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Objective: There is a complex interaction between nervous and cardiovascular systems, but sparse data exist on brain-heart electrophysiological responses to cardiac arrest resuscitation. Our aim was to investigate dynamic changes in autonomic and cortical function during hyperacute stage post-resuscitation., Methods: Ten rats were resuscitated from 7-min cardiac arrest, as indicators of autonomic response, heart rate (HR), and its variability (HRV) were measured. HR was monitored through continuous electrocardiography, while HRV was assessed via spectral analysis, whereby the ratio of low-/high-frequency (LF/HF) power indicates the balance between sympathetic/parasympathetic activities. Cortical response was evaluated by continuous electroencephalography and quantitative analysis. Parameters were quantified at 5-min intervals over the first-hour post-resuscitation. Neurological outcome was assessed by Neurological Deficit Score (NDS, range 0-80, higher = better outcomes) at 4-h post-resuscitation., Results: A significant increase in HR was noted over 15-30 min post-resuscitation (p < 0.01 vs.15-min, respectively) and correlated with higher NDS (rs = 0.56, p < 0.01). LF/HF ratio over 15-20 min was positively correlated with NDS (rs = 0.75, p < 0.05). Gamma band power surged over 15-30 min post-resuscitation (p < 0.05 vs. 0-15 min, respectively), and gamma band fraction during this period was associated with NDS (rs ≥0.70, p < 0.05, respectively). Significant correlations were identified between increased HR and gamma band power during 15-30 min (rs ≥0.83, p < 0.01, respectively) and between gamma band fraction and LF/HF ratio over 15-20 min post-resuscitation (rs = 0.85, p < 0.01)., Interpretations: Hyperacute recovery of autonomic and cortical function is associated with favorable functional outcomes. While this observation needs further validation, it presents a translational opportunity for better autonomic and neurologic monitoring during early periods post-resuscitation to develop novel interventions., (© 2023 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.)

Abstract Best practice guidelines have advanced severe traumatic brain injury (TBI) care; however, there is little that currently informs goals of care decisions and processes despite their importance and frequency. Panelists from the S eattle I nternational severe traumatic B rain I njury C onsensus C onference (SIBICC) participated in a survey consisting of 24 questions. Questions queried use of prognostic calculators, variability in and responsibility for goals of care decisions, and acceptability of neurological outcomes, as well as putative means of improving decisions that might limit care. A total of 97.6% of the 42 SIBICC panelists completed the survey. Responses to most questions were highly variable. Overall, panelists reported infrequent use of prognostic calculators, and observed variability in patient prognostication and goals of care decisions. They felt that it would be beneficial for physicians to improve consensus on what constitutes an acceptable neurological outcome as well as what chance of achieving that outcome is acceptable. Panelists felt that the public should help to define what constitutes a good outcome and expressed some support for a "nihilism guard." More than 50% of panelists felt that if it was certain to be permanent, a vegetative state or lower severe disability would justify a withdrawal of care decision, whereas 15% felt that upper severe disability justified such a decision. Whether conceptualizing an ideal or existing prognostic calculator to predict death or an unacceptable outcome, on average a 64-69% chance of a poor outcome was felt to justify treatment withdrawal. These results demonstrate important variability in goals of care decision making and a desire to reduce this variability. Our panel of recognized TBI experts opined on the neurological outcomes and chances of those outcomes that might prompt consideration of care withdrawal; however, imprecision of prognostication and existing prognostication tools is a significant impediment to standardizing the approach to care-limiting decisions.

Extracorporeal membrane oxygenation (ECMO), in conjunction with its life-saving benefits, carries a significant risk of acute brain injury (ABI). Hypoxic-ischemic brain injury (HIBI) is one of the most common types of ABI in ECMO patients. Various risk factors, such as history of hypertension, high day 1 lactate level, low pH, cannulation technique, large peri-cannulation PaCO 2 drop (∆PaCO 2 ), and early low pulse pressure, have been associated with the development of HIBI in ECMO patients. The pathogenic mechanisms of HIBI in ECMO are complex and multifactorial, attributing to the underlying pathology requiring initiation of ECMO and the risk of HIBI associated with ECMO itself. HIBI is likely to occur in the peri-cannulation or peri-decannulation time secondary to underlying refractory cardiopulmonary failure before or after ECMO. Current therapeutics target pathological mechanisms, cerebral hypoxia and ischemia, by employing targeted temperature management in the case of extracorporeal cardiopulmonary resuscitation (eCPR), and optimizing cerebral O 2 saturations and cerebral perfusion. This review describes the pathophysiology, neuromonitoring, and therapeutic techniques to improve neurological outcomes in ECMO patients in order to prevent and minimize the morbidity of HIBI. Further studies aimed at standardizing the most relevant neuromonitoring techniques, optimizing cerebral perfusion, and minimizing the severity of HIBI once it occurs will improve long-term neurological outcomes in ECMO patients.

