Neurology of cardiopulmonary resuscitation.

This chapter aims to provide an up-to-date review of the science and clinical practice pertaining to neurologic injury after successful cardiopulmonary resuscitation. The past two decades have seen a major shift in the science and practice of cardiopulmonary resuscitation, with a major emphasis on postresuscitation neurologic care. This chapter provides a nuanced and thoughtful historic and bench-to-bedside overview of the neurologic aspects of cardiopulmonary resuscitation. A particular emphasis is made on the anatomy and pathophysiology of hypoxic-ischemic encephalopathy, up-to-date management of survivors of cardiopulmonary resuscitation, and a careful discussion on neurologic outcome prediction. Guidance to practice evidence-based clinical care when able and thoughtful, pragmatic suggestions for care where evidence is lacking are also provided. This chapter serves as both a useful clinical guide and an updated, thorough, and state-of-the-art reference on the topic for advanced students and experienced practitioners in the field.

Electroencephalographic sleep elements and outcome in acute encephalopathic patients: a 4-year cohort study.

BACKGROUND AND PURPOSE: Acute encephalopathy in hospitalized patients is common and associated with high mortality. Preservation of physiological sleep has been associated with favorable outcomes in acute brain injury. It is hypothesized that electroencephalographic presence of sleep elements is associated with good outcome in encephalopathic adults. METHODS: This observational study was performed at an academic tertiary medical care center. Clinical data, electroencephalogram (EEG) characteristics and outcome of critically ill patients with acute encephalopathy were assessed. EEGs were interpreted regarding the presence of sleep elements (K-complexes, vertex sharp-waves and sleep spindles). Associations between sleep elements and outcome (graded by the Glasgow Outcome Scale, GOS) were analyzed. RESULTS: One hundred and forty-two consecutive patients with a median age of 64.5 years (range 18-98) and mean Glasgow Coma Scale 10.4 (± 3.8) were included. Leading etiologies were infections (47.2%), intracranial hemorrhages (14.1%) and ischaemic strokes (10.6%). All EEGs demonstrated encephalopathy patterns and 38% had ≥ 1 sleep element (27.5% K-complexes, 31.7% vertex sharp-waves and 33.8% sleep spindles). Patients without sleep elements were older (P = 0.010) and septic shock was more common (P = 0.014). Amongst sleep elements, K-complexes were significantly associated with good outcome, even after adjusting for possible confounders (odds ratio for GOS 5 = 2.79, 95% confidence interval 1.16-6.69) and without significant effect modification across subgroups. CONCLUSIONS: Whilst EEG sleep elements were detected more frequently in patients with favorable outcome, only K-complexes were significantly and independently associated with good outcome in intensive care unit patients with acute encephalopathy, findings that need to be confirmed in larger prospective studies.

Neurocritical care education during neurology residency: AAN survey of US program directors.

OBJECTIVE: Limited information is available regarding the current state of neurocritical care education for neurology residents. The goal of our survey was to assess the need and current state of neurocritical care training for neurology residents. METHODS: A survey instrument was developed and, with the support of the American Academy of Neurology, distributed to residency program directors of 132 accredited neurology programs in the United States in 2011. RESULTS: A response rate of 74% (98 of 132) was achieved. A dedicated neuroscience intensive care unit (neuro-ICU) existed in 64%. Fifty-six percent of residency programs offer a dedicated rotation in the neuro-ICU, lasting 4 weeks on average. Where available, the neuro-ICU rotation was required in the vast majority (91%) of programs. Neurology residents' exposure to the fundamental principles of neurocritical care was obtained through a variety of mechanisms. Of program directors, 37% indicated that residents would be interested in performing away rotations in a neuro-ICU. From 2005 to 2010, the number of programs sending at least one resident into a neuro-ICU fellowship increased from 14% to 35%. CONCLUSIONS: Despite the expansion of neurocritical care, large proportions of US neurology residents have limited exposure to a neuro-ICU and neurointensivists. Formal training in the principles of neurocritical care may be highly variable. The results of this survey suggest a charge to address the variability of resident education and to develop standardized curricula in neurocritical care for neurology residents.

The neurocritical care research network: NCRN.

