Schmidek and Sweet: Operative Neurosurgical Techniques [2, 7 ed.] 0323414796, 9780323414791

Citation preview

SCHMIDEK & SWEET

Operative Neurosurgical Techniques Seventh Edition

Indications, Methods, and Results ALFREDO QUIÑONES-­H INOJOSA, MD

WILLIAM J. AND CHARLES H. MAYO PROFESSOR CHAIR, NEUROLOGIC SURGERY DEPARTMENT OF NEUROSURGERY MAYO CLINIC JACKSONVILLE, FLORIDA

Elsevier 1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-­2899

SCHMIDEK & SWEET OPERATIVE NEUROSURGICAL TECHNIQUES: ISBN: 978-­0-­323-­41479-­1 INDICATIONS, METHODS, AND RESULTS,  Volume 1: 978-0-323-84721-6 SEVENTH EDITION Volume 2: 978-0-323-84722-3 Copyright © 2022, 2012, 2006, 2000, 1995, 1988, 1982 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Control Number: 2021930850

Content Strategist: Belinda Kuhn Director, Content Development: Laurie K. Gower Senior Content Development Manager: Laura Schmidt Content Development Specialist: Denise Roslonski Publishing Services Manager: Julie Eddy Senior Project Manager: Cindy Thoms Book Designer: Brian Salisbury Printed in Canada Last digit is the print number:  9  8  7  6  5  4  3  2  1

DEDICATION

I dedicated the 6th edition (the first edition where I served as Chief Editor) to Dr. Henry Schmidek, who was undoubtedly an extraordinary and visionary man. Dr. Schmidek was intellectually gifted with a voracious curiosity and never-­ ending gusto for knowledge and life. His immense love of his family was apparent to everyone who had the pleasure of his company. Dr. Schmidek died in the fall of 2008, but his legacy has continued through the 6th and now the 7th editions of this book. This book continues to be the most universal text in neurosurgery. This new 7th edition of Schmidek & Sweet Operative Neurosurgical Techniques is part of a legacy of academic excellence. I tried to keep the same spirit that characterized the prior editions of this book and made it a favorite among students, residents, health care providers, and faculty alike since its first printing. As I edited this text with the help of a superb team of section editors and contributors in the middle of the most extraordinary life-­altering COVID-­19 pandemic, I reflected on the many lives we have lost in the world and came to realize that it is not about how long we live but the contributions we make to this world, the people we touch, and the legacy we leave behind. I would like to thank my wife, Anna, and our children, Gabriella, David, and Olivia, for their extraordinary patience, love, and dedication to my career and life and, ultimately, their commitment to our patients, who are also part of our family. Our children keep me young, grounded,

and humble by asking me questions to which I do not have answers. Thanks to all my mentors thorough the decades since I came to the United States and special gratitude to our extraordinary team of nurses, administrators, anesthesiologists, neurologists, neurosurgeons, otolaryngologists, radiologists, endocrinologists, residents, fellows, and medical students who have dedicated their lives to the pursuit of perfection and patient care and who are an integral part of these advances in surgery—they all have helped me become a better surgeon and a compassionate physician. I have been given guidance and light during moments when the room was dark and the visibility was dimmed by moments of doubt and fear. A million thanks to my amazing patients and their families—they are the true unsung heroes who day after day stay positive and filled with hope despite their health struggles and often put their lives in our hands, ask questions, and constantly push us to be better physicians, surgeons, and human beings. Much gratitude and thanks also to Elsevier, Karim ReFaey, Laurie Gower, Denise Roslonski, Laura Schmidt, Belinda Kuhn, Cindy Thoms, and the extraordinary team who made this book possible. It has taken many years of work, many years’ experience and knowledge to produce this book. It would not have been possible without all of you. Alfredo Quiñones-­Hinojosa

iii

SECTION EDITORS

Section One

Section Four

Alfredo Quiñones-­Hinojosa, MD William J. and Charles H. Mayo Professor Chair, Neurologic Surgery Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Daniele Rigamonti, MD Professor, Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland CEO Johns Hopkins Aramco Healthcare Dhahran, Eastern Province, Saudi Arabia

Surgical Management of Brain and Skull Base Tumors

Maryam Rahman, MD, MS Assistant Professor Neurosurgery University of Florida Gainesville, Florida

Abnormalities of Cerebrospinal Fluid Dynamics

Section Five

Stereotactic Radiosurgery

Vascular Diseases

Cesare Giorgi, MD Consultant Neurosurgeon Gamma Knife Unit Fondazione Poliambulanza Brescis, Italy

Michael T. Lawton, MD Professor and Chair, Department of Neurosurgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona

Daniel M. Trifiletti, MD Associate Professor Radiation Oncology Mayo Clinic Jacksonville, Florida

Rabih G. Tawk, MD Associate Professor Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Section Six

Section Two

Brian L. Hoh, MD James & Brigitte Marino Family Professor and Chair Neurosurgery University of Florida Gainesville, Florida

Section Three

Operative Techniques in Pediatric Neurosurgery George I. Jallo, MD Professor, Neurosurgery, Pediatrics, and Oncology Division of Pediatric Neurosurgery Director, Institute for Brain Protection Sciences Johns Hopkins All Children’s Hospital St Petersburg, Florida

Functional Neurosurgery Emad N. Eskandar, MD Associate Professor, Neurosurgery Massachusetts General Hospital and Harvard Medical School Director, Stereotactic and Functional Neurosurgery Director, Neurosurgery Residency Program Massachusetts General Hospital Boston, Massachusetts Edward F. Chang, MD Associate Professor, Neurological Surgery School of Medicine University of California San Francisco, California

ix

x

SECTION EDITORS

Section Seven

Section Nine

Trauma

Neurosurgical Management of Spinal Disorders

J. Marc Simard, MD, PhD Professor Neurosurgery, Pathology, and Physiology School of Medicine University of Maryland Baltimore, Maryland

Ziya L. Gokaslan, MD, FAANS, FACS Julius Stoll, MD Professor and Chair, Department of Neurosurgery The Warren Alpert Medical School of Brown University Neurosurgeon-­in-­Chief, Rhode Island Hospital and The Miriam Hospital Clinical Director, Norman Prince Neurosciences Institute President, Brown Neurosurgery Foundation Providence, Rhode Island

Section Eight

Surgical Management of Nervous System Infections Rodrigo Ramos-­Zuniga Sr., MD, PhD Professor of Neurosciences Institute of Translational Neurosciences. Department of Neurosciences University of Guadalajara Guadalajara, Jalisco, Mexico Mohamed E. El-­Fiki, MBBCh, MS, MD, DNCh Professor, Neurosurgery University of Alexandria Alexandria, Egypt

Mohamad Bydon, MD Associate Professor Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota

Section Ten

Surgical Management of the Peripheral Nervous System Robert J. Spinner, MD Chair, Department of Neurologic Surgery Neurosurgery Professor Departments of Anatomy, Neurologic Surgery, and Orthopedic Surgery Mayo Clinic Rochester, Minnesota

IN MEMORIAM

Frank Lugo Acosta Jr., MD

Edward H. Oldfield, MD

1975-2020

1947-2017

Dr. Frank Lugo Acosta Jr., MD, age 45, passed away on November 21, 2020. Frank grew up in East Los Angeles/ Montebello. As a kid, Frank was smart, loved science, and enjoyed soccer. He went to Don Bosco Tech for high school and excelled in science, counting units, and chess. He got accepted to every Ivy League school in the country, choosing Harvard University to pursue his passion in chemistry, math, and physics. Frank matriculated at Harvard Medical School where he completed an HHMI Research fellowship. Frank went to the University of California at San Francisco for his neurosurgical training. Frank specialized in complex spine surgeries, and he was known around the world for his clinical and scientific contributions to deformity and complex spine neurosurgery. He was a top spine neurosurgeon in the county, an amazingly gifted, talented, and a very educated young man. Frank was a beloved son, brother, husband, father, colleague, and friend who loved to make others laugh. He will be deeply missed by his family, daughter, friends, colleagues, and all who knew him.

Edward H. Oldfield, MD, passed away on September 1, 2017. His death was a significant loss to everyone who knew him, including the over 100 trainees he mentored worldwide. While neurosurgery has lost a giant, Ed’s life left an indelible mark through scientific discovery and surgical innovation, as well as generations of trainees and colleagues. Ed was born in the small town of Mount Sterling, Kentucky, on November 22, 1947, to Ellis and Amanda (née Miller) Oldfield. He was the second of five children, with one older sister, two younger brothers, and one younger sister. Ed’s father was a decorated World War II veteran, having been awarded two Bronze Stars and a Purple Heart. Ed continued to study physics at the University of Kentucky, during which he met Susan, the love of his life and future wife. Upon completing three years of college, Ed joined the University of Kentucky College of Medicine. Afterward, he joined Vanderbilt University Medical Center for his neurosurgical training. Dr. Oldfield made significant clinical and scientific contributions to neurosurgery. He excelled in spinal vascular malformations, Chiari I malformation and syringomyelia, pituitary adenomas, drug delivery, nervous system neoplasia, gene therapy, and vasospasm, which led to over 500 peer-­reviewed publications, an H-­index over 100, and over 43,000 citations.

v

vi

IN MEMORIAM

Evandro de Oliveira, MD, PhD 1944-2021

Dr. Evandro De Oliveira passed away on February 11, 2021. Evandro was from Santa Catarina, Brazil, and completed medical school at the Federal University of Santa Catarina and then Neurosurgery Residency at the Universidad del Republica, in Montevideo, Uruguay. He spent time with Al

Rhoton, Jr. and M. Gazi Yasargil, which led to a lifelong friendship and collaborations. Evandro led a philosophy based on the mastery of anatomy and microneurosurgery, where the anatomy learned in the lab must be applied in the operative room, in a clean, beautiful, and effective manner. Evandro was a uniquely dedicated surgeon-­artist in chase of perfection. Nothing but the best was acceptable. He took Brazilian neurosurgery to the next level and inspired generations. Through his multiple positions, including Director of Institute of Neurological Sciences, Sao Paulo, he mentored 92 clinical fellows, over 600 visiting fellows, and additional 7000 surgeons, who attended one or more of the 350 courses held in his lab in Sao Paulo. Evandro was passionate about his family, his friends, and about neurosurgery. He always cared for his personal and “surgical” families, including during his battle against ALS. He remains alive through his wife, daughters, and granddaughter and through his disciples. Undoubtedly, Evandro was “The Unbelievable” surgeon, mentor, and master and will be forever missed.

ABOUT THE AUTHOR/EDITOR

Dr. Alfredo Quiñones-­Hinojosa, commonly known as Dr. Q, received his medical degree from Harvard University where he graduated cum laude. He completed his residency in neurosurgery at the University of California, San Francisco, where he also completed a postdoctoral fellowship in developmental and stem cell biology. His career began at the Johns Hopkins University School of Medicine, where he became Professor of Neurosurgery and Oncology, Neurology, and Cellular and Molecular Medicine and Director of the Brain Tumor Stem Cell Laboratory. Nowadays, he is the “William J. and Charles H. Mayo Professor” and Chair of Neurologic Surgery at the Mayo Clinic in Jacksonville, Florida.

Dr. Q is an internationally renowned neurosurgeon and neuroscientist who leads NIH-­ funded research to cure brain cancer. He is the principal investigator at the Brain Tumors Stem Cell Laboratory at the Mayo Clinic. He has published more than 450 peer-­reviewed papers and 100 book chapters, edited 14 high-­impact neurosurgical textbooks, and published his memoir, Becoming Dr. Q, in both English and Spanish. Dr. Q is the founder and president of the nonprofit organization Mission:BRAIN, providing patients in need access to advanced neurosurgical procedures around the world. For all his work, Dr. Q has also been recognized with several prestigious awards, including being named as one of the 100 most influential Hispanics in the U.S. by Hispanic Business Journal; as 2014 Neurosurgeon of the Year by Voices Against Brain Cancer, where he was also recognized with the Gary Lichtenstein Humanitarian Award; and by the 2015 Forbes magazine as one of Mexico’s most brilliant minds in the world; he was also selected by Popular Science magazine as one of their 6th Annual Brilliant Ten in their search for young genius influencing the course of science. He has received honorary degrees from Southern Vermont College, Lackawanna College, Dominican University, University of Notre Dame, Loyola University, and Universidad Anahuac Mexico. He was awarded the Cortes de Cadiz Prize in the category of surgery by the city council of Cadiz, Spain, and was also named by Forbes as one of the most creative Mexicans. Dr. Q’s story was featured on the BBC and Netflix show “The Surgeon’s Cut” in December 2020, and more recently Annapurna Pictures and Plan B Entertainment productions announced that his inspirational life story is going to be featured in a movie.

vii

VIDEO AND CONTENT ASSOCIATE EDITOR

Qatari Royal Family and most recently by grants from the National Institutes of Health. Dr. ReFaey’s research focuses on gliomas and awake brain mapping to preserve speech and motor functions and preserve the crucial areas of the brain. Dr. ReFaey has published in clinical and translational research, producing close to 40 peer-­reviewed publications and more than 30 book chapters. His work involving the design and utilization of high-­density electrocorticography (HD-ECoG) in intraoperative monitoring during awake craniotomies and its effect on the patient’s outcome led to national invited presentations, high-tier clinical publications, as well as five US patents complementing this technology (one issued, PCT/US2018/039956; two pending, # 2019-388; # 2017-113; and two in submission). He has been recognized by the American Epilepsy Society for the impact of his work and was awarded the Young Investigator Award of the Year in 2017. Dr. ReFaey is applying for neurosurgery residency to pursue his career as a neurosurgeon-­scientist.

Dr. Karim ReFaey earned his medical degree from Ain Shams University in Cairo, Egypt. He conducts cutting-­ edge research in neurosurgery, neuro-­oncology, and oncoepilepsy, sponsored originally by a generous grant from the

viii

CONTRIBUTORS

Marlien W. Aalbers, MD, PhD Department of Neurosurgery University of Groningen University Medical Center Groningen Groningen, the Netherlands Hadi Abou-­El-­Hassan, MD Research Fellow Department of Neurological Surgery Mayo Clinic Jacksonville, Florida Frank Acosta, MD Associate Professor of Neurological Surgery University of Southern California Los Angeles, California P. David Adelson, MD Director, Barrow Neurological Institute at Phoenix Children’s Hospital Diane and Bruce Halle Chair of Pediatric Neurosciences Chief, Pediatric Neurosurgery, Phoenix Children’s Hospital Professor, Department of Child Health University of Arizona College of Medicine Phoenix, Arizona, Professor, Neurosurgery Mayo Clinic Scottsdale, Arizona John R. Adler Jr., MD Professor, Department of Neurosurgery Stanford University Stanford, California Vijay Agarwal, MD Director, Skull Base Center Assistant Professor, Department of Neurosurgery Montefiore Medical Center University Hospital for the Albert Einstein College of Medicine New York, New York Manish K. Aghi, MD, PhD Professor in Neurological Surgery University of California, San Francisco San Francisco, California

Manmeet S. Ahluwalia, MD Brain Tumor and Neuro-­Oncology Center Neurological Institute Taussig Cancer Institute Cleveland Clinic Department of Medicine Cleveland Clinic Lerner College of Medicine Case Western University Cleveland, Ohio A. Karim Ahmed, BS MD Candidate, Neurosurgery Research Fellow Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland Pablo Ajler, MD Neurosurgery Hospital Italiano Buenos Aires, Argentina Oluwaseun O. Akinduro, MD Resident Physician, Department of Neurological Surgery Mayo Clinic Jacksonville, Florida Felipe C. Albuquerque, MD Assistant Director, Endovascular Surgery Professor of Neurosurgery Department of Neurosurgery Barrow Neurological Institute Phoenix, Arizona Philipp R. Aldana, MD Professor, Neurosurgery and Pediatric Neurosurgery Division of Pediatric Neurosurgery University of Florida Health Jacksonville Jacksonville, Florida Ram K. Alluri, MD Orthopaedic Surgery Resident Keck School of Medicine University of Southern California Los Angeles, California

xi

xii

CONTRIBUTORS

Mohammed Ali Alvi, MD Research Fellow, Department of Neurologic Surgery Mayo Clinic Neuro-­Informatics Laboratory Mayo Clinic Rochester, Minnesota Luca Amendola, MD Orthopaedic Surgery and Traumatology Unit Maggiore Hospital Regional Trauma Center Bologna Local Health District Bologna, Italy Sepideh Amin-­Hanjani, MD Professor and Program Director, Department of Neurosurgery Co-­Director, Neurovascular Surgery University of Illinois at Chicago Chicago, Illinois Joshua M. Ammerman, MD Chief, Section of Neurosurgery Chairman, Department of Surgery Sibley Memorial Hospital Assistant Clinical Professor of Neurosurgery George Washington University School of Medicine Washington, DC Adjunct Assistant Professor of Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland William Anderson, MD Associate Professor of Neurosurgery Associate Professor of Biomedical Engineering Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland Hugo Andrade-­Barazarte, MD, PhD Consultant Neurosurgeon Department of Neurosurgery and Cerebrovascular Diseases Henan Provincial People’s Hospital Zhengzhou, PR China Geoff Appelboom, MD, PhD Department of Neurosurgery Stanford University School of Medicine Stanford, California Paul M. Arnold, MD, FACS Professor and Chairman, Department of Neurosurgery Carle Illinois College of Medicine Urbana, Illinois Ashok Asthagiri, MD Associate Professor, Department of Neurological Surgery University of Virginia Health System Charlottesville, Virginia

Sonikpreet Aulakh, MBBS, MD Assistant Professor, Medicine Division of Hematology-­Oncology Department of Internal Medicine Department of Neurosciences West Virginia University School of Medicine Morgantown, West Virginia Khaled M. Aziz, MD Assistant Professor of Neurosurgery Director, Division of Complex Intracranial Surgery Neurosurgery Allegheny General Hospital Pittsburgh, Pennsylvania Tipu Aziz, F.Med.Sci Professor of Neurosurgery Nuffield Department of Surgical Sciences University of Oxford Oxford, England United Kingdom Joshua Bakhsheshian, MD Department of Neurological Surgery Keck School of Medicine University of Southern California Los Angeles, California Perry A. Ball, MD Professor Departments of Surgery and Anesthesiology Geisel School of Medicine Dartmouth-­Hitchcock Medical Center Lebanon, New Hampshire Stefano Bandiera, MD Coordinator of Specialist Reference Centre Spine Surgery prevalently Oncologic and Degenerative Istituto Ortopedico Rizzoli Bologna, Italy Nicholas M. Barbaro, MD Neurosurgeon Mulva Clinic for the Neurosciences Professor of Neurosurgery Dell Medical School University of Texas at Austin Austin, Texas Zachary R. Barnard, MD, MS Resident, Neurosurgery Cedars-­Sinai Medical Center Los Angeles, California Daniel L. Barrow, MD Pamela R. Rollins Professor and Chairman Department of Neurosurgery Emory University School of Medicine Atlanta, Georgia

CONTRIBUTORS

Thomas L. Beaumont, MD, PhD Department of Neurosurgery The Ohio State University Wexner Medical Center Columbus, Ohio Joshua Bederson, MD Professor and System Chair of Neurosurgery Department of Neurosurgery Icahn School of Medicine at Mount Sinai New York, New York Alexandra D. Beier, DO Associate Professor, Neurosurgery and Pediatrics Division of Pediatric Neurosurgery University of Florida Health Jacksonville Jacksonville, Florida Carlo Bellabarba, MD Professor and Vice Chair Department of Orthopaedics and Sports Medicine Joint Professor Department of Neurological Surgery University of Washington School of Medicine Chief of Orthopaedics Harborview Medical Center Seattle, Washington Lorenzo Bello, MD Professor, Neurosurgery Oncology and Hemato-­Oncology Neuro-­Oncological Surgery Università degli Studi di Milano Milano, Italy Alan J. Belzberg, MD Professor Neurosurgery Johns Hopkins Hospital Baltimore, Maryland Sharona Ben-­Haim, MD Assistant Professor, Department of Neurosurgery University of California–San Diego San Diego, California Netanel Ben-­Shalom, MD Department of Neurosurgery Rabin Medical Center Beilinson Campus New York, New York Matthew T. Bender, MD Assistant Professor, Department of Neurosurgery and Neurology University of Rochester Rochester, New York Bernard R. Bendok, MD Chair, Neurological Surgery in Arizona William J. and Charles H. Mayo Professor Professor of Neurosurgery Department of Neurosurgery Mayo Clinic Phoenix, Arizona

Ludwig Benes, MD Head, Department of Neurosurgery Klinikum Arnsberg Arnsberg, Germany Edward C. Benzel, MD Emeritus Chairman and Professor Department of Neurosurgery Lerner College of Medicine Neurological Institute Cleveland Clinic Cleveland, Ohio Helmut Bertalanffy, MD, PhD Professor, Neurosurgery Director of Vascular Neurosurgery International Neuroscience Institute Hannover, Germany Chetan Bettegowda, MD, PhD Professor, Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland Priyal Vinod Bhagat, DO Department of Orthopaedic Surgery New York University Medical Center New York, New York Wenya Linda Bi, MD, PhD Department of Neurosurgery Brigham and Women’s Hospital Boston, Massachusetts Harvard Medical School Cambridge, Massachusetts Kelly Bijanki, PhD Assistant Professor Department of Neurosurgery Baylor College of Medicine Houston, Texas Allen T. Bishop, MD Division of Hand Surgery Department of Orthopedics Professor, Orthopedics and Neurosurgery Mayo Clinic Rochester Minnesota Erica F. Bisson, MD, MPH Professor of Neurosurgery Department of Neurosurgery University of Utah Salt Lake City, Utah Keith L. Black, MD Chair and Professor Department of Neurosurgery Director Maxine Dunitz Neurosurgical Institute Cedars-­Sinai Medical Center Los Angeles, California

xiii

xiv

CONTRIBUTORS

Benjamin Blondel, MD Aix Marseille University Timone Hospital Department of Paediatric Orthopaedics Marseille, France Kofi Boahene, MD Professor of Otolaryngology–Head and Neck Surgery Johns Hopkins Medicine Baltimore, Maryland Angela M. Bohnen, MD Neurosurgeon NeurosurgeryOne Denver, Colorado Robert J. Bollo, MD, MS Associate Professor University of Utah Salt Lake City, Utah Markus Bookland, MD Associate Director of Academic Affairs Department of Pediatric Neurosurgery Connecticut Children’s Medical Center Hartford, Connecticut Assistant Professor Department of Surgery University of Connecticut School of Medicine Farmington, Connecticut Alireza Borghei, MD Post-­Doctorate Fellow Department of Neurosurgery Rush University Chicago, Illinois Hamid Borghei-­Razavi, MD Assistant Professor, Neurological Surgery Department of Neurosurgery Pauline Braathen Neurological Center Cleveland Clinic Florida Weston, Florida Stefano Boriani, MD GSpine4 Spine Surgery Division IRCCS Istituto Ortopedico Galeazzi Milan, Italy Sachin A. Borkar, MBBS, MCh, DNB, MNAMS Consultant and Associate Professor, Neurosurgery All India Institute of Medical Sciences and Jai Prakash Narain Apex Trauma Center New Delhi, India Weston, Florida Frank J. Bova, PhD Professor Department of Neurological Surgery University of Florida Gainesville, Florida

Bledi C. Brahimaj, MD Resident, Department of Neurosurgery Rush University Medical Center Chicago, Illinois Ryan J. Brandt, MD Assistant Professor Department of Radiology Dartmouth-­Hitchcock Medical Center Lebanon, New Hampshire Richard J. Bransford, MD Professor and Director of Spine Fellowship Department of Orthopaedics and Sport Medicine Joint Professor Department of Neurological Surgery University of Washington School of Medicine Seattle, Washington Jacques Brotchi, MD, PhD Emeritus Professor Department of Neurosurgery Erasme Hospital Brussels, Belgium Benjamin L. Brown, MD Assistant Professor, Department of Neurosurgery Mayo Clinic Jacksonville, Florida Jeffrey N. Bruce, MD Edgar M. Housepian Professor of Neurological Surgery Vice Chairman of Academic Affairs Neurological Surgery New York-­Presbyterian Columbia University Medical Center New York, New York Michael Bruneau, MD, PhD Professor Department of Neurosurgery Erasme Hospital Brussels, Belgium Ian A. Buchanan, MD Department of Neurological Surgery Keck School of Medicine University of Southern California Los Angeles, California Kim J. Burchiel, MD, FACS John Raaf Professor Department of Neurological Surgery Oregon Health & Science University Portland, Oregon

CONTRIBUTORS

Timothy G. Burke, MD Chairman Department of Neurosurgery Anne Arundel Medical Center Annapolis, Maryland Associate Professor Department of Neurosurgery The George Washington University Washington, DC

Ricardo L. Carrau, MD Professor Departments of Otolaryngology Head and Neck Surgery and Neurosurgery The Ohio State University Wexner Medical Center Columbus, Ohio

Ali Bydon, MD Professor of Neurosurgery Department of Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland

Bob S. Carter, MD, PhD Neurosurgeon Chair, Department of Neurosurgery William and Elizabeth Sweet Professor of Neurosurgery Harvard Medical School Massachusetts General Hospital Boston, Massachusetts

Mohamad Bydon, MD Associate Professor Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota

Laura Castana, MD “Claudio Munari” Epilepsy Surgery Center Department of Neuroscience ASST Grande Ospedale Metropolitano Niguarda Milan, Italy

Richard W. Byrne, MD Professor and Chair Department of Neurosurgery Rush University Medical Center Chicago, Illinois

Gabriel Castillo-Velazquez, MD Neurosurgeon Puerta de Hierro Medical Center Guadalajara, Mexico

Gustavo Augusto Porto Sereno Cabral Assistant, Neurosurgery Department Gaelão Air Force Hospital Rio de Janeiro, Brazil

Kaisorn L. Chaichana, MD Professor, Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Francesco Cacciola, MD Consultant Neurosurgeon Department of Neurosurgery University Hospital of Siena Siena, Italy

Asher Chanan-­Khan, MBBS, MD Professor, Medicine Division of Hematology-­Oncology Department of Medicine Mayo Clinic Jacksonville, Florida

Jessica K. Campos, MD Department of Neurosurgery University of California–Irvine Irvine, California

Edward F. Chang, MD Professor of Neurological Surgery University of California–San Francisco San Francisco, California

Justin M. Caplan, MD Department of Neurosurgery Johns Hopkins Hospital Baltimore, Maryland

Steven D. Chang, MD Robert C. and Jeannette Powell Professor in the Neurosciences Department of Neurosurgery Stanford School of Medicine Stanford, California

Anthony J. Caputy, MD Hugo V. Rizzoli Professor of Neurosurgery The George Washington University Washington, DC Francesco Cardinale, MD “Claudio Munari” Epilepsy Surgery Center Department of Neuroscience ASST Grande Ospedale Metropolitano Niguarda Milan, Italy Lucas P. Carlstrom, MD, PhD Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota

Aswin Chari, MA, BMBCh, MRCS GOSH Charity Surgeon-­Scientist Fellow and Neurosurgical Registrar Department of Neurosurgery Great Ormond Street Hospital London, United Kingdom Ching-­Jen Chen, MD Resident Physician, Neurological Surgery University of Virginia Charlottesville, Virginia

xv

xvi

CONTRIBUTORS

Douglas Chen, MD Neurotology Specialist Allegheny General Hospital Pittsburgh, Pennsylvania

Ray M. Chu, MD Clinical Chief, Neurosurgery Cedars-­Sinai Medical Center Los Angeles, California

James Chen, MD Interventional Radiology Charlotte Radiology Charlotte, North Carolina

William Clifton, MD Resident Physician Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Selby Chen, MD Department of Neurologic Surgery Mayo Clinic Jacksonville, Florida Joshua J. Chern, MD, PhD Section of Pediatric Neurosurgery Riley Hospital for Children Department of Neurosurgery Indiana University School of Medicine Goodman Campbell Brain and Spine Indianapolis, Indiana John H. Chi, MD, MPH Director, Neurosurgical Spinal Oncology Department of Neurosurgery Brigham and Women’s Hospital Associate Professor, Neurosurgery Harvard Medical School Boston, Massachusetts E. Antonio Chiocca, MD, PhD Harvey W. Cushing Professor of Neurosurgery Neurosurgeon-­in-­Chief and Chairman Department of Neurosurgery Brigham and Women’s Hospital Boston, Massachusetts Rohan Chitale, MD Assistant Professor, Department of Neurological Surgery Residency Associate Program Director Neurological Surgery Vanderbilt University Medical Center Nashville, Tennessee Bhupal Chitnavis, BSc(Hons), MBBS, FRCS(Eng), FRCS(SN) Consultant Neurosurgeon Department of Neurosurgery London Bridge Hospital London, United Kingdom Omar A. Choudhri, MD Assistant Professor, Neurosurgery and Radiology University of Pennsylvania Director, Penn Center for Cerebral Revascularization Co-­Director Cerebrovascular and Endovascular Neurosurgery Philadelphia, Pennsylvania

Alan R. Cohen, MD Professor, Neurosurgery, Oncology, and Pediatrics Chief of Pediatric Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Salomon Cohen, MD Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota Geoffrey P. Colby, MD, PhD Associate Professor, Neurosurgery and Radiology Director of Cerebrovascular Neurosurgery University of California, Los Angeles Los Angeles, California Tyler S. Cole, MD Resident Physician Department of Neurosurgery Barrow Neurological Institute Phoenix, Arizona Alessandro Consales, MD Department of Pediatric Neurosurgery Istituto Giannina Gaslini Genoa, Italy Alexander L. Coon, MD Director, Endovascular and Cerebrovascular Neurosurgery Carondelet Neurological Institute Tucson, Arizona Jared B. Cooper, BA, MS, MD Resident, Neurosurgery Westchester Medical Center Valhalla, New York William R. Copeland, MD Department of Neurologic Surgery Tenwek Hospital Bomet, Kenya Domagoj Coric, MD Chief, Department of Neurosurgery Carolinas Medical Center Chief, Spine Division Atrium Healthcare Musculoskeletal Institute Carolina Neurosurgery and Spine Associates Charlotte, North Carolina

CONTRIBUTORS

Frank M. Corl, MD Assistant Professor Biomedical Communications Mayo Clinic Rochester, Minnesota Brian M. Corliss, MD Department of Neurological Surgery University of Florida Gainesville, Florida Marcelo Corti, MD Chairman Division of HIV AIDS Infection Diseases FJ Muñiz Hospital University of Buenos Aires Buenos Aires, Argentina Massimo Cossu, MD “C. Munari” Epilepsy Surgery Center Department of Neuroscience ASST Grande Ospedale Metropolitano Niguarda Milan, Italy Bradford L. Currier, MD Professor Department of Orthopedic Surgery Professor Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota William T. Curry, MD Co-­Director, Mass General Neuroscience Director of Neurosurgical Oncology Massachusetts General Hospital Boston, Massachusetts Guilherme Dabus, MD, FAHA Director, Fellowship Department of Neurointerventional Surgery Miami Cardiac and Vascular Institute Baptist Neuroscience Center Miami, Florida

Ronan M. Dardis, MD Consultant Department of Neurosciences University Hospitals Coventry and Warwickshire NHS Trust Coventry, United Kingdom Sunit Das, MD Associate Professor Department of Surgery University of Toronto Toronto, Ontario, Canada Hormuzdiyar H. Dasenbrock, MD, MPH Department of Neurosurgery Boston University School of Medicine Boston, Massachusetts Arthur L. Day, MD Professor and Co-­Chairman Department of Neurosurgery University of Texas Houston Health Science Center Houston, Texas Gaetano De Biase, MD Department of Neurologic Surgery Mayo Clinic Jacksonville, Florida Rafael De la Garza Ramos, MD Neurological Surgery Resident Department of Neurosurgery Montefiore Medical Center New York, New York H. Gordon Deen, MD Department of Neurological Surgery Mayo Clinic Jacksonville, Florida Vedran Deletis, MD, PhD Department of Neurosurgery University Hospital Dubrava Zagreb, Croatia, Albert Einstein College of Medicine New York, New York

Nader S. Dahdaleh, MD Associate Professor, Department of Neurosurgery Northwestern University Feinberg School of Medicine Chicago, Illinois

Jay Detsky, MD Assistant Professor Odette Cancer Centre Sunnybrook Health Science Centre Toronto, Ontario, Canada

Andrew T. Dailey, MD Professor of Neurosurgery Department of Neurosurgery University of Utah School of Medicine Salt Lake City, Utah

Brian J. Dlouhy, MD Assistant Professor Department of Neurosurgery University of Iowa Hospitals and Clinics University of Iowa Stead Family Children’s Hospital Iowa City, Iowa

David J. Daniels, MD, PhD Associate Professor, Pediatric Neurosurgery Assistant Professor of Pharmacology Mayo Clinic Rochester, Minnesota

Ricardo A. Domingo, MD Postdoctoral Fellow Clinical Neurosurgery Team Mayo Clinic Jacksonville, Florida

xvii

xviii

CONTRIBUTORS

Joseph Domino, MD, MPH Resident Physician Department of Neurosurgery University of Kansas Medical Center Kansas City, Kansas Angela M. Donaldson, MD Senior Associate Consultant Otorhinolaryngology Head and Neck Surgery Mayo Clinic Jacksonville, Florida David Dornbos, MD Open Vascular and Endovascular Fellow Department of Neurosurgery Semmes-­Murphey Clinic University of Tennessee Health Science Center Memphis, Tennessee Michael J. Dorsi, MD Assistant Professor of Neurosurgery Ronald Reagan UCLA Medical Center Los Angeles, California Cassius Vinicius Corrêa Dos Reis, MD, PhD Chairman, Neurosurgery Hospital das Clinicas Universidade Federal de Minas Gerais Belo Horizonte, Brazil Thomas B. Ducker, MD Founder (Retired) Maryland Brain and Spine; Partner Emeritus Annapolis, Maryland Hugues Duffau, MD, PhD Professor and Chairman Neurosurgery and INSERM 1191 Montpellier University Medical Center Montpellier, France Ian F. Dunn, MD Department of Neurosurgery University of Oklahoma Health Sciences Center Oklahoma City, Oklahoma Randy S. D’Amico, MD Assistant Professor, Neurological Surgery Department of Neurosurgery Lenox Hill Hospital, Northwell Health Donald and Barbara Zucker School of Medicine at Hofstra/ Northwell New York, New York Eric R. Eggenberger, DO Professor, Neuro-­Ophthalmology Department of Neurology and Ophthalmology Mayo Clinic Jacksonville, Florida Jeff Ehresman, BS Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland

Ashraf N. El Naga, MD Assistant Clinical Professor and Co-­Director of Spine Trauma Service Department of Orthopaedics University of California, San Francisco School of Medicine San Francisco, California Turki Elarjani, MD Pre-­residency Fellow Department of Neurosurgery University of Miami Miami, Florida Benjamin D. Elder, MD, PhD Associate Professor Neurosurgery, Orthopaedic Surgery, and Biomedical Engineering Mayo Clinic School of Medicine Rochester, Minnesota Ahmed Elsharkawy, MD, PhD Senior Consultant Neurosurgeon Department of Neurosurgery Tanta University Tanta, Egypt Nancy E. Epstein, MD Clinical Professor, Neurological Surgery School of Medicine State University of New York at Stony Brook Editor-­in-­Chief Surgical Neurology International Garden City, New York Kadir Erkmen, MD Professor and Vice Chairman, Neurosurgery Lewis Katz School of Medicine Philadelphia, Pennsylvania Thomas J. Errico, MD Chief of Spine Orthopaedics New York University New York, New York Clifford J. Eskey, MD, PhD Professor of Radiology and Surgery Department of Radiology Dartmouth-­Hitchcock Medical Center Lebanon, New Hampshire Linton Evans, MD Neurosurgical Oncology Fellow Department of Neurosurgery The University of Texas MD Anderson Cancer Center Houston, Texas Megan C. Everson, MD Resident Physician Department of Neurosurgery Mayo Clinic Rochester, Minnesota

CONTRIBUTORS

Naomi Fei, MD PGY6 Hematology-­Oncology Fellow Division of Hematology-­Oncology Department of Internal Medicine West Virginia University School of Medicine Morgantown, West Virginia Richard G. Fessler, MD Professor Department of Neurosurgery Rush Medical College Chicago, Illinois Aaron G. Filler, MD, PhD, JD, FRCS Attending Physician Department of Neurosurgery Cedars Sinai Medical Center Los Angeles, California Bruno C. Flores, MD Department of Neurosurgery Barrow Neurological Institute Phoenix, Arizona Kevin T. Foley, MD Professor Neurosurgery, Orthopedic Surgery, and Biomedical Engineering University of Tennessee Health Science Center Chairman Semmes-­Murphey Clinic Memphis, Tennessee Roberto I. Foroni, PhD Department of Medical Physics University Hospital Verona, Italy Antonio J. Forte, MD, PhD Associate Professor of Plastic Surgery Division of Plastic and Hand Surgery Mayo Clinic Jacksonville, Florida Kostas N. Fountas, MD, PhD Director and Chairman Department of Neurosurgery Faculty of Medicine University of Thessaly Larisa, Greece W. Christopher Fox, MD Associate Professor Department of Neurologic Surgery Mayo Clinic Jacksonville, Florida William David Freeman, MD Neurologic Surgery, Neurology, and Critical Care Mayo Clinic Jacksonville, Florida

William Alan Friedman, MD Professor and Chairman Department of Neurological Surgery University of Florida Gainesville, Florida David M. Frim, MD, PhD Professor, Department of Surgery Section of Neurosurgery The University of Chicago Chicago, Illinois Fabio Frisoli, MD Department of Neurological Surgery New York University School of Medicine New York, New York Miki Fujimura, MD Director Department of Neurosurgery Kohnan Hospital Sendai, Japan Sara Ganaha, MD Postdoctoral Fellow, Department of Neurosurgery Mayo Clinic Jacksonville, Florida Dheeraj Gandhi, MBBS, MD Professor, Director of Interventional Neuroradiology Radiology, Neurology, and Neurosurgery Clinical Director, Center of Metabolic Imaging and Therapeutics Radiology University of Maryland School of Medicine Baltimore, Maryland Sirin Gandhi, MD Clinical Research Fellow Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona Mark Garrett, MD Neurosurgeon Partner Barrow Brain and Spine Director of Neurotrauma Chandler Regional Medical Center Chandler, Arizona Tomas Garzon-­Muvdi, MD, MSc Assistant Professor, Neurosurgery University of Texas Southwestern Dallas, Texas Alessandro Gasbarrini, MD Medical Director with Organisational duties at the Vertebral Surgery Department Spine Surgery prevalently Oncologic and Degenerative Istituto Ortopedico Rizzoli Bologna, Italy

xix

xx

CONTRIBUTORS

Kelly Gassie, MD Neurosurgery Resident Department of Neurosurgery Mayo Clinic Jacksonville, Florida Fred H. Geisler, MD, PhD Adjunct Professor Department of Medical Imaging College of Medicine at the University of Saskatchewan Saskatoon, Saskatchewan, Canada President Copernicus Dynamics Group, L.P. Chicago, Illinois George Georgoulis, MD Neurosurgeon Neurosurgery General Hospital of Athens “G.Gennimatas” Athens, Greece Brian J. A. Gill, MD Department of Neurological Surgery Columbia University New York, New York Felix Goehre, MD, PhD Adjunct Professor of Neurosurgery Department of Neurosurgery BG Hospital Bergmannstrost Halle Halle, Germany Atul Goel, MCh (Neurosurgery) Professor and Head Department of Neurosurgery Seth G. S. Medical College and K.E.M Hospital Mumbai, India Gunjan Goel, MD Neurosurgeon Neurosurgical Medical Clinic San Diego, California Ziya L. Gokaslan, MD, FAANS, FACS Julius Stoll, MD Professor and Chair Department of Neurosurgery The Warren Alpert Medical School of Brown University Neurosurgeon-­in-­Chief Rhode Island Hospital and The Miriam Hospital Clinical Director Norman Prince Neurosciences Institute President Brown Neurosurgery Foundation Providence, Rhode Island Katherine G. Gold, MD Assistant Professor Department of Ophthalmology Mayo Clinic Jacksonville, Florida

Diego F. Gomez, MD Neurologic Surgery Hospital Universitario Fundación Santa Fe de Bogotá, Colombia L. Fernando Gonzalez, MD Associate Professor, Neurosurgery Duke University Durham, North Carolina C. Rory Goodwin, MD Neurosurgeon, Spine Surgeon Duke Cancer Center Durham, North Carolina Chad R. Gordon, DO, FACS Professor and Director, Neuroplastic and Reconstructive Surgery Department of Plastic and Reconstructive Surgery Fellowship Director, Neuroplastic and Reconstructive Surgery Departments of Plastic Surgery and Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Anshit Goyal, MBBS, MS Research Fellow Department of Neurosurgery Mayo Clinic Rochester, Minnesota C. S. Graffeo, MD Resident, Department of Neurosurgery Mayo Clinic Rochester, Minnesota Andrew W. Grande, MD Associate Professor and Co-Director Earl Grande, Vel, V. Richard Zerling Stroke, Stem Cell, and Neuroimaging Laboratory Department of Neurosurgery University of Minnesota Minneapolis, Minnesota Ramesh Grandhi, MD Assistant Professor Department of Neurosurgery Clinical Neurosciences Center University of Utah Salt Lake City, Utah Alexander L. Green, FRCS(SN), MB BS, BSc Oxford Functional Neurosurgery Nuffield Department of Surgery University of Oxford Department of Neurological Surgery The West Wing The John Radcliffe Hospital Oxford, England United Kingdom

