscitated by the multiple teams activated prior to his arrival. He eventually had sustained return of circulation, was taken to the catheterization lab for emergent percutaneous coronary intervention, and recovered with a good neurologic outcome. Conclusion: Cardiac arrest centers may be capable of advanced interventions including ECPR. However, the systems of care offered by these centers is itself a lifesaving intervention. As this case highlights, despite not receiving the specified intervention (ECPR) the systems of care required to offer such a resource led to this favorable outcome. [ABSTRACT FROM AUTHOR]

Abstract Emergency clinicians often resuscitate cardiac arrest patients, and after acute resuscitation, clinicians face multiple decisions regarding disposition. Recent evidence suggests that out‐of‐hospital cardiac arrest patients with return of spontaneous circulation have higher odds of survival to hospital discharge, long‐term survival, and improved functional outcomes when treated at centers that can provide advanced multidisciplinary care. For community clinicians, a high volume cardiac arrest center may be hours away. While current guidelines recommend against neurological prognostication in the first hours or days after return of spontaneous circulation, there are early findings suggestive of irrecoverable brain injury in which the patient would receive no benefit from transfer. In this Concepts article, we describe a simplified approach to quickly evaluate neurological status in cardiac arrest patients and identify findings concerning for irrecoverable brain injury. Characteristics of the arrest and resuscitation, initial neurological assessment, and brain computed tomography together can identify patients with high likelihood of irrecoverable anoxic injury. Patients who may benefit from centers with access to continuous electroencephalography are discussed. This approach can be used to identify patients who may benefit from rapid transfer to cardiac arrest centers versus those who may benefit from care close to home. Risk stratification also can provide realistic expectations for recovery to families.

Background: Electroencephalography (EEG) is commonly used after cardiac arrest. Burst suppression with identical bursts (BSIB) has been reported as a perfectly specific predictor of poor outcome but published case series are small. We describe two patients with BSIB who awakened from coma after cardiac arrest. Methods: We identified two out-of-hospital cardiac arrest (OHCA) patients with coma and BSIB. We determined the etiology of arrest, presenting neurological examination, potential confounders to neurological assessment, neurodiagnostics and time to awakening. We reviewed and interpreted EEGs using 2021 American Clinical Neurophysiology Society guidelines. We quantified identicality of bursts by calculating pairwise correlation coefficients between the first 500 ms of each aligned burst. Results: In case one we present a 62-year-old man with OHCA secondary to septic shock. EEG showed burst suppression pattern, with bursts consisted of high amplitude generalized spike waves in lock-step with myoclonus (inter-burst correlation = 0.86). He followed commands 3 days after arrest, when repeat EEG showed a continuous, variable and reactive background without epileptiform activity. Case two was a 49-year-old woman with OHCA secondary to polysubstance overdose. Initial EEG revealed burst suppression with high amplitude generalized polyspike-wave bursts with associated myoclonus. She followed commands on post-arrest day 4, when repeat EEG showed a continuous, variable and reactive background with frequent runs of bifrontal predominant sharply contoured rhythmic delta activity. Conclusion: These cases highlight the perils of prognosticating with a single modality in comatose cardiac arrest patients.

Anoxic brain injury following cardiac arrest causes serious neurological sequela and mortality. Cortical blindness is a known manifestation of anoxic brain injury. However, its delayed‐onset presentation is very rare. Here, we report two patients with an anoxic brain injury who were effectively resuscitated after cardiac arrest, and subsequently developed delayed‐onset cortical blindness and movement disorders. We also provide a literature review of previously reported similar cases. These cases highlight that even in successfully revived patients, anoxic brain injury‐related neurological deficits could appear late in the course and may be permanent in 25% of the cases. [ABSTRACT FROM AUTHOR]