Neurocritical care diseases carry a high morbidity and mortality. Therapeutic and technological advances in neurocritical care have greatly improved the outcome of a variety of life-threatening disorders including traumatic brain injury, acute ischemic stroke, intracerebral and subarachnoid hemorrhage, and anoxic injury following cardiac arrest. These advances have stemmed from a better understanding of the physiology of neurocritical care illnesses, improved neuromonitoring techniques, and the introduction of more efficacious treatments. Despite all the advances in neuromonitoring, diagnostic imaging, and emerging treatments, much research needs to be undertaken in neurocritical care. Many of the clinical trials carried out in the general critical care population have excluded neurocritical care patients. For instance, the landmark ARDSNET trial that demonstrated the beneficial effects of low tidal volume ventilation in patients with ARDS cannot be directly applied to neurocritical care patients who frequently may experience this pulmonary complication. There is a need for a more cohesive and integrated research system or network to establish a track record for high-quality, investigator-initiated clinical research in neurocritical care. Such a system may help us overcome potential impediments to the future advancement of neurocritical care research. We propose the creation of the neurocritical care research network. The mission of the Network is to facilitate multicenter and multidisciplinary collaboration and patient enrollment in clinical trials of specific neurocritical care diseases.

Research priorities in neurocritical care.

This summary of the last session of the First Neurocritical Care Research Conference reviews the discussions about research priorities in neurocritical care. The first presentation reviewed current projects funded by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health and potential models to follow including an independent Neurocritical Care Network or the creation of such a network with the goal of collaborating with already existing ones. Experienced neurointensivists then presented their views on the most common and important research questions that need to be answered and investigated in the field. Finally, utility of clinical registries was discussed emphasizing their importance as hypothesis generators. During the group discussion, interests in comparative effectiveness research, the use of physiological endpoints from monitoring and alternate trial design were expressed.

Clinical trial design in the neurocritical care unit.

Clinical trials provide a robust mechanism to advance science and change clinical practice across the widest possible spectrum. Fundamental in the Neurocritical Care Society's mission is to promote Quality Patient Care by identifying and implementing best medical practices for acute neurological disorders that are consistent with the current scientific knowledge. The next logical step will be to foster rapid growth of our scientific body of evidence, to establish and disseminate these best practices. In this manuscript, five invited experts were impaneled to address questions, identified by the conference organizing committee as fundamental issues for the design of clinical trials in the neurological intensive care unit setting.

The critical care research networks experience.

Neurocritical care is a subspecialty of critical care medicine, dedicated to the care and the advancement of care of critically ill patients with neurosurgical or neurological diseases. Neurocritical care patients are heterogeneous, in both their disease process and the therapies they receive, however, several studies demonstrate that care of these patients in dedicated NeuroIntensive Care Units (neuroICUs) by neurointensivists, who coordinate their care is associated with reduced mortality and resource utilization. NeuroICUs foster innovation, and yet despite all the recent advances, much research needs to be undertaken in neurocritical care to better understand the disease pathophysiology and to demonstrate improved outcome with the use of goal-directed therapy based on evolving techniques and therapies.

Research and technology in neurocritical care.

The daily practice of neurointensivists focuses on the recognition of subtle changes in the neurological examination, interactions between the brain and systemic derangements, and brain physiology. Common alterations such as fever, hyperglycemia, and hypotension have different consequences in patients with brain insults compared with patients of general medical illness. Various technologies have become available or are currently being developed. The session on "research and technology" of the first neurocritical care research conference held in Houston in September of 2009 was devoted to the discussion of the current status, and the research role of state-of-the art technologies in neurocritical patients including multi-modality neuromonitoring, biomarkers, neuroimaging, and "omics" research (proteomix, genomics, and metabolomics). We have summarized the topics discussed in this session. We have provided a brief overview of the current status of these technologies, and put forward recommendations for future research applications in the field of neurocritical care.

Reversal of transtentorial herniation with hypertonic saline.