CONTRIBUTORS

Jeffrey P. Greenfield, MD, PhD Vice Chairman for Academic Affairs Associate Professor, Neurological Surgery Associate Professor, Pediatric Neurosurgery Associate Residency Director Department of Neurosurgery New York Presbyterian Hospital New York, New York Sanjeet S. Grewal, MD Assistant Professor, Department of Neurosurgery Mayo Clinic Florida Jacksonville, Florida Mari L. Groves, MD Assistant Professor Department of Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Jian Guan, MD Pacific Neuroscience Institute Torrance, California Gerardo Guinto, MD Neurosurgeon Centro Neurologico ABC Mexico City, Mexico Richard Gullan, MD Consultant Neurosurgeon King’s College Hospital London, England, United Kingdom Gaurav Gupta, MD Associate Professor, Neurosurgery Director, Cerebrovascular and Endovascular Neurosurgery Rutgers Robert Wood Johnson Medical School New Brunswick, New Jersey Nalin Gupta, MD, PhD Professor, Neurological Surgery and Pediatrics University of California San Francisco Chief, Division of Pediatric Neurosurgery UCSF Benioff Children’s Hospital San Francisco, California Vivek Gupta, MD Associate Professor Department of Radiology Mayo Clinic Jacksonville, Florida Raymond J. Hah, MD Assistant Professor, Orthopaedic Surgery and Neurosurgery Keck School of Medicine University of Southern California Los Angeles, California

Fernando Hakim, MD Chair, Neurologic Surgery Hospital Universitario Fundación Santa Fe de Bogotá, Colombia, Associate Professor of Neurologic Surgery Universidad de Bosque Professor Universidad de los Andes Bogotá, Colombia Dia Radi Halalmeh, MD Research Fellow Michigan Head and Spine Institute Department of Neurosurgery Southfield, Michigan Clayton L. Haldeman, MD, MHS Resident Department of Neurosurgery University of Wisconsin Hospitals and Clinics Madison, Wisconsin Neil Haranhalli, MD Assistant Professor Departments of Neurosurgery and Radiology Montefiore Medical Center Albert Einstein College of Medicine New York, New York Douglas A. Hardesty, MD Department of Neurosurgery The Ohio State University Wexner Medical Center Columbus, Ohio Trevor Hardigan, MD, PhD Resident Physician Department of Neurosurgery Icahn School of Medicine at Mount Sinai Hospital New York, New York James S. Harrop, MD, MSHQS, FACS Professor of Neurological Surgery and Orthopedics Sidney Kimmel Medical College at Thomas Jefferson University Section Chief, Division of Spine and Peripheral Nerve Disorders Thomas Jefferson University Hospital Philadelphia, Pennsylvania Sara Hartnett, MD Resident Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine Tampa, Florida Stefan Heinze, MD Neurosurgeon Department of Neurosurgery Philips University Marburg Marburg, Germany

xxi

xxii

CONTRIBUTORS

Juha Hernesniemi, MD, PhD Emeritus Professor, Department of Neurosurgery Helsinki University Hospital and University of Helsinki Helsinki, Finland, Professor and Chairman, Department of Neurosurgery Henan Provincial People’s Hospital Zhengzhou, PR China David S. Hersh, MD Assistant Professor Division of Pediatric Neurosurgery Connecticut Children’s Harford, Connecticut Joaquin Hidalgo, MD Fellow Division of Pediatric Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Travis Hill, MD, PhD Department of Neurological Surgery New York University School of Medicine New York, New York Kevork N. Hindoyan, MD Orthopedic Surgery Huntington Hospital Pasadena, California Olivia Ho, MD, MMSc, FRCSC Senior Associate Consultant Plastic and Reconstructive Surgery Mayo Clinic Jacksonville, Florida Brian L. Hoh, MD James & Brigitte Marino Family Professor and Chair Department of Neurosurgery University of Florida Gainesville, Florida L. Nelson Hopkins, MD Departments of Neurosurgery and Radiology Jacobs School of Medicine and Biomedical Sciences University at Buffalo Department of Neurosurgery Gates Vascular Institute at Kaleida Health Canon Stroke and Vascular Research Center University at Buffalo Buffalo, New York Wesley Hsu, MD, FAANS Associate Professor, Division of Neurosurgery Director of Spinal Oncology Wake Forest Baptist Medical Center Winston-­Salem, North Carolina

Judy Huang, MD Professor and Vice Chair, Neurosurgery Director, Neurosurgery Residency Program Fellowship Director, Cerebrovascular Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Michael Huang, MD Department of Neurological Surgery Brain and Spinal Injury Center University of California San Francisco San Francisco, California Wei X. Huff, MD, PhD Section of Pediatric Neurosurgery Riley Hospital for Children Department of Neurosurgery Indiana University School of Medicine Goodman Campbell Brain and Spine Indianapolis, Indiana Sakibul Huq, BS Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland Zain Hussain, MD Dermatologist and Mohs Micrographic Surgeon New Jersey Dermatology and Aesthetics Center Marlboro, New Jersey Natasha Ironside, MBChB Research Fellow Department of Neurological Surgery Columbia University College of Physicians and Surgeons New York, New York Rajiv R. Iyer, MD Department of Orthopedic Surgery Columbia University Medical Center Morgan Stanley Children’s Hospital of New York-­ Presbyterian New York, New York Pascal M. Jabbour, MD Professor, Neurosurgery Director, Division of Neurovascular Surgery and Endovascular Neurosurgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Christina Jackson, MD Resident Department of Neurosurgery Johns Hopkins Hospital Baltimore, Maryland

CONTRIBUTORS

xxiii

Christopher M. Jackson, MD Department of Neurosurgery Johns Hopkins Hospital Baltimore, Maryland

Bowen Jiang, MD Department of Neurosurgery Johns Hopkins University Baltimore, Maryland

Behnam Rezai Jahromi, MD Department of Neurosurgery and Neurosurgery Research Group Helsinki University Hospital and University of Helsinki Helsinki, Finland

Evan Joyce, MD, MS Neurosurgical Resident, Department of Neurological Surgery University of Utah School of Medicine Salt Lake City, Utah

George I. Jallo, MD Professor of Neurosurgery, Pediatrics, and Oncology Division of Pediatric Neurosurgery Director, Institute for Brain Protection Sciences Johns Hopkins All Children’s Hospital St Petersburg, Florida Alejandra Jaume, MD Neurosurgeon Neurosurgery Department Hospital Maciel Montevideo, Uruguay Mohsen Javadpour, MD Consultant Neurosurgeon Clinical Director of the National Neurosurgical Centre Beaumont Hospital Dublin, Ireland Andrew Jea, MD Professor and Chief, Section of Pediatric Neurosurgery Riley Hospital for Children Department of Neurosurgery Indiana University School of Medicine Goodman Campbell Brain and Spine Indianapolis, Indiana Mark Jentoft, MD Assistant Professor, Laboratory Medicine and Pathology Department of Pathology Mayo Clinic Jacksonville, Florida David H. Jho, MD, PhD Assistant Professor, Neurosurgery Departments of Neuroendoscopy and Neurosurgery Allegheny General Hospital (Allegheny Health Network) Pittsburgh, Pennsylvania

M. Yashar S. Kalani, MD, PhD Vice Chair and Associate Professor, Neurological Surgery University of Virginia School of Medicine Charlottesville, Virginias Eftychia Z. Kapsalaki, MD, PhD Professor, Department of Diagnostic Radiology Faculty of Medicine University of Thessaly Larisa, Greece Michael G. Kaplitt, MD, PhD Professor, Neurological Surgery Vice Chairman for Research Director of Stereotactic and Functional Neurosurgery Weill Cornell Medical College New York, New York Patrick Karas, MD Resident Physician Department of Neurosurgery Baylor College of Medicine Houston, Texas Selmin Karatayli-­Ozgursoy, MD Research Fellow Otorhinolaryngology Mayo Clinic Florida Jacksonville, Florida Takeshi Kawase, MD, PhD Honorary Professor, Neurosurgery School of Medicine Keio University Tokyo, Japan Uwe Kehler, PhD Department of Neurosurgery Asklepios Klinik Altona Hamburg, Germany

Diana H. Jho, MD Assistant Professor, Neurosurgery Department of Neurosurgery Milton S. Hershey Medical Center (Penn State Health) Hershey, Pennsylvania

Panagiotis Kerezoudis, MD, MS Resident Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota

Hae-­Dong Jho, MD, PhD Professor and Chairman, Neuroendoscopy Departments of Neuroendoscopy and Neurosurgery Allegheny General Hospital (Allegheny Health Network) Pittsburgh, Pennsylvania

Drew S. Kern, MD, MS, FAAN Assistant Professor Movement Disorders Center Departments of Neurology and Neurosurgery University of Colorado School of Medicine Aurora, Colorado

xxiv

CONTRIBUTORS

Farhan A. Khan, BS Department of Neurological Surgery Columbia University New York, New York Nickalus R. Khan, MD Department of Neurosurgery Semmes-­Murphey Clinic Memphis, Tennessee Kathleen Khu, MD Clinical Associate Professor Division of Neurosurgery Department of Neurosciences College of Medicine and Philippine General Hospital University of the Philippines Manila Ermita, Manila, Philippines Daniel H. Kim, MD, FAAN, FACS Professor Department of Neurosurgery UT Health Science Center Houston, Texas Matthias Kirsch, Prof, MD Klinik für Neurochirurgie Asklepios Schildautalkliniken Seesen Karl-­Herold-­Str. 1, 38723 Seesen, Germany Molecular Neuroimaging Laboratory Medizinische Fakultät, Technische Universität Dresden Fetscherstraße, Dresden, Germany Petra Klinge, MD, PhD Lifespan Physician Group Pediatric Neurosurgery Providence, Rhode Island Matthew J. Koch, MD Resident Department of Neurosurgery Massachusetts General Hospital Boston, Massachusetts Michael Kogan, MD, PhD Fellow Department of Neurosurgery Thomas Jefferson University Philadelphia, Pennsylvania John Paul G. Kolcun, MD Resident Department of Neurological Surgery Rush University Medical Center Chicago, Illinois Douglas Kondziolka, MD Professor, Department of Neurological Surgery New York University School of Medicine New York, New York

Marcus Christopher Korinth, MD, PhD Prof. Dr. Med Neurosurgery University Hospital Aachen, Germany Rupesh Kotecha, MD Radiation Oncologist Miami Cancer Institute Miami, Florida Dietmar Krex Prof, MD Klinik und Poliklinik für Neurochirurgie Universitätsklinikum Carl Gustav Carus Dresden an der Technischen Universität Dresden Fetscherstraße, Dresden, Germany Chandan Krishna, MD Department of Neurological Surgery Precision Neuro-Therapeutics Innovation Lab Neurosurgery Simulation and Innovation Lab Mayo Clinic Phoenix, Arizona Kartik G. Krishnan, MD, PhD Department of Neurosurgery Center for Clinical Neurosciences Johann Wolfgang Goethe University Frankfurt, Germany Ajit Krishnaney, MD Department of Neurosurgery Neurologic Institute Cleveland Clinic Cleveland, Ohio Varun R. Kshettry, MD Assistant Professor, Neurological Surgery Cleveland Clinic Lerner College of Medicine of Case Western Reserve University Cleveland Director of Advanced Endoscopic and Microscopic Neurosurgery Laboratory Cleveland Clinic Cleveland, Ohio Maureen Lacy, PhD Professor Department of Psychiatry and Behavioral Neuroscience The University of Chicago Chicago, Illinois Travis R. Ladner, MD Resident Physician Department of Neurosurgery Icahn School of Medicine at Mount Sinai Hospital New York, New York Jose Alberto Landeiro, MD, PhD Chairman Neurosurgery Department Hospital Universitario Antonio Pedro Niteroi, Rio de Janeiro, Brazil

CONTRIBUTORS

Frederick F. Lang, MD Professor and Chair Department of Neurosurgery The University of Texas MD Anderson Cancer Center Houston, Texas Michael J. Lang, MD Assistant Professor Department of Neurosurgery University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania Alexandra Giantini Larsen, BA Department of Neurosurgery Brigham and Women’s Hospital Boston, Massachusetts, Harvard Medical School Cambridge, Massachusetts Dimitri Laurent, MD Resident Physician Lillian S. Wells Department of Neurosurgery University of Florida Gainesville, Florida Michael T. Lawton, MD Professor and Chair Department of Neurosurgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona Bryan S. Lee, MD Neurosurgeon Department of Neurosurgery Barrow Neurological Institute Barrow Brain and Spine Phoenix, Arizona Allan Levi, MD, PhD, FACS Chair, Department of Neurological Surgery Professor of Neurological Surgery, Orthopedics, and Rehabilitation Medicine University of Miami Miller School of Medicine Chief of Neurosurgery Jackson Memorial Hospital Miami, Florida Marc Levivier, MD, PhD, IFAANS Department of Clinical Neurosciences Neurosurgery Service and Gamma Knife Center Centre Hospitalier Universitaire Vaudois (CHUV) University of Lausanne Faculty of Biology and Medicine (FBM) Lausanne, Switzerland Elad I. Levy, MD, MBA Departments of Neurosurgery and Radiology Jacobs School of Medicine and Biomedical Sciences Department of Neurosurgery Gates Vascular Institute at Kaleida Health Canon Stroke and Vascular Research Center University at Buffalo Buffalo, New York

Michael Lim, MD Professor and Chair, Department of Neurosurgery Stanford University School of Medicine Stanford, California Li-­Mei Lin, MD Carondelet Neurological Institute Tucson, Arizona Michelle Lin, MD Department of Neurosurgery Mayo Clinic Jacksonville, Florida Göran Erland Lind, MD, PhD Senior Consultant Neurosurgeon Department of Neurosurgery Karolinska University Hospital Karolinska Institutet Stockholm, Sweden Bengt Linderoth, MD, PhD Professor Emeritus, Neurosurgery Karolinska Institutet Stockholm, Sweden Michael J. Link, MD Professor Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota Giorgio Lo Russo, MD “Claudio Munari” Epilepsy Surgery Center Department of Neuroscience ASST Grande Ospedale Metropolitano Niguarda Milan, Italy Christopher M. Loftus, MD, DHC(Hon), FACS First Vice President - Immediate Past World Federation of Neurosurgical Societies Professor and Former Chairman Temple University Lewis Katz School of Medicine Philadelphia, Pennsylvania Michele Longhi, MD, PhD Radiosurgery and Stereotactic Neurosurgery Section Department of Neuroscience University Hospital Verona, Italy Russell R. Lonser, MD Professor and Chairman Department of Neurological Surgery The Ohio State University Wexner Medical Center Columbus, Ohio Christopher E. Louie, MB, MPH Resident, Department of Surgery University of California, San Diego San Diego, California

xxv

xxvi

CONTRIBUTORS

Daniel C. Lu, MD, PhD Professor and Vice Chair, Research Department of Neurosurgery University of California Los Angeles, California

Justin R. Mascitelli, MD Cerebrovascular Fellow Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona

Christopher Ludtka, BEng J. Crayton Pruitt Family Department of Biomedical Engineering University of Florida Gainesville, Florida

Marcus D. Mazur, MD Assistant Professor of Neurosurgery Department of Neurosurgery University of Utah School of Medicine Salt Lake City, Utah

Larry B. Lundy, MD Associate Professor Otolaryngology and Neurosurgery Otolaryngology–Head and Neck Surgery Mayo Clinic Jacksonville, Florida

Paul C. McCormick, Jr., MD Resident Physician, Psychiatry New York Presbyterian Weill Cornell Medical Center New York, New York

Subu N. Magge, MD Vice Chair Department of Neurosurgery Lahey Hospital and Medical Center Burlington, Massachusetts Assistant Professor, Neurosurgery Tufts University Boston, Massachusetts Martijn J. A. Malessy, MD, PhD Professor of Nerve Surgery Department of Neurosurgery Leiden University Medical Center Leiden, The Netherlands Allen H. Maniker, MD Chief Department of Neurosurgery Beth Israel Medical Center New York, New York Geoffrey T. Manley, MD, PhD Department of Neurological Surgery Brain and Spinal Injury Center University of California San Francisco San Francisco, California Peiman Maralani, MD Affiliate Scientist Sunnybrook Health Sciences Centre Toronto, Ontario, Canada Lina Marenco-­Hillembrand, MD Department of Neurosurgery Mayo Clinic Jacksonville, Florida Meleine Martinez-­Sosa, MD Fellow, Pediatric Neurosurgery Institute for Brain Protection Sciences Johns Hopkins All Children’s Hospital St. Petersburg, Florida

Paul C. McCormick, MD, MPH Herbert and Linda Gallen Professor of Neurological Surgery Department of Neurosurgery Columbia University College of Physicians and Surgeons New York, New York José Hinojosa Mena-Bernal, MD Chief, Department of Neurosurgery Hospital Sant Joan de Deu (Barcelona) Barcelona, Spain Arnold H. Menezes, MD Professor and Vice Chairman Department of Neurosurgery University of Iowa Hospitals and Clinics Iowa City, Iowa Fredric B. Meyer, MD Uihlein Professor and Enterprise Chair Dean of Education Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota Erik H. Middlebrooks, MD Associate Professor, Neuroradiology Department of Radiology Mayo Clinic Jacksonville, Florida Rajiv Midha, MD, MSc, FRCSC Professor of Neurosurgery and Head Department of Clinical Neurosciences University of Calgary Calgary, Alberta, Canada Anthony Mikula, MD Resident, Department of Neurological Surgery Mayo Clinic Rochester, Minnesota

CONTRIBUTORS

David Miller, MD Departments of Neurosurgery and Radiology Mayo Clinic Jacksonville, Florida

Yagmur Muftuoglu, PhD Department of Neurosurgery Stanford University School of Medicine Stanford, California

Jonathan P. Miller, MD Professor, Neurosurgery Department of Neurosurgery Case Western Reserve University Cleveland, Ohio

Sten Myrehaug, MD Assistant Professor of Radiation Oncology Sunnybrook Health Sciences Centre Toronto, Ontario, Canada

Bilal Mirza, MD, PHD Department of Neurosurgery Royal Hallamshire Hospital Sheffield, United Kingdom Zaman Mirzadeh, MD, PhD Assistant Professor, Neurosurgery Barrow Neurological Institute Phoenix, Arizona J. Mocco, MD, MS Professor and System Vice Chair Department of Neurosurgery Icahn School of Medicine at Mount Sinai Hospital New York, New York Camilo A. Molina, MD Assistant Professor of Neurosurgery and Orthopedic Surgery Deputy Director of Spine Innovation Center for Innovation in Neuroscience and Technology Washington University School of Medicine St. Louis, Missouri Alaa S. Montaser, MD Department of Neurosurgery The Ohio State University Wexner Medical Center Columbus, Ohio Jacques J. Morcos, MD, FRCS(Eng), FRCS(Ed), FAANS Professor and Co-­Chairman Department of Neurological Surgery Professor of Clinical Neurosurgery and Otolaryngology Director, Cerebrovascular Surgery Director, Skull Base Surgery University of Miami Division Chief, Cranial Neurosurgery Jackson Memorial Hospital Miami, Florida Chad J. Morgan, MD Neurosurgeon Springfield Neurological and Spine Institute Springfield, Missouri Abteen Mostofi, MA, MB, BChir, PhD, MRCS Clinical Lecturer in Neurosurgery Atkinson Morley Neurosciences Unit St George’s, University of London London, England, United Kingdom

xxvii

Arya Nabavi, MD, PhD, MaHM, IFAANS Professor and Director, Neurosurgery KRH Hanover Nordstadt Hannover, Germany Michael J. Nanaszko, MD Neurosurgery Barrow Neurological Institute Phoenix, Arizona Pranav Nanda, MD, MPhil Resident Physician, Department of Neurosurgery Massachusetts General Hospital Boston, Massachusetts Varun Naragum, MD Assistant Professor of Radiology University of Massachusetts Medical School Worcester, Massachusetts Rani Nasser, MD Assistant Professor of Neurosurgery University of Cincinnati Medical Center Cincinnati, Ohio Edgar Nathal, MD, DMSc Head, Department of Neurosurgery National Institute of Neurology and Neurosurgery “Manuel Velasco Suárez” Professor of Vascular Neurosurgery Universidad Nacional Autónoma de México Professor of Vascular Neurosurgery National Institute of Neurology and Neurosurgery Chief of Service, Neurosurgery National Institute of Medical and Nutricional Sciences “Salvador Subirán” Mexico City, Mexico Timothy K. Nguyen, MD Radiation Oncologist Department of Radiation Oncology London Health Sciences Centre London, Ontario, Canada Marco Conti Nibali, MD Oncology and Hemato-­Oncology Neuro-­Oncological Surgery Università degli Studi di Milano Milano, Italy

xxviii

CONTRIBUTORS

Antonio Nicolato, MD Radiosurgery and Stereotactic Neurosurgery Section Department of Neuroscience University Hospital Verona, Italy Anitha Nimmagadda, MD Division of Occupational and Environmental Medicine University of Chicago Chicago, Illinois Richard B. North, MD Professor (ret.) Departments of Neurosurgery, Anesthesiology and Critical Care Medicine Johns Hopkins University School of Medicine President Neuromodulation Foundation, Inc. Baltimore, Maryland President Institute of Neuromodulation Chicago, Illinois Eric Nottmeier, MD Professor of Neurosurgery Department of Neurosurgery Mayo Clinic Jacksonville, Florida Mohammad Hassan A. Noureldine, MD, MSc Postdoctoral Research Fellow, Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Postdoctoral Research Fellow Institute for Brain Protection Sciences Johns Hopkins All Children’s Hospital St. Petersburg, Florida W. Jerry Oakes, MD Hendley Professor of Pediatric Neurosurgery University of Alabama Birmingham School of Medicine Children’s of Alabama Birmingham, Alabama Christopher S. Ogilvy, MD Professor of Neurosurgery Department of Neurosurgery Harvard Medical School Director, BIDMC Brain Aneurysm Institute Director, Endovascular and Operative Neurovascular Surgery Beth Israel Deaconess Medical Center Boston, Massachusetts Jeffrey G. Ojemann, MD Professor of Neurological Surgery University of Washington Seattle, Washington Steven Ojemann, MD Associate Professor Department of Neurosurgery University of Colorado School of Medicine Aurora, Colorado

David O. Okonkwo, MD, PhD Professor, Neurological Surgery University of Pittsburgh Pittsburgh, Pennsylvania Alessandro Olivi, MD Institute of Neurosurgery Fondazione Policlinico A. Gemelli IRCSS Catholic University of Rome Rome, Italy Osarenoma U. Olomu, BA, MD Assistant Professor Otolaryngology–Head and Neck Surgery Mayo Clinic Jacksonville, Florida Alon Orlev, MD Department of Neurosurgery Rabin Medical Center Israel Brooks Osburn, MD Resident, Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine Tampa, Florida Nakao Ota, MD, PhD Consultant Neurosurgeon Department of Neurosurgery Sapporo Teishinkai Hospital Sapporo, Japan Bradley A. Otto, MD Departments of Otolaryngology Head and Neck Surgery and Neurosurgery The Ohio State University Wexner Medical Center Columbus, Ohio Dachling Pang, MD Consultant Paediatric Neurosurgeon Great Ormond Street Hospital for Children NHS Trust London, United Kingdom Professor of Pediatric Neurosurgery University of California, Davis Sacramento, California Ian Parney, MD, PhD Professor and Vice-­Chair (Research), Neurological Surgery Mayo Clinic Rochester, Minnesota José María Pascual, MD, PhD Consultant Neurosurgeon Department of Neurosurgery La Princesa University Hospital Madrid, Spain

CONTRIBUTORS

Aman B. Patel, MD Director of Cerebrovascular and Endovascular Neurosurgery Co-Director of the Neuroendovascular Program Department of Neurosurgery Massachusetts General Hospital Boston, Massachusetts Anoop Patel, MD Assistant Professor, Neurosurgery University of Washington Seattle, Washington Smruti K. Patel, MD Resident Physician Department of Neurosurgery University of Cincinnati College of Medicine Cincinnati, Ohio Rana Patir, MBBS, MS, MCh Chairman and Head of Department Department of Neurosurgery Fortis Memorial Research Institute New Delhi, India Richard D. Penn, MD Adjunct Professor, Bioengineering University of Illinois–Chicago Chicago, Illinois Zachary Pennington, BS Medical Student Department of Neurosurgery Johns Hopkins Hospital Baltimore, Maryland Giuseppe Maria Della Pepa, MD Institute of Neurosurgery Fondazione Policlinico A. Gemelli IRCSS Catholic University of Rome Rome, Italy Alexander Perdomo-­Pantoja, MD Department of Neurosurgery The Johns Hopkins Hospital Baltimore, Maryland Erlick A. C. Pereira, MA, BMBCh, DM, FRCS(SN) Senior Lecturer and Honorary Consultant in Neurosurgeon Department of Neurosurgery St. George’s University Hospitals London, England, United Kingdom Mick J. Perez-­Cruet, MD, MS Vice Chairman and Professor Director Minimally Invasive and Spine Program Department of Neurosurgery Oakland University William Beaumont Medical School Royal Oak, Michigan, Michigan Head and Spine Institute Southfield, Michigan

Maria Peris-­Celda, MD, PhD Associate Professor Department of Neurosurgery Mayo Clinic Rochester, Minnesota A. Perry, MD Resident Department of Neurosurgery Mayo Clinic Rochester, Minnesota Avital Perry, MD Department of Neurosurgery Sheba Medical Center Tel-­Aviv University Ramat-­Gan, Israel Federico Pessina, MD Neurosurgery Unit Humanitas Research Hospital Rozzano, Italy Jennifer L. Peterson, MD Associate Professor Radiation Oncology Mayo Clinic Jacksonville, Florida Martin H. Pham, MD Department of Neurological Surgery University of Southern California San Diego School of Medicine San Diego, California Mark Pichelmann, MD Assistant Professor of Neurologic Surgery Spine and Neurosurgery Mayo Clinic Health System Eau Claire, Wisconsin Carlos D. Pinheiro-­Neto, MD, PhD Associate Professor Department of Otolaryngology Mayo Clinic Rochester, Minnesota Phillip Pirgousis, MD Associate Professor Otolaryngology – Head and Neck Surgery Reconstructive Surgery Neurological Surgery Mayo Clinic Jacksonville, Florida Lawrence H. Pitts, MD Department of Neurological Surgery Brain and Spinal Injury Center University of California San Francisco San Francisco, California

xxix

xxx

CONTRIBUTORS

Rick J. Placide, MD Professor Department of Orthopaedic Surgery Medical College of Virginia Virginia Commonwealth University Richmond, Virginia

Pablo A. Quevedo-Valdes, MD, PhD Department of Neurosurgery Brigham and Women’s Hospital Boston, Massachusetts Harvard Medical School Cambridge, Massachusetts

Puneet Plaha, MBBS, PhD, FRCS(SN) Consultant Neurosurgeon Oxford University Hospitals Oxford, United Kingdom

Alfredo Quiñones-­Hinojosa, MD William J. and Charles H. Mayo Professor Chair, Neurologic Surgery Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Adam J. Polifka, MD Assistant Professor Lillian S. Wells Department of Neurosurgery University of Florida Gainesville, Florida Willem Pondaag, MD, PhD Neurosurgeon Department of Neurosurgery Leiden University Medical Center Leiden, the Netherlands Kalmon D. Post, MD Professor of Neurosurgery Department of Neurosurgery Icahn School of Medicine at Mount Sinai New York, New York Matthew B. Potts, MD Department of Neurological Surgery Northwestern University Feinberg School of Medicine Chicago, Illinois Lars Poulsgaard, MD Neurosurgeon, Director of Skull Base Surgery Department of Neurosurgery Rigshospitalet, Copenhagen, Denmark Alessandro Prete, MD Clinical Research Fellow Institute of Metabolism and Systems Research University of Birmingham Birmingham, United Kingdom Daniel M. Prevedello, MD Professor Department of Neurosurgery The Ohio State University Wexner Medical Center Columbus, Ohio Ruth Prieto, MD, PhD Consultant Neurosurgeon Department of Neurosurgery Puerta de Hierro University Hospital Madrid, Spain Ross C. Puffer, MD Staff Neurosurgeon Walter Reed National Military Medical Center Bethesda, Maryland

Leonidas M. Quintana, Sr., Professor Department of Neurosurgery Faculty of Medicine Valparaíso University Valparaiso, Chile Gazanfar Rahmathulla, MBBS (MD), FACS, IFAANS, MBA Medical Director, Neurosurgery Trauma Department of Neurosurgery University of Florida College of Medicine Clinical Assistant Professor Department of Neurosurgery University of Florida Jacksonville, Florida Rudy J. Rahme, MD Resident Physician Department of Neurological Surgery Northwestern University Feinberg School of Medicine and McGaw Medical Center Chicago, Illinois Seba Ramhmdani, MD Department of Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland Juan F. Ramon, MD, MS Neurologic Surgery Hospital Universitario Fundación Santa Fe de Bogotá, Colombia Andres Ramos-Fresnedo, MD Postdoctoral Fellow Department of Neurosurgery Mayo Clinic Jacksonville, Florida Rodrigo Ramos-­Zuniga Sr., MD, PhD Professor of Neurosciences Institute of Translational Neurosciences Department of Neurosciences University of Guadalajara Guadalajara, Jalisco, Mexico

CONTRIBUTORS

Nathan J. Ranalli, MD Assistant Professor Departments of Neurosurgery and Pediatrics University of Florida Health Science Center Jacksonville Jacksonville, Florida

Angela M. Richardson, MD, PhD Cerebrovascular and Skull Base Fellow Department of Neurosurgery University of Wisconsin–Madison Madison, Wisconsin

Manish Ranjan, MD Neurosurgery Fellow Rockefeller Neuroscience Institute West Virginia University Morgantown, West Virginia

Daniele Rigamonti, MD Professor, Neurosurgery Johns Hopkins School of Medicine Baltimore, Maryland CEO Johns Hopkins Aramco Healthcare Dhahran, Eastern Province Saudi Arabia

Aaron Rapp, MD Resident Department of Neurosurgery Oakland University William Beaumont School of Medicine Royal Oak, Michigan United States Vijay M. Ravindra, MD, MSPH Adult and Pediatric Neurosurgery Department of Neurosurgery Naval Medical Center San Diego San Diego, California Pablo F. Recinos, MD Associate Professor Department of Neurological Surgery Cleveland Clinic Lerner College of Medicine of Case Western Reserve University Cleveland Section Head,­Skull Base Surgery Cleveland Clinic Cleveland, Ohio Karim ReFaey, MD Postdoctoral Fellow, Neurosurgery Mayo Clinic Hospital Jacksonville, Florida Jean Régis, MD Stereotactic and Functional Neurosurgery Service and Gamma Knife Unit CHU Timone Marseille, France Katherine Relyea, MS Section of Pediatric Neurosurgery Riley Hospital for Children Department of Neurosurgery Indiana University School of Medicine Goodman Campbell Brain and Spine Indianapolis, Indiana Daniel K. Resnick, MD, MS Professor and Vice Chairman Department of Neurosurgery University of Wisconsin School of Medicine and Public Health Madison, Wisconsin

xxxi

Marco Riva, MD Oncology and Hemato-­Oncology Neuro-­Oncological Surgery Università degli Studi di Milano Milano, Italy Matteo Riva, MD Specialist in Neurosurgery KU Leuven Cancer Institute Leuven, Belgium Michele Rizzi, MD “C. Munari” Epilepsy Surgery Center Department of Neuroscience ASST Grande Ospedale Metropolitano Niguarda Milan, Italy Shimon Rochkind, MD, PhD Director, Division of Peripheral Nerve Reconstruction Head, Translational Medicine and Clinical Research Center for Nerve Reconstruction Tel Aviv Sourasky Medical Center Tel Aviv, Israel John D. Rolston, MD, PhD Assistant Professor Department of Neurosurgery University of Utah Salt Lake City, Utah William S. Rosenberg, MD Director Center for the Relief of Pain Research Medical Center Kansas City, Missouri Robert H. Rosenwasser, MD Professor and Chair, Department of Neurological Surgery Thomas Jefferson University and Hospitals Philadelphia, Pennsylvania Florian Roser, MD Professor and Chairman Neurological Institute Cleveland Clinic Abu Dhabi, Abu Dhabi United Arab Emirates

xxxii

CONTRIBUTORS

Marco Rossi, MD Oncology and Hemato-­Oncology Neuro-­Oncological Surgery Università degli Studi di Milano Milano, Italy Nathan C. Rowland, MD, PhD Neurosurgeon Medical University of South Carolina Charleston, South Carolina James T. Rutka, MD, PhD Director of The Arthur and Sonia Labatt Brain Tumour Research Centre Division of Neurosurgery The Hospital for Sick Children RS McLaughlin Professor and Chair Department of Surgery University of Toronto Toronto, Ontario, Canada George N. Rymarczuk, MD Fellow Spinal Neurosurgery Thomas Jefferson University Philadelphia, Pennsylvania Arjun Sahgal, MD Professor of Radiation Oncology and Surgery Deputy Chief, Department of Radiation Oncology Sunnybrook Health Sciences Centre Toronto, Ontario, Canada Francesco Sala, MD Professor of Neurosurgery Neurosciences, Biomedicine, and Movement Sciences Neurosurgery Verona, Italy Federico Salle, MD, MSc Neurosurgeon, University of the Republic Neurosurgery Department Hospital Maciel President of the Uruguayan Society of Neurosurgery Montevideo, Uruguay Sepehr Sani, MD Associate Professor, Neurosurgery Rush University Medical Center Chicago, Illinois LCDR. Gabriel F. Santiago, MD, MC USN Division Chief, Neuroplastic and Reconstructive Surgery Department of Otolaryngology – Head and Neck Surgery Naval Medical Center Portsmouth Assistant Professor, Surgery F. Edward Herbert School of Medicine Uniformed Services University of Health Sciences Bethesda, Maryland

Roberto Salvatori, MD Professor, Medicine and Neurosurgery Medical Director Pituitary Center Johns Hopkins University Baltimore, Maryland Jaime L. Martinez Santos, MD Neurosurgery Resident Department of Neurosurgery Medical University of South Carolina Charleston, South Carolina Christina E. Sarris, MD Resident Physician, Neurosurgery Barrow Neurological Institute Phoenix, Arizona Luis E. Savastano, MD, PhD Resident Neurosurgeon, Neurosurgery University of Michigan Ann Arbor, Michigan Amar Saxena, MBBS, MS, MCh(Neurosurgery), FRCS(Eng), FRCS(Surg Neurol) Chairman Higher Surgical Committee in Neurosurgery for West Midlands University Hospitals Coventry and Warwickshire Coventry, United Kingdom Gabriele Schackert, Prof, MD Klinik und Poliklinik für Neurochirurgie Universitätsklinikum Carl Gustav Carus Dresden an der Technischen Universität Dresden Fetscherstraße, Dresden, Germany Meic H. Schmidt, MD, MBA Professor and Chair, Department of Neurosurgery University of New Mexico Albuquerque, New Mexico Henry W. S. Schroeder, Prof, MD Universitätsmedizin Greifswald Klinik für Neurochirurgie Greifswald, Germany Joseph Schwab, MD, MS Chief, Orthopaedic Spine Surgery Director, Spine Oncology Co-Director, Stephan L. Harris Chordoma Center Associate Professor of Orthopedic Surgery Harvard Medical School Massachusetts General Hospital Boston, Massachusetts

CONTRIBUTORS

Theodore H. Schwartz, MD David and Ursel Barnes Professor in Minimally Invasive Surgery Professor of Neurosurgery, Neurology, and Otolaryngology Director, Center for Epilepsy and Pituitary Surgery Co-­Director, Surgical Neuro-­oncology Department of Neurosurgery New York Presbyterian Hospital New York, New York Tommaso Sciortino, MD Oncology and Hemato-­Oncology Neuro-­Oncological Surgery Università degli Studi di Milano Milano, Italy Daniel M. Sciubba, MD Professor Departments of Neurosurgery, Oncology, Orthopaedic Surgery, and Radiation Oncology Director Spine Tumor and Spine Deformity Research Johns Hopkins University School of Medicine Baltimore, Maryland Kyle W. Scott, BS College of Medicine University of Florida Gainesville, Florida Jonathan P. Scoville, MD Resident Department of Neurosurgery University of Utah Salt Lake City, Utah Alfred P. See, MD Department of Neurosurgery Barrow Neurological Institute Phoenix, Arizona Raymond F. Sekula, Jr., MD Professor Director, Cranial Nerve Disorders Program Director, Residency Training Program Vice Chair, UPMC Central Pa University of Pittsburgh Pittsburgh, Pennsylvania Amjad Shad, MBBS, FRCS(Ed), FRCS(SN)MR Department of Neurosurgery Radcliffe Infirmary Oxford, United Kingdom Jugal Shah, MD Department of Neurological Surgery New York University School of Medicine New York, New York Ali Shaibani, MD Departments of Radiology and Neurosurgery Northwestern University Feinberg School of Medicine Department of Medical Imaging Children’s Memorial Hospital Chicago, Illinois

xxxiii

Ammar Shaikhouni, MD, PhD Assistant Professor Department of Neurological Surgery The Ohio State University Wexner Medical Center Columbus, Ohio Manish S. Sharma, MBBS Chair Department of Neurosurgery Mankato Hospital Mankato, Minnesota Associate Professor Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota Jason Sheehan, MD Professor, Neurosurgery University of Virginia Charlottesville, Virginia John Paul Sheehy, MD Assistant Professor Department of Neurosurgery University of Cincinnati Cincinnati, Ohio Sameer Sheth, MD, PhD Associate Professor Neurosurgery, Psychiatry and Behavioral Sciences, Neuroscience McNair Scholar Baylor College of Medicine Adjunct Associate Professor Department of Electrical and Computer Engineering Rice University Houston, Texas Changbin Shi, MD Department of Neurosurgery Harbin Medical University Harbin, China Nir Shimony, MD Geisinger Medical Center Neurosurgery Neuroscience Institute Danville, Pennsylvania, Geisinger Commonwealth School of Medicine Neurosurgery Geisinger Commonwealth School of Medicine Scranton, Pennsylvania, Johns Hopkins University School of Medicine Neurosurgery Institute for Brain Protection Sciences St. Petersburg, Florida Alexander Y. Shin, MD Division of Hand Surgery Department of Orthopedics Professor of Orthopedics and Neurosurgery Mayo Clinic Rochester, Minnesota

xxxiv

CONTRIBUTORS

Adnan H. Siddiqui, MD, PhD Departments of Neurosurgery and Radiology Jacobs School of Medicine and Biomedical Science Department of Neurosurgery Gates Vascular Institute at Kaleida Health Canon Stroke and Vascular Research Center University at Buffalo Buffalo, New York Roberto Leal Silveira, MD, PhD Skull Base Neurosurgery and Neurooncology Madre Teresa Institue Belo Horizonte, Brazil Nathan Simmons, MD Section of Neurosurgery Dartmouth-­Hitchcock Medical Center Lebanon, New Hampshire Marc Sindou, MD, DSc Professor Emeritus of Neurosurgery Neurosurgery University of Lyon Lyon, France Marco Sinisi, MD Neurosurgery The Wellington Hospital St. Johns Wood, London United Kingdom Edward R. Smith, MD Department of Neurosurgery Boston Children’s Hospital Harvard Medical School Boston, Massachusetts Joseph R. Smith, MD† Professor Emeritus, Department of Neurosurgery Augusta University Augusta, Georgia Kyle A. Smith, MD Assistant Professor, Department of Neurosurgery Semmes-­Murphey Clinic University of Tennessee Health Sciences Center Memphis, Tennessee Matthew D. Smyth, MD, FACS, FAAP Appoline Blair Professor of Pediatric Neurosurgery Professor of Neurological Surgery and Pediatrics Co-­Director, Washington University Pediatric Epilepsy Center at St. Louis Children’s Hospital Director, St. Louis Children’s Hospital Pediatric Neurosurgery Fellowship St. Louis, Missouri Hany Soliman, MD Affiliate Scientist Sunnybrook Research Institute Toronto, Ontario, Canada † Deceased