Cardiac arrest (CA) remains the leading cause of coma, and early arousal recovery indicators are needed to allocate critical care resources properly. High-frequency oscillations (HFOs) of somatosensory evoked potentials (SSEPs) have been shown to indicate responsive wakefulness days following CA. Nonetheless, their potential in the acute recovery phase, where the injury is reversible, has not been tested. We hypothesize that time-frequency (TF) analysis of HFOs can determine arousal recovery in the acute recovery phase. To test our hypothesis, eleven adult male Wistar rats were subjected to asphyxial CA (five with 3-min mild and six with 7-min moderate to severe CA) and SSEPs were recorded for 60 min post-resuscitation. Arousal level was quantified by the neurological deficit scale (NDS) at 4 h. Our results demonstrated that continuous wavelet transform (CWT) of SSEPs localizes HFOs in the TF domain under baseline conditions. The energy dispersed immediately after injury and gradually recovered. We proposed a novel TF-domain measure of HFO: the total power in the normal time-frequency space (NTFS) of HFO. We found that the NTFS power significantly separated the favorable and unfavorable outcome groups. We conclude that the NTFS power of HFOs provides earlier and objective determination of arousal recovery after CA.

Objective assessment of the brain's responsiveness in comatose patients on Extracorporeal Membrane Oxygenation (ECMO) support is essential to clinical care, but current approaches are limited by subjective methodology and inter-rater disagreement. Quantitative electroencephalogram (EEG) algorithms could potentially assist clinicians, improving diagnostic accuracy. We developed a quantitative, stimulus-based algorithm to assess EEG reactivity features in comatose patients on ECMO support. Patients underwent a stimulation protocol of increasing intensity (auditory, peripheral, and nostril stimulation). A total of 129 20-s EEG epochs were collected from 24 patients (age [Formula: see text], 10 females, 14 males) on ECMO support with a Glasgow Coma Scale[Formula: see text]8. EEG reactivity scores ([Formula: see text]-scores) were calculated using aggregated spectral power and permutation entropy for each of five frequency bands ([Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text]. Parameter estimation techniques were applied to [Formula: see text]-scores to identify properties that replicate the decision process of experienced clinicians performing visual analysis. Spectral power changes from audio stimulation were concentrated in the [Formula: see text] band, whereas peripheral stimulation elicited an increase in spectral power across multiple bands, and nostril stimulation changed the entropy of the [Formula: see text] band. The findings of this pilot study on [Formula: see text]-score lay a foundation for a future prediction tool with clinical applications.

Since the 1960s, EEG has been used to assess the neurologic function of patients in the hours and days after cardiac arrest. Accurate and reliable prognostication after cardiac arrest is vital for tailoring aggressive patient care for those with a high likelihood of recovery and setting appropriate goals of care for those who have a high likelihood of a poor outcome. Attempts to define EEG's role in this process has evolved over the years. In this review, we provide important historical context about EEG's use, it's perceived unreliability in the post-cardiac arrest patient in the past and provide a detailed analysis of how this role has changed recently. A review of the 71 most recent and highest quality studies demonstrates that the introduction of a uniform classification and a timed approach to EEG analysis have positioned EEG as a complementary tool in the multimodal approach for prognostication. The review was created and intended for medical staff in the intensive care units and emphasizes EEG patterns and timing which portend both favorable and poor prognoses. Also, the review addresses the overall quality of the existing studies and discusses future directions to address the knowledge gaps in this field., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 The Authors.)