Background: Cerebral edema after cardiac arrest may be a modifiable cause of secondary brain injury. We aimed to identify processes of care associated with recovery in a cohort of patients with mild to moderate edema.Methods: We conducted a retrospective cohort study of adults resuscitated from out-of-hospital arrest (OHCA) at a single center from 2010 to 2018. We included those with cerebral edema ranging from mild to moderate (gray to white matter attenuation ratio (GWR) 1.2 to 1.3 on initial brain computerized tomography (CT). We used Pittsburgh Cardiac Arrest Category (PCAC) to adjust for illness severity and considered the following values in the first 24 h of admission as additional predictors: GWR, lab values affecting serum osmolality (sodium, glucose, blood urea nitrogen (BUN)), total osmolality, change in osmolality from 0 to 24 h, cardiac etiology of arrest, targeted temperature to 33 °C (vs 36 °C), time-weighted mean arterial pressure (MAP), partial pressures of arterial oxygen and carbon dioxide and select medications. Our primary outcome was discharge with cerebral performance category 1-3. We used unadjusted and adjusted logistic regression for analysis.Results: We included 214 patients for whom CT was performed median 3.8 [IQR 2.4-5.2] hours after collapse. Median age was 57 [IQR 48-67] years, 82 (38%) were female, and 68 (32%) arrested from ventricular tachycardia or fibrillation. In adjusted models, modifiable processes of care were not associated with outcome.Conclusions: Illness severity, but not modifiable processes of care, were associated with recovery among post-arrest patients with mild-to-moderate cerebral edema. [ABSTRACT FROM AUTHOR]

Grey-white ratio (GWR) can estimate severity of cytotoxic cerebral edema secondary to hypoxic-ischemic brain injury after cardiac arrest and predict progression to death by neurologic criteria (DNC). Current approaches to calculating GWR are not standardized and have variable interrater reliability. We tested if measures of variance of brain density on early computed tomographic (CT) imaging after cardiac arrest could predict DNC. We performed a retrospective cohort study, identifying post-arrest patients treated between 2011 and 2020 at our single center. We extracted demographic data from our registry and Digital Imaging and Communication in Medicine (DICOM) files for each patient's first brain CT. We analyzed slices 15–20 of each DICOM, corresponding to the level of the basal ganglia while accommodating differences in patient anatomy. We extracted pixel arrays and converted the radiodensities to Hounsfield units (HU). To focus on brain tissue densities, we excluded HU > 60 and < 10. We calculated the variance of each patient's HU distribution and the difference between the means of a two-group Gaussian finite mixture model. We compared these novel metrics to existing measures of cerebral edema, then randomly divided our data into 80% training and 20% test sets and used logistic regression to predict DNC. Of 1,133 included subjects, 457 (40%) were female, mean (standard deviation) age was 58 (16) years, and 115 (10%) progressed to DNC. CTs were obtained a median [interquartile range] of 4.2 [2.8–5.7] hours post-arrest. Our novel measures correlated weakly with GWR. HU variance, but not difference between mixture model means, differed significantly between subjects with and without sulcal or cistern effacement. GWR outperformed our novel measures in predicting progression to DNC with an area under the receiver operating characteristic curve (AUC) of 0.82, compared to HU variance (AUC = 0.73) and the difference between mixture model means (AUC = 0.56). There are differences in the distribution of HU on post-arrest CT in patients with qualitative measures of cerebral edema. Current methods to quantify cerebral edema outperform simple measures of attenuation variance on early brain CT. Further analyses could investigate if these measures of variance, or other distributional characteristics of brain density, have improved predictive performance on brain CTs obtained later in the clinical course or derived from discrete regions of anatomical interest. [ABSTRACT FROM AUTHOR]

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Anoxic brain injury (ABI) is an important cause of prolonged hospital stay and morbidity across the globe. It is a sequel of major systemic insults resulting from various etiologies, such as reduced oxygen availability, insufficient cerebral blood flow, reduced oxygen carriage, or any metabolic condition that can interfere with the utilization of oxygen. A varying combination of pathophysiologic mechanisms leads to a spectrum of clinical manifestations, the understanding of which will significantly help in prognostication of patients. Neuroprognostication helps both the clinician and the patient's family in planning future course and is further aided by various neuromonitoring modalities, biomarkers, and imaging. Targeted temperature management still remains a therapeutic tool in ABI and along with other neuroprotective measures may improve the survival. Continuing research in ABI may uncover more promising treatment strategies.