Mark M. Souweidane, MD Vice Chairman, Neurological Surgery Director of Pediatric Neurological Surgery Department of Neurosurgery New York Presbyterian Hospital New York, New York Edgardo Spagnuolo, MD Assistant Professor, Chairman Neurosurgical Department Maciel Hospital Honorary President Latin American Federation of Neurosurgical Societies Member of the WANS World Academy of Neurosurgeons Ex-­Vice President WFNS Montevideo, Uruguay Robert F. Spetzler, MD Director and J.N. Harber Chair of Neurological Surgery Barrow Neurological Institute St. Joseph’s Hospital and Medical Center Phoenix, Arizona Professor of Neurosurgery Department of Surgery University of Arizona College of Medicine Tucson, Arizona Robert J. Spinner, MD Chair, Department of Neurologic Surgery Neurosurgery Professor Departments of Anatomy, Neurologic Surgery, and Orthopedic Surgery Mayo Clinic Rochester, Minnesota Christopher J. Stapleton, MD Neurosurgeon Cerebrovascular and Endovascular Neurosurgery Department of Neurosurgery Massachusetts General Hospital Boston, Massachusetts Rachel Stein, MD Neurosurgery Resident Mayo Clinic Jacksonville, Florida Michael P. Steinmetz, MD Professor and Chairman Department of Neurosurgery Cleveland Clinic Lerner College of Medicine Cleveland, Ohio Scellig Stone, MD, PhD Department of Neurosurgery Boston Children’s Hospital Harvard Medical School Boston, Massachusetts

CONTRIBUTORS

xxxv

Geoffrey P. Stricsek, MD Resident Physician Neurological Surgery Thomas Jefferson University Philadelphia, Pennsylvania

Rabih G. Tawk, MD Associate Professor Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Paola Suarez-Meade, MD Post-Doctoral fellow Department of Neurosurgery Mayo Clinic Jacksonville, Florida

John M. Tew, Jr., MD Professor of Neurosurgery Executive Director, Community Affairs Vice President of Community Affairs University of Cincinnati Gardner Neuroscience Institute Cincinnati, Ohio

Michael E. Sughrue, MD Centre for Minimally Invasive Neurosurgery Prince of Wales Private Hospital Randwick, NSW, Australia Ian Suk, MD Department of Art as Applied to Medicine Department of Neurosurgery Johns Hopkins University School of Medicine Baltimore, Maryland

Nicholas Theodore, MD Professor of Neurosurgery, Orthopaedic Surgery, and Biomedical Engineering Neurosurgery Johns Hopkins University School of Medicine Director, Neurosurgical Spine Center Co-­Director, Carnegie Center for Surgical Innovation Johns Hopkins University Baltimore, Maryland

Daniel Q. Sun, MD Assistant Professor Department of Otolaryngology Johns Hopkins University School of Medicine Baltimore, Maryland

B. Gregory Thompson Jr., MD Professor and Program Director Department of Neurosurgery University of Michigan Ann Arbor, Michigan

Samir Sur, MD Department of Neurosurgery MedStar Washington Hospital Center Assistant Professor of Neurosurgery Georgetown University School of Medicine Washington, District of Columbia

John A. Thompson, PhD Departments of Neurosurgery and Neurology University of Colorado Anschutz Medical Campus Aurora, Colorado

Ulrich Sure, MD Neurosurgeon Department of Neurosurgery Philipps University Marburg, Germany Ahmad Sweid, MD Postdoctoral Research Fellow, Neurosurgery Thomas Jefferson University Philadelphia, Pennsylvania Ian Tafel, MD Neurosurgery Resident Department of Neurosurgery Brigham and Women’s and Boston Children’s Hospitals Harvard Medical School Boston, Massachusetts Rafael J. Tamargo, MD Department of Neurosurgery Johns Hopkins Hospital Baltimore, Maryland

Fucheng Tian, MD Precision Neuro-Therapeutics Innovation Lab Neurosurgery Simulation and Innovation Lab Mayo Clinic Phoenix, Arizona, Department of Neurosurgery Harbin Medical University Harbin, China Wuttipong Tirakotai, MD, MSc Doctor, Department of Neurosurgery Prasat Neurological Institute Bangkok, Thailand Stavropoula Tjoumakaris, MD Professor, Neurological Surgery Thomas Jefferson University Philadelphia, Pennsylvania Nathan Todnem, MD Department of Neurosurgery Montefiore Medical Center Albert Einstein College of Medicine New York, New York

xxxvi

CONTRIBUTORS

Teiji Tominaga, MD Professor and Chairman Department of Neurosurgery Tohoku University Graduate School of Medicine Sendai, Japan

Jamie J. Van Gompel, MD Associate Professor Departments of Neurosurgery and Otolaryngology Mayo Clinic Rochester, Minnesota

Daniel M. Trifiletti, MD Associate Professor, Radiation Oncology Mayo Clinic Jacksonville, Florida

Viren S. Vasudeva, MD Staff Neurosurgeon Georgia Neurological Surgery and Comprehensive Spine Center St. Mary’s Medical Group Athens, Georgia

Shashwat Tripathi, BSA MD, PhD Candidate 2027’ Feinberg School of Medicine Northwestern University Chicago, Illinois Eric Tseng, MD Affiliate Scientist Assistant Professor, Radiation Oncology Sunnybrook Health Sciences Centre Toronto, Ontario, Canada R. Shane Tubbs, MS, PA-­C, PhD Professor Department of Neurosurgery Tulane University School of Medicine New Orleans, Louisiana Riikka Tulamo, MD, PhD Adjunct Professor, Consultant Vascular Surgeon Department of Vascular Surgery Neurosurgery Research Group University of Helsinki and Helsinki University Hospital Helsinki, Finland Constantin Tuleasca, MD-­PhD Department of Clinical Neurosciences, Neurosurgery Service, and Gamma Knife Center Centre Hospitalier Universitaire Vaudois (CHUV) University of Lausanne, Faculty of Biology and Medicine (FBM) Swiss Federal Institute of Technology (EPFL), LTS-­5 Lausanne, Switzerland Ali H. Turkmani, MD Department of Neurological Surgery Precision Neuro-Therapeutics Innovation Lab Neurosurgery Simulation and Innovation Lab Mayo Clinic Phoenix, Arizona Kunal Vakharia, MD Department of Neurosurgery Jacobs School of Medicine and Biomedical Sciences University at Buffalo Department of Neurosurgery Gates Vascular Institute at Kaleida Health Buffalo, New York

Ana Luisa Velasco, MD, PhD Head of Neurology Head of the Epilepsy Clinic General Hospital Mexico Eduardo Liceaga Mexico City, Mexico Francisco Velasco, MD Unite for Stereotactic and Functional Neurosurgery General Hospital of Mexico Mexico City, Mexico Gregory J. Velat, MD Clinician, Department of Neurological Surgery Florida Hospital Memorial Medical Center Daytona Beach, Florida Vyshak Alva Venur, MD Alvord Brain Tumor Center Seattle Cancer Care Alliance Assistant Professor Division of Medical Oncology University of Washington School of Medicine UW Medicine Assistant Member Clinical Research Division Fred Hutchinson Cancer Research Seattle, Washington Angela Verlicchi, MD Neurology Service Anemos Neuroscience Reggio Emilia, Italy Tito Vivas-­Buitrago, MD Post-­Doctoral Fellow Department of Neurosurgery Mayo Clinic Jacksonville, Florida Alexander L. Vlasak, MD Resident Physician Department of Neurosurgery Mayo Clinic Hospital Jacksonville, Florida

CONTRIBUTORS

Frank D. Vrionis, MD, MPH, PhD Senior Member and Director, Spinal and Skull Base Oncology H. Lee Moffitt Cancer Center Professor of Neurosurgery, Orthopedics, and Oncology Department of Neurosurgery University of South Florida Tampa, Florida John Varmaa Wainwright, MD, MS Neurological Surgery Chief Resident Neurosurgical Spine Surgery Westchester Medical Center New York Medical College Valhalla, New York M. Christopher Wallace, MD Professor of Surgery Chair and Section Chief, Division of Neurosurgery Queen’s University School of Medicine Kingston General Hospital Kingston, Ontario, Canada Muhammad Waqas, MBBS Department of Neurosurgery Jacobs School of Medicine and Biomedical Sciences University at Buffalo Department of Neurosurgery Gates Vascular Institute at Kaleida Health Buffalo, New York Clarence B. Watridge, MD Professor Emeritus Department of Neurosurgery Mayo Clinic Jacksonville, Florida

xxxvii

David M. Wildrick, PhD Surgery Publications Program Manager Department of Neurosurgery The University of Texas MD Anderson Cancer Center Houston, Texas D. Andrew Wilkinson, MD, MS Resident Neurosurgeon Neurosurgery University of Michigan Ann Arbor, Michigan Christopher J. Winfree, MD, FAANS Assistant Professor Department of Neurological Surgery Columbia University College of Physicians & Surgeons New York, New York Timothy Witham, MD Professor of Neurological and Orthopedic Surgery Director, Johns Hopkins Neurosurgery Spinal Fusion Laboratory Director, Johns Hopkins Bayview Medical Center’s Spine Program Co-­Program Director, Johns Hopkins Neurosurgery Residency Program Department of Neurosurgery Johns Hopkins University Baltimore, Maryland Amir Wolff, DMD Department of Maxillofacial Surgery Rambam Health Care Center Haifa, Israel

Nirit Weiss, MD Assistant Professor of Neurosurgery Neurosurgery Icahn School of Medicine at Mount Sinai New York, New York

Jean-­Paul Wolinsky, MD Professor of Neurosurgery and Orthopedic Surgery Vice Chairman of Neurosurgery Director of Spinal Oncology Northwestern University Feinberg School of Medicine Chicago, Illinois

Matthew E. Welz, MD Department of Neurological Surgery Precision Neuro-Therapeutics Innovation Lab Neurosurgery Simulation and Innovation Lab Mayo Clinic Phoenix, Arizona

Kyle C. Wu, MD Neurosurgery Resident Department of Neurosurgery Brigham and Women’s and Boston Children’s Hospitals Harvard Medical School Boston, Massachusetts

Erick M. Westbroek, MD Senior Resident Department of Neurosurgery Johns Hopkins University Baltimore, Maryland

Shaun Xavier, MD Department of Orthopaedic Surgery New York University New York, New York

Robert E. Wharen, MD Professor Emeritus Department of Neurosurgery Mayo Clinic Jacksonville, Florida

Kurt Yaeger, BS, MD Resident Physician Department of Neurosurgery Icahn School of Medicine at Mount Sinai Hospital New York, New York

xxxviii

CONTRIBUTORS

Claudio Yampolsky, MD Chairman Neurosurgery Hospital Italiano Buenos Aires, Argentina

Eric L. Zager, MD Professor, Neurosurgery Perelman School of Medicine at the University of Pennsylvania Philadelphia, Pennsylvania

Reza Yassari, MD MS Professor of Neurosurgery Division Chief, Neurosurgery Spine Program Leo Davidoff Department of Neurosurgery Montefiore Medical Center Albert Einstein College of Medicine Bronx, New York

Bruno Zanotti, MD Neurosurgery Unit Neuroscience Department Carlo Poma Hospital Mantova, Italy

Yagiz Ugur Yolcu, MD Department of Neurologic Surgery Mayo Clinic Rochester, Minnesota Alexander K. Yu, MD Neurological Surgery Allegheny General Hospital Pittsburgh, Pennsylvania

Mehmet Zileli, MD Professor Department of Neurosurgery Ege University Izmir, Turkey Emanuele Zivelonghi, PhD Department of Medical Physics University Hospital Verona, Italy

VIDEO CONTENTS

Chapter 7

Chapter 17

Video 1: Right-sided Awake Craniotomy With ECoG and Brain Mapping for Glioma Resection Courtesy of Karim ReFaey and Alfredo Quiñones-­Hinojosa

Video: Endoscopic Endonasal Resection of Recurrent Craniopharyngioma Courtesy of Thomas Beaumont, Kyle VanKoevering, Ricardo Carrau, and Daniel Prevedello

Current Surgical Management of High-­Grade Gliomas; New and Recurrent

Video 2: Right-sided Redo Awake Craniotomy With ECoG and Brain Mapping for Recurrent Glioma Resection Courtesy of Karim ReFaey and Alfredo Quiñones-­Hinojosa

Chapter 9

Management of Primary Central Nervous System Lymphomas Video: Right-sided Stereotactic Needle Biopsy for Primary-CNS Lymphoma Courtesy of Karim ReFaey, Mark Jentoft, Erik H. Middlebrooks, and Alfredo Quiñones-­Hinojosa

Chapter 12

Endoscopic Endonasal Approach to Sellar, Parasellar, and Suprasellar Surgery Video 1: Endoscopic Trans-­sphenoidal Approach, Sphenoidotomy, and Septectomy Courtesy of Angela M. Bohnen, Angela M. Donaldson, Osarenoma U. Olomu, and Alfredo Quiñones-­Hinojosa

The Endoscopic Endonasal Approach for Craniopharyngiomas

Chapter 18

Minimally Invasive Surgeries for Deep-­Seated Brain Lesions Video: Minimally Invasive Exoscope-Assisted Trans-­sulcal Approach Courtesy of Kaisorn L. Chaichana, Sanjeet Grewal, and Alfredo Quiñones-­Hinojosa

Chapter 19

Surgical Approaches to Lateral and Third Ventricular Tumors Video: Endoscopic Transforaminal-­Transchoroidal Approach Courtesy of Oluwaseun O. Akinduro, Kaisorn L. Chaichana, Rabih G. Tawk, and Ronald Reimer

Chapter 20

Transcallosal and Endoscopic Approach to Intraventricular Brain Tumors

Video 2: Nasoseptal Flap Courtesy of Angela M. Bohnen, Angela M. Donaldson, Osarenoma U. Olomu, and Alfredo Quiñones-­Hinojosa

Video: Intraventricular Neuroendoscopy Courtesy of Gunjan Goel, Jeffrey P. Greenfield, Mark M. Souweidane, and Theodore H. Schwartz

Chapter 13

Chapter 22

Endoscopic Endonasal Approach to Lateral Cavernous Sinus Video: Endoscopic Endonasal Approach for Left-­Sided Cavernous Sinus Tumor Courtesy of Douglas A. Hardesty, Alaa S. Montaser, Bradley A. Otto, Ricardo L. Carrau, and Daniel M. Prevedello

Chapter 16

Transcranial Surgery for Pituitary Macroadenomas Video: Intraoperative Left Middle Cerebral Artery Injury in Case 3 and the Proper Management Courtesy of Hamid Borghei-­Razavi, Varun R. Kshettry, Florian Roser, Alfredo Quiñones-­Hinojosa, and Pablo F. Recinos

Management of Tumors of the Fourth Ventricle Video: Exophytic Brainstem Fourth Ventricle Pilomyxoid Astrocytoma Courtesy of Rajiv R. Iyer and Alan R. Cohen

Chapter 24

Surgical Approach to Falcine Meningiomas Video: Left Supratentorial Craniotomy for Resection of Falcine Meningioma Courtesy of Paola Suarez-­Meade, Karim ReFaey, and Alfredo Quiñones-­Hinojosa

xlvii

xlviii

VIDEO CONTENTS

Chapter 26

Chapter 45

Supraorbital Approach Variants for Intracranial Tumors

Surgical Treatment of Moyamoya Disease in Adults

Video: Right Supraorbital Craniotomy With Eyelid Approach Courtesy of Karim ReFaey, Kelly Gassie, Olivia A. Ho, Antonio Jorge Forte, and Alfredo Quiñones-­Hinojosa

Video 1: Left Direct Bypass for Adult Moyamoya Disease Courtesy of Leonidas Quintana, Miki Fujimura, and Teiji Tominaga

Chapter 27

Video 2: Left Wide Encephaloduroarteriosynangiosis (EDAS) for Adult Moyamoya Disease Courtesy of Leonidas Quintana, Miki Fujimura, and Teiji Tominaga

Surgical Management of Sphenoid Wing Meningiomas Video 1: Giant Sphenoid Wing Meningioma Courtesy of Gerardo Guinto Video 2: Small Sphenoid Wing Meningioma Courtesy of Gerardo Guinto

Chapter 34

The OZ Chapter: Original OZ, Modified for Parietal, Modified for Frontal Cosmetic Results of the OZ Video: Orbitozygomatic Approach for Tumor Resection Courtesy of Karim ReFaey, Shashwat Tripathi, Andres Ramos-Fresnedo, Jaime L. Martinez Santos, Paola Meade-Suarez and Alfredo Quiñones-­Hinojosa

Chapter 38

Bypass Techniques Video: Dual STA-­MCA Bypass Courtesy of Oluwaseun O. Akinduro, Neil Haranhalli, Ricardo A. Domingo, Hadi Abou-­El-­Hassan, and Rabih G. Tawk

Chapter 39

Previously Coiled Aneurysms Video: Endoscopic-Assisted Clipping of Previously Coiled Pcomm Aneurysm Courtesy of Lina Marenco-­Hillembrand, Nathan Todnem, Neil Haranhalli, David Miller, and Rabih G. Tawk

Chapter 42

Management of Unruptured Intracranial Aneurysms Video 1: Acomm Aneurysm Clipping Courtesy of Omar A. Choudhri Video 2: PICA Aneurysm Clipping Courtesy of Omar A. Choudhri

Chapter 46

Surgical Treatment of Paraclinoid Aneurysms Video: Mini-­Pterional Approach for Ruptured Dorsal Proximal (Ophthalmic) Aneurysm Courtesy of Edgar Nathal, Oluwaseun O. Akinduro, Gabriel Castillo, and Rabih G. Tawk

Chapter 50

Surgical Management of Terminal Basilar and Posterior Cerebral Artery Aneurysms Video 1: Microsurgical Clipping of MCA and Basilar Tip Aneurysms Courtesy of Vijay Agarwal and Daniel L. Barrow Video 2: Subtemporal Approach to Basilar Tip Aneurysm Courtesy of Vijay Agarwal and Daniel L. Barrow

Chapter 57

Surgical Management of Cerebral Arteriovenous Malformations Video 1: Surgical Resection of Left Frontal AVM Courtesy of Edgardo Spagnuolo, Alejandra Jaume, and Federico Salle Video 2: Surgical Resection of Left Fronto-­Parietal AVM Courtesy of Edgardo Spagnuolo, Alejandra Jaume, and Federico Salle Video 3: Surgical Resection of Left Temporal Lobe AVM Courtesy of Edgardo Spagnuolo, Alejandra Jaume, and Federico Salle

Chapter 58

Surgical Management of Cerebral Arteriovenous Malformations Video 1: Microcatheterization of Unruptured Pcomm Artery Aneurysm Courtesy of D. Andrew Wilkinson, Luis E. Savastano, and B. Gregory Thompson, Jr.

VIDEO CONTENTS

xlix

Video 2: Partial Coil Deployment Within the Aneurysm Courtesy of D. Andrew Wilkinson, Luis E. Savastano, and B. Gregory Thompson, Jr.

Chapter 81

Video 3: Stent Deployment Across Aneurysm Neck, Jailing the Coiling Microcatheter Courtesy of D. Andrew Wilkinson, Luis E. Savastano, and B. Gregory Thompson, Jr.

Video: Technical Nuances of Ventriculo-­atrial Shunt Placement Courtesy of Tito Vivas-­Buitrago and Daniele Rigamonti

Chapter 61

Endovascular Treatment of Intracranial Occlusive Disease Video 1: Deployment of Wingspan Stent System Across the MCA Courtesy of Kunal Vakharia, Muhammad Waqas, L. Nelson Hopkins, Adnan H. Siddiqui, and Elad I. Levy Video 2: Navigation of Wingspan Stent System Across the MCA Courtesy of Kunal Vakharia, Muhammad Waqas, L. Nelson Hopkins, Adnan H. Siddiqui, and Elad I. Levy

Chapter 62

Endovascular Treatment of Extracranial Occlusive Disease Video: Carotid Artery Stenting Courtesy of Matthew John Koch

Chapter 64

Endovascular Management of Dural Arteriovenous Fistulas Video: Carotid Artery Stenting Courtesy of Bowen Jiang, Matthew T. Bender, Erick M. Westbroek, Jessica K. Campos, Li-­Mei Lin, Alexander L. Coon, and Geoffrey P. Colby

Chapter 66

Principles for Surgical Management of Hydrocephalus in the Adult

Chapter 83

Endoscopic Treatment of Hyrdrocephalus: Third Ventriculostomy, Aquaductoplasty, Septostomy Video: Endoscopic Third Ventriculostomy Courtesy of Anthony L. Mikula, Benjamin D. Elder, Tito Vivas-­Buitrago, and Daniele Rigamonti

Chapter 84

Surgical Management of Cysts: Intraventricular Cysts, Intraventricular Septations, and Extraventricular Arachnoid Cysts Video: Endoscopic Colloid Cyst Resection, ETV, and Septum Pellucidotomy Courtesy of Kelly Gassie and Alfredo Quiñones-­Hinojosa

Chapter 85

Management of Shunt Complications Video: Surgical Management of Shunt Infections Courtesy of Claudio Yampolsky and P. Ajler

Chapter 86

Management of Cerebrospinal Fluid Leaks Video: Management of Cerebrospinal Fluid Leaks Courtesy of Angela Bohnen, Christopher Louie, Ricardo A. Domingo, Gaetano De Biase, Angela M. Donaldson, Osarenoma U. Olomu, and Alfredo Quiñones-­Hinojosa

Endovascular Treatment of Head and Neck Bleeding

Chapter 98

Video 1: Bilateral Sphenopalatine Artery Embolization for Intractable Epistaxis Courtesy of Dimitri Laurent, Adam J. Polifka, and W. Christopher Fox

Video: Laser-­Ablation Techniques Courtesy of Tito Vivas-­Buitrago, Sanjeet S. Grewal, and Robert E. Wharen, Jr.

Video 2: Posttraumatic Vertebral Artery Jugular Venous Fistula Courtesy of Dimitri Laurent, Adam J. Polifka, and W. Christopher Fox

Chapter 74

Surgical Management of Spinal Dysraphism Video: L1-­5 Laminoplasty for Resection of Lipoma and Detethering of Spinal Cord Courtesy of Oluwaseun O. Akinduro and Philipp R. Aldana

Laser-­Ablation Techniques

Chapter 105

Implantation of Deep Brain Stimulation Electrodes Under General Anesthesia for Parkinson’s Disease and Essential Tremor Video: DREZ (Dorsal Root Entry Zone) Lesions for Brachial Plexus Avulsion Pain Courtesy of Kim J. Burchiel

l

VIDEO CONTENTS

Chapter 109

Lesion Procedures for Psychiatric Disorders Video: Stereotactic Lesion Procedures Courtesy of Kelly Bijanki, Patrick Karas, and Sameer Sheth

Video 2: Midline Suboccipital Craniotomy for Fourth Ventricular Cysticercosis Courtesy of Rodrigo Ramos-­Zúñiga, Tomás Garzón-­Muvdi, and Kaisorn L. Chaichana

Chapter 148

Chapter 112

Thoracoscopic Sympathectomy for Hyperhidrosis

Lumbar Spinal Arthroplasty: Clinical Experiences of Motion Preservation

Video: Bilateral Thoracoscopic Sympathotomy at T2 Courtesy of Karim ReFaey, Sanjeet Grewal, Mathew Thomas, and Robert E. Wharen, Jr.

Video: Total Disc Replacement (TDR) at L5-­S1 with Activ-­l TDR, and 11 Degrees of Lordosis Courtesy of Fred H. Geisler and Domagoj Coric

Chapter 113

Surgery for Intractable Spasticity Video: Surgery for Intractable Spasticity Courtesy of Marc Sindou and George Georgoulis

Chapter 120

Surgery for Intractable Spasticity Spinal Cord Stimulation and Intraspinal Infusions for Pain Video: Surgical Placement of Spinal Cord Internal Pulse Generator for Intractable Pain Courtesy of Karim ReFaey, Alexander Vlasak, Andres Ramos-­Fresnedo, Perry A. Ball, Ronald Reimer, and Eric Nottmeier

Chapter 126

Principles of Neuroplastic Surgery: Management of Scalp Defects and Neurocranial Reconstruction Video: Principles of Neuroplastic Surgery and Surgical Aspects of Cranioplasty Reconstruction Courtesy of Netanel Ben-­Shalom and Chad R. Gordon

Chapter 131

Neurocysticercosis Video 1: Intraventricular Resection of Cysticercosis Courtesy of Rodrigo Ramos-­Zúñiga, Tomás Garzón-­Muvdi, and Kaisorn L. Chaichana

Chapter 167

Management of Chiari Malformations and Syringomyelia Video: C1 Laminectomy for Chiari Malformation Revision Courtesy of Karim ReFaey, William Clifton, and Alfredo Quiñones-­Hinojosa

Chapter 174

Intradural Extramedullary Tumors Video 1: Thoracic Laminectomy Courtesy of Oluwaseun O. Akinduro and H. Gordon Deen Video 2: Surgical Resection of Lumbar Intradural Extramedullary Schwannoma Courtesy of Mohamad Bydon, Megan C. Everson, Anshit Goyal

Chapter 194

Robotic Spine Surgery Video: Robotically Assisted MIS L4-­S1 TLIF Courtesy of Selby Chen   

PREFACE

What we write today becomes history tomorrow. Books that continue to be updated are a testament that the concept stands strong but the field has continued to move, and the need for contemporary knowledge and updates is crucial to keep the concept alive and thriving. Drs. Schmidek and Sweet co­edited the first single volume entitled Current Techniques in Operative Neurosurgery in 1977. At the time, that first edition reflected their own interests in contemporary neurosurgical procedures. So much has changed in the field and in the world since then, but what has not changed is the thirst for knowledge and the need to make patient surgical care better and more efficient. In this new edition, in the middle of an enormous and life-­changing COVID-­19 pandemic, this book has continued the same tradition: to provide the working neurosurgeon and health care provider with information that would be useful when carrying for a patient with a neurosurgical disorder and/or taking a patient to the operating room. The chapters provided an overview of the topic, a discussion of available options, and results. In many cases, alternative surgical and nonsurgical options were included for dealing with a particular clinical situation. The goal from the inception of this book has been to provide a single source that would allow a neurosurgeon to develop a surgical plan for the patient and at the same time understand the nuances, potential complications, and expectations of surgery so the care of the patient is improved. The chapter references would be up to date and allow further immersion in the topic as needed. The success of these volumes places Operative Neurosurgical Techniques: Indications, Methods, and Results among the most widely used neurosurgical texts worldwide with an extraordinary number of authors from all over the world. Now in its seventh edition, this title is dedicated to all those unsung heroes around the world that despite monumental challenges as surgery stopped in many corners of the world due to the pandemic, they continued to provide care for patients and continued to put down their ideas in this new edition. The field of neurological surgery has experienced a tremendous evolution since I did the 6th edition and it fills me with pride and pleasure to know that our field continues to be innovative, exhilarating, and courageous. In this 7th edition, I continued the tradition that was started in the last edition to add multiple section editors,

which has allowed us to keep the current edition as contemporary as possible. The 7th edition continues to reflect the same underlying vision for the book and attempts to keep up to date with the rapidly evolving changes in neurosurgery. This new and improved edition consists of 10 sections and 193 chapters authored by 445 contributors representing neurosurgical services from several different countries. It was the original intention of Dr. Schmidek in the first five editions to reflect the ongoing worldwide changes, to include contributions of internationally renowned doctors, and to perpetuate the idea of a worldwide text in neurosurgery and we have continued this tradition in the 6th and 7th editions. This 7th edition has lived up to that goal with a more modern utilization of video and new surgical techniques. In this edition a large percentage of the chapters deal with material not previously addressed, including topics of pediatric neurosurgery, endovascular surgery, robotic spine, innovation, skull base minimally invasive techniques, and the updates of peripheral nerve management and surgery. Where appropriate, chapters published in earlier editions have been extensively rewritten. All the chapters have been reviewed by myself and my coeditors to ensure that they reflect the current state of the art. This edition could not have been accomplished without the enthusiastic participation of the section editors and contributors who put in extraordinary efforts to complete their chapters on time. Every effort has been made to produce a product worthy of the contributions. This could only have been accomplished with the professionalism of Laurie Gower, Denise Roslonski, Laura Schmidt, Belinda Kuhn, and Cindy Thoms at Elsevier, and my Fellow, Dr. Karim ReFaey. I extend to all the section editors, contributors, and staff members from Elsevier and Mayo Clinic Florida my most sincere thanks for a tremendous job, which was incredibly well done. I also thank our families and loved ones who have made tremendous sacrifices, as many of us write and edit our chapters during mornings, nights, and weekends and often take time away from our families who are there supporting us and encouraging us continuously—a big thank you! Alfredo Quiñones-­Hinojosa, MD, FACS, FAANS

xxxix

SURGICAL MANAGEMENT OF MEDICALLY ENTRACTABLE EPILEPSY CHAPTER 98

Laser Interstitial Thermal Therapy for Epilepsy TITO VIVAS-­BUITRAGO  •  SANJEET SINGH GREWAL  •  ROBERT E. WHAREN, JR.

Introduction Laser interstitial thermal therapy (LITT) is a minimally invasive percutaneous procedure that involves the stereotactic insertion of a fiberoptic catheter and delivery of non-­ ionized photons into a predetermined intracranial location to thermally ablate specific anatomical structures or lesions. Laser technology for intracranial ablation has been available since 1960, with the use of ruby and CO2 lasers for the treatment of malignant gliomas.1,2 This technology was cumbersome, given the bulky nature of the systems, and was not practical for the ablation of deep brain structures. LITT was first described by Bown in 19833 and used in a clinical setting by Sugiyama et al. in 1990,4 with the development of a thin fiberoptic catheter that allowed for an intracranial insertion to reach deep brain structures, becoming more practical than previous attempts. Despite these improvements, the lack of real-­time monitoring and accurate control over the ablation volume limited the acceptance of this technique. The development of magnetic resonance thermography (MRT) allows for continuous monitoring of thermal damage in near real time. LITT guided by MRT is known as magnetic resonance guided LITT (MRgLITT) and has been gaining acceptance among surgeons, given its accuracy and near real-­time monitoring.5–7 MRgLITT is currently used as a minimally invasive option in the treatment of gliomas, brain metastasis, radiation necrosis, deep-­seated high-­grade gliomas (HHG), and epilepsy.60 Although surgical resection of an intracranial lesion is still generally considered the first line of treatment, there are scenarios in which MRgLITT can be beneficial. Patients with low preoperative functional scores, medical comorbidities with a high risk of peri-­and postoperative complications, deep-­ seated lesions, and patients with medically refractory epilepsy that are hesitant to pursue a craniotomy for open resection of the epileptogenic tissue often benefit from MRgLITT, with less associated risk than an open resection.8,9 The need for a minimally invasive approach for epilepsy has arisen from the underutilization of surgery due to multiple factors, one of which is the perceived complication rates and morbidity associated with open surgical resection.10 There are approximately 300,000 patients with medically refractory epilepsy in the United States; however, only 7000 procedures for the surgical treatment of epilepsy are performed annually and less than 10% of potentially eligible patients currently receive an

intervention.11 The role of minimally invasive approaches is to limit the morbidity and recovery associated with open resections, with the goal of offering treatment to additional cohorts of eligible patients.12 This chapter explores the technical aspects and the science behind MRgLITT technology, reviews the most recent data for cases and scenarios in which LITT is indicated as a treatment for epilepsy, and provides a detailed technical description of the surgical procedure. 

The Science of Laser Interstitial Thermal Therapy LASER (light amplification by stimulated emission of radiation) is the main component of this technique, in which photons are emitted from a fiberoptic probe and are absorbed by tissue molecules called chromophores.13,14 Photon energy is absorbed by chromophores in the tissue, resulting in a release of thermal energy causing heating of the target area.13,14 Temperatures between 46°C and 60°C will cause irreversible enzyme induction, DNA and protein denaturation, membrane dissolution, vessel sclerosis, and coagulative necrosis, leading to cell death.15,16 Temperatures above 60°C cause instantaneous coagulation necrosis.14,16 Absorption coefficients vary between tissue types and composition; the higher the absorption coefficient of the target zone, the faster the tissue temperature rises.17 The dissipation of heat in the targeted regions is affected by the close proximity of blood vessels and cerebrospinal fluid (CSF) that function as heat sinks.18–20 In most cases, pathological tissue has a greater absorption coefficient that translates to faster denaturation/ablation than healthy parenchyma, favoring surrounding healthy tissue preservation.17 Temperature limits are often set, with an automatic shut-­off mechanism as high as 90°C at the tip of the catheter (enough to perform an appropriate ablation but also low enough to avoid carbonization/vaporization) and to 50°C at the periphery of the target zone, to avoid damage to the adjacent parenchyma.21,22 This mechanism is utilized to optimize the lesioning near the tip of the laser fiber while preserving the integrity of the surrounding structures.17,21,22 The most commonly used and commercially available LITT systems are the Visualase (Medtronic, US, Minneapolis, MN), which uses a 15W, 980-­nm diode laser, and the NeuroBlate (Monteris Medical, Plymouth, MN), which uses a 12W, 1064-­ nm Nd:YAG

1151

1152

Section Six  •  FUNCTIONAL NEUROSURGERY

Table 98.1  Visualase and NeuroBlate Characteristics Component

Visualase

NeuroBlate

Silica within polymer sheath 1.65 Diffusing 15 CW 980 (diode) Saline N/A Frame-­based or frameless Yes

Silica within Sapphire capsule 2.2 and 3.3 Diffusing or directional Up to 12, pulsed 1064 (diose) CO2 with temperature feedback control Advanced (APD) and Robotic (RPD) Frame-­based or frameless Yes

Medtronic Automatica and manual

Ma Vision Pro Automaticb and manual

Patient interface platform Laser probe Composition Diameter (mm) Direction Output (W) Wavelength Cooling mechanism Probe driver Frame MRI-­compatible

Physician workstation Software Shut-­off mechanism aAutomatic

shut-­off in the Visualase System engages if a surgeon selected temperature limit is reached near a critical structure. shut-­off in the NeuroBlate System engages if patient movement in the MRI is detected. Adapted from Lagman C, Chung LK, Pelargos PE, et al. Laser neurosurgery: a systematic analysis of magnetic resonance-­guided laser interstitial thermal therapies. J Clin Neurosci 2017;36:20–26. bAutomatic

laser. The specifications of and differences between these two systems are summarized in Table 98.1. The NeuroBlate probe comes with a tip that can be rotated, retracted, and advanced with a calibrated driver, which can be particularly helpful for targets that have an irregular geometry. A potential advantage of the Visualase is its capability to generate a uniform ellipsoid field of heating around the tip of the probe that produces a constant area of coverage ideal for lesions with a homogenous shape. MRT is utilized for a continuous monitoring of the area of ablation. Temperature data is incorporated into a mathematical model (Arrhenius model)23 that provides an estimation of the ablation/necrosis zone in near real time (with imaging updated every 3 to 9 seconds, depending upon the number of planes that are being monitored) by displaying a colored zone of heating overlaid on the brain MRT image. The usage of MRT in LITT procedures is revolutionizing the acceptance of this technique, due to the capability to monitor the ablation in near real time.24–27 

Surgical Procedure Preoperative MRT imaging is obtained prior to the procedure for anatomy registration, trajectory planning, and intraoperative guidance. Trajectory assessment includes several variables, including skull thickness, dural anatomy, blood vessels, parenchyma, sulci, and ventricles. Implantation techniques vary between institutions, available equipment, and surgeon preference, including stereotactic frames, frameless systems, and robotic-­assisted guidance that can provide an accurate intraoperative execution of the preplanned trajectory. In this chapter, we describe (Fig. 98.1) the placement of the catheter using the ClearPoint System (a video description of the procedure is available in the online version of this chapter). MRgLITT procedure can be performed under light sedation or general anesthesia, depending on the surgeon’s preference after assessing for positioning, comfort, and procedure time length, always prioritizing safety and the patient’s comfort (see Fig. 98.1.A). All medications

and instrumentation must be MRI compatible. Chemical paralysis is recommended in general anesthesia to avoid unexpected movements during the procedure. Special care during positioning should be taken to avoid the restriction of venous outflow. After the scalp is prepped and draped in the usual fashion, the alignment grid is placed at the region of interest (see Fig. 98.1B). The intraoperative MR machine is then advanced to the operating table to obtain a trajectory planning scan. A target and the entry site are chosen, and the trajectory is determined. The MR scanner is removed, and the ClearPoint base and tower are secured to the outer table of the skull, centered on the chosen entry site (see Fig. 98.1C and D). The MR scanner is again returned to the operative field for an alignment scan. The ClearPoint system is aligned along the chosen trajectory to the target, and the MR scanner removed. After infiltration with a local anesthetic, a stab incision is made and (see Fig. 98.1E) a twist drill is made for skull penetration. The dura is coagulated with a stereotactic coagulator, and then a ceramic stylet is inserted and advanced to the target site. A new MR scan is obtained to confirm appropriate localization of the stylet to the target site. After accurate positioning is confirmed, the stylet is removed and the laser fiber is inserted into the target site. Correct positioning of the fiber is verified via MR scan (see Fig. 98.1F) and the fiber connected to the computer system. LITT temperature limits are programmed into the monitoring system, and an initial low dose of laser energy is administered to verify the proper functioning of the system. After adequate functioning is confirmed, target ablation is carried out with continuous monitoring of the ablation volume and tissue temperatures that are visualized as a colored overlay on the MR image. After the ablation is completed, MR imaging (post-­contrast T1, T2, T2-­FLAIR, and diffusion images) is acquired to verify the ablation zone. The MR machine is then removed, and the skin incision is closed.

TEMPORAL LOBE EPILEPSY Temporal lobe epilepsy (TLE) is the most common form of medically refractory epilepsy in adults, with mesial temporal

98  •  Laser Interstitial Thermal Therapy for Epilepsy

A

D

B

C

E

F

1153

G FIGURE 98.1  Figure illustrating the steps taken during MRgLITT ablation. (A) Positioning and scalp preparation. (B) Alignment grid placement. (C and D) ClearPoint base and tower placement. (E) Scalp incision. (F) Alignment of the cannula. (G) Laser catheter placement and ablation at the most anterior portion of the amygdala, with subsequent withdraw of the catheter and additional ablation along the hippocampal axis.

1154

Section Six  •  FUNCTIONAL NEUROSURGERY

A

B

FIGURE 98.2  3T seizure protocol MRI. Red circle shows abnormal asymmetric increased T2 signal intensity in the right hippocampal head and body, with loss of internal architecture and minimal atrophy.

lobe sclerosis (MTS; Fig. 98.2) being the leading cause in mesial temporal lobe epilepsy (MTLE).28–32 Surgical treatment with anterior temporal lobectomy (ATL) and selective amygdalohippocampectomy (SAH) has been demonstrated as the most effective type of treatment, with Engle I seizure-­free outcomes of 55% to 70% at 1 year and 40% at 10 years for all ATL patients, and 65% to 67% and 50% at one and 10 years, respectively, for patients with MTS.10,11,33,34 Although ATL surgery is considered the current gold standard for the treatment of refractory MTLE, it is also associated with variable postoperative cognitive decline, including deficits in verbal and nonverbal memory, word finding, recognition, and naming, depending on language dominance.35–39 Visual field defects (VFDs) are also commonly found after open temporal resection. A retrospective study from Schmeiser et al. reported an incidence of VFDs of 83% after ATL, 74% after selective transsylvian amygdalohippocampectomy, and 56% after subtemporal selective amygdalohippocampectomy.40 These reported complications, in addition to a patient’s perception of the invasiveness of an open craniotomy, have necessitated a need for less invasive procedures like MRgLITT. MR-­guided selective laser amygdalohippocampectomy (SLAH) is indicated in cases of isolated mesial pathologies without further evidence of temporal alterations.39,41 An occipital insertion of the LITT catheter is performed as described in the surgical procedure section, following an extraventricular trajectory along the axis of the hippocampus (see Fig. 98.1G). Ablation of the hippocampus and amygdala are performed using as many ablation targets as necessary to achieve an appropriate ablation volume. At this time, there is no class I data comparing the Engle seizure outcomes and/or complication rates between ATL and SLAH. Available literature from case series studies (class III data) suggest an efficacy rate almost comparable with ATL, along with surgical complication rates for SLAH that are less than ATL (Table 98.2).39,41–45 Volumetric analyses of patients with persistent seizures following SLAH suggest an association of mesial hippocampal head sparing with persistent disabling seizures.46 SLAH can be repeated for patients who fail to obtain an Engel Class I outcome. 

ILLUSTRATIVE CASE A 28-­year-­old right-­handed woman has a history of infantile seizures, first presenting as a generalized tonic-­clonic episode at the age of 10. The patient suffered from three types of seizures. The first type consisted of nausea and a gagging sensation, and the second type consisted of biting motions, mild alterations of consciousness, and humming. The third type consisted of a loss of awareness and unresponsiveness. A prolonged monitoring session demonstrated simple and complex partial seizures arising from the left medial temporal lobe. MR imaging revealed findings of left medial temporal sclerosis. Multiple AEDs failed to control her seizures. Wada testing demonstrated bilateral memory representation, and she was considered at increased risk for surgical resection. Responsive neurostimulation was performed, resulting in improved but incomplete seizure control over a 5-­year period. MRgLITT ablation of the left amygdala and hippocampus was thus performed (Fig. 98.3). The first ablation was performed for 2 minutes, obtaining a temperature of 62 degrees centigrade at the target site. A second lesion was then made 15 mm posterior to the initial lesion. Finally, a third lesion was made halfway in between the first two lesions. A post-­ablation MRI scan demonstrated a satisfactory ablation (Fig. 98.4, orange circles). There were no complications, and the patient was discharged the morning after surgery. The patient has been seizure-­free since the ablation. 