Objective: To review practices of brain death (BD) determination in patients on extracorporeal membrane oxygenation (ECMO)., Methods: A systematic search was applied to PubMed and 6 electronic databases from inception to May 22, 2019. Studies reporting methods of BD assessment in adult patients (>18 years old) while on ECMO were included, after which data regarding BD assessment were extracted., Results: Twenty-two studies (n = 177 patients) met the inclusion criteria. Eighty-eight patients (50%) in 19 studies underwent the apnea test (AT); most commonly through decreasing the ECMO sweep flow in 14 studies (n = 42, 48%), followed by providing CO 2 through the ventilator in 2 studies (n = 6, 7%), and providing CO 2 through the ECMO oxygenator in 1 study (n = 1, 1%). The details of the AT were not reported in 2 studies (n = 39, 44%). In 19 patients (22%), the AT was nonconfirmatory due to hemodynamic instability, hypoxia, insufficient CO 2 rise, or unreliability of the AT. A total of 157 ancillary tests were performed, including electroencephalogram (62%), computed tomography angiography (22%), transcranial Doppler ultrasound (6%), cerebral blood flow nuclear study (5%), cerebral angiography (4%), and other (1%). Forty-seven patients (53% of patients with AT) with confirmatory AT still underwent additional ancillary for BD confirmation. Only 21 patients (12% of all patients) were declared brain-dead using confirmatory ATs alone without ancillary testing., Conclusions: Performing AT for patients with ECMO was associated with high failure rate and hemodynamic complications. Our study highlights the variability in practice in regard to the AT and supports the use of ancillary tests to determine BD in patients on ECMO., (Copyright © 2020 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)

Objectives: Prolonged cardiac arrest is known to cause global ischemic brain injury and functional impairment. Upon resuscitation, electroencephalographic recordings of brain activity begin to resume and can potentially be used to monitor neurologic recovery. We have previously shown that intrathecal orexin shows promise as a restorative drug and arousal agent in rodents. Our goal is to determine the electrophysiology effects of orexin in a rodent model of asphyxial cardiac arrest, focusing on the electroencephalographic activity in the gamma and super-gamma bands (indicative of return of higher brain function)., Design: Experimental animal study., Setting: University-based animal research laboratory., Subjects: Adult male Wistar rats., Interventions: In an established model of asphyxial cardiac arrest ( n = 24), we treated half of Wistar rats with orexin administered intranasally by atomizer 30 minutes post return of spontaneous circulation in one of two dose levels (10 and 50 µM); the rest were treated with saline as control. Continuous electroencephalographic recording was obtained and quantitatively analyzed for the gamma fraction. Gamma and high-frequency super-gamma band measures were compared against clinical recovery according to Neuro-Deficit Score., Measurements and Main Results: Compared with the control cohort, the high-dose orexin cohort showed significantly better Neuro-Deficit Score 4 hours after return of spontaneous circulation (55.17 vs 47.58; p < 0.02) and significantly higher mean gamma fraction (0.251 vs 0.177; p < 0.02) in cerebral regions surveyed by rostral electrodes for the first 170 minutes after administration of orexin., Conclusions: Our findings support early and continuous monitoring of electroencephalography-based gamma activity as a marker of better functional recovery after intranasal administration of orexin as measured by Neuro-Deficit Score in an established animal model of asphyxial cardiac arrest., Competing Interests: The authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)

Cardiac arrest systems of care are successfully coordinating community, emergency medical services, and hospital efforts to improve the process of care for patients who have had a cardiac arrest. As a result, the number of people surviving sudden cardiac arrest is increasing. However, physical, cognitive, and emotional effects of surviving cardiac arrest may linger for months or years. Systematic recommendations stop short of addressing partnerships needed to care for patients and caregivers after medical stabilization. This document expands the cardiac arrest resuscitation system of care to include patients, caregivers, and rehabilitative healthcare partnerships, which are central to cardiac arrest survivorship.

Cerebral edema is commonly associated with cerebral pathology, and the clinical manifestation is largely related to the underlying lesioned tissue. Brain edema usually amplifies the dysfunction of the lesioned tissue and the burden of cerebral edema correlates with increased morbidity and mortality across diseases. Our modern-day approach to the medical management of cerebral edema has largely revolved around, an increasingly artificial distinction between cytotoxic and vasogenic cerebral edema. These nontargeted interventions such as hyperosmolar agents and sedation have been the mainstay in clinical practice and offer noneloquent solutions to a dire problem. Our current understanding of the underlying molecular mechanisms driving cerebral edema is becoming much more advanced, with differences being identified across diseases and populations. As our understanding of the underlying molecular mechanisms in neuronal injury continues to expand, so too is the list of targeted therapies in the pipeline. Here we present a brief review of the molecular mechanisms driving cerebral edema and a current overview of our understanding of the molecular targets being investigated.