This article highlights the possibility of positive outcomes associated with prolonged CPR and anoxic brain injury contesting the idea that such patients will invariably end up in a persistent vegetative state. [ABSTRACT FROM AUTHOR]

BACKGROUND: Hypoxic brain injury results in severe disabilities that require extensive acute inpatient and outpatient rehabilitation to promote maximal functional and cognitive recovery. Brain hypoxemia can result from a multitude of causes, including but not limited to cardiac arrest, drug overdose, and/or shock. While recovery from a hypoxic brain injury alone can be challenging, dealing with concurrent debilitative diagnoses such as Guillain Barré Syndrome (GBS) further complicates the recovery and rehabilitation course. CASE REPORT: The current case study highlights the acute inpatient rehabilitation course of a 16 year old male who presented with cerebral hypoxia secondary to strangulation and subsequently developed GBS. Physical examination of the patient upon rehabilitation consult was inconsistent with a purely hypoxic brain injury, including the absence of rectal tone. This prompted further potential spinal cord injury evaluation and work up, with diagnostic testing confirmatory of GBS. RELEVANCE: This case is important as, to our knowledge from literature review, the first known documented instance of hypoxic brain injury complicated by GBS. Moreover, it highlights the importance of identifying all potential causes of functional disability, particularly when presented with physical exam findings inconsistent with chief diagnosis, in order to maximize functional recovery and rehabilitative gains during acute inpatient rehabilitation. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate racial and ethnic disparities in postcardiac arrest outcomes in patients undergoing targeted temperature management.Design: Retrospective study.Setting: ICUs in a single tertiary care hospital.Patients: Three-hundred sixty-seven patients undergoing postcardiac arrest targeted temperature management, including continuous electroencephalogram monitoring.Interventions: None.Measurements and Main Results: Clinical variables examined in our clinical cohort included race/ethnicity, age, time to return of spontaneous circulation, cardiac rhythm at time of arrest, insurance status, Charlson Comorbidity Index, and time to withdrawal of life-sustaining therapy. CT at admission and continuous electroencephalogram monitoring during the first 24 hours were used as markers of early injury. Outcome was assessed as good (Cerebral Performance Category 1-2) versus poor (Cerebral Performance Category 3-5) at hospital discharge. White non-Hispanic ("White") patients were more likely to have good outcomes than white Hispanic/nonwhite ("Non-white") patients (34.4 vs 21.7%; p = 0.015). In a multivariate model that included age, time to return of spontaneous circulation, initial rhythm, combined electroencephalogram/CT findings, Charlson Comorbidity Index, and insurance status, race/ethnicity was still independently associated with poor outcome (odds ratio, 3.32; p = 0.003). Comorbidities were lower in white patients but did not fully explain outcomes differences. Nonwhite patients were more likely to exhibit signs of early severe anoxic changes on CT or electroencephalogram, higher creatinine levels and receive dialysis, but had longer duration to withdrawal of lifesustaining therapy. There was no significant difference in catheterizations or MRI scans. Subgroup analysis performed with patients without early electroencephalogram or CT changes still revealed better outcome in white patients.Conclusions: Racial/ethnic disparity in outcome persists despite a strictly protocoled targeted temperature management. Nonwhite patients are more likely to arrive with more severe anoxic brain injury, but this does not account for all the disparity. [ABSTRACT FROM AUTHOR]

This is a retrospective study to investigate the results of using zolpidem and lorazepam in persons with disorders of consciousness (DoC) and to provide practical information for clinical application and further studies. The cohort included 146 patients (11 hemorrhagic stroke, 87 traumatic brain injury (TBI), 48 anoxic brain injury (ABI)) admitted to a specialized DoC rehabilitation program. A positive trial indicated a patient responded to either zolpidem or lorazepam with prominent functional improvements necessitating routine use of the medication. Non-responders had equivocal or negative (i.e., went to sleep) responses. Eleven patients with a stroke who had either medication were all non-responders. Of the remaining 135 patients, 95 received at least one medication trial. The overall positive rate was 11.6% (11/95), with 6.3% (5/79) for zolpidem and 14.0% (6/43) for lorazepam. Among TBI patients, the positive rate of the zolpidem trial (10.2%, 5/49) was slightly higher than that of the lorazepam trial (6.9%, 2/29; p > 0.05). Among ABI patients, the positive rate of the lorazepam trial (28.6%, 4/14) was significantly higher than that of the zolpidem trial (0%, 0/30; p = 0.007). Following a positive trial, most patients were continued on the medications on a regular basis before eventual discontinuation. Our results suggested the etiology of DoC, considering traumatic vs. anoxic injuries, may serve in guiding the clinical application of these medications in the treatment of DoC and in future prospective studies. We advocate for screening all patients with DoC using zolpidem and/or lorazepam.