Nodular Heterotopias Periventricular nodular heterotopias (PVNH) occur when there is a migratory deficit in groups of neurons from the germinal zone of the periventricular matrix, forming sub-­ ependymal gray matter nodules that can vary in size and cause focal medically refractory epilepsy.47–49 Surgical resection of PVNH can be challenging, given their deep location and close proximity to eloquent brain and important white matter tracts. Less ­invasive procedures like radiosurgery and radiofrequency thermocoagulation have been implemented

Table 98.2  Selective Laser Ablation Case Series Literature Review Year

Design

Location in Brain of Surgery

Cuny DJ et al.

5 pediatrics

2012

Retrospective

Multiple sites

Wilfong A et al Willie JT et al.

14 pediatrics 13 adults

201 3

Retrospective

Hypothalamus

2014

Retrospective

Esquenazi Y et al. Drane DL et al.

2 adults

2014

39 resected vs. 19 SLA adults 17 pediatrics

2014

Retrospective case Retrospective compared

Lesional and nonlesional mTLE Periventricular white Temporal lobe

2015

Retrospective chart

Temporal and extratemporal

Waseem H et al.

7 AMTL resection 7 SLA Adults

2015

Prospective

Kang JY et al. Luedke MW et al.

20 adults (2 pediatrics) 2 adults

2016

Rolston JD et al.

2 adults

2016

Dredla BK et al.

2 adults

Jeimakowicz WJ et al. Gross RE et al.

Lewis Evan Cole et al.

Follow-­Up

Outcome and Complications

Cingulate tuber/TSC, MTS/MTLE, hypothalamic hamartoma (n = 2), focal cortical dysplasia Hypothalamic hamartoma

2–13 months

All seizure-­free (1 patient SF after resuming ASDs at 12 months)

1–24 months

79% SF initially (after 1 patient underwent repeat SLA,86% SF)

MTS, mesial temporal atrophy, mesial temporal signal change, normal Left frontal PNH, bilateral temporal PVNH Amygdala and hippocampus (SLA) vs. transcortical amygdalohippocampectomy Mixed

5–26 months

8/13 patients SF

1–16 months

Patient 1: seizures reoccurred after 1 month. Patient 2: underwent TL after failed SLA and became SF 57.9% SLAH SF; stable or slight improvement in cognitive

Anterior mesial temporal lobe (all)

TL resection: 5/7 MTS 2/7 normal SLA 5/7 MTS 2/7 normal

9–1 2 months

Prospective review Retrospective case report of 2 patients Pre and postop ECoGby Retrospective, case

Mesial temporal lobe Left mesial temporal lobe

2/7 normal SLA

6 months

Patient 1, subtle increased T2 signal in the left mesial temporal lobe. Patient 2, left MTS

Patient 1, 1 year Patient 2, 1 year

Hypothalamic hamartoma

Hypothalamic hamartoma

2016

Retrospective, case

Patients 1 and 2, left amygdala and hippocampus

Patients 1 and 2 MRI+/ PET− Left TLE (unknown cause) Localized with iEEG

Patient 1, most recent follow-­up: 5 months Patient 1–2 years Patient 2–4 months

23 adults

201 7

Prospective

Mesial temporal lobe

1 8/2 3 MTS1 patient, MTS and atrial heterotopia, 2 ablations

22.4 ± 7 months

58

201 8

Retrospective

Mesial temporal lobe

43/58 MTS 3/58 signal hippocampus increase on T2 and/or FLAIR

12

2016

SLAH, 6 months Resection, 1 year 3.5–35.9 months

7 patients SF, 1 Class II; 3 Class III, 6 Class IV, Complications: inaccurate fiber placement (2); laser cooling mechanism failure (1); post-­ablation edema (1), left quadrant TL resection: 7/7 Class I Complications: 1 aseptic meningitis-­ resolved SLA: 4/7 Class I; 1/7l Class II 2/7 inadequate follow-­up time (t < 12 months) Complications: 2/7 partial visual field deficit 1/7 Postop seizures resulting in repeat hospitalization 1/7 extended stay (N1 day) due to headaches 11 patients SF; 2 Class II; 7 Class IV, 4 patients (Class IV) underwent subsequent lobectomy Patient 1, Class II Patient 2, Class II Reduction in epileptiform discharges in the intra-­ablation contacts compared with extra-­ ablation contacts Patient 1, SF at most recent follow-­up; had transient hyperphagia and amnesia after the ablation, resolved by Patient 1, SF Decline in verbal memory and semantic verbal fluency Patient 2, SF except 3 seizures in first month due to low ASD levels but remains SF since Decline in verbal and visual memory and semantic verbal fluency 1 5/23 SF 4/23 Engel Class II 2/23 Engel Class III 2/23 Engel Class IV Complications: headache, nausea, unsteady gait (resolved), left homonymous hemianopia (partially resolved) Engel I all, 31/58 (53.4%) Non-­MTS, 5/15 (33.3%) MTS, 26/43 (60.5%) Complications: 3 VFD (2 superior quadrantanopia and 1 homonymous hemianopsia after repeat SLAH, 1 acute SDH and 1 acute IPH with no neurodeficits, 4 transient partial CNP (1 third nerve and 3 fourth nerve)

AMTL, Anterior mesial temporal lobe; ATL, anterior temporal lobectomy; ECoG, electrocorticography; MTLE, mesial temporal lobe epilepsy; MTS, mesial temporal lobe sclerosis; PVNH, periventricular nodular heterotopia; SLAH, selective laser amygdalohippocampectomy; TLE, temporal lobe epilepsy; TSC, tuberous sclerosis complex; VFD, visual field defects. Adapted from Petito GT, Wharen RE, Feyissa AM, et al. The impact of stereotactic laser ablation at a typical epilepsy center. Epilepsy Behav. 2018;78:37–44.

1155

Etiology

98  •  Laser Interstitial Thermal Therapy for Epilepsy

Number of Patients

Author

1156

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 98.3  Axial T1 MRI illustrating the correct placement of the catheter pre-­ablation (blue circle). Coronal and axial MR images showing post-­ ablation extension at different views and levels (orange circles).

98  •  Laser Interstitial Thermal Therapy for Epilepsy

A

1157

B

C

D

E

FIGURE 98.4  (A) Axial T2-­weighted brain MR image initially interpreted as normal. (B) Magnetoencephalography (MEG) study with spike dipole estimates (magenta), with suggestive posterior mesial parietal location of the source generator. Somatosensory dipole estimates for hand digits (green) indicate source generators in the expected homuncular region of the Rolandic cortex, anterior, and lateral to spike sources. (C) Upon further review of the initial MR image, a small area of cortical dysplasia is identified (red circle) that correlates in terms of location with the potential source generator identified with MEG. (D) Placement of depth electrodes and confirmation of the seizure onset zone. (E) Post-­ablation axial T2-­ weighted MR image (6 months postoperatively).

in the treatment of heterotopias. However, none of these techniques can monitor lesioning in real time, which is crucial for obtaining an appropriate ablation while minimizing potential complications, particularly near the eloquent brain. 

Illustrative Case A 28-­year-­old right-­handed man has a 24-­year history of focal onset seizures with rare generalization to tonic-­clonic seizures. Seizure onset was at age four, described as episodes of alteration of responsiveness with lip smacking and dystonic posturing. Seizures frequency had increased to twice per month despite trials of five antiepileptic medications (AEDs). MRI was initially considered nonlesional (see Fig. 98.4A), but after magnetoencephalography (MEG) was suggestive of posterior mesial parietal source generators (see Fig. 98.4B), further evaluation of MRI imaging revealed a small nodular heterotopia corresponding to the site of the MEG findings (Fig. 98.4C). Placement of depth electrodes confirmed this site as the seizure onset zone (see Fig. 98.4D).

MRgLITT was thus used to ablate the nodular heterotopia (see Fig. 98.4E). There were no perioperative or postoperative complications. The patient had an Engel class I outcome and has returned to driving and is now employed teaching English to international students. 

Hypothalamic Hamartomas Hypothalamic hamartomas (HH) are rare developmental hamartomatous non-­neoplastic lesions composed of normal neurons located in or around the hypothalamus.50 Patients with HH present with gelastic or laughing seizures often starting in childhood and can have developmental delay.51,52 Open surgery for intractable seizures from HH has been associated with significant morbidity and moderate efficacy.50,53–55 MRgLITT ablation of HH can significantly decrease procedure-­related complications, while achieving 86% to 93% seizure-­free outcomes at 1 year in retrospective studies, representing a significant increase in efficacy when compared with open procedures.56 

1158

Section Six  •  FUNCTIONAL NEUROSURGERY

A

B

FIGURE 98.5  (A) Axial MR image showing a small ovoid 5-mm non-­enhancing soft tissue lesion, isointense to the gray matter, arising from the right lateral wall of the left ventricle, compatible with a hypothalamic hamartoma (orange circle). (B) Axial MR image illustrating the post-­ablation zone matching the boundaries of the lesion.

Illustrative Case A 33-­year-­old male has medically intractable seizures consisting of drop attacks, jerking, and gelastic seizures. EMU findings were consistent with a seizure onset from a 6-­mm right-­sided hypothalamic lesion, consistent with a hypothalamic hamartoma (Fig. 98.5A). The patient had previously received Gamma Knife treatment at 18 Gy to the 80% isodose line. This did not help improve his seizure frequency, and he had a placement of a Vagus Nerve Stimulator (VNS), which also failed to help control his seizures. He was having drop attacks monthly and gelastic seizures on almost a weekly basis. The patient underwent a single ablation using MRgLITT (see Fig. 98.5B). A temperature cutoff marker was placed at the junction with the ipsilateral mamillary body, to limit injury to this structure. After completion of the ablation, a contrast scan was performed, revealing a satisfactory ablation (see Fig. 98.5C). The patient remains seizure-­free as of his last follow-­up. 

Corpus Callosotomy Corpus callosotomy is an effective procedure to treat atonic seizures in medically refractory nonfocal epilepsy. Sectioning the anterior two-­thirds of the corpus callosum and interrupting the crossing fibers between hemispheres can decrease both the magnitude and the frequency of the seizures. The callosotomy can be further expanded with the resection of the fibers in the posterior corpus callosum, if necessary.57 Different systems, including CO2 lasers and very recently MRgLITT, have been utilized for minimal invasive callosotomy with successful reports, including one

in which the patient was initially presenting 15 to 25 seizures per day, and 1 to 2 drop attacks per day, with seizure decline over 50% and complete resolution of atonic seizures after the procedure.58,59 While open corpus callosotomy is a very effective procedure to eliminate drop-­attacks, there can be transient neurological deficits, such as akinetic mutism secondary to retraction of the supplementary motor area (SMA) of the brain. The use of MRgLITT eliminates the need for retraction, allowing focused ablation of the corpus callosum. 

Summary MRgLITT is undoubtedly gaining more acceptance among the neurosurgical field, given the minimal invasiveness of the procedure, which can translate into shorter procedure times, a faster recovery, potentially decreased procedure-­related complications, and seizure-­ free outcome nearly comparable to the open surgical resection. Although there are no Level I data yet available comparing the efficacy between MRgLITT and open surgery, it is a very appealing alternative for patients who are at high risk of complications for an open resection but have proven to be medically refractory. KEY REFERENCES

Anzai Y, Lufkin R, DeSalles A, Hamilton DR, Farahani K, Black KL. Preliminary experience with MR-­guided thermal ablation of brain tumors. Am J Neuroradiol. 1995;16:39–48. Berg AT. Identification of pharmacoresistant epilepsy. Neurol Clin. 2009;27:1003–1013. Bown S. Phototherapy of tumors. World J Surg. 1983;7:700–709. Englot D, Ouyang D, Garcia P, Barbaro N, Chang E. Epilepsy surgery trends in the United States, 1990–2008. Neurology. 2012;78: 1200–1206. Englot DJ. The persistent under-­utilization of epilepsy surgery. Epilepsy Res. 2015;118:68.

98  •  Laser Interstitial Thermal Therapy for Epilepsy

Franck P, Henderson PW, Rothaus KO. Basics of lasers: history, physics, and clinical applications. Clin Plast Surg. 2016;43: ­ 505–513. Goldberg SN, Gazelle GS, Mueller PR. Thermal ablation therapy for focal malignancy: a unified approach to underlying principles, techniques, and diagnostic imaging guidance. Am J Roentgenol. 2000;174:323–331. Heisterkamp J, van Hillegersberg R, Zondervan P, IJzermans JN. Metabolic activity and DNA integrity in human hepatic metas­ tases after interstitial laser coagulation (ILC). Lasers Surg Med. 2001;28:80–86. Jolesz FA, Bleier AR, Jakab P, Ruenzel PW, Huttl K, Jako G. MR imaging of laser-­tissue interactions. Radiology. 1988;168:249–253. Kaiboriboon K, Malkhachroum AM, Zrik A, et al. Epilepsy surgery in the United States: analysis of data from the National Association of Epilepsy Centers. Epilepsy Res. 2015;116:105–109. Kwan P, Arzimanoglou A, Berg AT, et al. Definition of drug resistant epilepsy: consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia. 2010;51: 1069–1077. Larson TR, Bostwick DG, Corica A. Temperature-­correlated histo pathologic changes following microwave thermoablation of obstructive tissue in patients with benign prostatic hyperplasia. Urology. 1996;47:463–469. Matsumoto R, Mulkern RV, Hushek SG, Jolesz FA. Tissue temperature monitoring for thermal interventional therapy: comparison of T1‐ weighted MR sequences. J Magnet Resonance Imag. 1994;4:65–70.

1159

McNichols RJ, Gowda A, Kangasniemi M, Bankson JM, Price RE, Ha­zle JD. MR thermometry-based feedback control of laser interstitial thermal therapy at 980 nm. Lasers Surg Med. 2004;34:48–55. Patel NV, Mian M, Stafford RJ, et al. Laser interstitial thermal therapy technology, physics of magnetic resonance imaging thermometry, and technical considerations for proper catheter placement during magnetic resonance imaging–guided laser interstitial thermal therapy. Neurosurgery. 2016;79:S8–S16. Ryan RW, Spetzler RF, Preul MC. Aura of technology and the cutting edge: a history of lasers in neurosurgery. Neurosurg Focus. 2009;27:E6. Rosomoff HL, Carroll F. Reaction of neoplasm and brain to laser. Archiv Neurol. 1966;14:143–148. Stafford RJ, Fuentes D, Elliott AA, Weinberg JS, Ahrar K. Laser-­ induced thermal therapy for tumor ablation. Crit Rev Biomed Eng. 2010;38. Sugiyama K, Sakai T, Fujishima I, Ryu H, Uemura K, Yokoyama T. Stereotactic interstitial laser-­hyperthermia using Nd-­YAG laser. Stereotact Function Neurosurg. 1990;54:501–505. Yaroslavsky A, Schulze P, Yaroslavsky I, Schober R, Ulrich F, Schwarzmaier H. Optical properties of selected native and coagulated human brain tissues in vitro in the visible and near infrared spectral range. Physics Med Biol. 2002;47:2059. Numbered references appear on Expert Consult.

REFERENCES

1. Ryan RW, Spetzler RF, Preul MC. Aura of technology and the cutting edge: a history of lasers in neurosurgery. Neurosurg Focus. 2009;27:E6. 2. Rosomoff HL, Carroll F. Reaction of neoplasm and brain to laser. Archiv Neurol. 1966;14:143–148. 3. Bown S. Phototherapy of tumors. World J Surg. 1983;7:700–709. 4. Sugiyama K, Sakai T, Fujishima I, Ryu H, Uemura K, Yokoyama T. Stereotactic interstitial laser-­hyperthermia using Nd-­YAG laser. Stereotact Function Neurosurg. 1990;54:501–505. 5. Jolesz FA, Bleier AR, Jakab P, Ruenzel PW, Huttl K, Jako G. MR imaging of laser-­tissue interactions. Radiology. 1988;168:249–253. 6. Anzai Y, Lufkin R, DeSalles A, Hamilton DR, Farahani K, Black KL. Preliminary experience with MR-­guided thermal ablation of brain tumors. Am J Neuroradiol. 1995;16:39–48. 7. Matsumoto R, Mulkern RV, Hushek SG, Jolesz FA. Tissue temperature monitoring for thermal interventional therapy: comparison of T1‐weighted MR sequences. J Magnet Resonance Imag. 1994;4:65–70. 8. Kwan P, Arzimanoglou A, Berg AT, et al. Definition of drug resistant epilepsy: consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia. 2010;51:1069–1077. 9. Berg AT. Identification of pharmacoresistant epilepsy. Neurol Clin. 2009;27:1003–1013. 10. Englot DJ. The persistent under-­utilization of epilepsy surgery. Epilepsy Res. 2015;118:68. 11. Kaiboriboon K, Malkhachroum AM, Zrik A, et al. Epilepsy surgery in the United States: analysis of data from the National Association of Epilepsy Centers. Epilepsy Res. 2015;116:105–109. 12. Englot D, Ouyang D, Garcia P, Barbaro N, Chang E. Epilepsy surgery trends in the United States, 1990–2008. Neurology. 2012;78:1200–1206. 13. Franck P, Henderson PW, Rothaus KO. Basics of lasers: history, Physics, and clinical applications. Clin Plast Surg. 2016;43:505– 513. 14. Larson TR, Bostwick DG, Corica A. Temperature-­correlated histo pathologic changes following microwave thermoablation of obstructive tissue in patients with benign prostatic hyperplasia. Urology. 1996;47:463–469. 15. Heisterkamp J, van Hillegersberg R, Zondervan P, IJzermans JN. Metabolic activity and DNA integrity in human hepatic metastases after interstitial laser coagulation (ILC). Lasers Surg Med. 2001;28:80–86. 16. Goldberg SN, Gazelle GS, Mueller PR. Thermal ablation therapy for focal malignancy: a unified approach to underlying principles, techniques, and diagnostic imaging guidance. Am J Roentgenol. 2000;174:323–331. 17. Yaroslavsky A, Schulze P, Yaroslavsky I, Schober R, Ulrich F, Schwarzmaier H. Optical properties of selected native and coagulated human brain tissues in vitro in the visible and near infrared spectral range. Physics Med Biol. 2002;47:2059. 18. Patel NV, Mian M, Stafford RJ, et al. Laser interstitial thermal therapy technology, physics of magnetic resonance imaging thermometry, and technical considerations for proper catheter placement during magnetic resonance imaging–guided laser interstitial thermal therapy. Neurosurgery. 2016;79:S8–S16. 19. Stafford RJ, Fuentes D, Elliott AA, Weinberg JS, Ahrar K. Laser-­ induced thermal therapy for tumor ablation. Crit Rev Biomed Eng. 2010;38. 20. McNichols RJ, Gowda A, Kangasniemi M, Bankson JA, Price RE, Hazle JD. MR thermometry‐based feedback control of laser interstitial thermal therapy at 980 nm. Lasers Surg Med. 2004;34:48–55. 21. Jethwa PR, Barrese JC, Gowda A, Shetty A, Danish SF. Magnetic resonance thermometry-­ guided laser-­ induced thermal therapy for intracranial neoplasms: initial experience. Operat Neurosurg. 2012;71:ons133–o145. 22. Patel PD, Patel NV, Davidson C, Danish SF. The role of MRgLITT in overcoming the challenges in managing infield recurrence after radiation for brain metastasis. Neurosurgery. 2016;79:S40–S58. 23. Carpentier A, McNichols RJ, Stafford RJ, et al. Real-­time magnetic resonance-­guided laser thermal therapy for focal metastatic brain tumors. Operat Neurosurg. 2008;63:ONS21–ONS9.

24. Sakai T, Fujishima I, Sugiyama K, Ryu H, Uemura K. Interstitial laserthermia in neurosurgery. J Clin Laser Med Surg. 1992;10:37– 40. 25. Norred SE, Johnson JA. Magnetic resonance-­guided laser induced thermal therapy for glioblastoma multiforme: a review. BioMed Res Intl. 2014;2014. 26. Sinha S, Hargreaves E, Patel NV, Danish SF. Assessment of irrigation dynamics in magnetic‐resonance guided laser induced thermal therapy (MRgLITT). Lasers Surg Med. 2015;47:273–280. 27. Hawasli AH, Kim AH, Dunn GP, Tran DD, Leuthardt EC. Stereotactic laser ablation of high-­ grade gliomas. Neurosurg Focus. 2014;37:E1. 28. Gastaut H, Gastaut J, Silva GE, Sanchez G. Relative frequency of different types of epilepsy: a study employing the classification of the International League against Epilepsy. Epilepsia. 1975;16:457– 461. 29. Labate A, Ventura P, Gambardella A, et al. MRI evidence of mesial temporal sclerosis in sporadic “benign” temporal lobe epilepsy. Neurology. 2006;66:562–565. 30. Kim WJ, Park SC, Lee SJ, et al. The prognosis for control of seizures with medications in patients with MRI evidence for mesial temporal sclerosis. Epilepsia. 1999;40:290–293. 31. Kurita T, Sakurai K, Takeda Y, Horinouchi T, Kusumi I. Very long-­term outcome of non-­surgically treated patients with temporal lobe epilepsy with hippocampal sclerosis: a retrospective study. PloS One. 2016;11:e0159464. 32. Picot MC, Baldy-Moulinier M, Daurès JP, Dujols P, Crespel A. The prevalence of epilepsy and pharmacoresistant epilepsy in adults: a population-based study in a Western European country. Epilepsia. 2008;49:1230–1238. 33. Wiebe S, Blume WT, Girvin JP, Eliasziw M. A randomized, controlled trial of surgery for temporal-­lobe epilepsy. N Engl J Med. 2001;345:311–318. 34. Engel J, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-­resistant temporal lobe epilepsy: a randomized trial. Jama. 2012;307:922–930. 35. Phillips NA, McGlone J. Grouped data do not tell the whole story: individual analysis of cognitive change after temporal lobectomy. J Clin Exp Neuropsychol. 1995;17:713–724. 36. Helmstaedter C. Cognitive outcomes of different surgical approaches in temporal lobe epilepsy. Epilep Dis. 2013;15:221–239. 37. Hermann BP, Wyler AR, Bush AJ, Tabatabai FR. Differential effects of left and right anterior temporal lobectomy on verbal learning and memory performance. Epilepsia. 1992;33:289–297. 38. Drane DL, Ojemann GA, Aylward E, et al. Category-­specific naming and recognition deficits in temporal lobe epilepsy surgical patients. Neuropsychologia. 2008;46:1242–1255. 39. Petito GT, Wharen RE, Feyissa AM, Grewal SS, Lucas JA, Tatum WO. The impact of stereotactic laser ablation at a typical epilepsy center. Epilepsy Behav: E&B. 2018;78:37–44. 40. Schmeiser B, Daniel M, Kogias E, et al. Visual field defects following different resective procedures for mesiotemporal lobe epilepsy. Epilepsy Behav. 2017;76:39–45. 41. Kang JY, Wu C, Tracy J, et al. Laser interstitial thermal therapy for medically intractable mesial temporal lobe epilepsy. Epilepsia. 2016;57:325–334. 42. Gross RE, Willie JT, Drane DL. The role of stereotactic laser amygdalohippocampotomy in mesial temporal lobe epilepsy. Neurosurg Clin North Am. 2016;27:37–50. 43. Drane DL, Loring DW, Voets NL, et al. Better object recognition and naming outcome with MRI-­ guided stereotactic laser amygdalohippocampotomy for temporal lobe epilepsy. Epilepsia. 2015;56:101–113. 44. Jermakowicz WJ, Kanner AM, Sur S, et al. Laser thermal ablation for mesiotemporal epilepsy: analysis of ablation volumes and trajectories. Epilepsia. 2017;58:801–810. 45. Waseem H, Osborn KE, Schoenberg MR, et al. Laser ablation therapy: an alternative treatment for medically resistant mesial temporal lobe epilepsy after age 50. Epilepsy Behav : E&B. 2015;51:152–157. 46. Jermakowicz WJ, Kanner AM, Sur S, et al. Laser thermal ablation for mesiotemporal epilepsy: analysis of ablation volumes and trajectories. Epilepsia. 2017;58:801–810.

1159.e1

1159.e2References 47. Esquenazi Y, Kalamangalam GP, Slater JD, et al. Stereotactic laser ablation of epileptogenic periventricular nodular heterotopia. Epilepsy Res. 2014;108:547–554. 48. Gonzalez-­Martinez J, Vadera S, Mullin J, et al. Robot-­assisted stereotactic laser ablation in medically intractable epilepsy: operative technique. Neurosurgery. 2014;10(suppl 2):167–172; discussion 172-173. 49. Battaglia G, Chiapparini L, Franceschetti S, et al. Periventricular nodular heterotopia: classification, epileptic history, and genesis of epileptic discharges. Epilepsia. 2006;47:86–97. 50. Wilfong AA, Curry DJ. Hypothalamic hamartomas: optimal approach to clinical evaluation and diagnosis. Epilepsia. 2013;54:109– 114. 51. Wagner K, Wethe JV, Schulze-­ Bonhage A, et al. Cognition in epilepsy patients with hypothalamic hamartomas. Epilepsia. 2017;58(suppl 2):85–93. 52. Wilfong AA, Curry DJ. Hypothalamic hamartomas: optimal approach to clinical evaluation and diagnosis. Epilepsia. 2013;54(suppl 9):109–114. 53. Ng YT, Rekate HL, Prenger EC, et al. Transcallosal resection of hypothalamic hamartoma for intractable epilepsy. Epilepsia. 2006;47:1192–1202.

54. Harvey AS, Freeman JL, Berkovic SF, Rosenfeld JV. Transcallosal resection of hypothalamic hamartomas in patients with intractable epilepsy. Epileptic Dis. 2003;5:257–265. 55. Abla AA, Rekate HL, Wilson DA, et al. Orbitozygomatic resection for hypothalamic hamartoma and epilepsy: patient selection and outcome. Child’s Nervous Sys. 2011;27:265–277. 56. Curry DJ, Raskin J, Ali I, Wilfong AA. MR-­guided laser ablation for the treatment of hypothalamic hamartomas. Epilepsy Res. 2018;142:131–134. 57. Schaller K, Cabrilo I. Corpus callosotomy. Acta Neurochirurgica. 2016;158:155–160. 58. Falowski S, Byrne R. Corpus callosotomy with the CO2 laser suction device: a technical note. Stereotact Funct Neurosurg. 2012;90:137–140. 59. Ho AL, Miller KJ, Cartmell S, Inoyama K, Fisher RS, Halpern CH. Stereotactic laser ablation of the splenium for intractable epilepsy. Epilepsy Behav Case Rep. 2016;5:23–26. 60. Lagman C, Chung LK, Pelargos PE, et al. Laser neurosurgery: a systematic analysis of magnetic resonance-­guided laser interstitial thermal therapies. J Clin Neurosci. 2017;36:20–26.

CHAPTER 99

Multidisciplinary Presurgical Evaluation for Epilepsy Surgery ANA LUISA VELASCO  •  FRANCISCO VELASCO

Introduction When we decide that surgery is an option for treating epilepsy, there are a number of considerations we have to make. First and most important, the decision of operating on a patient with seizures does not reside in one person, it is the result of a multidisciplinary team: epileptologist, neurophysiologist, neuropsychologist, neuroradiologist, and neurosurgeons play an important role in selecting, studying, and, above all, tailoring the best surgery for the patient. Despite the advances in medical treatment, 30% of epileptic patients do not respond to adequate antiepileptic treatment.1 We consider that a patient has medically uncontrollable (or refractory) epilepsy when satisfactory seizure control cannot be achieved with any of the potentially available effective antiepileptic drugs (AEDs), alone or in combination, at doses or levels not associated with unacceptable side effects. On the other hand, surgery has a success rate of about 75%, depending on the site of surgery, the type of surgery performed, and the underlying etiology.3–5 In spite of this, surgical treatment of medically uncontrollable epilepsy is often delayed or withheld. Referral for epilepsy surgery takes an average of 20 to 25 years, resulting in a number of avoidable seizure-­related deaths, including drowning, motor vehicle accident, fatal status epilepticus, and sudden unexpected death in epilepsy.6 In children, appropriate timing for surgical procedures is critical, as seizure control may interfere with consolidation of cognitive and motor functions in a developing brain. On the other hand, brain maturation may decrease epileptogenesis, and a nonprogressive brain lesion like a scar or dysplasia may be associated to transient epileptogenesis.7 Other than lack of efficacy, causes of poor response to medical treatment are noncompliance, pseudo-­ epileptic seizures or a combination of epileptic and pseudo-­epileptic seizures, incorrect classification of seizures, and incorrect pharmacological treatment (either drug or dosage).8 So, the first action in evaluating surgical candidates is to confirm that a proper diagnosis and an appropriate medical treatment have been offered. A patient’s satisfaction with the results achieved with medical treatment often depends on their professional and social circumstances, as well as the type of seizures and the

1160

time of day in which they occur.8 Some patients seek surgical treatment for reasons other than medical intractability; intolerable side effects of AEDs, avoidance of congenital malformations in women who desire to get pregnant, and avoidance of the social stigmata of the disease are some of the reasons patients have expressed when coming to our clinic. Self-­assessment of quality of life is an important step in evaluating the patient’s perception of their disease. At our clinic we use the questionnaires QOLIE-­31 for adults9,10 and QOLIE-­48-­AD for adolescents.11,12 When epilepsy surgery is planned, we have three goals: 1. Eliminate or decrease epileptic seizures, 2. Prevent neurologic deficit due to surgery, 3. Improve the quality of life. In order to be able to reach the best surgical choice for the epileptic patient, a multidisciplinary team has to work to solve the surgical questions: Where do the patient’s seizures start? Are there functional or eloquent areas involved? What is the prognosis after surgery? Answering these questions will permit us to know what type of surgery is indicated and to be able to customize the procedure according to our patient’s needs. Nowadays, we have a great number of studies that can be performed, but it is important to remember that there is not a single one that can be considered the golden standard for diagnosis by itself. It is the clinician’s ability to interpret and find the concordance between studies that will lead us to a correct diagnosis and a successful surgery.13 The diagnostic workup can be divided into noninvasive and invasive phases: 

Phase I Testing: Noninvasive Studies CLINICAL DIAGNOSIS: SEIZURE DESCRIPTION Probably the most important part of the noninvasive studies is the seizure description. We must try to compile data that will lead us to the most probable diagnosis. Special attention should be paid to what both family and patient have to report. Aura: specific auras have been described in different types of seizures. For example, the manifestations of fear and ascending epigastric sensation direct us toward mesial

99  •  Multidisciplinary Presurgical Evaluation for Epilepsy Surgery

temporal epilepsy; simple visual auras toward occipital foci, levitation to somatosensory areas; insular foci manifest as sympathetic symptoms such as perspiration, difficulty in swallowing, and salivation.14 The sequence of symptoms that the patient has is also important; epigastric and psychic auras followed by behavioral arrest and automatisms (ocular, oral, hands, ambulatory) indicate a mesial temporal onset of seizures.15 A different sequence or visual, auditory, and somatic auras at the beginning orient us to extratemporal foci with propagation to the mesial temporal lobe.16 Dystonic positions of hands as an initial symptom can orient us to the contralateral frontal area, while if present after behavioral arrest and automatisms, they lose their localizing precision. If a tonic-clonic seizure occurs after auras or the symptoms previously mentioned, they are probably the result of propagation of a partial seizure, but if it is not preceded at all by any symptom, it is reasonable to presume that they are primary generalized seizures. Postictal symptoms have to be taken into consideration; for example, if there is amnesia and sleepiness during several hours, we suspect mesial temporal lobe seizures. If, on the contrary, there is an immediate recovery, frontal origin is more probable. Interictal behavioral changes must also be explored, since conduct abnormalities such as perseverance and aggressiveness (frontal lobe symptoms), depression, anxiety, and memory problems (mesial temporal lobe symptoms) can orient us to a specific area. Together with the neuropsychology team we can design the appropriate testing for each patient.

Surface Electroencephalogram The electroencephalogram (EEG) is considered the most important test for diagnosis since its initial description. Indeed, when abnormal, EEG provides valuable information. Interictal data: Focal discharges consisting of spikes and acute waves, usually localized to the epileptic area are suggestive of focus location; if a focal discharge occurs at or near one of the electrodes common to two channels, we will observe a phase reversal, pointing to the focus localization. If a discharge occurs midway between two electrodes, each will be equipotential and the channel connected between them will not show an abnormality. Some patients have bilateral secondary synchrony. This occurs when seizure activity starts in a cortical or mesial focus and spreads by the way of the thalamic reticular formation. A careful analysis will show that activity starts in a specific area and then spreads to other areas. Ictal data: Ictal recordings usually show acute and rhythmic theta activity, which starts in the affected region and afterward propagates to other areas. The postictal activity can be slow and unilateral indicating the affected hemisphere.17 A normal EEG does not mean that a patient does not have epilepsy; it is also true that the same patient might have different data in several EEG recordings taken on different days. One patient can have a normal EEG one day, abnormal right data another day, and contralateral data in another recording. This is part of the challenge of the epileptologist, to find concordance. Ictal recordings usually show acute and rhythmic theta activity, which starts in the epileptic zone (EZ, area where seizures are initiated) and afterward propagates to other

1161

areas. The postictal activity can be slow and unilateral indicating the affected hemisphere.17 

Continuous Video/Electroencephalogram Monitoring This technique consists in recording simultaneously the EEG as well as the behavior of the patient for a period that can last up to several days.18 This method allows for the confirmation of the clinical type of seizures and their correlation with the onset of abnormal EEG activity, particularly ictal activity, and detection of those cases with pseudo-­epileptic seizures. Both EEG and video/EEG recordings have their limitations. In spite of the length of the registration period, sometimes seizures do not occur, or multiple movement artifacts do not permit proper visualization of the abnormalities. The spatial resolution is not specific enough to permit the precise localization of the EZ and the clinical seizure type and EEG recordings do not always coincide so that sometimes intracranial recording becomes necessary. 

Neuropsychological Assessment in Surgical Candidates The overall objective of neuropsychological assessment in candidates to surgery for epilepsy is to seek evidence of cognitive deficits and their relationship with other studies (clinical and electrophysiological).2–5,8 Neuropsychological testing answers specific questions that other specialists of the epilepsy clinic have made and whose response has a significant impact on surgical decision. (1) What is the patient’s overall neuropsychological status? (2) Which is the hemispheric dominance for language? (3) If cognitive deficit exists, is it lateralized? (4) Is there concordance between neuropsychological findings and structural and electrophysiological results? (5) Should the patient have any sequelae from surgery, can we predict the degree of recovery? There are specific tests for each of the above questions. We will focus on questions two and three of the above, with particular attention to those adult patients with temporal lobe epilepsy (TLE). 

Hemispheric Dominance for Language Determining the lateralization of language can have a significant impact in surgical planning. It has been established10,28 that 95% to 99% of right-­handed subjects and 15% to 19% of left-­handed have a left cerebral hemispheric dominance for language. Due to the small percentage of subjects who may have a right hemisphere dominance, it is very important to clarify each case.12,13 This statement brings up another important fact: a right-­ handed patient who presents with difficulties of language might be mistakenly classified as having a left hemisphere affection when in fact he could have dysphasia of the dominant hemisphere, which is not necessarily the left. For decades, the Wada test has been the gold standard for determining hemispheric language dominance (HLL).10,14,15,17,18,22,32 Recently, a growing number of publications report that other techniques such as functional magnetic resonance imaging (fMRI) may have the same degree

1162

Section Six  •  FUNCTIONAL NEUROSURGERY

R

L

L

L 4

2

0

of reliability17,23–25,27,35 without the disadvantages of cost, risk, and complexity of other techniques.19,29 found a 91.3% concordance between the Wada test and fMRI. Other authors have also found correlation between these two methods, even in cases with bilateral representation of language.15 New noninvasive techniques are evolving to substitute Wada test, however, they still present limitations.20–23 To determine the HLL using fMRI, most authors use the task of evoking words silently30,34 based on a semantic category (e.g., names of animals) to activate temporal regions, or a phonological category (words beginning with same letter) for activating frontal regions of the dominant hemisphere.21,36 Fig. 99.1 illustrates a fMRI study using a phonological category. Dichotic listening technique (DLT) has also been proved useful in determining the HLL.9,31,33,37 It consists of simultaneous presentation of two words (one in each ear) with the same characteristics in terms of sound, number of syllables, and common use, with the intention to present some competition for processing stimuli between the two hemispheres. With this methodology it has been shown that the majority of right-­and left-­handed subjects have right ear advantages as a reflection of a left HLL.33 Fig. 99.2 shows the variability in the index of HLL according to the dichotic listening test in right-­handed healthy subjects. The lateralization index language (LI) is a predictor of postoperative verbal memory deficit as shown by some studies.20 

Lateralization of Memory Deficits Lateralization of memory deficits (LMDs) is another objective of preoperative neuropsychological assessment. Table 99.1 presents some of the available memory tests. At our Clinic we use the Battery of Learning and Memory and the Visuospatial Learning and Memory tests. When the LMD is found in the

FIGURE 99.1  Functional magnetic resonance imaging study showing left cerebral hemispheric dominance for language in a healthy subject using a phonological category (see text).

same hemisphere where the EZ has been localized through clinical, EEG, and imaging data, the decision for surgery is strengthened, otherwise the complete testing described in Table 99.1 is applied.2,5,8 Evaluation of memory is performed by well-­established tests (Fig. 99.3) that may vary slightly from one center to another.8 In approximately 50% of patients it is not possible to determine the LMD through neuropsychological studies alone,2 but that percentage decreases information provided by neuropsychological testing is concordance with other studies. A major problem in LDM is that there is a high error rate due to language dominance, as discussed above: that is, verbal memory deficit does not always indicate affection of the left cerebral hemisphere. 

Imaging Studies The best imaging method to study epilepsy is magnetic resonance imaging (MRI) because of its excellent spatial resolution employing basic sequences such as T1WI, T2WI, and FLAIR, due to its capacity to characterize signal intensity of normal and pathologic brain tissue with high sensitivity to detect cerebral lesions and very good specificity to suggest neoplasic, vascular, atrophic, dysplastic, infectious, and degenerative etiology. MRI allows the differentiation of edema, demyelinating diseases, heterotopic gray matter (see Fig. 99.3), and space-­occupying lesions involving anatomical structures causing epilepsy. In a series of 40 patients with refractory focal epilepsy, Knake et al.24 found that studies with 3T phased array surface coil (PA-­MRI) yielded additional diagnostic information in 48% of the studies (19/40) when compared to routine clinical reads at 1.5T. In the subgroup of patients with previous 1.5T MRIs interpreted as normal, 3T PA-­MRI resulted

99  •  Multidisciplinary Presurgical Evaluation for Epilepsy Surgery

INDEX OF LANGUAGE LATERALITY IN RIGHT-HANDED HEALTHY SUBJECTS (n = 53) 60

Frecuency (%)

50 40 30 20 10 0 SLL

WLL

B

WRL

SRL

FIGURE 99.2  Variability in language laterality in right-­handed healthy subjects using the dichotic-­listening test. The laterality index (LI) is obtained as follows (36): (L − R)/(L + R) = LI, where L = number of words heard with the left ear, R = number of words heard with the right ear. A positive LI corresponds to a left-­predominant lateralization and a negative LI corresponds to a right-­predominant lateralization, as follows: SLL = strong left lateralization (+0.50 to +1). WLL = weak left lateralization (+0.25 to +0.50). B = bilateral representation (+0.25 to −0.25). WRL = weak right lateralization (−0.25 to −0.50). SRL = strong right lateralization (−0.50 to −1).

1163

in the detection of a new lesion in 65% (15/23). In the subgroup of 15 patients with known lesions, 3T PA-­MRI better defined the lesion in 33% (5/15). On the other hand, Zijlmans et al.25 stated that patients studied with 1.5T show loss of cerebral tissue and mesial temporal sclerosis better than 3T, while those patients with cerebral dysplasias are better studied with 3T. High-­resolution 3T MRI (HR 3T MRI) and surface coils applied over the suspected epileptogenic zone are useful to detect lesions in patients suffering refractory epilepsy to medical treatment especially in cortical development malformations (CDMs).26 Successful surgery is possible even with normal MRI, but it requires adequate clinical and electrophysiological evidence of seizure onset. In order to optimize diagnosis of mesial temporal sclerosis and the severity of hippocampal atrophy, it is important to realize a precise hippocampal evaluation with axial and coronal images in MRI. Axial images oriented perpendicular to the axis of the clivus, 2 mm thick without any gap provide an adequate view of the hippocampal structures. Coronal images are taken perpendicular to axial sections. Hippocampal areas can be evaluated with region of interest (ROI) measurement to define possible differences in volumetric areas indicating hippocampal atrophy (Fig. 99.4A). Flair sequences offer an objective method to evaluate hippocampal area signal intensity in order to define hippocampal atrophy and mesial temporal sclerosis (see Fig. 99.4B), which may be associated to ipsilateral mammillary body and fornix atrophy (Fig. 99.5).

