(BQ) Part 1 book Current clinical neurology has contents: mpact of seizures on outcome, status epilepticus - lessons and challenges from animal models, spreading depolarizations and seizures in clinical subdural electrocorticographic recordings,... and other contents.
Current Clinical Neurology Series Editor: Daniel Tarsy Panayiotis N Varelas Jan Claassen Editors Seizures in Critical Care A Guide to Diagnosis and Therapeutics Third Edition Current Clinical Neurology Series Editor Daniel Tarsy, MD Department of Neurology Beth Israel Deaconness Hospital Boston, MA USA More information about this series at http://www.springer.com/series/7630 Panayiotis N Varelas • Jan Claassen Editors Seizures in Critical Care A Guide to Diagnosis and Therapeutics Third Edition Editors Panayiotis N Varelas, MD, PhD, FNCS Departments of Neurology and Neurosurgery Henry Ford Hospital Detroit, MI, USA Department of Neurology Wayne State University Detroit, MI, USA Jan Claassen, MD, Ph.D, FNCS Neurocritical Care Columbia University College of Physicians & Surgeons New York, NY, USA Division of Critical Care and Hospitalist Neurology Department of Neurology Columbia University Medical Center New York Presbyterian Hospital New York, NY, USA Current Clinical Neurology ISBN 978-3-319-49555-2 ISBN 978-3-319-49557-6 (eBook) DOI 10.1007/978-3-319-49557-6 Library of Congress Control Number: 2017934697 © Springer International Publishing AG 2017 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations Printed on acid-free paper This Humana Press imprint is published by Springer Nature The registered company is Springer International Publishing AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Series Editor Introduction The first two editions of Seizures in Critical Care: A Guide to Diagnosis and Therapeutics were published in 2005 and 2010 Both of these volumes provided much needed support for medical, neurological, and neurosurgical intensive care specialists who deal with critically ill patients who suffer seizures in the ICU setting At one time seizures, especially of the nonconvulsive type, were quite often poorly recognized in unresponsive ICU patients This situation has certainly been remedied over the past couple of decades, due in large part to the wealth of information summarized in these volumes As stated in my introductions to the first two volumes, seizures in ICU patients are typically secondary phenomena indicative of underlying medical and neurological complications in individuals with serious medical and surgical illness Rapid identification of the cause of these seizures, analysis of various contributing factors, and providing appropriate and rapid management and treatment are crucial to the survival of these patients Dr Varelas, together with his co-editor Dr Jan Claasen, has now recruited a larger number of new experts in various aspects of the field in order to provide additional information concerning basic pathophysiology as learned both from animal models and from new clinical technologies such as quantitative EEG and multimodal monitoring which have improved the care of these patients New clinical chapters in this third edition include an overview of the management of critical care seizures which is then followed by a series of chapters on the many clinical situations in which seizures occur in the ICU Many of these appeared in the earlier volumes but have been updated with several of these written by newly recruited authors These issues are all addressed in great depth and with much sophistication by the very impressive array of contributors to this volume Boston, MA, USA Daniel Tarsy, MD v Contents Part I General Section Status Epilepticus - Lessons and Challenges from Animal Models 3 Inna Keselman, Claude G Wasterlain, Jerome Niquet, and James W.Y Chen Impact of Seizures on Outcome 19 Iván Sánchez Fernández and Tobias Loddenkemper Diagnosing and Monitoring Seizures in the ICU: The Role of Continuous EEG for Detection and Management of Seizures in Critically Ill Patients, Including the Ictal-Interictal Continuum 31 Gamaleldin Osman, Daniel Friedman, and Lawrence J Hirsch Seizures and Quantitative EEG 51 Jennifer A Kim, Lidia M.V.R Moura, Craig