OBJECTIVE: To evaluate the role of 23.4% saline in the management of transtentorial herniation (TTH) in patients with supratentorial lesions. METHODS: Consecutive patients with clinically defined TTH treated with 23.4% saline (30 to 60 mL) were included in a retrospective cohort. Factors associated with successful reversal of TTH were determined. RESULTS: Seventy-six TTH events occurred in 68 patients admitted with intracerebral hemorrhage (n = 29), subarachnoid hemorrhage (n = 16), stroke (n = 8), brain tumor (n = 8), subdural hematoma (n = 5), epidural hematoma (n = 1), and meningitis (n = 1). In addition to 23.4% saline, TTH management included hyperventilation (70% of events), mannitol (57%), propofol (62%), pentobarbital (15%), ventriculostomy drainage (27%), and decompressive hemicraniectomy (18%). Reversal of TTH occurred in 57/76 events (75%). Intracranial pressure decreased from 23 +/- 16 mm Hg at the time of TTH to 14 +/- 10 mm Hg at 1 hour (p = 0.002), and 11 +/- 12 mm Hg at 24 hours (p = 0.001) among 22 patients with intracranial pressure monitors. Reversal of TTH was predicted by a >/=5 mmol/L rise in serum sodium concentration (p = 0.001) or an absolute serum sodium of >/=145 mmol/L (p = 0.007) 1 hour after 23.4% saline. Adverse effects included transient hypotension in 13 events (17%); no evidence of central pontine myelinolysis was detected on post-herniation MRI (n = 18). Twenty-two patients (32%) survived to discharge, with severe disability in 17 and mild to moderate disability in 5. CONCLUSION: Treatment with 23.4% saline was associated with rapid reversal of transtentorial herniation (TTH) and reduced intracranial pressure, and had few adverse effects. Outcomes of TTH were poor, but medical reversal may extend the window for adjunctive treatments.

Neurologic prognosis and withdrawal of life support after resuscitation from cardiac arrest.

OBJECTIVE: To study the impact of neurologic prognostication on the decision to withdraw life-sustaining therapies (LST) in comatose patients resuscitated after cardiac arrest. METHODS: The authors prospectively studied a consecutive series of post-resuscitation comatose patients referred for neurologic prognostication at a single center for 4 years. For most patients, neurologic prognostication was not sought due to early death or rapid return to consciousness. Prognostication was based on Glasgow Coma Score (GCS) and Brainstem Reflex Score (BRS), with EEG and cortical evoked potentials (CEP), which were graded as benign, uncertain, and malignant. The outcomes were as follows: survivors (Group S), brain or cardiac death (Group D), and death from withdrawal of life sustaining therapy (Group W). In Group W, the time interval to withdrawal of LST was analyzed by EEG and CEP grades. RESULTS: Of 58 patients studied, 10 were in Group S, 8 in Group D, and 40 in Group W. Initial median GCS and BRS was similar for all groups with significant improvement noted in Group S, but not in Group D or Group W. In Group W, CEP grade correlated with the median duration of continued therapy before a decision to withdraw LST: 7 days for benign CEP, 2 days for uncertain CEP, and 1 day for malignant CEP, p = 0.0004. CONCLUSION: In patients with poor neurologic recovery early after resuscitation from cardiac arrest, physicians appear to use the cortical evoked potential grade to estimate prognosis. Cortical evoked potential grade correlated with the waiting time until life sustaining therapies were withdrawn after no improvement in neurologic examination was seen.

Investigation of the effects of ischemic preconditioning on the HRV response to transient global ischemia using linear and nonlinear methods.

Ischemic preconditioning (IP) has been used as a strategy to prevent cell death in various organs, including the brain and the heart. Investigation of the effects of ischemic preconditioning mostly employed models with reduced complexity, such as cell cultures, tissue slices or perfused organ preparations. Although such models can provide valuable insight into the protective mechanism of preconditioning, the functional (re)organization of the control mechanisms at the level of the living organism cannot be assessed. The purpose of the present animal model study was to evaluate the effect of global ischemic preconditioning on the heart rate variability (HRV) response to the asphyxia insult. The data consisted of 4 h RR interval measurements recorded in five preconditioned and five non-preconditioned Wistar rats. Using linear (time and frequency domain) and nonlinear (approximate entropy and parameters of Poincare plots) measures, we evaluated the dynamic time course of the HRV response to the asphyxia insult and the effect of preconditioning on the autonomic neurocardiac control. Both the linear and nonlinear parameters indicate a faster recovery of the baseline HRV corresponding to the preconditioned groups, though only the spectral analysis identifies a statistically significant difference between the two groups. For the preconditioned group, at about 90 min after the asphyxic insult, the autonomic neural balance (measured by LF/HF ratio) appears fully recovered. The small variation of the rest of the parameters indicates the necessity of further investigation including the design of a larger study with a higher statistical power. Our results show for the first time that global ischemic preconditioning influences the HRV response to the asphyxia injury. The neuroprotective effect of preconditioning translates into a faster recovery of the basal HRV and the autonomic modulation of the heart.

Utility of CSF pressure monitoring to identify idiopathic intracranial hypertension without papilledema in patients with chronic daily headache.