Table 99.1  Most Frequently Used Tests in Epilepsy

MAGNETIC RESONANCE SPECTROSCOPY

General Batteries Wechsler Intelligence Scale Halstead-­Reitan Battery Hemispheric lateralization Wada Test

MRI was primarily employed to obtain structural images of the brain. In TLE, the most common pathologic finding is mesial temporal sclerosis. The characteristic pattern of hippocampal neuronal loss and gliosis is found in most patients undergoing epilepsy surgery. Magnetic resonance spectroscopy (MRS) is now employed to assess regional cell loss through determination of the concentrations of intermediate metabolites, including glutamate and glutamine.27 This noninvasive technique includes measures of other metabolites of cellular activity such as N-­acetyl-­aspartate (NAA), creatine (Cr), and choline (Ch) that give indirect information of cellularity of the ROI. MRS also provides a broad range of useful functional information as cerebral concentrations of GABA and glutamate, usually associated to increase in pH and inorganic phosphate and reduction of phosphate monoesters. Several studies in patients with epilepsy have documented neuronal loss and alterations in energy, lipid metabolism, acid-­base homeostasis, and amino acid neurotransmitter metabolism.28 Proton MRS imaging studies consistently demonstrate decreased NAA in the epileptogenic temporal lobe (Fig. 99.6). 

Dichotic Listening Functional Magnetic Resonance Imaging Attention Trail Making Test Cancelation Test Language Boston Diagnostic Aphasia Examination Boston Naming Test Token Test Visuospatial and Perceptual Hooper Visual Organization Test Constructional Apraxia Benton Judgment of Line Orientation Motor and Reaction Time Finger Oscillation Hand Dynamometer

Problem Solving, Flexibility Wisconsin Card Sorting Test Word Fluency Stroop Test Battery of Learning and Memory Wechsler Memory Scale Verbal Learning and Memory Story Recall Paired Word Learning Rey Auditory Verbal Learning Test California Verbal Learning Test Visuospatial Learning and Memory Simple Designs Recall Rey-­Osterrieth Complex Figure Benton Visual Retention Test Others Beck Depression Inventory Quality of Life in Epilepsia (QOLIE-­31) International Neuropsychiatric Interview (MINI)

FUNCTIONAL MAGNETIC RESONANCE IMAGING This is a noninvasive functional brain mapping technique assessed on blood oxygen level dependent (BOLD) signal with echo planar images (EPIs). It is obtained during T2* weighted imaging MRI studies, offering a map of physiologic and metabolic functions of cerebral activity during ictal and interictal discharges on images with spatial resolution of a few millimeters and a few seconds of temporal resolution.29,30 One of the first clinical applications of fMRI was presurgical evaluation of cerebral function in patients

1164

Section Six  •  FUNCTIONAL NEUROSURGERY

A

B

1

2

A

FIGURE 99.3  (A and B) Axial and coronal images, showing migration and sulcation disorders, with gray matter nodular heterotopy. Notice the abnormal localization of gray matter in deep white matter lateral to right ventricle with ependymal extension (arrows).

offers information to help therapeutic decisions including those relative to cost-­benefit of the treatment. In patients with refractory epilepsy to medical treatment fMRI evaluates the resection feasibility in 70% of cases, planning the surgical procedure in 43% and a better patient selection for invasive mapping in 52%.31 This diagnostic information allows a surgical resection preserving cerebral functions (Fig. 99.7).9 To date, intracarotid amobarbital testing remains the gold standard in evaluating memory before planning surgery in patients with refractory TLE, when neuropsychological testing is not contributive. Functional MRI holds great promise as a powerful tool in memory evaluation.23 In the future, fMRI will certainly contribute to partially replacing the Wada test in evaluating the hippocampal memory capacities.32 fMRI aids in the localization of language and motor function for patient candidates for epilepsy surgery and has up to a 90% concordance with the WADA test (Fig 99.8).33 

DIFFUSION TENSOR IMAGING TRACTOGRAPHY

B FIGURE 99.4  (A) T2 coronal image with region of interest measurement of the hippocampus. There is atrophy and hyperintensity on the left due to hippocampal sclerosis (arrow). (B) Flair sequence of coronal image showing left hippocampal hyperintensity (arrow), corresponding to sclerosis and atrophy.

with epilepsy and neoplasic lesions near eloquent areas. This technique detects the localization of the representative corporal zones in the primary motor and sensorimotor cortex or language zones prior to surgery. fMRI offers a noninvasive preoperative brain mapping with high sensitivity to detect cerebral lesions defining the margin of the lesion and normal brain tissue with functional expressions. It also predicts possible deficits on motor and sensory or language functions due to expansion of the lesion or surgical procedures and

Diffusion tensor imaging (DTI) allows the detection and examination, integrity, and orientation of discrete white matter fiber bundles not optimally evaluated with conventional MRI. Recently DTI and tractography have been applied to the study of epilepsy and have demonstrated diffusion changes in gray and white matter tissue. DTI gives information on the path of axonic fibers in the white matter as a support to surgical planning.34 It is particularly useful in determining the location of visual pathways in cases proposed for mesiotemporal lobe resection (Fig. 99.9). Intractable TLE is marked by widespread involvement of fiber tracts and asymmetries of white matter fibers, with lower fiber FA ipsilateral versus contralateral to the seizure focus. Image fusion (CT-­ MRI-­anatomic atlas) is used for implanting deep brain electrodes into precise anatomical structures using stereotactic surgical techniques. Image fusion may include angiography, angio CT, or angio-­MRI that allows elaborating electrodes trajectories that avoid cortical and subcortical blood vessel and eloquent areas (see below). Finally, postoperative MRI confirms the place and extension of surgical resection and the correct placement of intracranial electrodes. 

A

B

FIGURE 99.5  T1 coronal images. Left hippocampal sclerosis is associated to widening of temporal horn and ipsilateral atrophy of fornix (A) and mammillary body (B) (arrows).

1

1

RIGHT

LEFT Naa

Naa Miu

Co

Co Cr

Miu Cr

4

3

2

1

0

FIGURE 99.6  Hippocampal univoxel spectroscopy. There is bilateral reduction of N-­acetyl-­aspartate (NAA) compatible with hippocampal sclerosis. Arrows indicate peak NAA values in studies.

A

B

FIGURE 99.7  Functional magnetic resonance imaging (fMRI) and electrophysiologic brain mapping (BM) in a case with partial removal of lowgrade astrocytoma, used to plan total surgical resection. A, Tridimensional MRI reconstruction showing the proximity of previous resection cavity (upper arrow) and residual tumor (lower arrow) to the central fissure. B, Superimposition of MRI, fMRI, and subdural 36–contact grid user for BM. Black zone indicates the place of previous resection, grey zone the tumor mass to be removed, and red zone the area of activation in fMRI using a contralateral hand motor paradigm. Circles correspond to contacts of subdural grids used for BM. Empty circles indicate contacts used silent to electrical high-frequency stimulation (130 Hz), yellow dots contacts from where sensory responses were elicited, and black dots contacts from where somatic-evoked responses were recorded by stimulation of contralateral median nerve. White circles indicate the electroencephalogramepileptic zone. BM, Brain mapping; fMRI, functional magnetic resonance imaging.

1166

Section Six  •  FUNCTIONAL NEUROSURGERY

less capital outlay, uses inexpensive perfusion tracers, and is readily available.39 

Invasive Studies When noninvasive procedures fail in determining the anatomical origin of partial epilepsies, either because results are equivocal or there is no concordance among them, invasive studies become necessary. This more often occurs in: 1. Patients without structural lesions in imaging studies. 2. Patients with bilateral homologous interictal discharges and/or alternative onset of ictal activity in both hemispheres in video EEG studies. 3. Discordance between clinical seizure type, EEG, and image studies on the localization of the EZ. 4. EZ located near eloquent areas, which may compromise surgical resection with possible neurological deficit.

SPHENOIDAL ELECTRODES FIGURE 99.8  Tractography of horizontal temporal-frontal and temporal-occipital (Meyer’s) tracts in a patient with left anterior temporal lobectomy associated with quadrantanopsia. On the side of surgery, there is interruption of fibers of Meyer’s loop (arrow).

POSITRON EMISSION TOMOGRAPHY The primarily use of positron emission tomography (PET) in epilepsy is presurgical localization of the epileptic focus in patients with complex partial seizures (CPSs). The role of PET is not limited to clinical benefits in presurgical evaluation of epilepsy but also has the ability to quantify cerebral metabolism, blood flow, oxygen extraction, and receptor kinetics in an attempt to understand the pathophysiology of epilepsy.34 The positron-­emitting radionuclides used most commonly in PET imaging are oxygen-­15 (15O), nitrogen-­13 (13N), carbon-­11 (11C), and fluorine-­18 (18F).35 The accuracy of PET quantification is based on understanding the physiologic process of interest and the radiotracer by which this process is measured. The radiotracer is a compound to which the radionuclide is attached. Glucose using 18F-­2-­deoxyglucose (FDG) and cerebral blood flow using H215O (O15) are the two most common physiologic processes measured by PET. Most PET images are the result of time-­dependent integration of metabolic activity. For FDG studies, this varies from 30 to 45 minutes.36 FDG PET has the highest sensitivity and specificity in nonlesional epilepsy evaluation by acting as a combined measure of metabolism and anatomy.37 

SINGLE PHOTON EMISSION COMPUTED TOMOGRAPHY Ictal single photon emission computed tomography (SPECT) has been extensively studied in patients with partial epilepsy, particularly temporal lobe seizures, driven primarily by the need for preoperative localization, the volume of patients affected, and the type of seizure activity. There is a pattern of markedly increased temporal lobe perfusion accompanying the ictus, involving the mesial and often to a greater extent the anterolateral neocortical structures.38 Perfusion follows changes in metabolism during seizures and in the normal brain; imaging interictal and ictal brain-­blood flow with SPECT is a feasible alternative to PET, requires

Performing a minimally invasive procedure under local anesthesia and guided by fluoroscopy, we can implant sphenoidal electrodes. The idea is to bring a percutaneous inserted electrode tip close to the bone window represented by the foramen ovale at the skull base and have a closer recording of mesial structures of the brain without performing intracranial surgery. With the patient positioned in dorsal decubitus, his head hyperextended, and the x-­ray beam angulated to take a skull base film, a 21-­gauge spinal tap needle is inserted 2 cm lateral to the lip commissure. Guided by fluoroscopy the needle is directed to the entrance of the foramen ovale. A fine stainless steel electrode is isolated but at its end is passed through the needle just to the level of the skull base. The needle is removed and the electrode left and taped in place (we use Microspore tape, 3M) to the cheek. Sphenoidal electrodes help to define the side of the mesiotemporal epileptic foci (MTE) in cases of equivocal scalp EEG recordings. They are sometimes used to rule out MTE in cases with pseudo-­epileptic attacks (Fig. 99.10). The reason for limiting the use of sphenoidal electrodes is that unfortunately EEG recordings can be contaminated with different artifacts and are uncomfortable for the patient. 

INTRACRANIAL ELECTRODES Intracranial electrodes are used to explore cortical and subcortical structures by recording spontaneous and evoked EEG activity and applying electric current to obtain clinical eng EEg responses. Intracranial electrodes may be of two types (Fig. 99.11):    1. Plate electrodes in the form of flexible grids containing from 20 to 64 rounded contacts or strips with 4 to 16 contacts. Plate electrodes are placed subdurally and are used to explore cortical areas in the convexity, base of the brain, and interhemispheric cortex. Their placement requires the exposure of the cortical area to be explored, therefore, for correct placement the size and location of the initial craniotomy are of paramount importance. When the epileptogenic area has been localized over the convexity by noninvasive studies, the placement of grids and strips to define its extension and proximity to eloquent areas requires a craniotomy large enough to allow

99  •  Multidisciplinary Presurgical Evaluation for Epilepsy Surgery

FO FR

1167

FO FR

FP2 R sph

F8 T4 A2 FP2

A2

F8 T4 T6 FP1

L sph

F7 T3 A1 FP1

A1

F7 T3 T5

FIGURE 99.9  Skull base radiogram showing implanted sphenoidal electrodes. The tip of the inserted electrodes is at the entrance of the foramen ovale (FO), which is placed anterior and medial to the foramen rotundum minor (FR). Recordings from the electrodes clearly show unilateral interictal spiking on the right sphenoidal electrode leads (R sph) when compared to scalp monopolar leads (A1–A2) and the left sphenoidal (L sph).

for direct visualization of all or as much of the grid’s contacts as possible. The worst scenario is that the epileptic focus is beyond the craniotomy’s edge, forcing the surgeon to extend the incision or to make a new one perpendicular to the original, thus creating acute edges and compromising skin and/or bone flap vascular supply. The craniotomy size and location and the size of the grid or strips depend mostly on the results of presurgical evaluation studies, namely ictal semiology, surface EEG, and imaging studies. Obviously, basal and mesial areas of the brain are

difficult to see directly regardless of craniotomy size. When the epileptic area is placed in cortical basal areas subdural grids are slipped under the brain through a craniotomy of a size that allows an entire lobectomy. This also applies for the placement of interhemispheric grids, which are often bilateral. We do not recommend burr holes to introduce electrode strips over the cerebral surface, since they provide a poor spatial resolution for epileptic foci location and brain mapping.40 For both strips and grids, subdural bridging veins

1168

Section Six  •  FUNCTIONAL NEUROSURGERY

2

3

4

1 FIGURE 99.10  Different types of intracranial electrodes: 1. Sphenoidal electrodes. 2. Grids and strips consisting in silicon plates containing round plate contacts, to be inserted subdurally. 3. Parasagittal intracerebral electrodes to explore longitudinal areas such as amygdale-­hippocampus complex. 4. Orthogonal placed electrodes to explore different cortical and subcortical structures in suspected multifocal epilepsy involving more than one cerebral lobe.

MRI

CT

FIGURE 99.11  Imaging fusion of per-­operative computed tomography (CT) (lower half) showing the planned trajectory to insert an amygdala-­hippocampal electrode (interrupted white lines). This image is superimposed to a postoperative magnetic resonance imaging (MRI) (upper half), showing the electrodes in place (black dots corresponding to electrodes contacts), in both the amygdala (anterior arrow) and the hippocampus (posterior arrow). CT-­MRI fusion provides the advantages of indirect targeting to a nondistorted CT image and direct target made with the anatomical detail of MRI studies.

or adhesions could constitute a problem for accurate placement.41 2. Deep brain electrodes are fine tubular (0.8 to 1.3 mm in diameter) devices with multiple contacts along their trajectories. They are inserted in different cortical and subcortical anatomical structures using stereotactic techniques, guided by different imaging modalities (x-­ ray ventriculography, angiography, CT, and MRI), and coupled with anatomical atlases by a fusion imaging software. Imaging fusion allows elaborating virtual trajectories to reach the targets precisely and traversing nonvascular territories (Fig. 99.12).42 Deep brain electrodes may be inserted through parasagittal frontal, parietal, and occipital approach, or perpendicular to the sagittal plane (orthogonal approach).    In the parasagittal approach, electrodes usually traverse larger distances to get to the subcortical targets, however, their trajectories may be easily planned to avoid vascular areas. This approach is used to explore longitudinal anatomical areas, such as the amygdale-­hippocampal complex when bilateral independent epileptic foci in this region are suspected (Fig. 99.13).14 Frontal and parietal parasagittal approaches are used to explore the insular cortex, avoiding the risk of orthogonal placement traversing the densely vascular Sylvian fissure.14,43 Orthogonal approach allows a better definition of EZ and the areas involved in the propagation of the epileptic seizure, either unilateral or bilateral. It is the most adequate method to be used in cases where multilobar participation in seizure genesis is suspected, like in frontal-­ temporal, frontal-­parietal, temporal-­occipital foci, as an almost unrestricted number of electrodes may be inserted with low morbidity.44 Through intracranial electrodes we record EEG from different structures of the brain that may be involved in the genesis and propagation of spontaneous seizures.44 The advantage of recording with intracranial electrodes is that they are not subjected to physiologic artifacts such as movement and sweating; they are much closer to the seizure origin; their spatial resolution is high and can show ictal onsets with specificity.45 When EEG recordings with intracranial electrodes are performed with simultaneous video-­telemetry, we can punctually determine the relationship between behavioral changes and EEG data. Interictal data: Unlike surface EEG, interictal elements detected with intracranial electrodes are very conspicuous, with high amplitude, acute and fast. It is common to find interictal spikes in several contacts and as such, it is difficult to base our focus localization without ictal activity, although sometimes they have high amplitude and show phase reversal which suggests the precise focus location as seen in the figure. Sleep studies are also useful, since during REM sleep, the interictal spikes are more localized to the seizure onset. Nevertheless, ictal activity is the golden standard to define focus location. In the hippocampus onset of seizures is anticipated by desynchronized fast activity occurring in the epileptic focus,45–48 the low-­ voltage fast one (see Fig. 99.2) or high-­voltage slow pattern.49 When ictal onset is found in one or two contacts it is considered a focal onset; if on the other hand ictal activity onset is observed in more than three contacts simultaneously, it is not a focal but a regional onset.50 If, as shown in Video 99.1, the ictal

99  •  Multidisciplinary Presurgical Evaluation for Epilepsy Surgery

A

B

C

1169

FIGURE 99.12  Bilateral parasagittal electrodes inserted through occipital approach to explore the amygdalae and hippocampi in a case suspected to have bilateral hippocampal independent foci. A, Coronal section showing electrodes within the hippocampus (arrows). B and C, Sagittal and axial sections showing the position of the two most anterior contacts in the amygdala (anterior arrows) and the last four contacts within the hippocampus (posterior arrow).

12–7

extend beyond the epileptic focus, although their pattern has not been described. There appears to be no association between the extent of HFOs and seizure count, but an association has been found between the rate of HFO and seizure count.25,52 On the other hand, electric current applied to different contacts of intracranial electrodes serve to identify the EZ as the place with lowest threshold to induce an EEG after discharge, accompanied by a clinical seizure similar to the spontaneous seizures the patient presents.53 

7–2

INTRACRANIAL ELECTRODES AND BRAIN MAPPING

FP2-F8 F8-T4 T4-T6 16–11 11–6 6–1 17–12

18–13 13–8 8–3 20–15 15–10 10–5 FIGURE 99.13  Shows interictal data in a patient with a right basotemporal grid. First three channels correspond to surface electroencephalogram and the rest to the temporal grid. Activity is restricted to two channels with phase reversal in contact six corresponding to anterior parahippocampus. Note that surface recording does not show epileptic activity.

EEG onset is focal and precedes several seconds the behavioral changes, the postsurgical results regarding seizure reduction are better.51 Epilepsy centers are now including the identification of high-­frequency oscillations (HFOs), known as ripples (80 to 250 Hz) and fast ripples (250 to 500 Hz), as part of the process of identification of the epileptic focus. Total rates of HFOs are significantly higher in the seizure-­onset zone than outside, their rate either increases or decreases before the onset of EEG and clinical seizures, and they

Electric current applied through intracranial electrodes is used to identify the location of eloquent areas (brain mapping or BM). BM is carried out with the patient awake and able to perform motor, speech, and cognitive tasks, as well as to report any distress elicited by electrical stimulation.54 The spatial precision is excellent if we stimulate with low intensities. Two types of pulses are used to map eloquent areas: Low-­ frequency (1 to 2 Hz), high-­amplitude (1.0 to 5.0 mA), and long pulse duration (1.0 to 3.0 ms) electric current is used to induce focal muscular contractions in contralateral extremities when applied to motor cortex. High-­frequency (50 to 130 Hz), low-­amplitude (0.5 to 10.0 mA), and short pulse width (0.21 to 1.0 ms) electric current interferes with spontaneous ongoing activity, such as speech or voluntary movements, or elicits sensory changes in the form of paresthesias.55 

TRANSOPERATIVE VERSUS EXTRAOPERATIVE ELECTROCORTICOGRAPHY (ECO) AND BRAIN MAPPING EEG recording and BM may be performed just before resection of the EZ in the same day or the craniotomy or the electrode implantation can be performed in a first operation and resection of EZ as a separated procedure. This allows the neurology-­neurophysiology-­neuropsychology team to carry on recordings and BM using as much time as necessary to accomplish the goal of precisely defining the location of EZ

1170

Section Six  •  FUNCTIONAL NEUROSURGERY

and eloquent areas, so the surgeon has all necessary information to establish the surgical plan.56 For the past 20 years we have used the two-­stage operation strategy and found it very convenient for the patient and for the surgical outcome. Most of the published reports focus on the results obtained with transoperative ECoG, while there are comparatively few reports on extra-­surgical ECoG. Although transoperative Eco and BM have the obvious advantage of reducing the study and treatment to a single procedure, thus giving the impression of being safer, in our experience the inconveniences outweigh the advantages. At our institution we do not use transoperative electrocorticography but rather an extraoperative long-­ lasting recording for a number of reasons: 1.  Time available to record electrical cortical activity is limited during surgical procedures resulting in a limited chance to record a seizure. More often one records only interictal epileptiform activity.57 2. The neurophysiologist must read and interpret recordings and BM as they are obtained, thus mandating the need for both the equipment and neurophysiologist to be either in the operating room or in an area where close communication with the surgeon is possible.57 If cognitive functions or language have to be explored, the presence of the neuropsychology team is also required. This often results in crowded operating areas where the sterility of the procedure is compromised and accidents are prone to occur (e.g., tripping on one of the many cables). 3. Spontaneous seizures seldom occur during neurophysiological (EEG) examination, so important decisions have to be taken based on interictal recordings or on seizures induced by a convulsing drug. Seizures induced with pentylenetetrazol or other methods do not necessarily originate at the epileptic focus. Besides, spontaneous seizures that may occur during the transoperative registration are not necessarily the ones that the patient presents most frequently. 4.  Transoperative ECoG recording is usually done with an awake patient because of concerns of interference of anesthetic agents with the recordings. Of note, sufentanil, fentanyl, alfentanil, propofol, and methohexital have been reported to produce epileptiform changes on ECoG, whereas propofol, halothane, barbiturates, and benzodiazepines may suppress the epileptic activity.57,58 5. Craniotomy in awake patient is particularly complicated in children, mentally retarded, anxious, or even tired patients. The surgical experience can generate unnecessary stress and poor cooperation, which is only augmented by the cortical mapping phase of the procedure. 6.  When comparing transoperative and extraoperative ECoG in 21 children, spike frequency was decreased by anesthetic agents; the spatial pattern of spikes was found to have a positive correlation in the 9 patients who had 10 or more spikes/min during intraoperative ECoG (mean ⍴ = 0.62; P < .01) and in 5/6 cases with 1 to 9 spikes/min (mean ⍴ = 0.50; P < .01).59 

SURGICAL TECHNIQUE FOR SUBDURAL ELECTRODE PLACEMENT Standard surgical techniques are used: general anesthesia is undertaken. Bony surfaces should be padded as necessary; microsurgical techniques are seldom necessary so head fixation is not mandatory. The skin flap is reflected and a bone

flap created, making sure a thorough hemostasis is obtained; placement of an epidural hemostatic agent below the craniotomy’s edges and dural tack-­up sutures should not be missed, and once the dura has been opened, the surgeon must look for and coagulate bleeding points on the dural edge. All of these precautions intend to prevent a subdural hematoma that could interpose itself between the arachnoid surface and the electrode grids resulting in movement of faulty recording from the latter. The electrode grids (and strips for that matter) should be soaked in non-­saline solution to allow for easier sliding over the arachnoid surface, particularly beyond the craniotomy’s edges. It is of utter importance that the surgeon identifies perfectly each cable of the grids used to ensure that proper connections with the EEG head mount and stimulator are established. Our practice is to write down the color codes of each cable and the cortical area they cover and use specific suture materials to tie together the cables of the same grid. Grids are fixed in position with a 4-­0 nylon suture from their edges to the dura. A drawing or sketch of the contacts of the grids and strips in relation to identified cortical landmarks helps the neurophysiologist in locating the epileptogenic and eloquent areas. The dura should be closed as watertight as the cables allow. We do not use stab wounds to externalize the cables to prevent contamination of the tunnel when the distal end of the cables is pulled for removal. Rather, we externalize them through the surgical wound. Galea and subdermal tissue are closed with an absorbable suture and the skin is closed with a nonabsorbable one. After surgery the patient is taken to his or her room and a postoperative MRI confirms the electrodes localization. Antibiotics are continued throughout the entire process of focus identification and cortical mapping; AEDs are usually discontinued the night of the surgery so that recording can begin the next day. Patients with a history of status epilepticus, abundant seizures, or severely altered surface EEG are not taken off medications until we have evaluated the first days of recordings and the need to gradually taper the medications. Head dressings are changed daily, giving us the chance to inspect the wound. When a CSF fistula occurs, additional stitches, head elevation, bed rest, and sometimes acetazolamide are used. Close neurological observation is mandatory, since patients with subdural grids may develop subdural hematomas (see complications later). Should a patient present three or more consecutive generalized seizures in close proximity, we administer 5 to 10 mg of diazepam to prevent status epilepticus. 

SURGICAL TECHNIQUE FOR INTRACEREBRAL ELECTRODES As mentioned above, intracerebral electrodes are implanted using stereotactic techniques. After the frame has been placed, a contrast CT or MRI is obtained. We prefer to obtain both and use image fusion to analyze the stereotactic position of the targeted structure. This gives the advantage of indirect calculation using the CT image that is not subject to distortion and the anatomical identification of the target using the more detailed MRI. Moreover, after CT and MRI have been fused, the target is analyzed on anatomical atlases provided with the fusion software (see Fig. 99.13).

99  •  Multidisciplinary Presurgical Evaluation for Epilepsy Surgery

For implanting the electrodes to explore the amygdala-­ hippocampal complex using an occipital approach, two burr holes are placed guided by the stereotactic trajectory. Electrodes are implanted and held in place with a plastic ring that fits the size of the burr hole and a cap. They are externalized through the wound to prevent contamination when explanting them. Orthogonally implanted electrodes require a much more sophisticated technique. CT and MRI images should be fused with an angiography to prevent lesioning vascular structures. Each electrode has four to eight contacts, and at least three of them are used to explore the hippocampus and amygdala. They offer the advantage of recording neocortical and paleocortical structures simultaneously, thus allowing the detection of extra-­mesial foci. Other areas of the brain anatomically related to the suspected EZ can be covered. This is the case of orbitofrontal and motor areas. Insular electrodes can be implanted but, as mentioned before, due to the high risk of lesion of the Sylvian vessels, orthogonal electrodes have been substituted by parasagittal, frontally or parietal-­inserted electrodes. Each orthogonal electrode requires a stereotactic-­planned burr hole and a separate stab wound. Moreover, when extraoperative recording is to be undertaken, implantation of a screw in the cranial vault is used to hold the electrodes in place. Hollow macro electrodes allow the implantation of microelectrodes in the same trajectory for unitary recording, used mainly for research purposes. In some cases restricted EZ or lesions causing epileptogenesis may be destroyed by radiofrequency lesions through the same orthogonal electrode used for recording.60 

FOCAL EPILEPSY DETECTED NEAR ELOQUENT AREAS Cortical stimulation is usually indicated when corticectomy will be in or adjacent to eloquent cortex. ECo and BM allow the identification of epileptic foci in or near eloquent cortical areas and permit tailoring the resection with satisfactory safety and seizure relief; this has been proved for pure insular lesions and those extending to adjacent lobes.61 In sensory-­motor cortices, an ECoG that demonstrates few postresectional spikes and no distant spikes predicts a better seizure control. 

Complications Infection rate has been reported as 3.9% and epidural hematomas and brain edema rates as 2%.62 It has been said that almost all patients subject to subdural grid placement for extraoperative recordings develop a subdural collection,63 but it has also been reported that only 7.8% of them require surgical drainage.62 Most require only conservative management, and neither volume, midline shift, or maximal thickness predict the clinical course of these patients, so a sound clinical judgment must be exercised to guide their care and need for evacuation.63 The artifact caused by electrodes on CT makes evaluation of electrode placement and complications difficult, and MRI is the preferred method to evaluate them.64 In a series of 21 pediatric patients a CSF leak was seen in 21 patients, 10 had positive subdural cultures, but only 1 of these had a positive lumbar CSF culture, and none developed clinical meningitis; 1 patient developed transient visual field loss after placement of grids over the occipital lobes.65 Another series of 112 children (122 procedures) revealed that placement of additional electrodes was necessary in 5.7% of patients, wound infection occurred in 2.4%

1171

of these patients, cerebrospinal fluid leak in 1.6%, and subdural hematoma, symptomatic pneumocephalus, bone flap osteomyelitis, or strip electrode fracture occurred in 0.8% each. There were four cases of transient neurological deficit (3.3%) and no permanent deficit or death.66

PARADIGM OF SURGICAL TREATMENT Once preoperative evaluation has been completed, the surgical treatment is decided in the following paradigm: 1. When EZ is not in an eloquent area, besides performing a lesionectomy, information derived from the ECo is used to tailor the resection of the EZ, which usually extends beyond the lesion margins. ECo also guides the resection of EZ in epilepsies not associated to lesions. 2. When EZ is near an eloquent area, fMRI and BM are imperative. If EZ is not in the eloquent area, carefully restricted cortical resection according to information obtained from BM is performed. If EZ is within an eloquent area, alternative techniques such as subpial transsection or chronic electrical stimulation of the epileptic focus are indicated. Preliminary results with this last technique are very promising.67 3.  Bilateral homologous foci, like bilateral independent temporal lobe foci with unilateral structural lesion (temporal sclerosis), operate the side of the lesion associated to vagus nerve stimulation in case of residual seizures. If there is no lesion, bilateral neuromodulation of epileptic foci is highly efficient.68 4. In cases of multiple bilateral EZ, centromedian thalamic bilateral stimulation provides 79% to 83% overall improvement,69,70 extended corpus callosum section up to 80%,71 and vagus nerve stimulation up to 56%.72 Numbered references appear on Expert Consult.

REFERENCES

1. *Kwan P, Arzimanoglou A, Berg AT, et al. Definition of drug resistant epilepsy: consensus proposal by the ad hoc Task Force of the ILAE Commission on therapeutic strategies. Epilepsia. 2009;51(6):1069–1077. 2. *Kwan P, Brodie MG. Early identification of refractory epilepsy. N Eng J Med. 2000;342(5):314–319. 3. *Devaux B, Chassoux F, Guenot M, et al. Epilepsy surgery in France. Neurochirurgie. 2008;54(3):453–465. 4. *Guenot M. Surgical treatment of epilepsy: outcomes of various surgical procedures in adults and children. Rev Neur (Paris). 2004;160 Spec No 1:5S241-5S250. 5. *Spencer SS. When should temporal lobe epilepsy be treated surgically? Lancet Neurol. 2002;1(6):375–382. 6. *Ryvlin P, Nashef L, Lhatoo SD, et al. Incidence and mechanisms of cardiorespiratory arrests in epilepsy monitoring units (MORTEMUS): a retrospective study. Lancet Neurol. 2013;12(10):966–977. 7. *Dulac O. Indications for surgery in childhood epilepsies: when and how should children be operated. Neurochirurgie. 2008;54(3):340–341. 8. Bauer J, Reuber M. Medical treatment of epilepsy. Expert Opin Emerg Drugs. 2003;8(2):457–467. 9. Cramer JA, Perrine K, Devinsky O, et al. Development and crosscultural translations of 31- item quality of life in epilepsy inventory. Epilepsia. 1998;39(1):81–88. 10. Torres X, Arroyo S, Araya S, et al. The Spanish version of the quality of life in epilepsy inventory (QOLIE-31): translation, validity and reliability. Epilepsia. 1999;40(9):1299–1304. 11. Brabcova DB, Belohlavkova A, Kohout J, et al. Psychometric properties of the Czech versions of the impact of pediatric epileptic scale (IPES) and Quality of life in epilepsy inventory for adolescents (QOLIE-AD-48). Epilepsy Behav. 2021;114(PtA):107629. 12. *Cramer JA, Westbrook LE, Devinsky O, et al. Development of Quality of life in epilepsy inventory for adolescents (QOLIEAD-48). Epilepsia. 1999;40(8):1114–1121.

1172

Section Six  •  FUNCTIONAL NEUROSURGERY

13. Velasco AL, Boleaga B, Brito F, et al. Absolute and relative predictor values of some non-invasive and invasive studies for the outcome of anterior temporal lobectomy. Arch Med Res. 2000;31(1):62–74. 14. Isnard J. Drug resistant partial epilepsy. Invasive electrophysiological explorations. Rev Neurol (Paris). 2004;160 Spec No 1:5S138-5S143. 15. Delgado-Escueta AV, Walsh GO. Type I complex partial seizures of hippocampal origin: excellent results of anterior temporal lobectomy. Neurology. 1985;35(2):143–154. 16. Walsh GO, Delgado-Escueta AV. Type II complex partial seizures: poor results of anterior temporal lobectomy. Neurology. 1984;34(1):1–13. 17. Williamson PD, French JA, Thadani VM, et al. Characteristics of medial temporal lobe epilepsy II: interictal and ictal scalp electroencephalography, neuropsychological testing, neuroimaging, surgical results and pathology. Ann Neurol. 1993;34(6):781–787. 18. Provincial Guidelines for the Management of Medically Refractory Epilepsy in Adults and Children who are not Candidates for Epilepsy surgery. Epilepsy Implementation Task-Force. Critical Services Ontario. American EEG Society Guidelines; 2016. 19. *Arora J, Pugh K, Westerveld Met al. Language lateralization in epilepsy patients: fMRI validated with the Wada procedure. Epilepsia. 2009;50(10):2225–2241. 20. *Pelletier I, Sauerwein HC, Lepore F, et al. Non-invasive alternatives to the Wada Test in the presurgical evaluation of language and memory functions in epilepsy patients. Epileptic Disord. 2007;9(2):111–126. 21. Abou-Khalil B. Methods for determination of language dominance: the Wada test and proposed non invasive alternatives. Curr Neurol Neurosci Rep. 2007;7(6):483–490. 22. *Baxendale S. The Wada test. Curr Opin Neurol. 2009;22(2):185–189. 23. *Kesavadas C, Thomas B. Clinical aplications of fMRI in epilepsy. Indian J Radiol Imaging. 2008;18(3):210–217. 24. *Knake S, Triantafyllou C, Wald LL, et al. 3T-phased array MRI improves the presurgical evaluation in focal epilepsies: a prospective study. Neurology. 2005;11(7):1026–1031. 65. 25. *Zijlmans M, de Kort GA, Witkamp TD, et al. 3T versus 1.5T phasedarray MRI in the presurgical workup of patients with partial epilepsy of uncertain focus. J Magn Reson Imaging. 2009;30(2):256–262. 26. *Strandberg EM, Backman S, Källén K, et al. Presurgical evaluation using 3T MRI. Do surface coils provide additional information? Epileptic Disord. 2008;10(2):83–92. 27. *Prichard JW, Rosen BR. Functional study of the brain by NMR. Cereb Blood Flow Metab. 1994;14(3):365–372. 28. *Hugg JW, Laxer KD, Matson GB, et al. Neural loss localizes human temporal lobe epilepsy by in vivo proton magnetic resonance spectroscopic imaging. Ann Neurol. 1993;34(6):788–794. 29. Kuzniecky R. Magnetic resonance and functional magnetic resonance imaging: tools for the study of human epilepsy. Curr Opin Neurol. 1997;10(2):88–91. 30. Ricci GB, De Carli D, Colonnese C, et al. Hemodynamic response (BOLD/fMRI) in focal epilepsy with reference to benzodiazepine effect. Magn Reson Imaging. 2004;22(10):1487–1492. 31. Baumgartner C, Koren JP, Britto-Arias M, et al. Presurgical evaluation and epilepsy surgery. F1000 Res. 2019;29:8:F1000 Faculty Rev-1818. 32. *Dupont S, Baulac M. Contribution of MRI to the exploration of partial refractory epilepsy. Rev Neurol (Paris). 2004;160 Spec No 1:5S91-5S97. 33. *Sell E. Functional magnetic resonance. Medicina (B Aires). 2007;67(6Pt 1):661–664. 34. *Ahmadi ME, Hagler Jr DJ, McDonald CR, et al. Side matters: diffusion tensor imaging tractography in left and right temporal lobe epilepsy. Am J Neuroradiol. 2009;30(9):1740–1747. 35. *Setoain X, Carreño M, Pavía J, et al. PET and SPECT in epilepsy. Rev Esp Med Nucl Imagen Mol. 2014;33(3):165–174. 36. *Lotan E, Friedman KP, Davidson T, et al. Brain FDG-PET: utility in the diagnosis of dementia and epilepsy. Isr Med Assoc J. 2020;22(3):178–184. 37. Theodore WH, Gaillard WD, Sato S, et al. Positron emission tomographic measurement of cerebral blood flow and temporal lobectomy. Ann Neurol. 1994;36(2):241–244. 38. Stefan H, Schneider S, Abraham-Fuchs K, et al. Magnetic source localization in focal epilepsy. Multichannel magnetoencephalography correlated with magnetic resonance brain imaging. Brain. 1990;113(pt 5):1347–1359. 39. *Stefan H, Pawlik G, Böcher-Schwarz HG, et al. J Neurol. 1987;234(6):377–384.

40. *Steven DA, Andrade-Souza YM, Burneo JG. J Neurosurg. 2007;106(6):1102–1106. 41. *Zumsteg D, Wieser HG. Presurgical evaluation: current role of invasive EEG. Epilepsia. 2000;41(suppl 3):S55–S60. 42. *Kelly PJ. Stereotactic navigation: J Tailarach and I. Neurosurgery. 2004;54(2):454–463. 43. *Afif:2008 44. Cossu:2008 45. Spencer 1992 46. *Park 1996 47. Spanneda 1997 48. Schiller et al. 1998 49. *Velasco AL 2000 50. *Engel 1995 51. *Velasco 2000 predictors 52. *Kelley MS, Jacobs MP, Lowenstein DH. The NINDS epilepsy Benchmarks. Epilepsia. 2009;50(3):579–582. 53. *Chauvel P, Landré E, Trottier S, et al. Electrica Stimulation with intracerebral electrodes to evoke seizures. Adv Neurol. 1993;63:115–121. 54. *Grande KM, Ihnen SKZ, Arya R. Electrical stimulation mapping of brain function: a comparison between subdural and stereo EEG. Front Hum Neurosci. 2020;7(14):611291. 55. *Goldring S and Gregorie EM: Surgical management of epilepsy using epidural recordings to localize the seizure focus. Review of 100 Cases. PMID:6699689. DOI:10.3171/jns.1984.60.3.0457 56. *Vakani R, Nair DR. Electrocorticography and functional mapping. Handb Clin Neurol. 2019;160:313–327. 57. *Keene DL, Whiting S, Ventureyra EC. Electrocorticography. Epileptic Disord. 2000;2(1):57–63. 58. Al-Ghanem SS, Al-Oweidi AS, Tamimi AF, et al. Middle East J Anaesthesiol. 2009;20(1):31–37. 59. *Asano E, Benedek K, Shah A, et al. Is intraoperative electrocorticography reliable in children with intractable neocortical epilepsy? Epilepsia. 2004;45(9):1091–1099. 60. Guenot M, Isnard J, Ryvlin P, et al. SEEG-guided RF thermocoagulation of epileptic foci: feasibility, safety and preliminary results. Epilepsia. 2004;45(11):1368–1374. 61. *Spena G, Schucht P, Seidel K, et al. Brain tumors in eloquent areas a European multicenter survey of intraoperative mapping techniques, intraoperative seizure occurrence and antiepileptic drug prophylaxis. J. Neurosurg Rev. 2017;40(2):287–298. 62. *Chauvel P, González Martínez J, Bulacio J. Presurgical intracraneal investigations in epilepsy surgery. Handb Clin Neurol. 2019;161:45–71. 63. *Mocco J, Komotar RJ, Ladoceur A, et al. Radiographic characteristics fail to predict clinical course after subdural electrode placement. Neurosurg. 2006;58(1):120–125. 64. *Silberbusch MA, Rothman MI, Bergey GK, et al. Subdural grid implantation for intracranial EEG recording: CT and MR appearance. AJNR. 1998;19(6):1089–1093. 65. *Simon SL, Telfeian A, Duhaime AC. Complications of invasive monitoring used in intractable pediatric epilepsy. Pediatr Neurosurg. 2003;38(1):47–52. 66. *Johnston Jr JM, Mangano FT, Ojemann JG, et al. Complications of invasive subdural electrode monitoring at Saint Louis Children's Hospital: 1994-2005. J Neurosurg. 2006;105(suppl 5):343–347. 67. *Velasco AL, Velasco M, Núñez JM, et al. Neuromodulation of the epileptic foci in patients with non-lesional refractory motor epilepsy. Int J Neural Syst. 2009;19(3):139–147. 68. *VelascoAL VF, Velasco M, et al. Electrical stimulation of the hippocampal foci for seizure control: a double blind, long term followup study. Epilepsia. 2007;48(10):1895–1903. 69. *Cukiert A, Burattini JA, Cukiert CM, et al. Centromedian stimulation yields additional seizure frequency and attention improvement in patients previously submitted to callosotomy. Seizure. 2009;18(8):588–592. 70. *Velasco F, Velasco M, Velasco AL, et al. 2009 Stimulation of the central median thalamic nucleus for epilepsy. Stereotact Funct Neurosurg. 2001;77(1–4):228–232. 71. *Cukiert A, Cukiert CM, Burattini JA, et al. Long term outcome after callosotomy or vagus nerve stimulation in consecutive prospective cohorts of children with Lennox-Gastaut or Lennox like syndrome and non specific MRI findings. Seizure. 2013;22(5):396–400. 72. Karceski S. Vagus nerve stimulation and Lennox-Gastaut syndrome: a review of the literature and data from the VNS patient registry. CNS Spectr. 2001;6(9):766–770.