Williamson, Edilberto Amorim, Sahar Zafar, Siddharth Biswal, and M.M Brandon Westover Spreading Depolarizations and Seizures in Clinical Subdural Electrocorticographic Recordings 77 Gajanan S Revankar, Maren K.L Winkler, Sebastian Major, Karl Schoknecht, Uwe Heinemann, Johannes Woitzik, Jan Claassen, Jed A Hartings, and Jens P Dreier Multimodality Monitoring Correlates of Seizures 91 Jens Witsch, Nicholas A Morris, David Roh, Hans-Peter Frey, and Jan Claassen Management of Critical Care Seizures 103 Christa B Swisher and Aatif M Husain Management of Status Epilepticus in the Intensive Care Unit 121 Panayiotis N Varelas and Jan Claassen Part II Etiology-Specific Section Ischemic Stroke, Hyperperfusion Syndrome, Cerebral Sinus Thrombosis, and Critical Care Seizures 155 Panayiotis N Varelas and Lotfi Hacein-Bey 10 Hemorrhagic Stroke and Critical Care Seizures 187 Ali Mahta and Jan Claassen 11 Traumatic Brain Injury and Critical Care Seizures 195 Georgia Korbakis, Paul M Vespa, and Andrew Beaumont 12 Brain Tumors and Critical Care Seizures 211 Panayiotis N Varelas, Jose Ignacio Suarez, and Marianna V Spanaki vii viii 13 Global Hypoxia-Ischemia and Critical Care Seizures 227 Lauren Koffman, Matthew A Koenig, and Romergryko Geocadin 14 Fulminant Hepatic Failure, Multiorgan Failure and Endocrine Crisis and Critical Care Seizures 243 Julian Macedo and Brandon Foreman 15 Organ Transplant Recipients and Critical Care Seizures 259 Deena M Nasr, Sara Hocker, and Eelco F.M Wijdicks 16 Extreme Hypertension, Eclampsia, and Critical Care Seizures 269 Michel T Torbey 17 Infection or Inflammation and Critical Care Seizures 277 Andrew C Schomer, Wendy Ziai, Mohammed Rehman, and Barnett R Nathan 18 Electrolyte Disturbances and Critical Care Seizures 291 Claudine Sculier and Nicolas Gaspard 19 Alcohol-Related Seizures in the Intensive Care Unit 311 Chandan Mehta, Mohammed Rehman, and Panayiotis N Varelas 20 Drug-Induced Seizures in Critically Ill Patients 321 Denise H Rhoney and Greene Shepherd 21 Illicit Drugs and Toxins and Critical Care Seizures 343 Maggie L McNulty, Andreas Luft, and Thomas P Bleck 22 Seizures and Status Epilepticus in Pediatric Critical Care 355 Nicholas S Abend Index 369 Contents Contributors Nicholas S Abend Department of Neurology and Pediatrics, Children’s Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA Edilberto Amorim Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, MA, USA Andrew Beaumont Department of Neurosurgery, Aspirus Spine and Neuroscience Institute, Aspirus Wausau Hospital, Wausau, WI, USA Siddharth Biswal Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, MA, USA Thomas P Bleck Department of Neurological Sciences, Neurosurgery, Anesthesiology, and Medicine, Rush Medical College, Chicago, IL, USA James W.Y Chen Department of Neurology, VA Greater Los Angeles Health Care System, Los Angeles, CA, USA Jan Claassen Neurocritical Care, Columbia University College of Physicians and Surgeons, New York, NY, USA Division of Critical Care and Hospitalist Neurology, Department of Neurology, Columbia University Medical Center, New York Presbyterian Hospital, New York, NY, USA Jens P Dreier Center for Stroke Research Berlin, Charité University Medicine Berlin, Berlin, Germany Department of Neurology, Charité University Medicine Berlin, Berlin, Germany Department of Experimental Neurology, Charité University Medicine Berlin, Berlin, Germany Iván Sánchez Fernández Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA Department of Child Neurology, Hospital Sant Joan de Déu, University of Barcelona, Barcelona, Spain Brandon Foreman University of Cincinnati Medical Center, Cincinnati, OH, USA Department of Neurology and Rehabilitation Medicine, University of Cincinnati, Cincinnati, OH, USA Hans-Peter Frey Division of Critical Care and Hospitalist Neurology, Department of Neurology, Columbia University Medical Center, New York Presbyterian Hospital, New York, NY, USA Daniel Friedman Comprehensive Epilepsy Center, Department of Neurology, New York University, New York, NY, USA ix x Nicolas Gaspard Service de Neurologie–Centre de Référence pour le Traitement de l’Epilepsie Réfractaire, Université Libre de Bruxelles–Hôpital