The aim of the present study was to report on the utility of continuous Pcsf monitoring in establishing the diagnosis of idiopathic intracranial hypertension without papilledema (IIHWOP) in chronic daily headache (CDH) patients. We report a series of patients (n = 10) with refractory headaches and suspected IIHWOP referred to us for continuous Pcsf monitoring between 1991 and 2000. Pcsf was measured via a lumbar catheter and analysed for mean, peak, highest pulse amplitude and abnormal waveforms. A 1-2 day trial of continuous controlled CSF drainage (10 cc/ h) followed Pcsf monitoring. Response to CSF drainage was defined as improvement in headache symptoms. Patients with abnormal waveforms underwent a ventriculoperitoneal (VPS) or lumboperitoneal (LPS) shunt insertion. All patients had normal resting Pcsf (8 +/- 1 mmHg) defined as ICP < 15 mmHg. During sleep, all patients had B-waves and 90% had plateau waves or near plateau waves. All patients underwent either a VPS or LPS procedure. All reported improvement of their headache after surgery. Demonstration of pathological Pcsf patterns by continuous Pcsf monitoring was essential in confirming the diagnosis of IIHWOP, and provided objective evidence to support the decision for shunt surgery. Increased Pcsf was seen mostly during sleep and was intermittent, suggesting that Pcsf elevation may be missed by a single spot-check LP measurement. The similarity between IIHWOP and CDH suggests that continuous Pcsf monitoring in CDH patients may have an important diagnostic role that should be further investigated.

Vulnerability of the thalamic somatosensory pathway after prolonged global hypoxic-ischemic injury.

The aim of this study was to test the hypothesis that under prolonged global ischemic injury, the somatosensory thalamus and the cortex would manifest differential susceptibility leading to varying degrees of thalamo-cortical dissociation. The thalamic electrical responses displayed increasing suppression with longer durations of ischemia leading to a significant thalamo-cortical electrical dissociation. The data also point to a selective vulnerability of the network oscillations involving the thalamic relay and reticular thalamic neurons. An adult rat model of asphyxial cardiac arrest involving three cohorts with 3 min (G1, n=5), 5 min (G2, n=5) and 7 min (G3, n=5) of asphyxia respectively was used. The cortical evoked response, as quantified by the peak amplitude at 20 ms in the cortical evoked potential, recovers to more than 60% of baseline in all the cases. The multi-unit responses to the somatosensory stimuli recorded from the thalamic ventral posterior lateral (VPL) nuclei consists typically of three components: (1). the ON response (<30 ms after stimulus), (2). the OFF response (period of inhibition, from 30 ms to 100 ms after stimulus) and (3). rhythmic spindles (beyond 100 ms after stimulus). Asphyxia has a significant effect on the VPL ON response at 30 min (P<0.025), 60 min (P<0.05) and 90 min (P<0.05) after asphyxia. Only animals in G3 show a significant suppression (P<0.05) of the VPL ON response when compared to the sham group at 30 min, 60 min and 90 min after asphyxia. There was no significant reduction in somatosensory cortical N20 (negative peak in the cortical response at 20 ms after stimulus) amplitude in any of the three groups with asphyxia indicating a thalamo-cortical dissociation in G3. Further, rhythmic spindle oscillations in the thalamic VPL nuclei that normally accompany the ON response recover either slowly after the recovery of ON response (in the case of G1 and G2) or do not recover at all (in the case of G3).We conclude that there is strong evidence for selective vulnerability of thalamic relay neurons and its network interactions with the inhibitory interneurons in the somatosensory pathway leading to a thalamo-cortical dissociation after prolonged durations of global ischemia.

Detection of asphyxia using heart rate variability.

The long-term aims of this study are to find a parameter derived from the ECG that has a high sensitivity and specificity to asphyxia and, once we know or suspect that asphyxia occurred, to estimate how severe it was. We carried out a pilot study in which 24 adult Wistar rats were anaesthetised and subjected to controlled asphyxia for specified durations. We measured the pH, 'neurological score' and the ECG, extracting from this heart rate and heart rate variability (HRV). We have developed a technique capable of detecting asphyxia in less than 1 min, based on monitoring the ECG and estimating HRV by measuring the standard deviation of normal RR intervals (the RR interval is the time interval between two consecutive R-points of the QRS complex). In all cases the heart rate decreased and HRV increased, by an average of 46 +/- 33 ms in relation to the baseline, at the onset of asphyxia. The comparison of the base level of HRV after and before asphyxia shows promise for the estimation of the severity of the episode; however, the limitations of this study should be noted as they include the small size of the cohort and the methods of analysis.