CHAPTER 100

Temporal Lobe Operations in Intractable Epilepsy SEPEHR SANI  •  BLEDI BRAHIMAJ  •  ALIREZA BORGHEI  •  RICHARD W. BYRNE Epilepsy affects 1% of the world’s population and incurs an enormous burden of disease.1 One-­third of patients with epilepsy fail to achieve adequate seizure control with antiepileptic drugs or cannot tolerate their side effects.2–4 In temporal lobe epilepsy, patients may experience dyscognitive or complex partial seizures, with auras, and possibly tonic-­ clonic seizures. Auras are generally characteristic in semiology, including epigastric sensation, automatisms, and taste or smell sensation, among others.5–8 There are significant alterations in daily living, disability, loss of work and overall quality of life in poorly controlled temporal lobe seizures. The timely and appropriate selection for patients to undergo surgical intervention following medically refractory epilepsy has proven superior to continued medical therapy alone in regard to seizure freedom.9–15 Surgical technique for anterior temporal lobectomy (ATL) has evolved over many years, with evolution of variable approaches. In this chapter, the foundational principles behind temporal lobe resection surgery are discussed as well as a detailed technical explanation on temporal lobectomy and its variances. The ATL is one of the most common operations for treatment of heavily epileptogenic temporal lobes. Mesial temporal lobe epilepsy (MTLE), defined by hippocampal sclerosis, is of the most pharmacoresistant forms of epilepsy. For a subset of patients with intractable MTLE, ATL offers the possibility of a seizure-­free life. With appropriate selection, validated Class I evidence has demonstrated seizure freedom rates ranging from 70% to 80% with surgical intervention.16–24 Seizure freedom has paramount implications in both the adult and pediatric populations.

History While the modern ATL has evolved over the years, the first applications and descriptions of the technique have existed for over a century. Jackson and Colman described seizures associated with “tasting movements” and a “dreamy state” related to a lesion in the mesial temporal lobe in 1898.25 Dr. Penfield at the Montreal Neurological Institute was one of the first to describe the methodical approach to temporal lobectomy. With better refinements in electroencephalograms (EEGs) and electrocorticography (ECoG), Penfield demonstrated that mesial limbic structures played a key role in what was described as “psychomotor epilepsy.”26 Advances in electrophysiology as well as anatomical and

functional neuroimaging techniques have allowed for more focal localization of seizure foci. This has led to more “selective” resections, with sparing of the temporal lobe neocortex and parts of the amygdalohippocampal complex. Falconer and Morris described early versions of such procedures and their initial experience that would form the basis for the modern ATL.27,28 Niemeyer soon proposed a mesial resection technique that spared the lateral cortex29; this was later adapted by Wieser, Yasargil, and colleagues30–32 and it was the forerunner of the contemporary selective amygdalohippocampectomy (SAH). 

Indications and Patient Selection The evaluation of a patient with intractable epilepsy begins with a thorough history. Assessment of seizure onset, semiology, timing, and duration of epilepsy are recorded. All prior treatments with antiepileptic drugs, including duration, dosages, and responses are noted. A family history of epilepsy, along with identification of any other etiologic factors (e.g., history of head trauma, infection of the nervous system, exposure to neurotoxins, and so on) are queried. Patient selection hinges on the concordance of data from several modalities, including high-resolution magnetic resonance imaging (MRI) with special attention to the mesial temporal lobe structures, EEG, single-­ photon emission computed tomography (SPECT), SPECT co-­registered to MRI (SISCOM), and magnetic encephalography (MEG). Additional testing including neuropsychological assessment, WADA, and functional MRI studies may be needed.33 In 25% of patients, additional data may be needed for seizure focus localization. Examples include cases involving possible bitemporal involvement and cases where the extent of neocortical temporal lobe involvement is not clearly defined. In such cases, invasive monitoring is indicated. Placement of epidural, subdural, and intraparenchymal electrodes can help elucidate and further refine the seizure focus in these patients.34–36 Stereo-­EEG, a technique where intraparenchymal electrodes are inserted through 3-­to-­5-­millimeter bony anchors placed through the skull openings have gained significant popularity recently, owing to advances in stereotactic techniques and intraoperative imaging that allow for precise localization and broad sampling of brain regions.37–39 It is the concordance of these tests that are used to (1) identify the patient as one with the “surgically remediable

1173

1174

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 100.1  Patient positioning and incisional marking for temporal lobectomy. (A) Patient is positioned supine and head fixated with the nose elevated 20 degrees above the horizontal sagittal plane. (B) A frontotemporal curvilinear incisional mark is preferred. In a left-­sided approach, a straighter curve is made (solid line), however, a larger curve with greater exposure is pursued in right-­sided surgery (dashed line).

syndrome” of MTLE,40 (2) localize a seizure focus suitable for resection, and (3) determine that the benefit obtained from resecting the elucidated epileptogenic zone would outweigh any language or memory deficit likely to be experienced. 

Surgical Procedure ANTERIOR TEMPORAL LOBECTOMY The “standard” ATL, in which the lateral neocortex and mesial hippocampal structures are removed in a single specimen, was developed in the early 1950s.41–43 More recently, a two-­part resection, in which the lateral and mesial portions are resected separately, has been favored by most surgeons.44–46 ATL refers to resection of all the neocortical temporal lobe structures, including the superior temporal gyrus (STG), middle temporal gyrus (MTG), inferior temporal gyrus (ITG), fusiform or occipitotemporal gyrus, parahippocampal gyrus and the uncus. However, more often a tailored approach is used to minimize removal of normal tissue. With the use of ECoG, functional imaging, and vascular anatomy, the extent of lateral neocortical resection is determined on a patient-­by-­patient basis. Thus preoperative patient data as well as intraoperative electrophysiology determines resection. This is often quantitated by the number of centimeters of the temporal lobe gyri resected as measured posteriorly from the temporal pole. The procedure is usually performed under general anesthesia, unless ECoG or language mapping are planned. In the former case, nitrous oxide should be discontinued during ECoG, but the patient should remain paralyzed with depolarizing muscle relaxants; in the latter, the procedure may be performed while the patient is awake.47,48 When ECoG is planned, perioperative use of anxiolytic medications (diazepam, midazolam, etc.) that might suppress EEG activity should be avoided. In temporal lobectomy surgery, the patient is positioned laterally in head fixation with the nose elevated 20 degrees above the horizontal sagittal plane. This allows for better long-­ axis visualization of the hippocampus. To assist in venous drainage, the head of the table is raised 20 degrees (Fig. 100.1A). At the author’s institution, a microscope is used for the mesial structure resection. Tissue aspiration and subpial dissection is performed with the use of an ultrasonic aspirator, although bipolar electrocautery is also acceptable. Use of neuronavigation is optional.

A

B

After proper positioning, the surgical area is shaved with clippers, prepared, and degreased utilizing alcohol solution. A frontotemporal curvilinear incisional mark is made (see Fig. 100.1B) being mindful not to extend past the posterior margin of the pinna to prevent necrosis. The surgical area that is marked off is prepared and draped in a sterile fashion. Skin incision is performed and soft tissue dissection is carried down to the root of the zygoma utilizing monopolar cautery. A myofascial flap with the temporalis muscle is reflected anteriorly. Three burr holes are made, one at the key hole, the second at the root of the zygoma, and one at the posteriormost extent of the squamous portion of the temporal bone, just below the superior temporal line. A craniotome is used to complete the frontotemporal craniotomy. Further exposure, if necessary, is gained by using a rongeur to trim down the greater sphenoid wing, and inferiorly, to access the middle fossa. A durotomy is made starting at the posterior edge of the craniotomy in a C-­shaped fashion and reflected anteriorly, anchored at the greater sphenoid wing. The cortical surface is inspected for any abnormalities, as well as for the presence of large draining veins such as the Labbé vein or the middle cerebral vein. At this time baseline ECoG activity can be recorded over the frontotemporal surface of the neocortical structures. A subdural strip may be inserted at the base of the temporal lobe in the coronal plane, placing the tip on the medial parahippocampal gyrus. Depth electrodes may alternatively be utilized to record the hippocampus through the MTG. The depth electrode is oriented perpendicular to the surface of the brain at the level of the MTG, inserted to a depth of 4 cm. This may be assisted by stereotactic image guidance. Neocortical resection may extend between 3 and 4.5 cm from the temporal tip along the sylvian fissure on the dominant side, and 3 to 5 cm on the nondominant hemispheres. However, there are critical considerations in tailoring the extent of anteroposterior resection. Alternations may need to be made with the information obtained from cortical stimulation mapping. Further, attention must also be paid to the neurovasculature. Particular note should be made of the vein of Labbé, which is identified on preoperative MRI and confirmed intraoperatively. Secondly, attention should be paid to the cortical M3 branches overlying the superior and middle temporal gyri. Some of these vessels may arise anteriorly, then curve posteriorly, beyond the limits of the resection and should be preserved.

100  •  Temporal Lobe Operations in Intractable Epilepsy

1175

Supramarginal gyrus Superior and inferior rami of posterior sylvian fissure

STG

Heschl’s gyrus

Am

Sylvian fissure Superior temporal sulcus Middle temporal gyrus

PHG

Inferior temporal gyrus

A

Superior temporal gyrus

MTG

H

Inferior temporal sulcus

B

FG

ITG

FIGURE 100.2  (A) Cortical surface anatomy of the left temporal lobe. (B) Cross-­sectional anatomy of the left temporal lobe at the level of the amygdala and head of the hippocampus. Am, Amygdala; FG, fusiform gyrus; H, hippocampus; Arrow showing temporal horn of the lateral ventricle; ITG, inferior temporal gyrus; MTG, middle temporal gyrus; PHG, parahippocampal gyrus; STG, superior temporal gyrus.

In nondominant cases, further posterior extension to 5 or 6 cm may possibly be achievable without significant impact on memory, language, or cognitive function. More generous lateral resections are typically reserved for situations in which there is suspicion of epileptogenicity in the neocortex. In these cases, ECoG and language mapping may be useful to tailor the resection to match the pathophysiology and to avoid postoperative language deficit.47–50 In most cases of standard MTLE, however, ECoG and large lateral resections are not necessary.46,51 A more sparing approach to the lateral resection was developed by Spencer and colleagues, in which only 3 to 3.5 cm of the temporal tip is removed, leaving the STG intact, regardless of laterality.46,52 Parenchymal resection is done in the subpial plane, emptying the cortical and subcortical structures starting with the STG or MTG (Fig. 100.2). In tailored resections, often the STG is spared. The superior temporal sulcus is coagulated using bipolar electrocautery after identification and sparing of arterial end-­branches. Dissection and aspiration is continued inferomedially through the white matter utilizing a bipolar or ultrasonic aspirator until the collateral sulcus is identified (Figs. 100.3 and 100.4). Once the collateral sulcus is identified, the next step is to establish the cortical-­pial incision line. The subpial cortical resection continues with the emptying of the middle and interior temporal gyri, as well as the fusiform gyrus (see Fig. 100.3). Anatomically, the medial wall of the fusiform gyrus is the previously identified collateral sulcus. Thus, the posterior and medial margins of the lateral resection are complete. To complete the resection of the neocortex, further dissection is undertaken along the white matter temporal stem at a 45-­degree angle, in an effort to avoid entrance into the temporal horn prematurely (Fig. 100.5). The collateral sulcus may be used again as a useful landmark, carrying out the dissection laterally and above the structure. This completes the en bloc resection of the neocortex.

Resection of the Uncus and Amygdala Next, using the ultrasonic aspirator (30% of maximum suction and intensity) or bipolar cautery and suction under microscopic guidance, the uncal gyrus is emptied. The resection starts anteriorly at the temporal pole and ensues

in a posterior direction. It is imperative that the mesial pia is identified and preserved during this process (Fig. 100.6). Once identified, attention is turned to the semilunar gyrus, which marks the antero-­superior limit of the uncus and runs parallel to the endorhinal sulcus. These anatomical structures may be difficult to identify initially, resulting in surgeon uncertainly on the extent of uncal resection, especially the superior border. Relevant vascular anatomy can be of great help at this stage, since it is often constant and aids in identifying a safe line of superior and posterior resection of the amygdala. As the uncal resection progresses, the supraclinoid carotid artery (ICA) is visualized through the mesial pia. Resection follows the ICA line until the takeoff of the posterior communicating artery (PCoA) and anterior choroidal (AChA) arteries are identified. The AChA runs in the endorhinal sulcus through the pia and can be used to identify this sulcus. NB: It is important to maintain the resection below the anatomic line of the endorhinal sulcus, as the anterior fibers of the optic radiations lie directly above. The ICA is identified again through the pia along with the third cranial nerve as the mesial dissection continues. Posteriorly, the free edge of the tentorium is identified. Keeping the mesial pia intact, the ICA is followed until the bifurcation. The M1 is then used as the superior margin of aspiration, allowing for safe radical resection of the uncus. Resection of the amygdala is completed after the identification of the posterosuperior point, the proximal M1 (see Fig. 100.6B). Attention is now turned away from the mesial pia. The posterior margin of the previous neocortical resection is identified under the microscope. The white matter immediately superior to the collateral sulcus (which corresponds to the subcortical white matter of the MTG) is identified and aspirated medially until the temporal horn of the lateral ventricle is entered. With the aid of a nerve hook, the lateral ventricular wall is opened posteriorly. Retractors are utilized to improve visualization of the ventricular structures. One retractor is placed on the roof of the temporal horn, elevating and protecting fibers of the optic radiation just superiorly. The second retractor, typically thinner, is placed in the temporal horn, retracting posteriorly in the long axis, parallel to the hippocampus. In order to preserve

1176

Section Six  •  FUNCTIONAL NEUROSURGERY

Anterior perforated substance Rhinal sulcus Tentorial notch

Inferior temporal gyrus

Uncal notch Uncus Rhinal sulcus

Uncinate gyrus Band of Giacomini

Parahippocampal gyrus

Intralimbic gyrus

Occipitotemporal sulcus Fusiform gyrus

Anterior Choroidal artery

Collateral sulcus Convergence of parahippocampal gyrus and cingulate gyrus

A

B

FIGURE 100.3  (A) Surface anatomy of the basal medial temporal lobe. Basal view of the left hemisphere. (B) Magnified basal view highlighting the uncal gyrus and relevant vascular anatomy. The uncal gyrus is adjacent to the carotid artery, posterior communicating artery, the anterior choroidal artery and the third cranial nerve. The superior aspect of the uncus consists mostly of the amygdala, which receives its blood supply from the anterior choroidal artery and descending perforators of the middle cerebral artery. Superior to the uncal gyrus lies the semilunar gyrus. This small gyrus marks the superior aspect of the uncus and runs in parallel to the endorhinal sulcus. Moving posteriorly, at the posterior medial aspect of the amygdala lies the intralimbic gyrus of the uncus. This small gyrus lies between the amygdala and the hippocampus along the crural cistern and is a critical surgical landmark. The crural cistern is only a potential space, separating the mesial temporal structures from the crus cerebri of the midbrain by a single layer of arachnoid. This rectangular-­shaped landmark is crucial during surgery, as it identifies a safe deep border of resection early on.

S Roof of temporal horn

10 1 13

11 12

Choroidal fissure

2 Choroid plexus

3 8 14

4 7

6

Choroidal point

T

5

B

9

A

A

P H

Intralimbic gyrus

Collateral emminence

B

I

FIGURE 100.4  (A) Coronal cross-­section of the left temporal lobe. The lateral wall of the hippocampus is in the temporal horn (4). Note the relationship of the collateral sulcus (5) bulging into the temporal horn, the collateral eminence. Inferiorly, the hippocampus is surrounded by the parahippocampal gyrus (9). The hippocampus proper is composed of the dentate gyrus (6), CA4 and 3 regions, as well as the CA2 (2), and CA1 (3) regions. The hippocampal sulcus (8) divides the hippocampus from the parahippocampal gyrus. The fimbria and fornix (1) carry the outflow of information from the hippocampus. 1, Fornix; 2, CA2 region; 3, CA1 region; 4, temporal horn; 5, collateral sulcus; 6, dentate gyrus; 7, subiculum; 8, hippocampal sulcus; 9, parahippocampal gyrus; 10, medial and lateral geniculate nuclei; 11, cerebral peduncle; 12, substantia nigra; 13, red nucleus; 14, posterior cerebral artery. (B) Right temporal horn demonstrating the structures of the mesial temporal lobe as viewed during surgery. The middle temporal gyrus has been opened and subcortical white matter dissected, with retractors placed on the roof of the temporal horn. When entering the temporal horn, the hippocampus is seen as a bulging structure with a crescent shape. The hippocampal head is wide and approximately 15 mm in length (H), containing digitations on its surface. The body (B) of the hippocampus begins at the choroidal point and is approximately 10 mm in length before narrowing and blending posteriorly to the tail. The tail (T) wraps around the ambient cistern into the trigone of the ventricle. The dorsal border of the hippocampus is formed by the choroidal fissure, an important landmark. The intralimbic gyrus is a rectangular structure that is identified immediately anterior to the velum terminale, as shown. The velum terminale is a thin triangular-­shaped membrane that is formed by the fibers of the fimbria and stria terminalis. This is also known as the inferior choroidal point. Immediately posterior to this structure is the choroidal point, a thin pinkish membrane that is visible upon retraction of the choroid plexus. The choroidal point is an extremely consistent structure which marks the entry point of the anterior choroidal artery. Its identification is one of the first steps after entering the temporal horn.

100  •  Temporal Lobe Operations in Intractable Epilepsy

1177

45˚ H

H PCA

CS

A

B

Medial & lateral geniculate bodies PCA

H

C

D

Cerebral peduncle

FIGURE 100.5  (A) Cross-­sectional view of sequential neocortical resection. The middle, inferior temporal, and fusiform gyri are removed at a 45-­degree angle. CS, Collateral Sulcus. (B) The temporal horn is entered. The hippocampal sulcus is exposed by rolling the hippocampus in the resection cavity, allowing for mesial division of perforator arteries. (Shown with arrows in C) (D) After hippocampal resection, the superior and mesial structures, including the PCA, cerebral peduncle, and geniculate nuclei, can be seen through the pia.

fibers of the Meyer loop, which project laterally and anteriorly from the lateral geniculate body, a low and anterior opening into the ventricle is preferred (see Fig. 100.6). Preservation of Meyer loop fibers is ideal; however, the resultant superior quadrontopsia from disruption of these fibers is well tolerated by patients and seldom interferes with reading, working, or driving. Once inside the temporal horn, the choroid plexus is visible. It is followed to the choroidal point, its anterior origin (see Figs. 100.4B and 100.6). This is an important intraventricular landmark, allowing the surgeon to navigate the surrounding anatomy. Anterior to the choroidal point is a triangular structure, the velum terminale. Anterior to the velum terminale lies the intralimbic gyrus of the uncus, identified as a white rectangle. The intralimbic gyrus is the most posterior and superior gyrus of the uncus, and has a close association with the cerebral peduncle mesially. The intralimbic gyrus is safely resectable using the intraventricular approach as follows: with great care, ultrasonic aspiration of the intralimbic gyrus is undertaken, identifying the

mesial pia that separates it from the cerebral peduncle. This should be done first, to provide the mesial landmark of safe resection. The mesial pia of the intralimbic gyrus marks the posterosuperior margin of safe resection for the amygdala. An imaginary line is drawn from the mesial pia of the intralimbic gyrus, to the pia of the proximal M1, which was previously identified. Connection of this imaginary line by subpial resection, proceeding caudally, allows for resection of the uncus and the caudal amygdala (see Fig. 100.6). 

Resection of the Hippocampus Resection of the hippocampus commences with the aspiration of the parahippocampal gyrus and subiculum, proceeding from the medial side of the collateral sulcus, moving medially. With preservation of the pia, the edge of the tentorium, ambient cistern, and the posterior cerebral artery are identified. Removal of the parahippocampal gyrus allows for the mobilization of the hippocampus inferolaterally in the resection cavity of the parahippocampal gyrus. The fimbra is visualized medially. Aspirating the fimbra and dentate

1178

Section Six  •  FUNCTIONAL NEUROSURGERY

A FIGURE 100.6  Intraoperative steps of right-­sided amygdalohippocampectomy after completion of neocortical resection. A, anterior; I, inferior; P, posterior; S, superior. (A) Defining the antero-­superior border of amygdala resection. The sylvian fissure (dotted line), inferior frontal gyrus (IFG) and partially removed superior temporal gyrus (STG) are seen. The mesial pia is now visible after complete resection of the anterior uncus (U). The M1 segment is visible through the pia, which marks the antero-­superior border of the resection. Once identified, the location is marked and attention is now turned to the temporal horn further posteriorly. (B) A panoramic view including the temporal horn with a retractor placed along the roof to protect the contents including the fibers of the optic radiation. The hippocampal head (H) is visible. Once choroidal point and velum terminale are identified, the intralimbic gyrus is readily identifiable as the next anterior anatomical structure. The intralimbic gyrus is aspirated subpially (**). This marks the posterosuperior border of amygdala resection and also serves as a medial landmark during amygdala resection. A line drawn (dotted line) from the intralimbic gyrus (**) to the location of M1 (*) is demonstrated by the bipolar forceps as the resection line for the amygdala. (C) The same view as B after resection of amygdala. The head of the hippocampus (H) is now readily visible. (D) Attention is now turned more posteriorly in order to resect the hippocampal head. Superficially, the posterior extent of neocortical resection is shown (white dotted line). Intraventricularly, the hippocampal head (HH) is severed (black dotted line) in the coronal plane from the body (HB). (E) Next the HH is laterally peeled off the pia (arrowheads). The coronal resection line and the hippocampus body (HB) are visible. (F) Attention is now turned to the medial side of the HH where the hippocampal sulcus (*) is identified and carefully coagulated and divided along the long axis of the hippocampus. This step leads to complete separation of the HH. (G) The resection cavity after removal of the HH. The hippocampal sulcus remnant (*) and mesial pia are seen. CP, choroid plexus. (H) Now attention is turned posteriorly and the retractor is adjusted along the axis of the temporal horn to remove the hippocampus body (HB). In this view, the collateral eminence (arrowheads) and the remainder of the parahippocampal gyrus (PHG) are seen. The dotted line shows the coronal resection line of the body from the now removed HH. (I) The HB is first separated subpially on the lateral side (black dotted lines). (J) Next the HB is severed from the tail by aspiration as shown (black dotted lines). (K) Lastly, attention is turned medially. The hippocampal sulcus is identified, coagulated, and divided along the axis of the HB (black dotted lines), allowing its complete removal. L) After removal of the HB, the medial pia is visible. The ambient cistern (*) and the posterior cerebral artery (arrowheads) can be seen through the pia.

A

I STG

I

Fetal PCA

U

H

Am

*

P

**

IFG

AS

B

P A

S

I

I A

H *

C

**

CP

HH

D

S

A

S

I

Pia

I

HH

P

HH

A

* * ****

HB

E

P

HB

P

HB

F

S

S I

I

PHG

P

HB

A *

P

* * HB * * CP

G

A

CP

H

S I

Pia

S

I

P

P Pia HB

HB

I

A

Pia

J

CP

I

K

I

P

HB

Pia

CP

Pia

P Pia

CP

*

A

A

gyrus transects the hippocampus. This exposes the hippocampal sulcus and the branches of the hippocampal artery as they enter the hippocampus. It is important to delineate bypassing branches of the PCA, while carefully coagulating relevant branches. Vascular transection should be performed in the anteroposterior direction, to allow the hippocampal head, body, and desired amount of tail to be removed en bloc (Fig. 100.7, see also Fig. 100.6). Variations in the vasculature may be encountered. A high-­riding superior cerebellar artery may come into the field. Alternatively, the PCA may have a major branch underneath the parahippocampal gyrus. Major anatomical vascular aberrations such as these can be identified on careful review of preoperative MRI. After meticulous hemostasis is achieved, the cavity is lined with oxidized cellulose, and the wound is closed in a standard fashion. 

Pia

L

S

SELECTIVE RESECTIONS Selective Amygdalohippocampectomy In cases of localized mesial temporal pathology, a selective approach may be employed to preserve the neocortical temporal lobe structures. For this resection, a focused incision is made centered on the MTG, approximately 3 cm from the temporal pole. Dissection is then carried out perpendicular to the cortical surface until the lateral ventricle is encountered. Two retractors are utilized, as described above, for proper visualization so that mesial structure resection can begin. In this selective approach, identifying the trans-­pial M1 as the superior-­anterior border of the amygdala resection is not possible, thus different landmarks are used to perform the

100  •  Temporal Lobe Operations in Intractable Epilepsy

H CP

Am

*

CA A1 M1

FIGURE 100.7  Intraoperative left-­sided resection of the mesial temporal structures. The sylvian fissure (black dotted line) and sylvian vein (arrowheads) are shown. Anteriorly and deeper, the uncus has been largely removed and the medial pia is visible. The internal carotid artery (ICA), and its bifurcation (M1, A1) are visible. The anterior choroidal artery is seen (small arrows) traveling along the groove of the now removed rhinal sulcus to the choroidal point (CP). Posteriorly, the retractor is placed along the roof of the temporal horn, visualizing the choroidal point and velum terminale (dotted line). Anterior to that is the now removed intralimbic gyrus (*). The cerebral peduncle is visible through the medial pia of the intralimbic gyrus. A line drawn (black solid line) from here to M1 marks the superior resection line of the amygdala (Am).

resection of the amygdala and uncus. The uncus is resected to the level of the anterior projection of the choroidal fissure. Again, intraventricularly, the choroidal point, velum terminale, and intralimbic gyrus are identified. Aspiration of the intralimbic gyrus and identification of the mesial pia adjacent to the cerebral peduncle is performed. The anterior choroidal artery can be used as a useful landmark here, similar to the superior resection line of the amygdala described earlier in the chapter. The anterior choroidal artery can be traced from the choroidal point forward to the endorhinal sulcus. As the resection is carried anteriorly, the endorhinal sulcus becomes the superior extent of the resection. The amygdala and the uncus can then be safely removed, including the mesial intracisternal portions of the uncus. At this juncture, the resection of the hippocampus is performed as previously described using the standard technique. 

Trans-­Sylvian Approach to Amygdalohippocampectomy Wieser, Yasargil, and colleagues developed the trans-­sylvian approach, a technique which leaves the lateral temporal neocortex intact.31,32 In the trans-­sylvian-­trans-­cisternal approach, a standard frontotemporal craniotomy is carried out. However, in order to facilitate proper visualization during resection, the sphenoid wing and the orbital roof are drilled smooth. After dural opening as previously described, subarachnoid dissection of the sylvian fissure is carried out. The middle cerebral artery (MCA) is encountered and traced down to its origin, where the arachnoid of the carotid cistern is sharply divided. Attention is turned to the sylvian vein, which is traced anteriorly. The sylvian vein should be preserved if possible, and especially if it appears dominant

1179

intraoperatively or on preoperative imaging. Mobilization of the temporal lobe allows for identification of the anterior choroidal (AChA) and posterior communicating (PCoA) arteries. The AChA is a landmark that is followed toward the inferior choroidal point. It may be necessary to perform a subpial dissection of the endorhinal sulcus to visualize the inferior choroidal point, as the visualization of the AChA is lost around the uncus. The parahippocampal gyrus is then visualized, including its superior border: the hippocampal sulcus and the hippocampal formation. Medially the PCoA, AChA, and occulomotor nerve are seen. The SAH is started by entering the border of the hippocampus and the uncal recess. The geniculate body or P2 bifurcation delineates the posterior edge of the resection. The superior limit is the optic tract, and the lateral limit, the margin of the hippocampus at the collateral sulcus or eminence. The major advantages of the trans-­ sylvian selective approach is the early visualization and proximal control of arterial vasculature. This approach also eliminates neocortical violation of the lateral temporal lobe. However, care should be taken with temporal lobe retraction, as it is possible to induce retraction injury during visualization of the mesial temporal and perimesencephalic structures. The trans-­sylvian-­trans-­cisternal approach for amygdalohippocampectomy has been described as part of an effort to spare the anterior optic radiation. Yet visualization of the choroidal fissure can be challenging. Thus there is a risk to the optic tract, optic radiations, and the occulomotor nerve, although this risk is small. A variety of subtemporal approaches have been described in further efforts to keep the lateral neocortex intact.53–55 Major disadvantages of this approach are temporal lobe retraction, risk of injury to venous drainage, including the vein of Labbé, and difficulties with surgical orientation. These approaches are reserved for mesial temporal lesionectomies requiring neocortical sparing. 

Outcomes SEIZURE REDUCTION Surgical intervention in epilepsy is thought to be an underutilized treatment approach in patients with medically refractory temporal lobe epilepsy. It is important to consider that the risk of surgery should be weighed heavily in relation to a favorable outcome, as only significant-­to-­complete resolution of seizures are associated with improved outcomes.56 The most commonly applied metric of efficacy is reduction in seizure frequency on the Engel classification scheme.57 Most studies cite rates of seizure freedom (Engel Class I), which has been shown to correlate with quality-­of-­life improvement following epilepsy surgery.58–60 Surgery may not appreciably improve quality of life unless patients are rendered free (or nearly free) of their seizures.56,61 In a randomized controlled trial by Wiebe and colleagues62 eighty patients with temporal lobe epilepsy were assigned to surgery or continued treatment with antiepileptics for 1 year. At 1 year after randomization, the surgical group had a 58% freedom from awareness-­impairing seizures, compared to 8% in the medical treatment arm. Further, the patients in the surgical group had a statistically significant better quality

1180

Section Six  •  FUNCTIONAL NEUROSURGERY

of life.62 Engel and colleagues queried 100 epilepsy centers and noted that 68% of ATL patients were seizure-­free following surgery.57 A meta-­analysis of recent series has also concluded that rates of seizure freedom following resection for MTLE approached 70%.24,63 Most studies are limited by short 1 or 2 years’ postoperative follow-­up, which limits information regarding long-­ term seizure recurrence. However, evidence suggests that 2-­year outcomes predict long-­term response.64 This has been corroborated by longer follow-­up studies which have 47% to 80% postoperative disabling seizure freedom up to the fifth postoperative year, along with improved quality of life.11,17,19,20,62,65–71 There is a subset of the population with epilepsy localized to the temporal lobe but without the MRI abnormalities typically associated with mesial temporal sclerosis. This population comprises approximately 20% to 30% of patients with temporal lobe epilepsy, and the rate of seizure freedom among these patients is lower, incurring a higher degree of postoperative outcome variability, ranging between 30% and 70%.72–77 At the authors’ institution, 21 patients with electrophysiologically localized MTLE with “negative” MRI underwent ATL. Of the 21 patients, 71% had an excellent outcome (Engel Class I) at 4.8 years’ follow-­up, and 62% at 8.3 years.66 

COMPLICATIONS The ATL and its surgical variances are well-­tolerated procedures. Major complications are exceedingly rare. Postoperative mortality has not been reported in any major series.78–81 In a single-center experience spanning 30 years, no mortalities were reported in all cases of epilepsy surgery. Looking specifically at temporal surgeries alone, in a cohort of 1232 patients, 0.3% had postoperative hematoma, rate of infection was 0.5%, and postoperative hydrocephalus developed in only one patient. The overall morbidity rate was 1.7%.81 Further meta-­ analyses reviewing all publishable works reporting complications in anterior temporal lobectomies found that since the 1980s, surgery has become safer, with a decrease in overall complications. Interestingly, the study found that the rate of infection increases significantly to 5.8% from 1.1%, as did the rate of hemorrhage, from 1.2% to 4.3%, in patients who underwent implantation of electrodes for seizure focus characterization.82 Careful attention must be paid intraoperatively to the manipulation and retraction of major vessels such as the MCA. Damage may lead to hemiparesis, the most common overt neurological deficit of ATL, at a rate of 0.4% to 1.5%.80,81 The incidence of cranial nerve injuries (those to cranial nerve III being more common than those to either cranial nerve IV or cranial nerve VII) resulting in a permanent deficit is less than 1%. As previously mentioned, this is an operation involving functional brain tissue. As such, the loops of Meyer are at risk during resection. Visual field cuts of the contralateral superior quadrant are a common deficit after the surgery, nearing an incidence of 65% in some series.83 While this deficit is typically well tolerated by patients with no overt clinical consequences, it has been associated with extent of resection. In resections reaching 7 cm from the temporal pole, the degree of visual loss is much greater, nearing full hemianopia, which may impair daily living and driving. Longitudinal studies have shown that approximately one-­ third of patients will have some visual field recovery.84–86

Postoperative psychiatric disturbances are common in the weeks and months following surgery, affecting up to 50% of patients.87–90 This population of patients is at risk for augmentation of baseline psychiatric disorders, given their high preoperative prevalence of depressive symptoms.91,92 New-­ onset depression often occurs in the postoperative period, associated with persistent seizures postoperatively.93,94 However, there has been an association between postoperative seizure freedom and decline in preexisting depression.88,95–97 Postoperative psychosis is a recognized but poorly understood phenomenon that affects up to 10% of patients.87,98–100

Neuropsychological Morbidity While the overall morbidity and mortality of ATL is relatively low, postoperative neuropsychological changes have been reported.81 Deficits, when noted, are often in the realm of memory and language. Patients with mesial temporal sclerosis and epilepsy commonly have baseline preoperative deficits in memory and language. Yet significant consideration must be given to patients undergoing surgical resection, as surgery has been shown to augment these deficits.101,102 Memory deficits following temporal resection range from global amnesia to subclinical declines in material-­specific memory. Global memory deficits are rare, with a frequency of 1%; however, material-­specific memory deficits are far more frequent, and include decrements in short-­term verbal and nonverbal memory. In dominant-­side resections, short-­term verbal memory is commonly impaired at an incidence of 25% to 50%.103 A series of ATL and SAH patients identified declines following 40% and 29% of left-­and right-­sided operations, respectively.104 On verbal semantic and memory tasks, left-­sided ATLs were associated with up to 50% decline from baseline, while right-­sided ATLs showed a one-­ third decrease. The postoperative verbal memory declines are not isolated to augmentation of preoperative deficits. Patients with mesial temporal sclerosis, with normal preoperative neuropsychological testing, could still demonstrate postoperative verbal memory deficits after left-sided ATL.103,105 Multiple studies, however, have also shown that the most significant decline occurs within the first 1 to 2 years after surgery, and then a plateau effect is observed.106–108 Previous study information has given rise to two main theories regarding the memory declines associated with ATL: (1) hippocampal atrophy on the side to be resected but impaired memory function on the contralateral side (the “functional reserve” model); and (2) both intact memory and normal-­appearing hippocampus on the resected side (the “functional adequacy” model).109–112 Language function compromise occurs in few patients. A study found that patients undergoing left-­sided operations tended to have preoperative language deficits that persisted postoperatively.113 Further studies have shown that patients with MTLE after ATL do not have significant language compromise. Furthermore, the deficits tended to be transient and improvements in overall language were associated with seizure freedom.114,115 The reported rate of transient postoperative dysnomia is 25% following dominant resection, and is permanent in 1% of cases. No difference in language deficits has been shown when resections are tailored with the use of intra-­or extra-­operative language mapping.116,117

100  •  Temporal Lobe Operations in Intractable Epilepsy

In regard to cognition there are mixed results among various studies.92–94 Intellectual function remains stable and, as with other neuropsychological deficits, is shown to improve with seizure freedom.70,118–122 Significant improvements in cognition postoperatively are likely associated with seizure freedom, and may also be related to the overall quality of life improvement from weaning of antiepileptic drugs.14 

EXTENT OF RESECTION The previous dogma of epilepsy surgery as it pertains to temporal lobectomy was aggressive anterolateral neocortical resection along with resection of the entire amygdalohippocampal complex. This approach, however, as is now appreciated, overlooked the importance of the mesial temporal structures as a main contributor to the seizure focus. Furthermore, no correlation has been established between seizure outcome and extent of neocortical resection. The same can be said about the violation and resection of the STG in respect to outcome and risk of adverse language deficits. Cascino and colleagues123 reported that extent of lateral resection does not correlate with surgical outcome. Later, a prospective, randomized trial found no difference in surgical outcome between patients in whom the STG was resected and those in whom it spared.124 As such, contemporary surgical planning incorporates resection of “seizure positive” temporal lobe cortices as demonstrated by pre-­or intraoperative electrophysiology in a tailored fashion.123–125 Extent of mesial hippocampal resection may or may not improve seizure outcome. Previously published studies do not correlate extent of posterior resection of the hippocampus to seizure freedom.126–129 Evidence in support of aggressive hippocampectomy arises from studies whereby residual hippocampus tail has been shown to be part of the seizure focus.130,131 Further evidence for more aggressive hippocampectomy, extending to the level of the superior colliculus, comes from a randomized trial conferring an almost two-­ fold increase of seizure control (69% vs. 38% at 1 year after surgery) without associated postoperative morbidity.132,133 Lastly, MRI volumetric studies have shown a positive correlation between mesio-­ basal and hippocampal resection extent with favorable seizure outcome.132,134,135

Tailored Resections A tailored approach to temporal lobectomy is the culmination of multiple modalities of information that are used to choose the best surgical plan for a patient. Tailored resections recognize the variability between patients in both inciting pathology and distribution of eloquent cortex and subcortical networks. The utilization of ECoG allows for real-­time tailoring of surgical resection. Such techniques have been used in two applications: (1) ECoG-­ detected interictal discharges for mapping the epileptogenic zone and (2) cortical stimulation for delineating areas of language. ECoG-­detected epileptiform abnormalities and seizure outcome studies are mixed. While early studies were confirmatory that interictal discharges, especially when absent before resection or abundant after resection, had a positive correlation with seizure outcome. Reports have suggested that preresection spikes predict outcomes,136 but others found no association.123,136–138 On the other hand, residual discharges postresection have been reported to be associated with persistent seizures.139–143 Other studies, however, do

1181

not support this conclusion.123,137,138,144–152 A meta-­analysis concluded that although ECoG may have a role in selected infrequent cases, there is no well-­ defined relationship between ECoG discharges and outcome within the MTLE population.24 Cortical stimulation mapping can aid the surgeon in tailoring the neocortical lateral resection to avoid detrimental language and memory deficits in dominant-­side ATL. This was established by Ojemann and colleagues, who showed that cortical stimulation and avoidance of regions that evoked changes in naming and memory during stimulation reduced postoperative language and memory measure decline.153 In comparison of tailored resection versus a standard ATL, verbal IQ and auditory comprehension have been associated with extent of STG resection, favoring a tailored approach with intraoperative language mapping.154 Looking at the addition of mesial temporal structure resection in a population of children with left temporal lobe epilepsy, there was a significant risk associated with resection of mesial temporal structures for verbal memory. This held true for children who had intact verbal memory preoperatively.155,156 Still, similar studies of cortical stimulation for tailored resections have not been able to demonstrate such results.113,114,124,157,158 This may be due to the localization of the language areas, rarely occurring within the typical 4.5 cm from the anterior temporal pole, and thus outside the typical resection boundaries.159 

SELECTIVE MESIAL RESECTION There have been no prospective, randomized trials comparing SAH to ATL with overall seizure outcome. There have been multiple studies including systemic reviews investigating the standard ATL in comparison to selective mesial resection alone. In a systemic review and meta-­analysis of ATL versus SAH, the patients who underwent ATL had a statistically significant greater degree of seizure freedom following surgery.160 This finding was corroborated in a similar study by Josephson and colleagues161 in a pooled population of 1203 patients, which revealed a statistically significant higher degree of Engel Class I outcome in patients undergoing ATL in comparison to SAH. A recent meta-­analysis which included 626 patients, with nearly equal patients in the standard ATL in comparison to selective mesial resection, did not show a statistically significant difference in seizure outcomes at 1-­year follow-­up, nor were they able to show an advantage in either resection method regarding verbal memory. The study concluded ultimately that (1) clinical presentation and (2) preoperative electrographic data are the most important deciding factors on which surgical approach to utilize.162 The SAH, be it trans-­sylvian or trans-­cortical, was born out of the desire to reduce possible neuropsychiatric sequelae of neocortical resection. Studies that looked into seizure outcomes between the selective and standard ATL have not shown significant differences in respect to neuropsychiatric data.125,133,163,164 Again, while a paucity of information exists on particular approach, trans-­sylvian or transcortical, a study conducted to elucidate the possible differential outcomes did not reveal differences in seizure or cognitive outcomes.164 With respect to overall neuropsychological performance, Clusmann and colleagues noted a higher rate of improvement and a lower rate of deterioration with a tailored approach.165

1182

Section Six  •  FUNCTIONAL NEUROSURGERY

Some studies also favored SAH in tests of recall,101 verbal memory, and verbal IQ.166–168 However, other studies have not found differences in functions including naming, general cognition,158 memory,169 and learning and retention.102 Thus, while there is evidence for better outcomes for SAH versus ATL on some neuropsychological measures,170 a prospective, randomized trial with standardized and thorough postoperative assessment is needed to adequately address this issue. KEY REFERENCES

Binder DK, Schramm J. Resective surgical techniques: mesial temporal lobe epilepsy. In: Luders H, ed. Textbook of Epilepsy Surgery. London: Informa Healthcare; 2008:1081–1092. Chelune GJ. Hippocampal adequacy versus functional reserve: predicting memory functions following temporal lobectomy. Arch Clin Neuropsychol. 1995;10(5):413–432. Engel Jr J. Etiology as a risk factor for medically refractory epilepsy: a case for early surgical intervention. Neurology. 1998;51(5):1243–1244. Engel Jr J, Cascino G, Shields W. Surgically remediable syndromes. In: Engel J, Pedley T, eds. Epilepsy: A Comprehensive Textbook. Philadelphia: Lippincott-­Raven; 1998:1687–1696. Engel Jr J, Van Ness P, Rasmussen T, et al. Outcome with respect to epileptic seizures. In: Engel J, ed. Surgical Treatment of the Epilepsies. New York: Raven Press; 1993:609–621. Engel Jr J, Wiebe S, French J, et al. Practice parameter: temporal lobe and localized neocortical resections for epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology, in association with the American Epilepsy Society and the American Association of Neurological Surgeons. Neurology. 2003;60(4):538–547. Engel Jr . J. Surgery for seizures. N Engl J Med. 1996;334(10):647–652. Hermann BP, Wyler AR, Ackerman B, et al. Short-­ term psychological outcome of anterior temporal lobectomy. J Neurosurg. 1989;71(3):327–334. Josephson CB, Dykeman J, Fiest KM, et al. Systematic review and meta-­analysis of standard vs selective temporal lobe epilepsy surgery. Neurology. 2013;80(18):1669–1676. Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med. 2000;342(5):314–319. McIntosh AM, Wilson SJ, Berkovic SF. Seizure outcome after temporal lobectomy: current research practice and findings. Epilepsia. 2001;42(10):1288–1307. Niemeyer P. The transventricular amygdalohippocampectomy in temporal lobe epilepsy. In: Baldwin M, Baily P, eds. Temporal Lobe Epilepsy. Springfield, IL: Charles C Thomas; 1958:461–482.