A 63-year-old woman was hospitalized for rehabilitation from the aftereffects of an anoxic brain injury. In addition to a general cognitive decline, agraphia of kana and kanji was noted at the time of admission, which had advanced to agraphia which is dominant in kanji at the time of hospital discharge. Brain magnetic resonance imaging revealed no stroke lesions, and brain perfusion scintigraphy found a decreased blood flow in the bilateral parietal lobes. We hereby report on this case because case reports on agraphia caused by anoxic brain injury are extremely rare.

Introduction: We tested the impact of antiepileptic drug (AED) administration on post-cardiac arrest epileptiform electroencephalographic (EEG) activity.Methods: We studied an observational cohort of comatose subjects treated at a single academic medical center after cardiac arrest from September 2010 to January 2018. We aggregated the observed EEG patterns into 5 categories: suppressed; discontinuous background with superimposed epileptiform activity; discontinuous background without epileptiform features; continuous background with epileptiform activity; and continuous background without epileptiform activity. We calculated overall probabilities of transitions between EEG states in a multistate model, then used Aalen's additive regression to test if AEDs or hypothermia are associated with a change in these probabilities.Results: Overall, 828 subjects had EEG-monitoring for 42,840 h with a median of 40 [IQR 23-64] h per subject. Among patients with epileptiform findings on initial monitoring, 50% transitioned at least once to a non-epileptiform, non-suppressed state. By contrast, 19% with non-epileptiform initial activity transitioned to an epileptiform state at least once. Overall, 568 (78%) patients received at least one AED. Among patients with continuous EEG background activity, valproate, levetiracetam and lower body temperature were each associated with an increased probability of transition from epileptiform states to non-epileptiform states, where patients with discontinuous EEG background activity no agent linked to an increased probability of transitioning from epileptiform states.Conclusion: After cardiac arrest, the impact of AEDs may depend on the presence of continuous cortical background activity. These data serve to inform experimental work to better define the opportunities to improve neurologic care post-cardiac arrest. [ABSTRACT FROM AUTHOR]

Highlights • The NSE ratio is a unique method to quantify NSE changes over time. • NSE ratio > 1.0 indicates increasing NSE and may reflect ongoing neuronal injury. • A 48:24 h NSE ratio >1.7 was 100% specific for poor outcome in this population. • The NSE ratio may be generalizable across populations and laboratories. Abstract Introduction Serum neuron-specific enolase (NSE) levels have been shown to correlate with neurologic outcome in comatose survivors of cardiac arrest but use of absolute NSE thresholds is limited. This study describes and evaluates a novel approach to analyzing NSE, the NSE ratio, and evaluates the prognostic utility of NSE absolute value thresholds and trends over time. Methods 100 consecutive adult comatose cardiac arrest survivors were prospectively enrolled. NSE levels were assessed at 24, 48, and 72 h post-arrest. Primary outcome was the Glasgow Outcome Score (GOS) at 6 months post-arrest; good outcome was defined as GOS 3–5. Absolute and relative NSE values (i.e. the NSE ratio), peak values, and the trend in NSE over 72 h were analyzed. Results 98 patients were included. 42 (43%) had a good outcome. Five good outcome patients had peak NSE >33 µg/L (34.9–46.4 µg/L). NSE trends between 24 and 48 h differed between outcome groups (decrease by 3.0 µg/L (0.9–7.0 µg/L) vs. increase by 13.4 µg/L (−3.7 to 69.4 µg/L), good vs. poor, p = 0.004). The 48:24 h NSE ratio differed between the good and poor outcome groups (0.8 (0.6–0.9) vs. 1.4 (0.8–2.5), p = 0.001), and a 48:24 h ratio of ≥1.7 was 100% specific for poor outcome. Conclusions The NSE ratio is a unique method to quantify NSE changes over time. Values greater than 1.0 indicate increasing NSE and may be reflective of ongoing neuronal injury. The NSE ratio obviates the need for an absolute value cut-off. [ABSTRACT FROM AUTHOR]