Cerebral vasculitis: diagnosis and follow-up with transcranial Doppler ultrasonography.

The authors report a patient with postpartum intracerebral hemorrhage associated with cerebral vasculitis. Cerebral circulation was assessed with transcranial Doppler (TCD) ultrasonography, magnetic resonance angiography, and conventional cerebral angiography. Initial TCD studies demonstrated bilateral patchy increased cerebral blood flow velocity (CBFV) in the anterior circulation with complete normalization during remission. This case report provides evidence that cerebral vasculitis leads to relevant CBFV changes and that the TCD technique may assist in diagnosis and follow-up of these patients.

Central nervous system infections: a critical care approach.

Central nervous system (CNS) infections are diverse. CNS infections can cause significant morbidity and mortality and are markedly different from systemic infections. The closed anatomic space of the CNS, its immunologic isolation from the rest of the body, and the often nonspecific nature of the key manifestations present a challenge to the clinician. Early recognition and aggressive management are essential to patient recovery and prevention of long-term neurologic sequelae. This review discusses the major types of CNS infections and focuses on critical care management, with emphasis on current epidemiologic trends.

A novel quantitative EEG injury measure of global cerebral ischemia.

OBJECTIVE: To develop a novel quantitative EEG (qEEG) based analysis method, cepstral distance (CD) and compare it to spectral distance (SD) in detecting EEG changes related to global ischemia in rats. METHODS: Adult Wistar rats were subjected to asphyxic-cardiac arrest for sham, 1, 3, 5 and 7 min (n=5 per group). The EEG signal was processed and fitted into an autoregressive (AR) model. A pre-injury baseline EEG was compared to selected data segments during asphyxia and recovery. The dissimilarities in the EEG segments were measured using CD and SD. A segment measured was considered abnormal when it exceeded 30% of baseline and its duration was used as the index of injury. A comprehensive Neurodeficit Score (NDS) at 24 h was used to assess outcome and was correlated with CD and SD measures. RESULTS: A higher correlation was found with CD and asphyxia time (r=0.81, P<0.001) compared to SD and asphyxia time (r=0.69, P<0.001). Correlation with cardiac arrest time (MAP<10 mmHg) showed that CD was superior (r=0.71, P<0.001) to SD (r=0.52, P=0.002). CD obtained during global ischemia and 90 min into recovery correlated significantly with NDS at 24 h after injury (Spearman coefficient=-0.83, P<0.005), and was more robust than the traditional SD (Spearman coefficient=-0.63, P<0.005). CONCLUSION: The novel qEEG-based injury index from CD was superior to SD in quantifying early cerebral dysfunction after cardiac arrest and in providing neurological prognosis at 24 h after global ischemia in adult rats. Studying early qEEG changes after asphyxic-cardiac arrest may provide new insights into the injury and recovery process, and present opportunities for therapy.

Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions.

OBJECTIVE: To determine the short- and long-term outcomes after successful reversal of transtentorial herniation by medical treatment. Although it has been recognized that aggressive medical management can reverse transtentorial herniation, it is believed that overall outcome in such patients is poor. DESIGN: Prospective cohort study. SETTING: Neurocritical care unit of a university hospital. PATIENTS: A total of 28 consecutive patients who underwent an episode of transtentorial herniation (defined as decrease in level of consciousness accompanied by pupillary dilation) secondary to a supratentorial mass lesion followed by successful reversal. INTERVENTION: Herniation was reversed by using a combination of hyperventilation, mannitol and hypertonic saline. MEASUREMENTS AND MAIN RESULTS: The following outcomes were analyzed: risk of second herniation, radiologic evidence of structural damage or vascular compromise related to herniation on post-herniation computed tomographic scan, in-hospital mortality, and long-term functional outcome using Rankin score and Barthel index. A total of 32 episodes of transtentorial herniations were reversed in 28 patients during a 14-month period. The most common precipitating cause were edema (n = 23) or new/expanding intracerebral hematoma (n = 5). After first reversal of transtentorial herniation in 28 patients, a second herniation episode was observed in 16 patients after a mean interval of 88.2 hrs (range, 23-432 hrs); four were successfully reversed. On follow-up computed tomographic scan, hypodense lesion in midbrain (n = 6), temporal lobe contusion (n = 2), posterior cerebral artery (n = 3), and middle cerebral artery (n = 1) infarction were visualized in a minority of patients. The in-hospital mortality was 60% (n = 15) with brain death being the cause of death in 13 patients; care was withdrawn in eight patients. Second episode of herniation (p = .002) and midbrain involvement during herniation (p = .02) were associated with in-hospital mortality. During a mean follow-up period of 11.4+/-4.2 months, two patients died of cerebral neoplasm and human immunodeficiency virus-related sepsis, respectively. Of the 11 survivors, 7 were functionally independent (Rankin score <3 and Barthel index >60). CONCLUSIONS: Although mortality after transtentorial herniation is high, we found a prominent potential for meaningful recovery with aggressive medical reversal of transtentorial herniation. Our study implies that timely medical intervention for reversing transtentorial herniation can result in preservation of neurologic function.