Ojemann GA. Intraoperative tailoring of temporal lobe resections. In: Engel J, ed. Surgical Treatment of the Epilepsies. New York, NY: Raven Press; 1993:481–488. Ojemann GA. Temporal lobectomy tailored to electrocorticography and functional mapping. In: Spencer SS, Spencer DD, eds. Surgery for Epilepsy. Boston, MA: Blackwell Scientific Publications; 1991:137–145. Penfield W. Henri Jasper H: Epilepsy and the functional anatomy of the human brain? London J. and A. Churchill. 1954:584–586. Schramm J. Temporal lobe epilepsy surgery and the quest for optimal extent of resection: a review. Epilepsia. 2008;49(8):1296–1307. Semah F, Picot MC, Adam C, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology. 1998;51(5):1256– 1262. Spencer DD. Anteromedial temporal lobectomy: directing the surgical approach to the pathologic substrate. In: Spencer SS, Spencer DD, eds. Surgery for Epilepsy. Boston, MA: Blackwell Scientific Publications; 1991:129–137. Spencer DD, Doyle WK. Temporal lobe operations for epilepsy: radical hippocampectomy. In: Schmidek HH, Sweet WH, eds. Operative Neurosurgical Techniques: Indications, Methods, and Results. Philadelphia, PA: WB Saunders Company; 1995:1305–1316. Spencer DD, Spencer SS, Mattson RH, et al. Access to the posterior medial temporal lobe structures in the surgical treatment of temporal lobe epilepsy. Neurosurgery. 1984;15(5):667–671. Sperling MR, O’Connor MJ, Saykin AJ, et al. Temporal lobectomy for refractory epilepsy. JAMA. 1996;276(6):470–475. Wiebe S, Blume WT, Girvin JP, et al. A randomized, controlled trial of surgery for temporal-­lobe epilepsy. N Engl J Med. 2001;345(5):311– 318. Wieser HG, Yasargil MG. Selective amygdalohippocampectomy as a surgical treatment of mesiobasal limbic epilepsy. Surg Neurol. 1982;17(6):445–457. Wyler AR, Hermann BP, Somes G. Extent of medial temporal resection on outcome from anterior temporal lobectomy: a randomized prospective study. Neurosurgery. 1995;37(5):982–990. Yam D, Nicolle D, Steven DA, et al. Visual field deficits following anterior temporal lobectomy: long-­term follow-­up and prognostic implications. Epilepsia. 2010;51(6):1018–1023. Yasargil MG, Teddy PJ, Roth P. Selective amygdalo-­hippocampectomy. Operative anatomy and surgical technique. Adv Tech Stand Neurosurg. 1985;12:93–123. Numbered references appear on Expert Consult.

REFERENCES

1. Engel J. Surgery for seizures. N Engl J Med. 1996;334(10):647– 652. 2. Cockerell OC, Johnson AL, Sander JW, Hart YM, Shorvon SD. Remission of epilepsy: results from the national general practice study of epilepsy. Lancet Lond. Engl. 1995;346(8968):140–144. 3. Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med. 2000;342(5):314–319. 4. Mohanraj R, Brodie MJ. Diagnosing refractory epilepsy: response to sequential treatment schedules. Eur J Neurol. 2006;13(3):277– 282. 5. Fogarasi A, Tuxhorn I, Janszky J, et al. Age-­dependent seizure semiology in temporal lobe epilepsy. Epilepsia. 2007;48(9):1697– 1702. 6. Kanemoto K, Takeuchi J, Kawasaki J, Kawai I. Characteristics of temporal lobe epilepsy with mesial temporal sclerosis, with special reference to psychotic episodes. Neurology. 1996;47(5):1199– 1203. 7. Sadler RM. The syndrome of mesial temporal lobe epilepsy with hippocampal sclerosis: clinical features and differential diagnosis. Adv Neurol. 2006;97:27–37. 8. Williamson PD, Thadani VM, French JA, et al. Medial temporal lobe epilepsy: videotape analysis of objective clinical seizure characteristics. Epilepsia. 1998;39(11):1182–1188. 9. Elliott RE, Bollo RJ, Berliner JL, et al. Anterior temporal lobectomy with amygdalohippocampectomy for mesial temporal sclerosis: predictors of long-­term seizure control. J Neurosurg. 2013;119(2):261–272. 10. Engel J, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-­resistant temporal lobe epilepsy: a randomized trial. J Am Med Assoc. 2012;307(9):922–930. 11. Elwes RD, Marshall J, Beattie A, Newman PK. Epilepsy and employment. A community based survey in an area of high unemployment. J Neurol Neurosurg Psychiatry. 1991;54(3):200– 203. 12. Walczak TS, Leppik IE, D’Amelio M, et al. Incidence and risk factors in sudden unexpected death in epilepsy: a prospective cohort study. Neurology. 2001;56(4):519–525. 13. Helmstaedter C, Kurthen M, Lux S, Reuber M, Elger CE. Chronic epilepsy and cognition: a longitudinal study in temporal lobe epilepsy. Ann Neurol. 2003;54(4):425–432. 14. Elger CE, Helmstaedter C, Kurthen M. Chronic epilepsy and cognition. Lancet Neurol. 2004;3(11):663–672. 15. Sperling MR. The consequences of uncontrolled epilepsy. CNS Spectr. 2004;9(2):98–101. 106–109. 16. Blumcke I, Spreafico R, Haaker G, et al. Histopathological findings in brain tissue obtained during epilepsy surgery. N Engl J Med. 2017;377(17):1648–1656. 17. Bien CG, Kurthen M, Baron K, et al. Long-­term seizure outcome and antiepileptic drug treatment in surgically treated temporal lobe epilepsy patients: a controlled study. Epilepsia. 2001;42(11):1416–1421. 18. Kwan P, Arzimanoglou A, Berg AT, et al. Definition of drug resistant epilepsy: consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia. 2010;51(6):1069–1077. 19. McIntosh AM, Kalnins RM, Mitchell LA, et al. Temporal lobectomy: long-­term seizure outcome, late recurrence and risks for seizure recurrence. Brain. 2004;127(9):2018–2030. 20. Schmidt D, Stavem K. Long-­term seizure outcome of surgery versus no surgery for drug-­resistant partial epilepsy: a review of controlled studies. Epilepsia. 2009;50(6):1301–1309. 21. Soeder BM, Gleissner U, Urbach H, et al. Causes, presentation and outcome of lesional adult onset mediotemporal lobe epilepsy. J Neurol Neurosurg Psychiatry. 2009;80(8):894–899. 22. Semah F, Picot MC, Adam C, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology. 1998;51(5):1256–1262. 23. Engel J, Wiebe S, French J, et al. Practice parameter: temporal lobe and localized neocortical resections for epilepsy: report of the quality standards subcommittee of the American Academy of Neurology, in association with the American Epilepsy Society and the American Association of Neurological Surgeons. Neurology. 2003;60(4):538–547.

24. McIntosh AM, Wilson SJ, Berkovic SF. Seizure outcome after temporal lobectomy: current research practice and findings. Epilepsia. 2001;42(10):1288–1307. 25. Jackson JH, Colman WS. Case of epilepsy with tasting movements adn “dreamy state”—very small patch of softening in the left uncinate gyrus. Brain. 1898;21(4):580–590. 26. Penfield W, Jasper HH, Penfield W. Epilepsy and the Functional Anatomy of the Human Brain. Boston: Little, Brown; 1954. 27. Falconer MA, Serafetinides EA. A follow-­ up study of surgery in temporal lobe epilepsy. J Neurol Neurosurg Psychiatry. 1963;26(2):154–165. 28. Morris AA. Temporal lobectomy with removal of uncus, hippocampus, and amygdala: results for psychomotor epilepsy three to nine years after operation. AMA Arch. Neurol. Psychiatry. 1956;76(5):479–496. 29. Neimeyer P. The transventriuclar amygdalohippocampectomy in temporal lobe epilepsy. In: BaileyP, Baldwin M, eds. Temporal Lobe Epilepsy. 1958:461–482. 30. Wieser HG. Selective amygdalo-­hippocampectomy for temporal lobe epilepsy. Epilepsia. 1988;29(suppl 2):S100–S113. 31. Wieser HG, Yaşargil MG. Selective amygdalohippocampectomy as a surgical treatment of mesiobasal limbic epilepsy. Surg Neurol. 1982;17(6):445–457. 32. Yaşargil MG, Teddy PJ, Roth P. Selective amygdalo-­ hippocampectomy. Operative anatomy and surgical technique. Adv Tech Stand Neurosurg. 1985;12:93–123. 33. So EL. Integration of EEG, MRI, and SPECT in localizing the seizure focus for epilepsy surgery. Epilepsia. 2000;41(suppl 3):S48–S54. 34. DiLorenzo DJ, Mangubat EZ, Rossi MA, Byrne RW. Chronic unlimited recording electrocorticography–guided resective epilepsy surgery: technology-­enabled enhanced fidelity in seizure focus localization with improved surgical efficacy: clinical article. J Neurosurg. 2014;120(6):1402–1414. 35. Lesser RP, Crone NE, Webber WRS. Using subdural electrodes to assess the safety of resections. Epilepsy Behav. 2011;20(2):223– 229. 36. Nair DR, Burgess R, McIntyre CC, Lüders H. Chronic subdural electrodes in the management of epilepsy. Clin Neurophysiol. 2008;119(1):11–28. 37. Alomar S, Jones J, Maldonado A, Gonzalez-­ Martinez J. The stereo-­electroencephalography methodology. Neurosurg. Clin. N. Am. 2016;27(1):83–95. 38. Enatsu R, Bulacio J, Najm I, et al. Combining stereo-­ electroencephalography and subdural electrodes in the diagnosis and treatment of medically intractable epilepsy. J. Clin. Neurosci. Off. J. Neurosurg. Soc. Australas. 2014;21(8):1441–1445. 39. Gonzalez-­Martinez J, Bulacio J, Alexopoulos A, et al. Stereoelectroencephalography in the “difficult to localize” refractory focal epilepsy: early experience from a North American epilepsy center. Epilepsia. 2013;54(2):323–330. 40. Engel Jr J, Cascino G, Shields W. Surgically remediable syndromes. Epilepsy Compr. Textbok. 1998:1687–1696. 41. Hill D, Falconer MA, Pampiglione G, Liddell DW. Discussion on the surgery of temporal lobe epilepsy. Proc. R. Soc. Med. 1953;46(11):965–976. 42. Falconer MA, Meyer A, Hill D, Mitchell W, Pond DA. Treatment of temporal-­lobe epilepsy by temporal lobectomy; a survey of findings and results. Lancet Lond. Engl. 1955;268(6869):827– 835. 43. Crandall P. Standard en bloc anterior temporal lobectomy. Surg. Epilepsy. 1991;118–129. 44. Binder DK, Schramm J. Resective surgical techniques: mesial temporal lobe epilepsy. Textb. Epilepsy Surg. 2008;1081–1092. 45. Oliver A. Surgery of epilepsy: overall procedure. Neurosurg. Asp. Epilepsy. 1990:117–148. 46. Spencer SS. Anteromedial temporal lobectomy: directing the surgical approach to the pathologic substrate. Surg. Epilepsy. 1991:129–137. 47. Grosssman R, Hamilton W. Temporal lobe operations for drug-­ resistant epilepsy. Oper. Neurosurg. Tech. Indic. Methods Results. 1995:1382–1393. 48. Ojemann RG. Temporal lobectomy tailored to electrocorticography and functional mapping. Surg. Epilepsy. 1991:137–145.

1182.e1

1182.e2References 49. Miles A, Ojemann RG. Tailored resections for epilepsy. Youmans Neurol. Surg. 2004:2615–2628. 50. Ojemann RG. Intraoperative tailoring of the temporal lobe resections. Surg. Treat. Epilepsies. 1993:481–488. 51. Spencer DD, Doyle WK. Temporal lobe operations for eilepsy: radical hippocampectomy. Oper. Neurosurg. Tech. Indic. Methods Results. 1995:1305–1316. 52. Spencer DD, Spencer SS, Mattson RH, Williamson PD, Novelly RA. Access to the posterior medial temporal lobe structures in the surgical treatment of temporal lobe epilepsy. Neurosurgery. 1984;15(5):667–671. 53. Hori T, Tabuchi S, Kurosaki M, et al. Subtemporal amygdalohippocampectomy for treating medically intractable temporal lobe epilepsy. Neurosurgery. 1993;33(1). 50-­56-­57. 54. Shimizu H, Suzuki I, Ishijima B. Zygomatic approach for resection of mesial temporal epileptic focus. Neurosurgery. 1989;25(5):798–801. 55. Park TS, Bourgeois BF, Silbergeld DL, Dodson WE. Subtemporal transparahippocampal amygdalohippocampectomy for surgical treatment of mesial temporal lobe epilepsy. Technical note. J Neurosurg. 1996;85(6):1172–1176. 56. Birbeck GL, Hays RD, Cui X, Vickrey BG. Seizure reduction and quality of life improvements in people with epilepsy. Epilepsia. 2002;43(5):535–538. 57. Engel Jr J, Van Ness P, Rasmussen T. Outcome with respect to epileptic seizures. Surg. Treat. Epilepsies. 1993:609–621. 58. Ferguson SM, Rayport M, Schell CA. Life after surgery for temporolimbic seizures. Int Rev Neurobiol. 2006;76:87–116. 59. Spencer SS, Berg AT, Vickrey BG, et al. Health-­related quality of life over time since resective epilepsy surgery. Ann Neurol. 2007;62(4):327–334. 60. Tanriverdi T, Poulin N, Olivier A. Life 12 years after temporal lobe epilepsy surgery: a long-­term, prospective clinical study. Seizure. 2008;17(4):339–349. 61. McLachlan RS, Rose KJ, Derry PA, et al. Health-­related quality of life and seizure control in temporal lobe epilepsy. Ann Neurol. 1997;41(4):482–489. 62. Wiebe S, Blume WT, Girvin JP, Eliasziw M. Effectiveness and efficiency of surgery for temporal lobe epilepsy study group. A randomized, controlled trial of surgery for temporal-­lobe epilepsy. N Engl J Med. 2001;345(5):311–318. 63. Kim R, Spencer D. Surgery for mesial temporal sclerosis. Oper. Neurosurg. Tech. 2000:1436–1444. 64. Foldvary N, Nashold B, Mascha E, et al. Seizure outcome after temporal lobectomy for temporal lobe epilepsy: a Kaplan-­Meier survival analysis. Neurology. 2000;54(3):630–634. 65. Falowski SM, Wallace D, Kanner A, et al. Tailored temporal lobectomy for medically intractable epilepsy: evaluation of pathology and predictors of outcome. Neurosurgery. 2012;71(3):703– 709; discussion 709. 66. Smith AP, Sani S, Kanner AM, et al. Medically intractable temporal lobe epilepsy in patients with normal MRI: surgical outcome in twenty-­ one consecutive patients. Seizure. 2011;20(6):475–479. 67. Sperling MR, Barshow S, Nei M, Asadi-­Pooya AA. A reappraisal of mortality after epilepsy surgery. Neurology. 2016;86(21):1938– 1944. 68. Téllez-­Zenteno JF, Dhar R, Wiebe S. Long-­term seizure outcomes following epilepsy surgery: a systematic review and meta-­ analysis. Brain J. Neurol. 2005;128(Pt 5):1188–1198. 69. Berkovic SF, McIntosh AM, Kalnins RM, et al. Preoperative MRI predicts outcome of temporal lobectomy: an actuarial analysis. Neurology. 1995;45(7):1358–1363. 70. Sperling MR, O’Connor MJ, Saykin AJ, Plummer C. Temporal lobectomy for refractory epilepsy. J Am Med Assoc. 1996;276(6):470–475. 71. So EL, Radhakrishnan K, Silbert PL, et al. Assessing changes over time in temporal lobectomy: outcome by scoring seizure frequency. Epilepsy Res. 1997;27(2):119–125. 72. Barry E, Sussman NM, O’Connor MJ, Harner RN. Presurgical electroencephalographic patterns and outcome from anterior temporal lobectomy. Arch Neurol. 1992;49(1):21–27. 73. Bell ML, Rao S, So EL, et al. Epilepsy surgery outcomes in temporal lobe epilepsy with a normal MRI. Epilepsia. 2009;50(9):2053– 2060.

74. Ivanovic J, Larsson PG, Østby Y, et al. Seizure outcomes of temporal lobe epilepsy surgery in patients with normal MRI and without specific histopathology. Acta Neurochir. 2017;159(5):757– 766. 75. Lee SK, Lee SY, Kim K-­K, et al. Surgical outcome and prognostic factors of cryptogenic neocortical epilepsy. Ann Neurol. 2005;58(4):525–532. 76. Siegel AM, Roberts DW, Thadani VM, et al. The role of intracranial electrode reevaluation in epilepsy patients after failed initial invasive monitoring. Epilepsia. 2000;41(5):571–580. 77. Siegel AM, Jobst BC, Thadani VM, et al. Medically intractable, localization-­related epilepsy with normal MRI: presurgical evaluation and surgical outcome in 43 patients. Epilepsia. 2001;42(7):883–888. 78. Behrens E, Schramm J, Zentner J, König R. Surgical and neurological complications in a series of 708 epilepsy surgery procedures. Neurosurgery. 1997;41(1). 1-­9-­10. 79. Rydenhag B, Silander HC. Complications of epilepsy surgery after 654 procedures in Sweden, September 1990-­1995: a multicenter study based on the Swedish National Epilepsy Surgery Register. Neurosurgery. 2001;49(1). 51-­56-­57. 80. Salanova V, Markand O, Worth R. Temporal lobe epilepsy surgery: outcome, complications, and late mortality rate in 215 patients. Epilepsia. 2002;43(2):170–174. 81. Tanriverdi T, Ajlan A, Poulin N, Olivier A. Morbidity in epilepsy surgery: an experience based on 2449 epilepsy surgery procedures from a single institution: clinical article. J Neurosurg. 2009;110(6):1111–1123. 82. Tebo CC, Evins AI, Christos PJ, Kwon J, Schwartz TH. Evolution of cranial epilepsy surgery complication rates: a 32-­year systematic review and meta-­ analysis: a review. J Neurosurg. 2014;120(6):1415–1427. 83. Yam D, Nicolle D, Steven DA, et al. Visual field deficits following anterior temporal lobectomy: long-­term follow-­up and prognostic implications. Epilepsia. 2010;51(6):1018–1023. 84. Barton JJS, Hefter R, Chang B, Schomer D, Drislane F. The field defects of anterior temporal lobectomy: a quantitative reassessment of Meyer’s loop. Brain. 2005;128(9):2123–2133. 85. Egan RA, Shults WT, So N, et al. Visual field deficits in conventional anterior temporal lobectomy versus amygdalohippocampectomy. Neurology. 2000;55(12):1818–1822. 86. Pathak-­Ray V, Ray A, Walters R, Hatfield R. Detection of visual field defects in patients after anterior temporal lobectomy for mesial temporal sclerosis—establishing eligibility to drive. Eye. 2002;16(6):744–748. 87. Fenwich PB, Fenwick PB. Psychiatric assessment and temporal lobectomy. Acta Neurol Scand Suppl. 1988;117:96–102. 88. Blumer D, Wakhlu S, Davies K, Hermann B. Psychiatric outcome of temporal lobectomy for epilepsy: incidence and treatment of psychiatric complications. Epilepsia. 1998;39(5):478–486. 89. Ring HA, Moriarty J, Trimble MR. A prospective study of the early postsurgical psychiatric associations of epilepsy surgery. J Neurol Neurosurg Psychiatry. 1998;64(5):601–604. 90. Inoue Y, Mihara T. Psychiatric disorders before and after surgery for epilepsy. Epilepsia. 2001;42(suppl 6):13–18. 91. Glosser G, Zwil A, Glosser D, O’Connor M, Sperling M. Psychiatric aspects of temporal lobe epilepsy before and after anterior temporal lobectomy. J Neurol Neurosurg Psychiatry. 2000;68(1):53–58. 92. Matsuura M. Indication for anterior temporal lobectomy in patients with temporal lobe epilepsy and psychopathology. Epilepsia. 2000;41(suppl 9):39–42. 93. Naylor AS, Bá R-­H, Kessing L, Kruse-­Larsen C. Psychiatric morbidity after surgery for epilepsy: short-­ term follow up of patients undergoing amygdalohippocampectomy. J Neurol Neurosurg Psychiatry. 1994;57(11):1375–1381. 94. Quigg M, Broshek DK, Heidal-­Schiltz S, Maedgen JW, Bertram EH. Depression in intractable partial epilepsy varies by laterality of focus and surgery. Epilepsia. 2003;44(3):419–424. 95. Altshuler L, Rausch R, Delrahim S, Kay J, Crandall P. Temporal lobe epilepsy, temporal lobectomy, and major depression. J Neuropsychiatry Clin Neurosci. 1999;11(4):436–443. 96. Hermann BP, Wyler AR, Ackerman B, Rosenthal T. Short-­term psychological outcome of anterior temporal lobectomy. J Neurosurg. 1989;71(3):327–334.

References1182.e3 97. Derry PA, Rose KJ, McLachlan RS. Moderators of the effect of preoperative emotional adjustment on postoperative depression after surgery for temporal lobe epilepsy. Epilepsia. 2000;41(2):177– 185. 98. Jensen I, Larsen JK. Mental aspects of temporal lobe epilepsy. Follow-­up of 74 patients after resection of a temporal lobe. J Neurol Neurosurg Psychiatry. 1979;42(3):256–265. 99. Mace CJ, Trimble MR. Psychosis following temporal lobe surgery: a report of six cases. J Neurol Neurosurg Psychiatry. 1991;54(7):639–644. 100. Christodoulou C, Koutroumanidis M, Hennessy MJ, et al. Postictal psychosis after temporal lobectomy. Neurology. 2002;59(9):1432–1435. 101. Helmstaedter C, Elger CE. Cognitive consequences of two-­thirds anterior temporal lobectomy on verbal memory in 144 patients: a three-­month follow-­up study. Epilepsia. 1996;37(2):171–180. 102. Jones-­Gotman M, Zatorre RJ, Olivier A, et al. Learning and retention of words and designs following excision from medial or lateral temporal-­ lobe structures. Neuropsychologia. 1997;35(7):963–973. 103. Martin RC, Sawrie SM, Roth DL, et al. Individual memory change after anterior temporal lobectomy: a base rate analysis using regression-­ based outcome methodology. Epilepsia. 1998;39(10):1075–1082. 104. Clusmann H, Schramm J, Kral T, et al. Prognostic factors and outcome after different types of resection for temporal lobe epilepsy. J Neurosurg. 2002;97(5):1131–1141. 105. LoGalbo A, Sawrie S, Roth DL, et al. Verbal memory outcome in patients with normal preoperative verbal memory and left mesial temporal sclerosis. Epilepsy Behav. EB. 2005;6(3):337–341. 106. Hamberger MJ, Drake EB. Cognitive functioning following epilepsy surgery. Curr Neurol Neurosci Rep. 2006;6(4):319–326. 107. Martin RC, Kretzmer T, Palmer C, et al. Risk to verbal memory following anterior temporal lobectomy in patients with severe left-­sided hippocampal sclerosis. Arch Neurol. 2002;59(12):1895– 1901. 108. Rausch R, Kraemer S, Pietras CJ, et al. Early and late cognitive changes following temporal lobe surgery for epilepsy. Neurology. 2003;60(6):951–959. 109. Trenerry MR, Jack CR, Ivnik RJ, et al. MRI hippocampal volumes and memory function before and after temporal lobectomy. Neurology. 1993;43(9):1800–1805. 110. Hermann BP, Seidenberg M, Dohan FC, et al. Reports by patients and their families of memory change after left anterior temporal lobectomy: relationship to degree of hippocampal sclerosis. Neurosurgery. 1995;36(1):39–45. 111. Davies KG, Bell BD, Bush AJ, et al. Naming decline after left anterior temporal lobectomy correlates with pathological status of resected hippocampus. Epilepsia. 1998;39(4):407–419. 112. Chelune GJ. Hippocampal adequacy versus functional reserve: predicting memory functions following temporal lobectomy. Arch. Clin. Neuropsychol. Off. J. Natl. Acad. Neuropsychol. 1995;10(5):413–432. 113. Davies KG, Maxwell RE, Beniak TE, Destafney E, Fiol ME. Language function after temporal lobectomy without stimulation mapping of cortical function. Epilepsia. 1995;36(2):130–136. 114. Hermann BP, Wyler AR, Somes G. Language function following anterior temporal lobectomy. J Neurosurg. 1991;74(4):560–566. 115. Hermann BP, Wyler AR. Comparative results of dominant temporal lobectomy under general or local anesthesia: language outcome. J Epilepsy. 1988;1(3):127–134. 116. Langfitt JT, Rausch R. Word-­finding deficits persist after left anterotemporal lobectomy. Arch Neurol. 1996;53(1):72–76. 117. Stafiniak P, Saykin AJ, Sperling MR, et al. Acute naming deficits following dominant temporal lobectomy: prediction by age at 1st risk for seizures. Neurology. 1990;40(10):1509–1512. 118. Novelly RA, Augustine EA, Mattson RH, et al. Selective memory improvement and impairment in temporal lobectomy for epilepsy. Ann Neurol. 1984;15(1):64–67. 119. Hermann BP, Wyler AR, Richey ET. Wisconsin Card Sorting Test performance in patients with complex partial seizures of temporal-­lobe origin. J Clin Exp Neuropsychol. 1988;10(4):467– 476. 120. Rausch R, Crandall PH. Psychological status related to surgical control of temporal lobe seizures. Epilepsia. 1982;23(2):191–202.

121. Olivier A. Risk and benefit in the surgery of epilepsy: complications and positive results on seizures tendency and intellectual function. Acta Neurol Scand Suppl. 1988;117:114–121. 122. Wachi M, Tomikawa M, Fukuda M, et al. Neuropsychological changes after surgical treatment for temporal lobe epilepsy. Epilepsia. 2001;42(suppl 6):4–8. 123. Cascino GD, Trenerry MR, Jack CR, et al. Electrocorticography and temporal lobe epilepsy: relationship to quantitative MRI and operative outcome. Epilepsia. 1995;36(7):692–696. 124. Hermann B, Davies K, Foley K, Bell B. Visual confrontation naming outcome after standard left anterior temporal lobectomy with sparing versus resection of the superior temporal gyrus: a randomized prospective clinical trial. Epilepsia. 1999;40(8):1070– 1076. 125. Schramm J, Lehmann TN, Zentner J, et al. Randomized controlled trial of 2.5-­cm versus 3.5-­cm mesial temporal resection—­ part 2: volumetric resection extent and subgroup analyses. Acta Neurochir. 2011;153(2):221–228. 126. Kanner AM, Kaydanova Y, deToledo-­Morrell L, et al. Tailored anterior temporal lobectomy. Relation between extent of resection of mesial structures and postsurgical seizure outcome. Arch Neurol. 1995;52(2):173–178. 127. Renowden SA, Matkovic Z, Adams CB, et al. Selective amygdalohippocampectomy for hippocampal sclerosis: postoperative MR appearance. AJNR Am. J. Neuroradiol. 1995;16(9):1855–1861. 128. Son EI, Howard MA, Ojemann GA, Lettich E. Comparing the extent of hippocampal removal to the outcome in terms of seizure control. Stereotact Funct Neurosurg. 1994;62(1–4):232– 237. 129. McKhann GM, Schoenfeld-­McNeill J, Born DE, Haglund MM, Ojemann GA. Intraoperative hippocampal electrocorticography to predict the extent of hippocampal resection in temporal lobe epilepsy surgery. J Neurosurg. 2000;93(1):44–52. 130. Hennessy MJ, Elwes RD, Binnie CD, Polkey CE. Failed surgery for epilepsy. A study of persistence and recurrence of ­seizures following temporal resection. Brain J. Neurol. 2000;123 (Pt 12):2445–2466. 131. Salanova V, Markand O, Worth R. Temporal lobe epilepsy: analysis of failures and the role of reoperation. Acta Neurol Scand. 2005;111(2):126–133. 132. Bonilha L, Yasuda CL, Rorden C, et al. Does resection of the medial temporal lobe improve the outcome of temporal lobe epilepsy surgery? Epilepsia. 2007;48(3):571–578. 133. Wyler AR, Hermann BP, Somes G. Extent of medial temporal resection on outcome from anterior temporal lobectomy: a randomized prospective study. Neurosurgery. 1995;37(5). 982-­990-­ 991. 134. Nayel MH, Awad IA, Luders H. Extent of mesiobasal resection determines outcome after temporal lobectomy for intractable complex partial seizures. Neurosurgery. 1991;29(1). 55-­60-­61. 135. Awad IA, Katz A, Hahn JF, et al. Extent of resection in temporal lobectomy for epilepsy. I. Interobserver analysis and correlation with seizure outcome. Epilepsia. 1989;30(6):756–762. 136. McBride MC, Binnie CD, Janota I, Polkey CE. Predictive value of intraoperative electrocorticograms in resective epilepsy surgery. Ann Neurol. 1991;30(4):526–532. 137. Tran TA, Spencer SS, Marks D, et al. Significance of spikes recorded on electrocorticography in nonlesional medial temporal lobe epilepsy. Ann Neurol. 1995;38(5):763–770. 138. Schwartz TH, Bazil CW, Walczak TS, et al. The predictive value of intraoperative electrocorticography in resections for limbic epilepsy associated with mesial temporal sclerosis. Neurosurgery. 1997;40(2). 302-­309-­311. 139. Bengzon AR, Rasmussen T, Gloor P, Dussault J, Stephens M. Prognostic factors in the surgical treatment of temporal lobe epileptics. Neurology. 1968;18(8):717–731. 140. So N, Olivier A, Andermann F, Gloor P, Quesney LF. Results of surgical treatment in patients with bitemporal epileptiform abnormalities. Ann Neurol. 1989;25(5):432–439. 141. Fiol ME, Gates JR, Torres F, Maxwell RE. The prognostic value of residual spikes in the postexcision electrocorticogram after temporal lobectomy. Neurology. 1991;41(4):512–516. 142. Stefan H, Quesney LF, Abou-­Khalil B, Olivier A. Electrocorticography in temporal lobe epilepsy surgery. Acta Neurol Scand. 1991;83(2):65–72.

1182.e4References 143. Salanova V, Andermann F, Rasmussen T, Olivier A, Quesney L. The running down phenomenon in temporal lobe epilepsy. Brain J. Neurol. 1996;119(Pt 3):989–996. 144. Tuunainen A, Nousiainen U, Mervaala E, et al. Postoperative EEG and electrocorticography: relation to clinical outcome in patients with temporal lobe surgery. Epilepsia. 1994;35(6):1165– 1173. 145. Kanazawa O, Blume WT, Girvin JP. Significance of spikes at temporal lobe electrocorticography. Epilepsia. 1996;37(1):50–55. 146. Radhakrishnan K, So EL, Silbert PL, et al. Predictors of outcome of anterior temporal lobectomy for intractable epilepsy: a multivariate study. Neurology. 1998;51(2):465–471. 147. Rasmussen TB. Surgical treatment of complex partial seizures: results, lessons, and problems. Epilepsia. 1983;24(suppl 1):S65– S76. 148. Wyllie E, Lüders H, Morris HH, et al. Clinical outcome after complete or partial cortical resection for intractable epilepsy. Neurology. 1987;37(10):1634–1641. 149. Fenyes I, Zoltan L, Fenyes G. Temporal epilepsies with deep-­ seated epileptogenic foci. Postoperative course. Arch Neurol. 1961;4:559–571. 150. Devinsky O, Canevini MP, Sato S, et al. Quantitative electrocorticography in patients undergoing temporal lobectomy. J Epilepsy. 1992;5(3):178–185. 151. Graf M, Niedermeyer E, Schiemann J, Uematsu S, Long DM. Electrocorticography: information derived from intraoperative recordings during seizure surgery. Clin. EEG Electroencephalogr. 1984;15(2):83–91. 152. Chatrian GE, Tsai ML, Temkin NR, et al. Role of the ECoG in tailored temporal lobe resection: the University of Washington experience. Electroencephalogr. Clin. Neurophysiol. Suppl. 1998;48:24–43. 153. Ojemann GA, Dodrill CB. Verbal memory deficits after left temporal lobectomy for epilepsy. Mechanism and intraoperative prediction. J Neurosurg. 1985;62(1):101–107. 154. Alpherts WCJ, Vermeulen J, van Rijen PC, et al. Standard versus tailored left temporal lobe resections: differences in cognitive outcome? Neuropsychologia. 2008;46(2):455–460. 155. Bujarski KA, Hirashima F, Roberts DW, et al. Long-­term seizure, cognitive, and psychiatric outcome following trans-­middle temporal gyrus amygdalohippocampectomy and standard temporal lobectomy. J Neurosurg. 2013;119(1):16–23. 156. Law N, Benifla M, Rutka J, Smith ML. Verbal memory after temporal lobe epilepsy surgery in children: do only mesial structures matter? Epilepsia. 2017;58(2):291–299. 157. Katz A, Awad IA, Kong AK, et al. Extent of resection in temporal lobectomy for epilepsy. II. Memory changes and neurologic complications. Epilepsia. 1989;30(6):763–771.

158. Wolf RL, Ivnik RJ, Hirschorn KA, et al. Neurocognitive efficiency following left temporal lobectomy: standard versus limited resection. J Neurosurg. 1993;79(1):76–83. 159. Ojemann G, Ojemann J, Lettich E, Berger M. Cortical language localization in left, dominant hemisphere. An electrical stimulation mapping investigation in 117 patients. J Neurosurg. 1989;71(3):316–326. 160. Hu W-­H, Zhang C, Zhang K, et al. Selective amygdalohippocampectomy versus anterior temporal lobectomy in the management of mesial temporal lobe epilepsy: a meta-­analysis of comparative studies. J Neurosurg. 2013;119(5):1089–1097. 161. Josephson CB, Dykeman J, Fiest KM, et al. Systematic review and meta-­analysis of standard vs selective temporal lobe epilepsy surgery. Neurology. 2013;80(18):1669–1676. 162. Kuang Y, Yang T, Gu J, Kong B, Cheng L. Comparison of therapeutic effects between selective amygdalohippocampectomy and anterior temporal lobectomy for the treatment of temporal lobe epilepsy: a meta-­analysis. Br J Neurosurg. 2014;28(3):374–377. 163. Sagher O, Thawani JP, Etame AB, Gomez-­Hassan DM. Seizure outcomes and mesial resection volumes following selective amygdalohippocampectomy and temporal lobectomy. Neurosurg Focus. 2012;32(3):E8. 164. Lutz MT, Clusmann H, Elger CE, Schramm J, Helmstaedter C. Neuropsychological outcome after selective amygdalohippocampectomy with transsylvian versus transcortical approach: a randomized prospective clinical trial of surgery for temporal lobe epilepsy. Epilepsia. 2004;45(7):809–816. 165. Clusmann H, Kral T, Gleissner U, et al. Analysis of different types of resection for pediatric patients with temporal lobe epilepsy. Neurosurgery. 2004;54(4). 847-­859-­860. 166. Pauli E, Pickel S, Schulemann H, Buchfelder M, Stefan H. Neuropsychologic findings depending on the type of the resection in temporal lobe epilepsy. Adv Neurol. 1999;81:371–377. 167. Paglioli E, Palmini A, Portuguez M, et al. Seizure and memory outcome following temporal lobe surgery: selective compared with nonselective approaches for hippocampal sclerosis. J Neurosurg. 2006;104(1):70–78. 168. Tanriverdi T, Olivier A. Cognitive changes after unilateral cortico-­ amygdalohippocampectomy unilateral selective-­ amygdalohippocampectomy mesial temporal lobe epilepsy. Turk. Neurosurg. 2007;17(2):91–99. 169. Gleissner U, Helmstaedter C, Schramm J, Elger CE. Memory outcome after selective amygdalohippocampectomy: a study in 140 patients with temporal lobe epilepsy. Epilepsia. 2002;43(1):87– 95. 170. Schramm J. Temporal lobe epilepsy surgery and the quest for optimal extent of resection: a review. Epilepsia. 2008;49(8):1296– 1307.

CHAPTER 101

Surgical Management of Extratemporal Lobe Epilepsy BILAL MIRZA  •  ALEXANDER L. GREEN  •  ERLICK A.C. PEREIRA

Introduction Extratemporal lobe epilepsy (ETLE) comprises debilitating conditions of heterogeneous symptomatology and pathology, both challenging to diagnose and to treat yet amenable to several surgical interventions. ETLE is defined as localization-­related epilepsy with the electrophysiological epileptogenic zone outside the temporal lobe of focal epilepsies with and without secondary generalization. ETLE include frontal lobe, parietal lobe, occipital lobe, and multilobar neocortical epilepsies. Depending on the presence or absence of a structural abnormality on MRI that is concordant with the epileptogenic zone, ETLE is denoted lesional and nonlesional, respectively. Extratemporal lesions on MRI, not necessarily epileptogenic, can coexist with mesial temporal sclerosis as dual pathology. Four percent to 15% of adult temporal lobe resections involve dual temporal and extratemporal pathology. The extratemporal pathology is most commonly cortical dysplasia followed by vascular malformations, infarction, and dysembryoplastic neuroepithelial tumors, in descending order of frequency.1–3 The higher childhood prevalence of dual pathology suggests earlier progression to intractable epilepsy and hence surgery.4 In this chapter, we consider adult extratemporal epilepsy surgery, childhood epilepsy surgery having been described in the pediatric section of this book. Available procedures account for less than half of all epilepsy surgery and can either be resective for an identified seizure-­generating region or palliative.5,6 In one highly specialized center, the surgical procedures for ETLE comprised 16% (147 interventions) of the epilepsy surgical workload over a 25-­year period.7 The management of ETLE is therefore tailored case-­ by-­ case and empirical although evidence-­based interventions and algorithms are being explored with technological advancement, for example, in imaging, neuronavigation, surgical robotics, and neuromodulation.8 Surgical ablative and resective procedures include topectomy (excision of nonlesional epileptogenic zone), lesionectomy, lobectomy, hemispherectomy; stereotactic ablative procedures; functional disconnective procedures including multiple subpial transections, corpus callosotomy, and hemispherotomy, all detailed in the following chapters. Neuromodulatory procedures include

deep brain stimulation (DBS) and vagus nerve stimulation, both modalities with availability of closed-­ loop responsive stimulation. Vagus nerve stimulation has also been described elsewhere in this section. We briefly review the above techniques before focusing upon DBS for epilepsy, describing its history, operative technique, and reviewing clinical outcomes and complications in the context of these other procedures. We do not review diagnostic intracranial electrode placement techniques and presurgical recording, which are covered in a preceding chapter.  