While autoimmune diseases have been frequently found to coexist in the same patients, the co-occurrence of myasthaeniagravis and antiphospholipid antibody syndrome (APAS) has only been reported in eight cases. We present a case of a 46-year-old Filipina who developed ischaemic stroke while admitted at the neurocritical unit for myasthaenic crisis. She was successfully thrombolysed with intravenous recombinant tissue plasminogen activator (rTPA), given a regimen of intravenous Ig and a dose of cyclophosphamide prior to discharge. Extensive workup revealed APAS to be the aetiology of her stroke. Twenty-one months into her follow-up, she is doing well with a modified Rankin Score of 0. Our case suggests that rTPA followed by immunomodulators may be given safely in myasthaenic crisis patients who develop ischaemic stroke. We emphasise the importance of doing a comprehensive neurological evaluation in agitated patients in the critical care unit., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Significant improvements have been achieved in cardiac arrest resuscitation and postarrest resuscitation care, but mortality remains high. Most of the poor outcomes and deaths of cardiac arrest survivors have been attributed to widespread brain injury. This brain injury, commonly manifested as a comatose state, is a marker of poor outcome and a major basis for unfavorable neurological prognostication. Accurate prognostication is important to avoid pursuing futile treatments when poor outcome is inevitable but also to avoid an inappropriate withdrawal of life-sustaining treatment in patients who may otherwise have a chance of achieving meaningful neurological recovery. Inaccurate neurological prognostication leading to withdrawal of life-sustaining treatment and deaths may significantly bias clinical studies, leading to failure in detecting the true study outcomes. The American Heart Association Emergency Cardiovascular Care Science Subcommittee organized a writing group composed of adult and pediatric experts from neurology, cardiology, emergency medicine, intensive care medicine, and nursing to review existing neurological prognostication studies, the practice of neurological prognostication, and withdrawal of life-sustaining treatment. The writing group determined that the overall quality of existing neurological prognostication studies is low. As a consequence, the degree of confidence in the predictors and the subsequent outcomes is also low. Therefore, the writing group suggests that neurological prognostication parameters need to be approached as index tests based on relevant neurological functions that are directly related to the functional outcome and contribute to the quality of life of cardiac arrest survivors. Suggestions to improve the quality of adult and pediatric neurological prognostication studies are provided.

The cessation (ischemia) and restoration (reperfusion) of cerebral blood flow after cardiac arrest (CA) induce inflammatory processes that can result in additional brain injury. Therapeutic hypothermia (TH) has been proven as a brain protective strategy after CA. In this article, the underlying pathophysiology of ischemia-reperfusion brain injury with emphasis on the role of inflammatory mechanisms is reviewed. Potential targets for immunomodulatory treatments and relevant effects of TH are also discussed. Further studies are needed to delineate the complex pathophysiology and interactions among different components of immune response after CA and identify appropriate targets for clinical investigations., Competing Interests: There are no conflicts of interest.

