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I NVITED R EVIEW Consensus Statement on Continuous EEG in Critically Ill Adults and Children, Part I: Indications Susan T. Herman,* Nicholas S. Abend,† Thomas P. Bleck,‡ Kevin E. Chapman,§ Frank W. Drislane,* Ronald G. Emerson,k Elizabeth E. Gerard,¶ Cecil D. Hahn,# Aatif M. Husain,**†† Peter W. Kaplan,‡‡ Suzette M. LaRoche,§§ Marc R. Nuwer,kk Mark Quigg,¶¶ James J. Riviello,## Sarah E. Schmitt,*** Liberty A. Simmons,††† Tammy N. Tsuchida,‡‡‡ and Lawrence J. Hirsch§§§ Introduction: Critical Care Continuous EEG (CCEEG) is a common procedure to monitor brain function in patients with altered mental status in intensive care units. There is significant variability in patient populations undergoing CCEEG and in technical specifications for CCEEG performance. Methods: The Critical Care Continuous EEG Task Force of the American Clinical Neurophysiology Society developed expert consensus recommenda- tions on the use of CCEEG in critically ill adults and children. Recommendations: The consensus panel recommends CCEEG for diagnosis of nonconvulsive seizures, nonconvulsive status epilepticus, and other paroxysmal events, and for assessment of the efficacy of therapy for seizures and status epilepticus. The consensus panel suggests CCEEG for identification of ischemia in patients at high risk for cerebral ischemia; for assessment of level of consciousness in patients receiving intravenous sedation or pharmacologically induced coma; and for prognostication in patients after cardiac arrest. For each indication, the consensus panel describes the patient populations for which CCEEG is From the *Comprehensive Epilepsy Program, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, U.S.A.; †Departments of Neurology and Pediatrics, Perelman School of Medicine, Children’s Hospital of Philadelphia, University of Pennsylvania, Philadelphia, Pennsylvania, U.S.A.; ‡Departments of Neurological Sciences, Neurosurgery, Medicine, and Anesthesiology, Rush Medical College, Chicago, Illinois, U.S.A.; §Department of Pediatrics and Neurology, University of Colorado, Boulder, Colorado, U.S.A.; kDepartment of Neurology, Hospital for Special Surgery, NewYork-Presbyterian Hospital/Weill Cornell Medical College, New York, New York, U.S.A.; ¶Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, U.S.A. #Division of Neurology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada; **Department of Neurology, Duke University Medical Center, Durham, North Carolina, U.S.A.; ††Neurodiagnostic Center, Veterans Affairs Medical Center, Durham, North Carolina, U.S.A.; ‡‡Department of Neurology, Johns Hopkins Bayview Medical Center, Baltimore, Maryland, U.S.A.; §§Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, U.S.A.; kkDepartment of Neurology, David Geffen School of Medicine and Clinical Neurophysiology, Ronald Reagan UCLA Medical Center, Los Angeles, California, U.S.A.; ¶¶FE Dreifuss Comprehensive Epilepsy Program, Department of Neurology, Univer- sity of Virginia, Charlottesville, Virginia, U.S.A.; ##NYU Division of Child Neurology, Columbia University Medical Center, New York, New York, U.S. A.; ***Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, U.S.A.; †††School of Clinical Neurophysiology, Crozer-Chester Medical Center, Upland, Pennsylvania, U.S. A.; ‡‡‡Department of Neurology and Pediatrics, Children’s National Medical Center, George Washington University School of Medicine, Washington, District of Columbia, U.S.A.; and §§§Department of Neurology, Yale Comprehensive Epilepsy Center, Yale School of Medicine, New Haven, Connecticut, U.S.A. Address correspondence and reprint requests to Susan T. Herman, MD, Beth Israel Deaconess Medical Center, Baker 5, 330 Brookline Avenue, Boston, MA 02215, U.S.A.; e-mail: sherman2@bidmc.harvard.edu. Copyright O 2015 by the American Clinical Neurophysiology Society ISSN: 0736-0258/15/3202-0087 indicated, evidence supporting use of CCEEG, utility of video and quantitative EEG trends, suggested timing and duration of CCEEG, and suggested frequency of review and interpretation. Conclusion: CCEEG has an important role in detection of secondary injuries such as seizures and ischemia in critically ill adults and children with altered mental status. Key Words: EEG, EEG monitoring, Quantitative EEG, Seizure, Nonconvulsive seizure, Status epilepticus, Nonconvulsive status, epilepticus, Intensive care unit, Critical care, Adults, Children. (J Clin Neurophysiol 2015;32: 87–95) C ritically ill patients are at high risk for a variety of neurologic insults, including seizures, ischemia, edema, infection, and increased intracranial pressure, which can result in permanent neurologic disability if untreated. Despite these risks, there are few techniques for continuously monitoring brain function. EEG measures the brain’s electrical activity, can be recorded continuously at the bedside, has good spatial and excellent temporal resolution, and is sensitive to changes in both brain structure and function (Nuwer, 1994). Over the past decade, technical advances have improved the efficiency of continuous EEG (CEEG) recording and remote review, leading to a greater than fourfold increase in the number of CEEGs performed in intensive care units (ICUs) (Ney et al., 2013). Recent surveys, however, show variability in why and how CEEG is performed in the ICU (Abend et al., 2010; Gavvala et al., 2014; Sanchez et al., 2013a), highlighting the need for clinical guidance on this expensive and labor-intensive procedure. Critical care continuous EEG (CCEEG) refers to the simul- taneous recording of EEG and clinical behavior (video) over extended time periods (hours to weeks) in critically ill patients at risk for secondary brain injury and neurologic deterioration. Critical care continuous EEG is usually performed in an ICU setting, but this varies by hospital and some patients may be in step-down units or general medical or surgical units. Critical care continuous EEG typically includes simultaneous video recording and may include graphical displays of quantitative EEG (QEEG) trends. The goal of CCEEG is to identify changes in brain function, such as non- convulsive seizures (NCS) or ischemia, which may not be evident by neurological examination alone, to facilitate early identification and management of these abnormalities. This consensus statement applies only to critically ill adult and pediatric patients. It does not apply to long-term monitoring of awake and alert patients with epilepsy, sleep monitoring, or intraoperative monitoring. Separate recommendations have been developed by the Journal of Clinical Neurophysiology Volume 32, Number 2, April 2015