Drowning is a leading cause of neurological morbidity and mortality in young children. Anoxic brain injury (ABI) can result from nonfatal drowning and typically entails substantial neurological impairment. The neuropathology of drowning-induced pediatric ABI is not well established. Specifically, quantitative characterization of the spatial extent and tissue distribution of anoxic damage in pediatric nonfatal drowning has not previously been reported but could clarify the underlying pathophysiological processes and inform clinical management. To this end, we used voxel-based morphometric (VBM) analyses to quantify the extent and spatial distribution of consistent, between-subject alterations in gray and white matter volume. Whole-brain, high-resolution T1-weighted MRI datasets were acquired in 11 children with chronic ABI and 11 age- and gender-matched neurotypical controls (4–12 years). Group-wise VBM analyses demonstrated predominantly central subcortical pathology in the ABI group in both gray matter (bilateral basal ganglia nuclei) and white matter (bilateral external and posterior internal capsules) (P

Out-of-hospital cardiac arrest (CA) remains a leading cause of sudden morbidity and mortality; however, outcomes have continued to improve in the era of targeted temperature management (TTM). In this review, we highlight the clinical use of TTM, and provide an updated summary of multimodality monitoring possible in a modern ICU. TTM is neuroprotective for survivors of CA by inhibiting multiple pathophysiologic processes caused by anoxic brain injury, with a final common pathway of neuronal death. Current guidelines recommend the use of TTM for out-of-hospital CA survivors who present with a shockable rhythm. Further studies are being completed to determine the optimal timing, depth and duration of hypothermia to optimize patient outcomes. Although a multidisciplinary approach is necessary in the CA population, neurologists and neurointensivists are central in selecting TTM candidates and guiding patient care and prognostic evaluation. Established prognostic tools include clinal exam, SSEP, EEG and MR imaging, while functional MRI and invasive monitoring is not validated to improve outcomes in CA or aid in prognosis. We recommend that an evidence-based TTM and prognostication algorithm be locally implemented, based on each institution's resources and limitations. Given the high incidence of CA and difficulty in predicting outcomes, further study is urgently needed to determine the utility of more recent multimodality devices and studies.

Liu et al. used continuous EEG and CBF velocity monitoring to investigate neurovascular coupling in patients with stroke from large vessel occlusion (LVO). All ABI patients experienced rScO SB 2 sb desaturation as compared with 42% patients without ABI ( I p i = 0.04). Distortion-product otoacoustic emissions (DPOAEs) and transient evoked otoacoustic emissions (TEOAEs) were measured in cardiac arrest patients and 10 patients with myocardial infarction as controls. [Extracted from the article]

Out-of-hospital cardiac arrest (CA) remains a leading cause of sudden morbidity and mortality; however, outcomes have continued to improve in the era of targeted temperature management (TTM). In this review, we highlight the clinical use of TTM, and provide an updated summary of multimodality monitoring possible in a modern ICU. TTM is neuroprotective for survivors of CA by inhibiting multiple pathophysiologic processes caused by anoxic brain injury, with a final common pathway of neuronal death. Current guidelines recommend the use of TTM for out-of-hospital CA survivors who present with a shockable rhythm. Further studies are being completed to determine the optimal timing, depth and duration of hypothermia to optimize patient outcomes. Although a multidisciplinary approach is necessary in the CA population, neurologists and neurointensivists are central in selecting TTM candidates and guiding patient care and prognostic evaluation. Established prognostic tools include clinal exam, SSEP, EEG and MR imaging, while functional MRI and invasive monitoring is not validated to improve outcomes in CA or aid in prognosis. We recommend that an evidence-based TTM and prognostication algorithm be locally implemented, based on each institution's resources and limitations. Given the high incidence of CA and difficulty in predicting outcomes, further study is urgently needed to determine the utility of more recent multimodality devices and studies. [ABSTRACT FROM AUTHOR]