Cardiac arrest (CA) entails significant risks of coma resulting in poor neurological and behavioral outcomes after resuscitation. Significant subsequent morbidity and mortality in post-CA patients are largely due to the cerebral and cardiac dysfunction that accompanies prolonged whole-body ischemia post-CA syndrome (PCAS). PCAS results in strong inflammatory responses including neuroinflammation response leading to poor outcome. Currently, there are no proven neuroprotective therapies to improve post-CA outcomes apart from therapeutic hypothermia. Furthermore, there are no acceptable approaches to promote cortical or cognitive arousal following successful return of spontaneous circulation (ROSC). Hypothalamic orexinergic pathway is responsible for arousal and it is negatively affected by neuroinflammation. However, whether activation of the orexinergic pathway can curtail neuroinflammation is unknown. We hypothesize that targeting the orexinergic pathway via intranasal orexin-A (ORXA) treatment will enhance arousal from coma and decrease the production of proinflammatory cytokines resulting in improved functional outcome after resuscitation. We used a highly validated CA rat model to determine the effects of intranasal ORXA treatment 30-minute post resuscitation. At 4hrs post-CA, the mRNA levels of proinflammatory markers (IL1β, iNOS, TNF-α, GFAP, CD11b) and orexin receptors (ORX1R and ORX2R) were examined in different brain regions. CA dramatically increased proinflammatory markers in all brain regions particularly in the prefrontal cortex, hippocampus and hypothalamus. Post-CA intranasal ORXA treatment significantly ameliorated the CA-induced neuroinflammatory markers in the hypothalamus. ORXA administration increased production of orexin receptors (ORX1R and ORX2R) particularly in hypothalamus. In addition, ORXA also resulted in early arousal as measured by quantitative electroencephalogram (EEG) markers, and recovery of the associated behavioral neurologic deficit scale score (NDS). Our results indicate that intranasal delivery of ORXA post-CA has an anti-inflammatory effect and accelerates cortical EEG and behavioral recovery. Beneficial outcomes from intranasal ORXA treatment lay the groundwork for therapeutic clinical approach to treating post-CA coma.

Nonconvulsive status epilepticus (NCSE) has rapidly expanded from classical features such as staring, repetitive blinking, chewing, swallowing, and automatism to include coma, prolonged apnea, cardiac arrest, dementia, and higher brain dysfunction, which were demonstrated mainly after the 2000s by us and other groups. This review details novel clinical features of NCSE as a manifestation of epilepsy, but one that is underdiagnosed, with the best available evidence. Also, we describe the new concept of epilepsy-related organ dysfunction (Epi-ROD) and a novel electrode and headset which enables prompt electroencephalography., Competing Interests: Competing interests: The authors declare that they have no competing interests.No competing interests were disclosed.No competing interests were disclosed.

This comprehensive review summarizes the evidence regarding use of cerebral autoregulation-directed therapy at the bedside and provides an evaluation of its impact on optimizing cerebral perfusion and associated functional outcomes. Multiple studies in adults and several in children have shown the feasibility of individualizing mean arterial blood pressure and cerebral perfusion pressure goals by using cerebral autoregulation monitoring to calculate optimal levels. Nine of these studies examined the association between cerebral perfusion pressure or mean arterial blood pressure being above or below their optimal levels and functional outcomes. Six of these nine studies (66%) showed that patients for whom median cerebral perfusion pressure or mean arterial blood pressure differed significantly from the optimum, defined by cerebral autoregulation monitoring, were more likely to have an unfavorable outcome. The evidence indicates that monitoring of continuous cerebral autoregulation at the bedside is feasible and has the potential to be used to direct blood pressure management in acutely ill patients.

A complex interaction exists between the nervous and cardiovascular systems. A large network of cortical and subcortical brain regions control cardiovascular function via the sympathetic and parasympathetic outflow. A dysfunction in one system may lead to changes in the function of the other. The effects of cardiovascular disease on the nervous system have been widely studied; however, our understanding of the effects of neurological disorders on the cardiovascular system has only expanded in the past 2 decades. Various pathologies of the nervous system can lead to a wide range of alterations in function and structure of the cardiovascular system ranging from transient and benign electrographic changes to myocardial injury, cardiomyopathy, and even cardiac death. In this article, we first review the anatomy and physiology of the central and autonomic nervous systems in regard to control of the cardiovascular function. The effects of neurological injury on cardiac function and structure will be summarized, and finally, we review neurological disorders commonly associated with cardiovascular manifestations., (© 2017 American Heart Association, Inc.)

Abnormal movements are frequently encountered in patients with brain injury hospitalized in intensive care units (ICUs), yet characterization of these movements and their underlying pathophysiology is difficult due to the comatose or uncooperative state of the patient. In addition, the available diagnostic approaches are largely derived from outpatients with neurodegenerative or developmental disorders frequently encountered in the outpatient setting, thereby limiting the applicability to inpatients with acute brain injuries. Thus, we reviewed the available literature regarding abnormal movements encountered in acutely ill patients with brain injuries. We classified the brain injury into the following categories: anoxic, vascular, infectious, inflammatory, traumatic, toxic-metabolic, tumor-related and seizures. Then, we identified the abnormal movements seen in each category as well as their epidemiologic, semiologic and clinicopathologic correlates. We propose a practical paradigm that can be applied at the bedside for diagnosing abnormal movements in the ICU. This model seeks to classify observed abnormal movements in light of various patient-specific factors. It begins with classifying the patient's level of consciousness. Then, it integrates the frequency and type of each movement with the availability of ancillary diagnostic tests and the specific etiology of brain injury.