Early electrophysiological and histologic changes after global cerebral ischemia in rats.

INTRODUCTION: Cerebral anoxia is fundamental to morbidity and mortality after resuscitation from cardiac arrest. With no proven effective primary therapy for post-anoxic brain injury, the goal of neurologic care are supportive, to provide prognosis and prevention of further complications. With the multifaceted approach using electroencephalography (EEG), somatosensory evoked potentials (SEP), multiunit recordings, behavioral and histologic assessment, we investigated the hyperacute recovery period after resuscitation from cardiac arrest in a rat model to define the value of EEG and SEP in assessing neurologic injury. METHODS: Two cohorts of rats were subjected to sham and graded asphyxic-cardiac arrest. EEG was collected during baseline, at injury, and 90 minutes into recovery in the first rat cohort. EEG bursting during the first 90 minutes of recovery was visually analyzed and correlated with the neurologic recovery at 24 hours after injury. The neurologic recovery was assessed using a neurodeficit score (NDS) with 80 as normal and 0 as brain dead. The next rat cohort subjected to asphyxic-cardiac arrest was studied using SEP and multiunit recording in the VPL; brain histologic studies were performed at 4 hours after the asphyxia. RESULTS: The first rat cohort subjected to graded asphyxic-cardiac arrest emerged from EEG isoelectricity by burst-suppression pattern during the first 90 minutes after asphyxia. Six rats in the good outcome group (NDS >60) showed increased frequency of bursting, leading to return of EEG background activity. Six rats with a bad outcome (NDS <60) had low-intensity and persistent bursting without return of EEG background activity within 90 minutes of observation. Visual assessment showed increased EEG peak burst counts during the first 90 minutes of recovery for the rats with a good outcome compared with the rats with a bad outcome. In the second cohort, the rats were subjected to 3 minutes, 5 minutes, and 7 minutes of asphyxia. The N20 recovered to 60% of baseline in all three cases. The recovery profile of VPL is similar to that of cortical N2O for the animal with 3 minutes of asphyxia. However, VPL response is suppressed after 7 minutes of asphyxia leading to a divergence in the rate of recovery of the cortical N20 and VPL response. In both the animals (with mild and intermediate injury) in which the early response in VPL recovered to more than 50% of baseline, the recovery profile was similar to the N20 in cortical evoked potential (EP). The rats were killed 4 hours after asphyxia and the hematoxylin and eosin stain performed on the brains showed evidence of neuronal injury in the thalamic reticular nucleus (TRN) which seemed to correlate with the duration of asphyxia. CONCLUSION: We present a multimodality assessment of early neurologic recovery following resuscitation from cardiac arrest. The recovery of bursting and high-frequency oscillations may be regulated by interneurons in the TRN. The early selective vulnerability of these interneurons in the TRN may be crucial to the early neurologic recovery as assessed by EP, multiunit recording, EEG, and neurologic behavioral recovery.

The burst-suppression electroencephalogram.

The burst-suppression (BS) pattern of the EEG occurs in a rather limited number of conditions. It has been observed in deep stages of general anesthesia and in conjunction with sedative overdoses. It is also known to occur in the wake of cardiorespiratory arrest. Undercutting of the cortex has been found to result in BS activity. Rare neonatal epileptic encephalopathies also give rise to BS. Our personal interest was prompted by the consistent finding of BS activity in rats following cerebral anoxia (nitrogen inhalation, airway obstruction): after periods of EEG flatness, BS activity developed, followed by periodic bursts and diffuse slowing. On the other hand, earlier literature (before 1960) showed virtually no observation of BS, neither in anoxic patients, nor in animal experiments. It is likely that the introduction of modern intensive care treatment has engineered episodes of BS activity, probably due to modifications of the anoxic cerebral pathology.