Erasme, Bruxelles, Belgium Department of Neurology, Comprehensive Epilepsy Center, Yale University School of Medicine, New Haven, CT, USA Romergryko Geocadin Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA Lotfi Hacein-Bey Sutter Imaging Division, Interventional and Diagnostic Neuroradiology, Sacramento, CA, USA Radiology Department, UC Davis School of Medicine, Sacramento, CA, USA Jed A Hartings Department of Neurosurgery, University of Cincinnati College of Medicine, Cincinnati, OH, USA Mayfield Clinic, Cincinnati, OH, USA Uwe Heinemann Neuroscience Research Center, Charité University Medicine Berlin, Berlin, Germany Lawrence J Hirsch Comprehensive Epilepsy Center, Department of Neurology, Yale University, New Haven, CT, USA Sara Hocker Division of Critical Care Neurology, Mayo Clinic, Rochester, MN, USA Aatif M Husain Department of Neurology, Duke University Medical Center, Durham, NC, USA Neurodiagnostic Center, Department of Veterans Affairs Medical Center, Durham, NC, USA Inna Keselman Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA Department of Neurology, VA Greater Los Angeles Health Care System, Los Angeles, CA, USA Jennifer A Kim Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, MA, USA Matthew A Koenig Neuroscience Institute, The Queens Medical Center, Honolulu, HI, USA Lauren Koffman Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA Georgia Korbakis Department of Neurosurgery, UCLA David Geffen School of Medicine, Los Angeles, CA, USA Tobias Loddenkemper Division of Epilepsy and Clinical Neurophysiology, Department of Neurology, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA Andreas Luft Department of Vascular Neurology and Rehabilitation, University Hospital of Zurich, Zurich, Switzerland Julian Macedo University of Cincinnati Medical Center, Cincinnati, OH, USA Ali Mahta Division of Neurological Intensive Care, Department of Neurology, Columbia University College of Physicians and Surgeon, New York, NY, USA Contributors Traumatic Brain Injury and Critical Care Seizures 11 Georgia Korbakis, Paul M. Vespa, and Andrew Beaumont Introduction Traumatic brain injury (TBI) is a serious public health concern in the United States An estimated 1.7 to million people suffer TBI annually leading to 1,365,000 emergency department visits per year Of these visits, 275,000 result in hospitalization and 52,000 in death [1–3] This incidence equates to one hospitalization per 1000 people each year [2] Many of these patients are admitted to the intensive care unit (ICU) for initial stabilization and monitoring The lifetime medical care costs of head injuries occurring in the United States in 1985 were estimated to total $4.5 billion, including $3.5 billion of hospital costs [4] Seizures are a well-known complication of TBI with reported incidences for convulsive seizures ranging from to 12% [5–13] and up to 33 % for nonconvulsive seizures [14, 15] The incidence of seizures is higher in severe TBI and also with penetrating injury [6, 16] Post-traumatic seizures are classified into immediate (5 mm (25.8%), and multiple cortical contusions (25%) In addition, Glasgow Coma Scale (GCS) was correlated with seizure incidence: GCS 3–8 had a cumulative seizure probability of 16.8%, whereas GCS 9–12 had 24.3% and GCS 13–15 had 8.0% In a large prospective, randomized, double-blind seizure prophylaxis study from Seattle, Temkin et al reported independent risk factors from Cox regression multivariate models Five factors emerged as increasing seizure risk in this population: early seizures (within days), coma for over week, dural penetration, depressed skull fracture not surgically treated, and one or more nonreactive pupil [22] These findings are in agreement with Annegers et al who described that brain contusion, skull fractures, and prolonged amnesia or unconsciousness (>24 h) are injury patterns associated with a higher incidence of seizures [6] Additionally, age ≥65 was also a risk factor for seizure development In a more recent study, an overall incidence of post-traumatic seizures of 6.33% (95% CI 3.96–8.69) was found in 411 patients followed for years with rates for early seizures of 1.95% and late seizures at 4.38% [23] The