Post-traumatic seizures develop in up to 20% of children following severe traumatic brain injury (TBI). Children ages 6-17 years with one or more risk factors for the development of post-traumatic epilepsy, including presence of intracranial hemorrhage, depressed skull fracture, penetrating injury or occurrence of post-traumatic seizure were recruited into this phase two study. Treatment subjects received levetiracetam 55mg/kg/day b.i.d. for 30 days, started within 8 hours post-injury. The recruitment goal was 20 treated patients. Twenty patients who presented within 8-24 hours post-TBI and otherwise met eligibility criteria were recruited for observation. Follow-up was for two years. 45 patients screened within 8 hours of head injury met eligibility criteria and 20 were recruited into the treatment arm. The most common risk factor present for pediatric inclusion following TBI was an immediate seizure. Medication compliance was 95%. No patients died; 19 of 20 treatment patients were retained; one observation patient was lost to follow-up. The most common severe adverse events in treatment subjects were headache, fatigue, drowsiness, and irritability. There was no higher incidence of infection, mood changes, or behavior problems among treatment subjects compared to observation subjects. Only 1 of 40 subjects (2.5%) developed post-traumatic epilepsy (defined as seizures > 7 days after trauma). This study demonstrates the feasibility of a pediatric post-traumatic epilepsy prevention study in an at-risk traumatic brain injury population. Levetiracetam was safe and well tolerated in this population. This study sets the stage for implementation of a prospective study to prevent post-traumatic epilepsy in an at-risk population.