Aim Of the Study: To determine the optimal mean arterial pressure (MAP) during the early-to-intermediate phase care of comatose survivors of out-of-hospital cardiac arrest (OHCA).Methods: We identified consecutive comatose survivors of OHCA with an initial shockable rhythm. Using blood pressure-over-time plots, we calculated the area below pre-specified MAP thresholds (ABT; mmHg*hours) during the first 96 h of admission. We used incremental MAP thresholds ranging between 65 and 85 mmHg. Logistic regression analyses were used to examine the association between ABT and clinical outcomes for each MAP threshold and to adjust for age, duration of cardiac arrest, and bystander CPR. The primary outcome was severe neurological dysfunction as defined by a cerebral performance category (CPC) ≥3.Results: We identified 122 consecutive OHCA patients meeting inclusion criteria. The rate of the primary outcome was 33%. There was a significant association between ABT and the rate of the primary outcome when MAP thresholds of 60 (p = 0.01), 65 (p < 0.01), 70 (p < 0.01), 75 (p < 0.01), and 80 mmHg (p < 0.01) were used. This association was lost once a MAP threshold of 85 mmHg was reached (p = 0.63). In the adjusted analysis, the association between ABT and the primary outcome was no longer present when the MAP threshold reached 75 mmHg.Conclusions: In comatose survivors of OHCA with an initial shockable rhythm, higher ABT is associated with increased rates of severe neurological dysfunction when MAP thresholds <75 mmHg are used. The current findings support the hypothesis that higher MAP targets (≥75 mmHg) may be indicated in this patient population. [ABSTRACT FROM AUTHOR]

Anoxic brain injury can manifest with various abnormal movements. We describe acute chorea in a young patient with anoxic brain injury due to chlordiazepoxide toxicity who had delayed radiographic lesions in bilateral globus pallidus. Although brain MRI 8 days after the anoxic event was unremarkable, repeat brain MRI 15 days after the event showed T2 hyperintensities and enhancement within the bilateral globus pallidi. It is possible that MRI brain findings of bilateral basal ganglia lesions may appear later than onset of chorea in anoxic brain injury. However, given the normal brain MRI in between, other etiologies cannot be excluded entirely. [ABSTRACT FROM AUTHOR]

Therapeutic hypothermia (TH) is a neuroprotective treatment post-cardiac arrest but is grossly underutilized. After TH induction, traditional biomarkers and parameters can no long predict clinical outcome due to a lack of understanding of hypothermic response. Innovative approaches to better understand the clinical effect of TH will help to prognosticate outcome and expand beneficial population. Protein glycosylation is an important extracellular post-translational modification, regulating various extracellular signaling pathways. Here, we used glycoproteomics to investigate the association of plasma glycoproteins with the prognosis of TH-treated cardiac arrest patients. Using lectin affinity chromatography and mass spectrometry, we identified 640 glycoproteins in the plasma of cardiac arrest patients undergoing TH treatment, of which 23 were up-regulated and 14 were down-regulated in good outcome patients as compared with poor outcome ones. Notably, two glycoproteins with antioxidant activity, ceruloplasmin (CP) and haptoglobin (HP), were found to be associated with favorable neurologic outcome. This was further supported by ELISA assay in a large patients cohort, in which glycosylated CP and HP enriched by concanavilin A (ConA) and wheat germ agglutinin (WGA) lectins were significantly increased in patients developing good outcome (ConA-CP: p = 0.033; ConA-HP: p = 0.04; WGA-HP: p = 0.021). Furthermore, ROC analysis demonstrated the predictive potential of ConA-CP, ConA-HP, and WGA-HP (ConA-CP: AUC = 0.732, p = 0.031; ConA-HP: AUC = 0.746, p = 0.022; WGA-HP: AUC = 0.714, p = 0.046) and combination of them improved the predictive power (AUC = 0.830, p = 0.002). Our results suggested that glycosylated CP and HP as well as other glycoproteins may play critical roles in neuroprotection and serve as sensitive prognostic markers for TH treatments. [ABSTRACT FROM AUTHOR]