patients with severe injury, defined as intracerebral hemorrhage/contusion, loss of con- G Korbakis et al sciousness, or amnesia >24 h, were more likely to develop post-traumatic seizures Interestingly, there were no statistically significant differences between age and GCS score The rates of post-traumatic seizures in the civilian population are lower than those based on military populations In the Vietnam Head Injury Study, 53 % of veterans who had penetrating head injuries developed post-traumatic epilepsy, and half of those patients still had seizures 15 years after injury However, the relative risk of developing epilepsy in these patients dropped from 580 times higher than the general age-matched population in the first year after TBI to 25 times higher after 10 years [8] A study looking at the more recent Afghanistan and Iraq war veterans again identified penetrating head injuries as having the strongest association of epilepsy development with an odds ratio of 18.77 (95 % CI 9.21–38.23) [24] Figure 11.1 shows examples of injuries associated with post-traumatic seizures Other factors that can predispose to the development of post-traumatic seizures include age (incidence is higher in the pediatric population [25] and the elderly [6]), history of alcohol abuse, previous seizures, and a family history of seizures [5] Genetic predisposition to post-TBI seizures is an interesting issue that has not been well addressed to date Similar injuries lead to a wide variety of seizure incidence and frequency Not all studies agree on the genetic predisposition Jennett found that family history of epilepsy was more common in patients aged less than 16 years with late post-TBI seizures [26] In the Vietnam Head Injury Study, this factor was not predictive of either early or late seizures [8] In another study examining genetic susceptibility to epilepsy, seizure incidence among relatives of patients with post-TBI seizures was not higher than among the general population [27] In a prospective study of late post-traumatic seizures after moderate and severe TBI, 106 patients were examined for the ApoE locus by restriction fragment length polymorphism analysis [28] Twenty-one patients had at least one late post-TBI seizure The relative risk of late post-TBI seizures for patients with the ε4 allele was 2.41 (95 % CI 1.15–5.07, p = 0.03) Of note, the presence of this allele was not associated with an unfavorable outcome Genetic variations of inhibitory neurotransmitters and pathways are also being evaluated as risk factors for post-traumatic seizure development A 2010 study by Wagner et al found certain adenosine A1 receptor gene variations to be associated with increased susceptibility of early and late seizures [29] Darrah et al found increased risk of post-traumatic seizures between week and months post-injury in patients with a particular polymorphism of the glutamic acid decarboxylase (GAD) gene [30] Identifying these genetic variations has important implications in both targeting the appropriate patient population to treat with anticonvulsants and helping to determine the pathophysiology of post-traumatic epilepsy In studies examining post-traumatic seizures, an arbitrary definition of early and late is commonly used Early seizures 11 Traumatic Brain Injury and Critical Care Seizures 197 Fig 11.1 CT examples of findings associated with post-traumatic seizures (a) Right subdural hematoma (b) Left frontal contusion (c) Multiple skull fractures are defined as occurring in the first days after injury and late seizures occur after this point Early seizure incidence ranges from 2.1 % to 16.9 % [6, 26, 31] The incidence of late seizures ranges from 1.9 to 30 % [17] However, this classification is potentially too restrictive Many TBI patients remain critical in the ICU for longer than days; it would be unreasonable to consider a seizure on the tenth hospital day a “late” seizure Some studies have extended the acute period to include the first month post-injury This approach, however, is not ideal, since the underlying cause of seizures in the first week after injury is most likely different from the cause of seizures occurring in the first month or indeed in