Objectives To evaluate the safety and tolerability of treatment with levetiracetam and determine the trough levels of levetiracetam in patients with traumatic brain injury (TBI) who are at high risk for posttraumatic epilepsy (PTE). Design Open-label, nonrandomized phase 2 study with 2 arms comparing levetiracetam treatment vs observation. Setting Two level 1 trauma centers. Patients A total of 422 participants 6 years or older with TBI who have a 20% risk for PTE were screened. Of these participants, 205 (48.6%) were eligible. A total of 126 participants were enrolled: 86 adults and 40 children. A total of 66 participants were in the treatment group (46 adults and 20 children), and a total of 60 participants were in the observation group (40 adults and 20 children). Participants presenting within 8 hours after TBI received treatment, and those presenting more than 8 to 24 hours after TBI did not. Intervention Treatment with levetiracetam (55 mg/kg/d) for 30 days starting within 8 hours after injury. Main outcome measures Number of adverse events, mood score, number of infections, trough level of levetiracetam, and PTE. Results Of the 66 participants treated with levetiracetam, 2 (3%) stopped treatment owing to toxicity (somnolence). The most common adverse events were fatigue, headache, and somnolence. Mood scores and number of infections did not differ between the treatment and observation groups. Mean trough levels of levetiracetam on days 2 to 30 ranged from 19.6 to 26.7 μg/mL. At 2 years, 13 of 86 adults (15.1%) and 1 of 40 children (2.5%) developed PTE. At 2 years, 5 of 46 treated adults (10.9%) and 8 of 40 untreated adults (20.0%) developed PTE (relative risk, 0.47; P=.18). Conclusion Treatment with 55 mg/kg/d of levetiracetam (a dose with an antiepileptogenic effect on animals) for patients with TBI at risk for PTE is safe and well tolerated, with plasma levels similar to those in animal studies. The findings support further evaluation of levetiracetam treatment for the prevention of PTE. Trial registration clinicaltrials.gov Identifier: NCT01463033.

Objective To determine if early serum S100B and neuron-specific enolase (NSE)levels are associated with neuroradiographic and clinical evidence of brain injury in newborns with encephalopathy. Study design Patients who received therapeutic whole-body hypothermia were prospectively enrolled in this observational study. Serum specimens were collected at 0, 12, 24, and 72 hours of cooling. S100B and NSE levels were measured by enzyme linked immunosorbent assay. Magnetic resonance imaging was performed in surviving infants at 7-10 days of life. Standardized neurologic examination was performed by a child neurologist at 14 days of life. Multiple linear regression analyses were performed to evaluate the association between S100B and NSE levels and unfavorable outcome (death or severe magnetic resonance imaging injury/significant neurologic deficit). Cutoff values were determined by receiver operating curve analysis. Results Newborns with moderate to severe encephalopathy were enrolled (n = 75). Median pH at presentation was 6.9 (range, 6.5-7.35), and median Apgar scores of 1 at 1 minute, 3 at 5 minutes, and 5 at 10 minutes. NSE and S100B levels were higher in patients with unfavorable outcomes across all time points. These results remained statistically significant after controlling for covariables, including encephalopathy grade at presentation, Apgar score at 5 minutes of life, initial pH, and clinical seizures. Conclusion Elevated serum S100B and NSE levels measured during hypothermia were associated with neuroradiographic and clinical evidence of brain injury in encephalopathic newborns. These brain-specific proteins may be useful immediate biomarkers of cerebral injury severity. (J Pediatr 2012;161:434-40).

This article offers the preferred methods and indications for longterm, conventional electroencephalography (EEG) monitoring for selected, high-risk neonates of postmenstrual age less than 48 weeks. The authors recognize that there may be significant practical barriers to the implementation of these recommendations for many caregivers and institutions, particularly with regard to the availability of equipment, and technical and interpretive personnel. A wide range of clinical circumstances dictates the implementation of EEG monitoring, frequency of EEG review, and the subsequent treatment of seizures or EEG background abnormalities detected by neonatal EEG. Consequently, this article should be considered as an expression of idealized goals and not as a mandated standard of care.

To investigate the presenting characteristics of new-onset afebrile seizures in infants (age 1-24 months) and the yield of neuroimaging.Prospective data were obtained from a standardized evaluation and management plan mandated by a critical care pathway. A total of 317 infants presented with new-onset afebrile seizures between 2001 and 2007. EEG was performed on 90.3%, head CT was obtained on 94%, and MRI was obtained on 57.4%.We found half of the infants had partial features to their seizures, yet evidence for primary generalized seizures was rare. The majority had more than 1 seizure upon presentation. Seizures in this age group tended to be brief, with 44% lasting less than 1 minute. EEG abnormalities were found in half. One-third of CTs were abnormal, with 9% of all CTs requiring acute medical management. Over half of MRIs were abnormal, with cerebral dysgenesis being the most common abnormality (p0.05). One-third of normal CTs had a subsequent abnormal MRI-only 1 resulted in altered medical management.Infantile seizures are usually brief, but commonly recurrent, and strong consideration should be made for inpatient observation. Acute imaging with CT can alter management in a small but important number of infants. Due to the superior yield, strong consideration for MRI should be given for all infants, as primary generalized seizures are rare, and there is a high rate of cerebral dysgenesis.