Encephalitis results in considerable morbidity and mortality in the United States and worldwide. Neurologists are often consulted or directly care for patients with encephalitis admitted to the hospital and must be able to discriminate between encephalitis and the many conditions that mimic it. Moreover, neurologists must be familiar with the myriad causes of encephalitis in order to develop a practical approach to diagnostic testing and treatment. An understanding of recent advances in management, particularly with respect to autoimmune etiologies and critical care approaches, is equally important. Here, we summarize a general approach to the care of adult patients with encephalitis.

Evoked potentials recorded from the somatosensory cortex have been shown to be an electrophysiological marker of brain injury in global hypoxic ischemia (HI). The evoked responses in somatosensory neurons carry information pertaining to signal from the ascending pathway in both the subcortical and cortical areas. In this study, origins of the subcortical and cortical signals are explored by decomposing the evoked neuronal activities into short- and long-latency responses (SLR and LLR), respectively. We evaluated the effect of therapeutic hypothermia on SLR and LLR during early recovery from cardiac arrest (CA)-induced HI in a rodent model. Twelve rats were subjected to CA, after which half of them were treated with hypothermia (32-34°C) and the rest were kept at normal temperature (36-37°C). Evoked neuronal activities from the primary somatosensory cortex, including multiunit activity (MUA) and local field potential (LFP), were continuously recorded during injury and early recovery. Results showed that upon initiation of injury, LLR disappeared first, followed by the disappearance of SLR, and after a period of isoelectric silence SLR reappeared prior to LLR. This suggests that cortical activity, which primarily underlies the LLR, may be more vulnerable to ischemic injury than SLR, which relates to subcortical activity. Hypothermia potentiated the SLR but suppressed the LLR by delaying its recovery after CA (hypothermia: 38.83 ± 5.86 min, normothermia: 23.33 ± 1.15 min; P < 0.05) and attenuating its amplitude, suggesting that hypothermia may selectively downregulate cortical activity as an approach to preserve the cerebral cortex. In summary, our study reveals the vulnerability of the somatosensory neural structures to global HI and the differential effects of hypothermia on these structures.

The goal of immediate post-cardiac arrest care is to optimize systemic perfusion, restore metabolic homeostasis, and support organ system function to increase the likelihood of intact neurological survival. The post-cardiac arrest period is often marked by hemodynamic instability as well as metabolic abnormalities. Support and treatment of acute myocardial dysfunction and acute myocardial ischemia can increase the probability of survival. Interventions to reduce secondary brain injury, such as therapeutic hypothermia, can improve survival and neurological recovery. Every organ system is at risk during this period, and patients are at risk of developing multiorgan dysfunction. The comprehensive treatment of diverse problems after cardiac arrest involves multidisciplinary aspects of critical care, cardiology, and neurology. For this reason, it is important to admit patients to appropriate critical-care units with a prospective plan of care to anticipate, monitor, and treat each of these diverse problems. It is also important to appreciate the relative strengths and weaknesses of different tools for estimating the prognosis of patients after cardiac arrest.

Neurological complications after cardiac arrest (CA) can be fatal. Although hypothermia has been shown to be beneficial, understanding the mechanism and establishing neurological outcomes remains challenging because effects of CA and hypothermia are not well characterized. This paper aims to analyze EEG (and the alpha-rhythms) using multiscale entropy (MSE) to demonstrate the ability of MSE in tracking changes due to hypothermia and compare MSE during early recovery with long-term neurological examinations. Ten Wistar rats, upon post-CA resuscitation, were randomly subjected to hypothermia (32 degrees C-34 degrees C, N = 5) or normothermia (36.5 degrees C-37.5 degrees C, N = 5). EEG was recorded and analyzed using MSE during seven recovery phases for each experiment: baseline, CA, and five early recovery phases (R1-R5). Postresuscitation neurological examination was performed at 6, 24, 48, and 72 h to obtain neurological deficit scores (NDSs). Results showed MSE to be a sensitive marker of changes in alpha-rhythms. Significant difference (p < 0.05) was found between the MSE for two groups during recovery, suggesting that MSE can successfully reflect temperature modulation. A comparison of short-term MSE and long-term NDS suggested that MSE could be used for predicting favorability of long-term outcome. These experiments point to the role of cortical rhythms in reporting early neurological response to ischemia and therapeutic hypothermia.