the first year after injury Seizures in the first week are more likely related to neurochemical and metabolic derangements, whereas later seizures may be related to the formation of glial scar leading to cortical irritation Also, there is a significant occurrence of seizures at the scene of both mild and severe TBIs [32, 33] These immediate seizures are more likely related to the direct disruption of cortical and subcortical connections as a result of percussive forces on the brain and less likely the result of neurochemical or metabolic derangements However, classifying the timing of onset of post-traumatic seizures is important for both trying to under- stand their pathophysiology and also in trying to define factors that can predict their occurrence A second important goal of dividing seizures by time of occurrence is to evaluate whether early seizures can predict the occurrence of late seizures or the development of a long- term seizure disorder Early seizures are linked with late seizure development The increased risk for late seizures after early seizures is independent of the actual number of seizures occurring during the first week after TBI [17] Not all studies, however, report an increased incidence of late seizures after early post-TBI seizures A large retrospective study by Annegers et al utilized multivariate analysis and found that early seizures are not an independent risk factor for late post-traumatic epilepsy, and most likely early seizures are a marker of injury severity sufficient to cause late epilepsy [5] Another interesting observation is that the incidence of late seizures after early post-TBI seizures is dependent on the age of the patient Children less than 16 years old may not be at increased risk for late seizures regardless of the early seizure type [5, 17] Additionally, there is some evidence that immediate seizures occurring at the scene of the trauma are not linked with any increased risk of developing late seizures [32] 198 The incidence of post-traumatic seizures differs in the pediatric population The overall incidence is higher than in adults [6, 25, 31] Early post-traumatic seizures occur slightly more commonly with reported incidence rates of 9–15% [12, 34–36] As with adults, there is a close correlation between injury severity and the incidence of any type of seizures Hahn et al demonstrated that the incidence of post-traumatic seizures was seven times greater in children with severe TBI and GCS 24 h Younger age (children) Older age (> 65 years) Diffuse cerebral edema (children) Depressed/linear skull fracture Metal fragment retention Focal neurological deficits Persistent EEG changes (>1 month) Early post-TBI seizures Chronic alcoholism Increased risk for seizures Early Late + + + + + + + + + + + + + + + + + + LOC loss of consciousness, + risk factor has been shown to increase the risk of seizures at the specified time point Adapted from Frey [17] Table 11.2 Summary of studies in the literature that examine prophylaxis against the risk of early and late seizures following traumatic brain injury and the anticonvulsant drug used (DPH, dilantin/phenytoin; CBZ, carbamazepine; PB, phenobarbital; VPA, valproic acid; LEV, levetiracetam) Study Young et al (1983) [90] Drug used DPH Young et al (1983) [108] McQueen et al (1983) [98] Glötzner et al (1983) [91] DPH DPH CBZ Temkin et al (1990) [11] DPH Pechadre et al (1991) [89] Manaka et al (1992) [99] Temkin et al (1999) [92] Szaflarski et al (2010) [97] Inaba et al (2013) [94] DPH PB VPA LEVt LEVt Early seizures 0.99 (0.27–3.61) 0.37 (0.18–0.78)* 0.25 (0.11–0.57)* 2.9 (0.7–13.3) 0.88 (0.24–3.28) (0.33-3.08) Late seizures 1.29 (0.56–3.0) 1.09 (0.41–2.86) 0.71 (0.39–1.3) 1.3 (0.82–2.08) 0.14 (0.03–0.55) 1.38 (0.54–3.5) 1.4 (0.8–2.4) Values represent relative risk with the 95 % confidence interval in parentheses * significant with p < 0.05 twhen compared to DPH References Sosin DM, Sniezek JE, Thurman DJ. 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Figure 1. 2a shows that mIPSCs recorded from granule cells in slices prepared h into SE showed a decreased peak amplitude to 61. 8 ± 11 .9% of controls (− 31. 5 ± 6 .1 picoAmpere (pA) for SE vs – 51. 0 ± 17 .0