We propose an improved quantitative measure of EEG during brain injury and recovery after cardiac arrest. In our previous studies, we proposed a measure, information quantity (IQ), to detect the early effects of temperature manipulation on the EEG signals recorded from the scalp. IQ incorporates the wavelet transform and the Shannon entropy in full bands from delta to gamma. Unlike IQ, here we separately calculate IQ in each subband, i.e., the new measure is IQ in each subband. We will call it subband IQ (SIQ). We demonstrate the performance of the proposed method by comparing SIQ with IQ in terms of how well the meausres predict actual neurological outcomes. Thirteen rats, based on 7-min cardiac arrest were used. The experimental results show that the proposed measure was more highly correlated to neurological outcome than IQ.

Object: The authors attempted to determine whether continuous intracranial pressure monitoring via the shunt reservoir identifies ventriculoperitoneal (VP) shunt malfunctions that are not identified by radionuclide shunt patency study or shunt tap in adults with hydrocephalus., Methods: During a 2-year period, 26 adults underwent 32 in-hospital continuous intracranial pressure (ICP) monitoring evaluations via needle access of a shunt reservoir. Monitoring was performed for 26.8 +/- 13.8 hours (mean +/- standard deviation). No ICP waveform abnormality was detected in 31% of the evaluations (10 of 32). In contrast, abnormalities were detected in 69% (22 of 32 evaluations), including B waves (nine of 22 evaluations), siphoning (nine of 22 evaluations), and variable ICP (two of 22 evaluations). In 20 (91%) of these 22 evaluations, the ICP abnormality was detected only after continuous ICP monitoring; in the other two evaluations, ICP became abnormal immediately on accessing the shunt reservoir. On the basis of the ICP monitoring results, shunt revision was performed in 66% (21 of 32 evaluations) and medical therapy was administered in 34% (11 of 32 evaluations). Shunt revision led to symptom improvement in 82% (18 of 22 patients) and no change in 18% (four of 22 patients); medical therapy led to improvement in 18% (two of 11 patients), worsening in 18% (two of 11 patients), and no change in 64% (seven of 11 patients; p < 0.05)., Conclusions: Continuous ICP monitoring via the shunt reservoir provides a more accurate assessment of shunt malfunction than transient ICP monitoring with a shunt tap or a radionuclide shunt patency study. It is a safe method for evaluating patients with suspected VP shunt malfunction, provides in vivo assessment of the effect of the shunt system on a patient's ICP, and can lead to more effective shunt revision.

In this paper, we provide a quantitative electroencephalogram (EEG) analysis to study the effect of hypothermia on the neurological recovery of brain after cardiac arrest. We hypothesize that the brain injury results in a reduction in information of the brain rhythm. To measure the information content of the EEG a new measure called information quantity (IQ), which is the Shannon entropy of decorrelated EEG signals, is developed. For decorrelating EEG signals, we use the discrete wavelet transform (DWT) which is known to have good decorrelating properties and to show a good match to the standard clinical bands in EEG. In measuring the amount of information, IQ shows better tracking capability for dynamic amplitude change and frequency component change than conventional entropy-based measures. Experiments are carried out in rodents (n = 30) to monitor the neurological recovery after cardiac arrest. In addition, EEG signal recovery under normothermic (37 degrees C) and hypothermic (33 degrees C) resuscitation following 5, 7, and 9 min of cardiac arrest is recorded and analyzed. Experimental results show that the IQ is greater for hypothermic than normothermic rats, with an IQ difference of more than 0.20 (0.20 +/- 0.11 is 95% condidence interval). The results quantitatively support the hypothesis that hypothermia accelerates the electrical recovery from brain injury after cardiac arrest.