History If the sufferer acts like a goat, and if he roars, or has convulsions involving the right side, they say the Mother of the Gods is responsible. If he utters a higher-­pitched and louder cry, they say he is like a horse and blame Poseidon. If the sufferer should be incontinent of faeces, as sometimes happens under the stress of an attack, Enodia is the name.10

HIPPOCRATES OF KOS (460–370 BC) Little was understood about anatomical localization of brain function and thus epilepsy until the late nineteenth century when David Ferrier and John Hughlings Jackson characterized cerebral functions in monkey and man, respectively.11,12 Hughlings Jackson rightly commented “a convulsion is but a symptom, and implies only that there is an occasional, an excessive, and a disorderly discharge of nerve tissue on the muscles. This discharge occurs in all degrees; it occurs with all sorts of conditions of ill health, at all ages, and under innumerable circumstances.” A prevailing British culture of cerebral localization emboldened first the Glaswegian William Macewen in 1879 and later the Englishman Sir Rickman Godlee in 1884 to perform exploratory craniotomies upon young patients with contralateral focal seizures.13,14 Both were vindicated, Macewen discovering of an acute subdural hematoma and Godlee finding a brain tumor. Sir Victor Horsley also performed extratemporal surgery for focal seizures in the late nineteenth century, describing in 10 cases a combination of subpial and lobar resections.15 Horsley’s cortical escharotomies

1183

1184

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 101.1  Irving Cooper’s cerebellar stimulator, consisting of internally implanted electrode plates and receiver (left), external antenna and transmitter (center), positioned over the internal receiver during stimulation (right).

of his patients led Hughlings Jackson to conclude of three cases that “there was in every case of epileptiform seizures a very local change of some kind,” and that because “the starting point of the fit was the sign to us of a discharging lesion, he would advise cutting out that lesion, whether it was produced by tumour or not.”16 Thus resective extratemporal epilepsy surgery was commenced. Corpus callosotomy arose in the 1930s from Van Wagenen’s serendipitous observation that patients with stroke involving the corpus callosum often had improvements in seizures. “It was decided to divide the corpus callosum surgically in an effort to limit the spread of a convulsive wave to one half of the cerebrum.”17 In both children and adults, corpus callosotomy appears, on average, to improve drop attacks and generalized tonic and tonic-­clonic seizure frequency by 80% in 70% of patients and complex partial, myoclonic, and absence seizure frequency by 50% in 50% of patients.18 Hemispherectomy was first described for infantile hemiplegia by Krynauw in 1950.19 Having late complications of hemosiderosis, hydrocephalus, brain shift, and hemorrhagic membrane formation, it was abandoned in the 1970s in favor of functional hemispherectomy advocated by Rasmussen.20 Most studies relate to children, three published adult studies reporting, respectively, 4 of 4, 5 of 9, and 5 of 12 patients becoming seizure free.21–23 Multiple subpial transection aims to limit the horizontal spread of epileptiform activity across functional columns of eloquent cortex. A meta-­ analysis of adults and children has shown more than 95% seizure frequency reduction in 87% of patients with generalized seizures and 68% with partial seizures, compared to cortical transections alone.24 It has been recommended for acquired epileptic aphasia (Landau-­ Kleffner syndrome).25 Late seizure recurrence in adults has however been reported in other adult groups.26 Electrical neuromodulatory approaches to extratemporal epilepsy are indicated where epilepsy persists despite

resection of epileptogenic foci or in the palliative circumstance where no seizure focus is demonstrated using scalp recording, noninvasive neuroimaging, and invasive recording described elsewhere. Vagus nerve stimulation has been approved in many countries for partial seizures with or without secondary generalization based upon trials showing differences in seizure frequency reduction between highfrequency (25% to 30% reduction) and low-frequency (6% to 15% reduction) stimulation groups.27 Median seizure reductions in 454 patients were 44% from baseline after 3 years, with 43% of patients having at least 50% seizure frequency reduction, although 20% had persisting hoarseness at 2 years’ follow-­up.28 Trigeminal nerve stimulation has also recently been reported, 12 patients having a median 66% seizure frequency reduction at 3 months with occasional side effects of orbicularis oculi twitching and dental discomfort and paresthesia. The results augur for larger trials given its advantage over vagus nerve stimulation of transcutaneous test stimulation.29 DBS for epilepsy is almost as old as human stereotactic surgery, having first been attempted acutely in 1952 by Heath. He recorded interictal spikes from the septum in a patient with complex partial seizures and then stimulated him. “Almost instantly, his behavioral state changed from one of disorganization, rage and persecution to one of happiness and mild euphoria.”30 Cooper first treated epilepsy with implantable DBS throughout the 1970s, targeting the superomedial cerebellar cortex and reporting seizure reduction first in 6 of 7, then later, 18 of 32 patients (Fig. 101.1).31 Eleven unblinded case series have reported benefits in 88 of 116 patients (76%),32 but two small double-­blinded studies comprising 14 patients have shown no benefit.33,34 Cerebellar stimulation therefore fell out of favor, with the exception of one recent report of five patients with generalized tonic-­ clonic seizures showing mean seizure frequency reduction of 59% at 6 months after surgery.34 Current deep brain targets under evaluation for epilepsy are the anterior thalamic

101  •  Surgical Management of Extratemporal Lobe Epilepsy

1185

Table 101.1  Case Series of Bilateral Anterior Thalamic Nucleus Deep Brain Stimulation for Partial or Secondarily Generalized Epilepsy Series Guan et al. (2017) Kim et al. (2017) Krishna et al. (2016) Lehtimäki et al. (2016) Piacentino et al. (2015)a Stillova et al. (2015) Van Goempel et al. (2015) SANTE; Salanova et al. (2015) SANTE; Fisher et al. (2010) Lee et al. (2012); Oh et al. (2012); Lee et al. (2006) Osorio et al. (2007) Lim et al. (2007) Andrade et al. (2006); Hodaie et al. (2002) Osorio et al. (2005) Kerrigan et al. (2004) Sussman et al. (1988) aOne

Responder (>50% Seizure Reduction)

Median Follow-­Up Months (Range)

% Seizure Frequency Reduction, Mean

17 29 16 15 6 3 2 105

9 of 17 (53%) 22 of 29 (75%) 11 of 16 (69%) 10 of 15 (67%) 1+4 of 6 (83%) NA 2 of 2 (100%) 69%

17 (12–25) 75 12–154 60 26 (12–48)a NA 3 60

56% 70% 54%–66% 68% 81% NA 53%, 80% 68%

110

54%

25

56%

12 of 15 (80%)

39 (24–67)

70%

4 of 4 (100) 1 of 4 (25%) 5 of 6 (83%) 2 of 7 (29%) 2 of 4 (50%) 4 of 5 (80%) 3 of 5 (75%)

36 (36) 44 (33–48) 60 (48–72) 15 10 days 18 (6–36) 12–18

76% 75% 64% 54% 72%–75% 78% Descriptive

Number of Patients

15 4 4 6 7 4 5 5

patient died day 40 after surgery.

nucleus, centromedian thalamus, subthalamic nucleus, posterior hypothalamus, caudal zona incerta, nucleus accumbens, hippocampus caudate, corpus callosum, and brainstem.35,36 We review current clinical outcomes information for these brain regions below. 

Anterior Thalamic Nucleus Stimulation Bilateral DBS of the anterior thalamic nuclei (ANT-­DBS) has been undertaken by several groups and reported in a total of 230 to 240 patients and include a long-­term followup multicenter, double-­ ­ blind, randomized clinical trial— stimulation of the anterior nucleus of the thalamus for epilepsy (SANTE), the first results of which were published in 2010.37 Results of the SANTE study and other clinical studies are summarized in Table 101.1. The pre-­SANTE trials pioneered ANT-­DBS for seizure control in small open-­labeled studies. In 1988, Sussman et al. in their preliminary report obtained seizure control in three of five patients at 12 to 18 months follow-­up.38 Kerrigan et al. reported four of five patients (80% responders) showing significant reductions in frequency (78% of baseline) and severity of seizures after 6 to 36 months.39 Hodaie et al. reported a mean reduction from baseline of 54% in seizure frequency at mean follow-­up of 15 months, also without adverse effects and with a stun effect reducing seizure frequency before turning on stimulation.40 Andrade et al. later described five of six patients from the latter center with improvements of at least 50% in their seizure frequency over a mean follow-­up period of 5 years.41 In 2005, ANT stimulation in a closed-­loop responsive system reduced seizure frequency to 72% to 75% in two of four patients.42 While the SANTE trial was going on, Lee et al. studied three patients, finding a 75% reduction in

seizure frequency at mean follow-­up of 13 months.43 Lim et al. found seizure frequency reduced to 75% from baseline in one of four patients.44 Osorio et al. showed seizure frequency reductions of 75% in four of four patients at 36 months delivering stimulation only with detection of EEG changes.45 In 2012, Lee et al. extended their previous findings and reported seizure control in 12 of 15 patients (80% responders) with seizure frequency of 70% at median follow-­up 39 months.46 Fisher et al., in their SANTE study, recruited 110 patients with medically refractory partial or secondarily generalized seizures.37 Bilateral ANT-­DBS was standardized to monopolar stimulation at a frequency of 145 Hz, pulse width of 90 μs, and cycle time on for 1 minute then off for 5 minutes using quadripolar electrodes (Medtronic Inc., Minneapolis, MN). After 1 month postsurgery patients were randomized in the blinded phase lasting for 3 months. The highest median seizure frequency reduction was 42.1% in the stimulated group at the second month. Significant seizure reduction from a median baseline of 19.5 seizures per month was seen in the group stimulated (33 of 54 patients, 61% responders) at amplitude of 5 V compared to the placebo group nonstimulated (29 of 55 patients, 53% responders) at 0 V, with a 29% seizure reduction in the last month of a 3-­month blinded phase. After this phase, all patients were transferred to 5 V DBS and enrolled in the open-­labeled and unblinded follow-­up. The greater than 50% responder rate was 43% (n = 99) at 13 months, 54% (n = 81) at 25 months, and 67% at 37 months (n = 42). The median seizure frequency reduction continued to improve with DBS throughout the trial: 41% at year 1 and 56% at year 2. The follow-­up report showed greater than 50% responder rate of 69% with median frequency seizure reduction of 68% at year 5.47 Six-­month seizure freedom after 5 years was reported by

1186

Section Six  •  FUNCTIONAL NEUROSURGERY

16% of the patients. The modest but significant improvement in quality of life in epilepsy from baseline reported by Fisher et al. remained unchanged at year 5. Cognition and mood changes have been subject to elaborate analysis as self-­reported changes during the blinded trial period were reported significantly higher in the stimulation group, although no significant changes were measured at objective neuropsychological testing. At 7-­year follow-­up no cognitive decline or worsening of mood was observed.48 Post-­ SANTE clinical reports of open-­ labeled small cohorts have emphasized technical aspects of the surgery such as imaging and intraoperative recording of evoked potentials and clinical correlation with respect to a “sweet-­ spot” for stimulation associated with seizure control. Stillova et al. reported three patients with ANT-­DBS and recorded hippocampal event–related potentials that suggested a role of the ANT in the memory of recognition.49 The effects on seizures were not available. Van Goempel et al. has suggested targeting the ANT with a posterior trajectory and recorded hippocampal-­ evoked potentials confirming ANT targeting obtained seizure reduction in both their patients with seizure reduction by 53% and 80%.50 Sun et al. recorded event-­related potentials and demonstrated that ANT stimulation increased the attention to emotional stimuli.51 Piacentino et al. showed in a heterogeneous case mix of patients, five of six responders with long-­term results more than 3 years in four patients achieving seizure reduction rates of 60% to 100%.52 Lahtimaki et al. reported 10 of 15 patients with mean seizure reduction of 68% after 5 years follow-­up and showed that favorable outcome was associated with contacts in the anterior aspect of the ANT.53 Kim et al. reported a long-­term cohort of 29 patients with 75% responders and overall 70% seizure reduction during the 11-­year follow-­up and did not find difference in outcome between focal and generalized epilepsies and between temporal lobe epilepsy and ETLE.54 Guan et al. reported 9 of 17 patients with 53% responders and mean seizure reduction 56% at 1 year after surgery.55 The mechanisms of anterior thalamic nucleus stimulation remain unclear. Animal models have shown seizure reduction in drug-­induced seizure models, postulating current dependent-­and serotonin-­mediated effects.56,57 Anatomical evidence suggests widespread limbic system sclerosis in epilepsy, including projections to and from anterior thalamic nucleus to cingulate cortex and hippocampus.58 Concurrent thalamic and scalp EEG recording studies after surgery suggest a recruiting rhythm, elicited with low-­frequency stimulation, correlating with clinical improvement.59 The nucleus is small and projects to and from many limbic and cortical structures, yet is less deep and proximal to subarachnoid vessels as the mammillary bodies, enabling safer targeting. Stereotactic ablation of the target demonstrated seizure reduction four decades ago,60 motivating its intensive experimental and clinical study. 

Centromedian Thalamic Stimulation Wilder Penfield first postulated that the centromedian thalamic nucleus could be modulated to ameliorate seizures, noting its diffuse projections from brainstem to cerebral cortex and proposing its role in their theory of centrocephalic propagation of seizures.61 In total, more than 39 patients

have undergone CM-­DBS, reported in seven studies from four groups. Velasco and colleagues introduced CM-­DBS in 1987. In this open-­labeled trial responder rate was 100% with 80% to 100% reduction in generalized tonic-­clonic seizures and a 60% to 100% reduction in partial complex seizures in five of five patients and in one case additional myoclonic and astatic seizures were reduced by 100% and 50%, respectively.62 In 1992, a double-­blinded, crossover-­design trial in seven patients by Fisher et al. revealed no clinical improvement in seizure frequency with CM-­DBS.63 In 2006, Velasco and colleagues have found seizure frequency reduction in 12 of 13 patients (92%) with Lennox-­Gastaut syndrome. At post hoc analysis they identified more than 80% responders (range 87% to 100%) had lead placed within the parvocellular subnucleus of CM in contrast to less than 79% responders (range 53% to 79%). Low-frequency (6 to 8 Hz) bipolar stimulation was delivered through pairs of adjacent quadripolar electrode contacts while assessing responses in concomitant scalp EEG. Implanted DBS settings were low frequency or high (130 Hz), pulse width 450 μs, and amplitude 6 to 10 V.64 In 2006, CM-­DBS failed to control seizures in two patients with longer-term follow-­up.41 In a subsequent study, four of four postcallosotomy patients with primary generalized seizures responded to CM-­DBS with a mean seizure reduction by 78% (range 65% to 98%) at 1 to 2 years follow-­up.65 Recently in 2013, a two-­center, single-­blinded controlled trial, six of six patients with generalized epilepsy and one of five patients with frontal lobe epilepsy obtained seizure frequency reduction greater than 50%. Two of six patients with generalized epilepsy remained seizure free postimplantation with DBS OFF for 12 and 50 months. At long-­term but unblinded, two in five patients with frontal lobe epilepsy and five in six patients with generalized epilepsy were responders (one became seizure free, one had >99% improvement, and three had 60% to 95% reduction in seizure frequency).66 The results with CM-­DBS showed most improvements in generalized seizures, less so in extratemporal lobe seizures, for example, complex partial seizures, temporal and frontal lobe seizures. Intraoperative corroboration of lead location with EEG appears to optimize clinical response and targeting the parvocellular subnucleus for CM-­DBS seems a “sweet spot” achieving this. 

Subthalamic Nucleus Stimulation The subthalamic nucleus has been established of late as the surgical target of choice in DBS for Parkinson disease and is therefore appealing, as functional neurosurgeons should have most experience with it. A mechanistic rationale for its stimulation has arisen from observations that the substantia nigra pars reticulata may gate seizures through inhibitory nigrotectal projections to the superior colliculi, its inhibition suppressing seizures in animal models.67 Subthalamic nucleus inhibition has also been shown to suppress seizures in animals.68 Clinically, in 2001, Benabid et al. introduced posterior STN-­ DBS for seizure control in a child with left focal centroparietal dysplasia treated with left STN stimulation resulting in 81% seizure reduction at 30 months follow­up.69 Chabardès et al. demonstrated 67% to 80% seizure frequency reduction in three of five patients with partial seizures and secondary generalization and 41% in one patient

101  •  Surgical Management of Extratemporal Lobe Epilepsy

with Dravet syndrome.70 Other small studies have also shown improvements, two of five patients, reported by Loddenkemper et al., as having 80% improvement in their partial seizures.71 Handforth et al. reported two patients indicating the challenges with epilepsy surgery. In one patient with bitemporal onset, seizures were reduced by 50% but with no meaningful change in fall injuries and in the second patient with frontal encephalomalacia seizures were reduced by 30% but meaningful reduction in seizure severity and related injury.72 In 2011, Wille et al. reported, in five of five patients with progressive myoclonic epilepsy, significant control of the myoclonic seizures with STN/SNpr DBS; however, the effect on generalized seizure in three of their patients remains unanswered.73,74 In 2012, Capecci et al. reported 65% seizure reduction in one postcallosotomy patient and no effect in one patient with absence and tonic-­clonic seizures postneonatal anoxia.75 In summary, the STN-­DBS appeared most effective in reducing partial seizures with and without secondary generalization and progressive myoclonic epilepsy, whereas primary generalizing tonic-­clonic seizures were less likely to respond. The clinical indications, optimal target region in the subthalamus, and overall efficacy of STN-­DBS in treatment of epilepsy is heterogeneous and remains to be established in larger and blinded trials. 

Other Deep Brain Targets The posterior hypothalamus has been targeted by DBS based upon observations that the mammillary bodies show epileptiform activity with depth electrode recording.76 A report of two patients with behavioral comorbidity and multifocal seizures by Franzini et al. showed seizure frequency reduced by 75% and 80% from baseline after 5 years and 9 months follow-­up, respectively.77 The mammillothalamic tract has also been stimulated to relieve gelastic seizures secondary to hypothalamic hamartomas in two patients with improvements in seizure frequency.78 Growing case series of DBS for cluster headache targeting the posterior hypothalamus increase our experience and confidence of this challenging deep brain target adjacent to the circle of Willis.79 DBS at the caudal zona incerta reduced seizures in focal sensorimotor seizures.77 DBS of the head of the caudate has been studied as an epilepsy treatment after non–human primate studies showing reductions in induced seizures with stimulation.80 Sramka et al. have published a study of 74 patients showing reduced interictal EEG activity with both caudate and dentate nucleus stimulation.81 Chkhenkeli et al. have stimulated the ventral caudate head at low frequency (4 to 8 Hz) in 38 patients, impressively eliminating seizures in 21 patients and improving 35 patients overall (92%).82 These results both encourage further, more controlled, clinical trials of caudate DBS. A recent single-­center randomized controlled cross-­over trial of quadruple DBS of the nucleus accumbens and anterior nucleus of thalamus showed seizure reduction to 50% and 85% in two of five patients with frontal and mesiotemporal epilepsy at 6 months with stimulation of only the nucleus accumbens.83 In their second study, three of four patients responded to NAC stimulation with seizure reduction range of 50% to 85% and with subsequent additional anterior nucleus stimulation no further improvement was observed.84 We will not discuss hippocampal DBS as it relates largely to mesial temporal rather

1187

than ETLE. However, two other deep brain targets deserve brief mention. The corpus callosum has been stimulated in 10 patients, perhaps unsurprisingly without benefit85 and the locus coeruleus has been stimulated unilaterally in two patients, seemingly improving seizure frequency.86 

Patient Selection Prevailing clinical indications for DBS in ETLE emerge from the clinical outcomes described above. They include partial onset epilepsy with or without secondary generalization, associated with frequent seizures poorly controlled by at least two antiepileptic medications trialed for at least 1 year. Recently we have proposed a pragmatic algorithm for selection of patients and available neuromodulatory treatment8 and reviewed the preoperative investigations guiding surgical treatment.87 Patients should ideally be without evidence of systemic disease, coagulopathy, ventriculomegaly, or evidence of other progressive neurologic disorders. Some might argue that they should have failed resective surgery and/or the less-­invasive treatment of vagus nerve stimulation. Scalp EEG combined with video telemetry should demonstrate bilateral and nonlocalizing findings, suggesting palliative rather than curative aims for the treatment. Preoperative neuroimaging should exclude lateralizing structural abnormalities amenable to resective surgery. The seizures should ideally be recognizable with a caregiver able to record a seizure diary to assess outcomes. 

Operative Technique Stereotactic techniques differ considerably between surgeons regarding frame used (if indeed used at all), targeting software used, whether the patient is awake or asleep, whether microelectrode recording is performed, and how DBS equipment is used. Our technique is detailed elsewhere.88,89 Details of how to perform stereotactic DBS procedures can be found elsewhere in this book. To summarize our technique, all patients now have several MRI scans prior to epilepsy surgery including T1, T2, FLAIR, inversion-­ recovery, and DTI sequences in 1-­mm-­thick axial slices. For surgery, a Cosman-­Roberts-­Wells (CRW) base ring is applied to the patient’s head under general anesthesia. A stereotactic CT scan is then performed and registered with the MRI dataset to eliminate spatial distortions, using MRI stereotaxy alone, that arise from magnetic field effects.90,91 The coordinates of the thalamic target are then calculated. Each electrode is passed to target via a twist drill craniostomy following a linear parasagittal scalp incision after impedance checks confirming an extraventricular approach. Implanted electrodes are then secured to the skull using bioplates (Codman, United States). All electrodes were externalized for a week of trial stimulation. During this period, video telemetry and dual deep brain electrode and scalp EEG recording is performed and seizure frequency, duration, and severity recorded. Stimulation settings are trialed and if efficacious and tolerated without side effects, the patient proceeds to full implantation of the device, including a subcutaneous implantable pulse generator. Typical coordinates for the anterior thalamic nucleus are 5 to 6 mm lateral to the midcommissural point, 8 mm

1188

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 101.2  Axial T2 MRI and Schaltenbrand and Wahren atlas section showing the anterior thalamic nucleus brain target. Coordinates are 5 to 6 mm lateral to the midcommissural point, 8 mm anterior to the posterior commissure and 12 mm above the anterior commissure/posterior commissure line. (Schaltenbrand G, Wahren W. Atlas for Stereotaxy of the Human Brain. Stuttgart: Thieme; 1977.)

FIGURE 101.3  Targeting the right anterior thalamic nucleus planning for bilateral deep brain stimulation. The ventricle is avoided in a transfrontal trajectory.

anterior to the posterior commissure and 12 mm above the anterior commissure/posterior commissure (AC/ PC) line, the angle of trajectory being approximately 60 degrees posteroinferiorly from the coronal plane (Figs. 101.2 and 101.3). As the anterior thalamic nuclei are visible in the floor of the lateral ventricles on MRI, direct localization is also possible. Common coordinates for the centromedian thalamic nucleus are 11 mm lateral to the

midcommissural point, 2 mm above the AC/PC line at the midpoint of the third ventricle (Figs. 101.4 and 101.5). We aim to place at least two electrode contacts in the parvocellular subdivision of the centromedian nucleus, its most lateral, anterior, and ventral part to optimize efficacy (see Fig. 101.4). Indirect localization of either nucleus is verified using the Schaltenbrand atlas (see Figs. 101.2 and 101.4).92 

101  •  Surgical Management of Extratemporal Lobe Epilepsy

1189

FIGURE 101.4  Axial T2 MRI and Schaltenbrand and Wahren atlas section showing the parvocellular division of the centromedian thalamic nucleus brain target. Coordinates are 11 mm lateral to the midcommissural point and 2 mm above the anterior commissure/posterior commissure line at the midpoint of the third ventricle. (Schaltenbrand G, Wahren W. Atlas for Stereotaxy of the Human Brain. Stuttgart: Thieme; 1977.)

FIGURE 101.5  Targeting the right centromedian thalamic nucleus planning for bilateral deep brain stimulation.

Complications While stereotactic ablation for epilepsy has been successfully performed in the past,60,93 DBS confers adjustability and reversibility such that unwanted adverse effects can be titrated out and avoided. DBS supersedes lesioning surgery due to lower mortality rates and reductions in both serious complications such as hemorrhage and adverse effects upon

cognition, speech, and swallowing.94 However, the DBS technique confers higher risks of infection due to the neuroprosthesis and of complications related to the frequently longer operative duration. Thalamic nucleus DBS for epilepsy appears safe and well tolerated with reported adverse effects being transient and mild. These include episodic nystagmus with cycling stimulation, auditory hallucinations,

1190

Section Six  •  FUNCTIONAL NEUROSURGERY

paranoid ideation, anorexia, and lethargy. Complications in the epilepsy case series cited above of an asymptomatic small right frontal hematoma, scalp erosion requiring DBS removal, implantable pulse generator infection, and accidental switching off of the stimulator are all well described in DBS for other conditions and do not seem to occur more frequently than the norm. Whether described as “neuromodulation,” “neurostimulation,” or “functional,” it should be emphasized that DBS is an intracranial surgical procedure that brings small but significant risks. Aside from multidisciplinary assessment to determine suitability for the procedure, the patient must be refractory to medical treatment and able to give informed consent (where appropriate) to risks of stroke (1% to 3%), worsening of seizures ( lateral geniculate > thalamus > visual cortex). In 1986, Brindley and colleagues first described direct stimulation of the visual cortex.60 This discovery came by way of an experiment placing electrodes in direct contact with the visual cortex of a blind patient’s occipital lobe. Following stimulation, the patient was able to “see” simple patterns (Fig. 111.11). A commercially available retinal prosthesis was approved by the FDA in 2013 (Argus II, Second Sight Medical products, Sylmar, CA). This BCI employs a camera and visual processing unit capable of converting light signals into electrical pulses, which are then transmitted wirelessly to an internal retinal implant (signals are sent to the occipital lobe’s visual cortex) (Fig. 111.12). Following implantation, recipients must learn to interpret signals received from the prosthesis as meaningful visual representations, which requires a significant amount of training. Continual improvements of this BCI, as well as similar visual BCIs in development, hold great promise that BCIs will soon provide patients with successful options for eradicating blindness.2,16,21,22,35,61,72 Motor-­oriented neuroprosthetics serve to interpret brain signals following a patient’s own desire to move, and then transforming his/her “will” into a functional, purposeful movement via a computerized prosthetic machine—such as an artificial arm or patient’s own limb (i.e., paraplegic patient’s leg moving via an exoskeleton).54 This type of configuration allows the signals to essentially bypass the patient’s damaged spinal cord. These devices use implanted surface electrodes to interpret motor cortex activity and relay the information to computers out of continuity with the EEG-­ sensing implant. As the signals pass onto another machine and/or to the intact peripheral nerves, purposeful movement within the paralyzed limb is possible.73 These advances are providing hope for paralyzed patients who are striving to

1. Camera 2. Transmitter Light

5. Wireless transmission 4. Transmitter antenna

3. Processor and battery

7. Electrode array

6. Receiver antenna 8. Capsule for 9. Optic receiver nerve electronics

FIGURE 111.12  The Argus II, an example of a brain-­computer interface designed to counteract and augment vision loss, is shown here. (Fighting blindness with microelectronics. Sci. Trans. Med. 2013, American Association for the Advancement of Science.)

gain increasing amounts of daily activity independence and to reverse extremity paralysis.21,37,53–56,63 Multielectrode arrays (MEAs) are devices that contain multiple electrodes or shanks through which neural signals are obtained/delivered, essentially serving as neural interfaces that connect neurons to man-­ made electronic circuitry. They record large populations of neurons, allowing neuroengineers to capture a broader range of unique neural signals. The fundamental unit of communication for the neuron is the action potential, which is an ion flux through the cellular membrane. This in turn generates a sharp change in voltage within the extracellular environment, which is what the MEA electrodes aim to detect. In 2012, Hochberg and colleagues demonstrated the ability of two people with long-­standing tetraplegia to use a neural interface system–based control of a robotic arm to perform three-­ dimensional reach and grasp movements using MEAs.39,43,50 Participants controlled the arm and hand over a broad space without explicit training, using signals decoded from a small, local population of motor cortex neurons recorded

111  •  Brain-Computer Interfacing: Prospects and Technical Aspects of Functional Cranial Implants

FIGURE 111.13  The BrainGate initiative produced a brain-­computer interface designed to counteract quadriplegia. The device shown here is using an implanted brain interface which controls an external robotic arm using cortical unit recordings derived from the paralyzed patient nearby. (Used with the permission of Brown University and Braingate.org. Retrieved from https://news.brown.edu/ articles/2012/05/braingate2.)

from a 96-­channel microelectrode array. One of the study participants, implanted with the sensor 5 years earlier, was able to use a robotic arm to drink coffee from a bottle (Fig. 111.13).5,8,9,22,35,39,42 In 2016, Bouton and colleagues showed that intracortically recorded signals can be linked in real time to muscle activation for movement restoration in a quadriplegic human. By way of an intracortical microelectrode array recording multiunit activity from the motor cortex, the researchers applied machine learning algorithms to decode the neuronal activity and control activation of the participant’s forearm muscles via a custom-­built, high-­resolution neuromuscular electrical stimulation system. The system provided isolated finger movements, and the participant achieved continuous cortical control of six different wrist and hand motions. He was able to use the system to complete functional tasks relevant to daily living (Fig. 111.14).74 From here, the next big step will be to create a wireless neural communication link connecting the brain and limb(s) to replace cables and enable full-­time, wireless BCI use. This future electrode array will detect one’s intention to move via the electrical activity of cortical motor neurons, and will then relay a neural signal pattern to a computer via a wireless cable connection.75 As the technology improves, it will be much safer to have everything housed within a single functional cranial implant, thereby eradicating the need to have any externalized hardware and/or foreign bodies protruding from the scalp. At this point, the implanted computerized cranial implant will translate the signal into digital commands capable of operating a computer, a robotic limb, or any other external device using his/her own will (Fig. 111.15).9,76–78 With recent advances in cranial implant design and manufacturing, it is now conceivable, as the BCI neurotechnology shrinks in size several-­fold secondary to improved/ condensed battery sources, we will soon witness transformation of the BCI, like the bag phone evolved into the modern cellular phone. The major determinant of efficacy will shift from technology composition to optimal delivery

1279

FIGURE 111.14  Functional movement task showing the participant opening his hand, grasping, lifting, transferring stir stick. (Copyright © Ohio State University, Retrieved from https://www.medgadget. com/2016/04/completely-paralyzed-man-moves-his-own-armfor-first-time.html.) Lower image is magnified view of Utah MEA system. (X. Xie et al., “Bi-layer encapsulation of utah array based nerual interfaces by atomic layer deposited Al2O3 and parylene C,” 2013 Transducers & Eurosensors XXVII: The 17th International Conference on Solid-State Sensors, Actuators and Microsystems (TRANSDUCERS & EUROSENSORS XXVII), Barcelona, Spain, 2013, pp. 1267-1270, doi: 10.1109/Transducers.2013.6627006.)

vehicle/anatomical placement location (i.e., complication risk). In other words, as BCIs become miniaturized and personalized in design, long-­term patient satisfaction and end-­user safety will have more to do with the surrounding bone and/or soft tissue contributing to patient appearance postimplantation, rather than the inherent function of the BCIs themselves (Fig. 111.16).2,3,5,17,18,39,41,46,49,50,57,62,72,79 

Neuroplastic and Reconstructive Surgery Modern cranioplasty, along with the burgeoning field of neuroplastic and reconstructive surgery, is undergoing a paradigm shift related to various techniques, surgical advancements, implantable neurotechnology, and improved biomaterials for cranial implant fabrication. These changes are challenged by preexisting silos and generational dogmas, which contribute to unacceptably high complication rates in cranioplasty. This was the main impetus behind this new field termed “neuroplastic surgery.”30 So far, many advancements have been made within the literature—including the introduction of various approaches for scalp/skull reconstruction, state-­ of-­ the-­ art cranial implant designs, and unprecedented success in housing BCIs and hydrocephalus shunt valves within cranial implants (Fig. 111.17).26 As the field of three-­dimensional printing advances and tissue engineering for autologous bone progresses, customized craniofacial implants with embedded neurotechnologies will become the gold standard for all BCI integration.55,56

1280

Section Six  •  FUNCTIONAL NEUROSURGERY

The first step to installing self-­ contained computers neighboring our brains is deciding where to put the hardware without distorting the skull and/or patient’s head shape.7 Implant accommodation for neuroprosthetics could be fitted with a multitude of functional parts, from drug-­ administrating ports to biosensing electronics. Technologies such as optogenetics, seeds for local radiation therapy, focused ultrasound probes, neurostimulation for epilepsy, and gene therapy (i.e., miRNA)/nanoparticle medicine therapeutics, can all be implanted into a patient-­specific functional cranial implant. Functional cranial implants will incorporate design inputs based on active clinical neurosurgical practice. They will eventually provide treatment and cures for spinal cord injury patients via the use of prosthetic arm systems, motorized wheelchair control, household interface systems, and emergency response systems. As previously mentioned, current design requirements for neuroprosthetics and neurotechnologies require transcranial hardwiring to external hardware, to allow activation of nearby external computers. Thus, the physical size parameters will be the key factor dictating success for the advance of low-­profile, intercranial implantable systems powering wireless functional devices, driving long-­ running data collection, and managing two-­way diagnostic/ therapeutic performance. Normal cranial bone will soon be removed by neurosurgeons, on an everyday basis, to make way for functional cranial implants housing multiple components for recording, amplifying, converting, and storing data, as well as wireless data transmission, solely dependent on each patient’s neuropathology. Together, these BCIs will

A

B

create a standard platform for integrating a wide spectrum of functional neurological devices, including but not limited to commercially available MEAs, ultrasound probes with multiple diagnostics and therapeutic purposes, intracranial pressure monitors, flow sensors, drug delivery systems, and tumor-­treating radiation fields.55,56 Concepts that drive the field of neuroscience research will be changed fundamentally with the actualization of additional “neurological real estate” for implanting functional BCIs by way of cranial implants. Several beneficial treatments will soon be realized such as (1) the reduction of complications associated with eliminating compression of surrounding soft tissue (which means less extrusion risk), (2) reducing the amount of revision surgery related to limited power supply (that is, increased room for multiple batteries), (3) eliminating a second surgical site often required to house the battery for currently marketed functional neurosurgical devices (i.e., prevent remote batteries like those placed on the chest wall), (4) the ability to monitor or map brain activity outside of an inpatient setting and be mobile/active during procedures that previously required tethering to external devices, and (5) collecting enough multiunit neural activity to provide treatment to spinal cord–injured patients for curing paralysis. In fact, the current neuromonitoring and neuromodulation systems placed above or below the cranium come with their own set of shortcomings. For example, the profile of implants placed between the scalp and cranium often cause pain and scalp/bone erosions due to local compression and ischemic sequelae, and increase the risk for infection due to the challenges of fixation and micromotion.

FIGURE 111.15  Solid, opaque cranial implants will soon be replaced with highly functional, clear-­ colored, custom cranial implants delivering personalized medicine via a multitude of imbedded neurotechnologies. (Johns Hopkins division of neuroplastic surgery.)

C

IN THE NOT TOO DISTANT FUTURE... GBM/BRAIN EPILEPSY TUMOR PATIENT? PATIENT?

HYDROCEPHALUS PATIENT?

PARKINSON’S PATIENT?

OR FIGURE 111.16  As brain-­computer interfaces become miniaturized, imbedded power sources improve, and the functional cranial implant industry expands, we will witness a dramatic advance in implantable neurotechnology in a way that removes all social stigma.

111  •  Brain-Computer Interfacing: Prospects and Technical Aspects of Functional Cranial Implants

1281

FIGURE 111.17  Right: State-­of-­the-­art cranial implant designs, housing brain-­computer interfaces and hydrocephalus shunt valves. Top Left: Pre-­ op skin breakdown above high profile shunt valve. Bottom left: 3D computed topography reconstruction demonstrating high versus low shunt valves. (From Gordon CR, et al. First in-human experience with integration of a hydrocephalus device within a customized cranial implant. Operative Neurosurgery, Volume 17, Issue 6, December 2019, Pages 608–615, https://doi.org/10.1093/ons/opz003.)

Existing technology requires components be wired to external devices, limits the amount of implantable parts, and can require a compromise on the density/volume of data collected. However, in the very near future, the development of implantable data storage and wireless management capabilities will overcome and eradicate these challenges.55,56 

Neuro-­Biohacking Whereas biohacking concentrates on the human body and the act of conscious hacking, neurohacking is focused on the mind-­brain interface—the intersection of neurology and consciousness. Specifically, neurohacking involves applying science and technology to influence the connections of brain and body in order to optimize subjective experience and thereby create a relative “superhuman” effect.80 Preliminary research suggests that targeted brain stimulation can improve recall in those with memory loss and cognitive enhancement, made possible by the formal, physical union of computer and brain (cerebral augmentation) (Fig. 111.18). The largest contributor to BCI development is the research arm of the DoD, known as the Defense Advanced Research Projects Agency (DARPA). This organization has a long track record of pushing scientists and engineers to

achieve the seemingly impossible. DARPA, in collaboration with Johns Hopkins Applied Physics Laboratory, birthed the Arpanet—which eventually became the internet—and also developed the global positioning system. Its medical research division has funded studies that on the use of neurological implants similar to the NeuroPace two-­way sensing device—treating everything from traumatic brain injury to psychosis. In simpler terms, a functional BCI for augmentation purposes, in theory, could turn an average human into a programmable, debuggable machine—like a computer or robot. What used to be accomplished through medicine, training, education, and psychotherapy could someday be achieved with BCIs. Neuralink, the latest startup from serial entrepreneur Elon Musk, is a direct cortical interface pursuing “neural lace technology,” which entails extensive brain mapping devices that may one day allow us to upload/download thoughts and/or communicate concepts without first expressing them in language.81 As the Wall Street Journal author Christopher Mimms stated in his article entitled “A Hardware Update for the Brain,” “Our reality is waiting” and BCIs/cranial implants are “the future of everything.” We agree. In fact, the more pressing questions now are, who will have access to technology once life-­changing, cognitive enhancement is realized? Will governments give it to their citizens and/or their

1282

Section Six  •  FUNCTIONAL NEUROSURGERY

A

B

C

D FIGURE 111.18  A, Bioluminescence using LED lights, delivers biometric data. (Northstar implant, photo courtesy of Ryan O’Shea.) B, Eyeborg project-­prosthetic camera and electronic eye shell housing, wirelessly transmit literal point of view images. (Rob Spence/Eyeborg Project.) C, RFID and NFC chips to replace keys, passwords, personal data storage, credit cards. (© John A. Rogers, from https://theconversation.com/ tattoo-you-the-stick-on-medical-revolution-2794.) D, Antenna capable of transposing colors to vibrations using a head mounted camera for overcoming achromatopsia. “hearing colors.” (Photo © Hector Adalid.)

military? Will businesses subsidize it for their employees? Will companies someday require brain-­computer interfaces for performance imrpovement? Like it or not, implanted neurotechnology, housed within functional cranial implants, is happening. Functional cranial implants, in combination with various BCIs, represent the ideal delivery vehicle, capitalizing on the biocompatible space once occupied by the human skull.36,51,52,70,73–78,81–84 

Conclusion This evolution of technical and clinical capabilities will involve necessary convergence of several disciplines, including basic neuroscience, neuroengineering, computer science, neurosurgery, and neuroplastic surgery. It will be an exciting era for biomedical/neuro-­engineering, one in which neurosurgeons and neuroplastic surgeons alike stand to make great contributions. These innovative advancements will help those patients who have succumbed to neurologic pathology, ranging from degenerative brain disease to trauma with extremity paralysis. Monumental changes in neurosurgery have included Wilhelm Röntgen’s discovery of x-­rays, Walter Dandy’s description of ventriculography and pneumoencephalography, António Egas Moniz’s achieving opacification of the carotid artery, and Sir Godfrey Hounsfield’s development of the computed topography scan.2 Implantable neurotechnology housed within functional

cranial implants will soon be added to this list. Without doubt, we agree wholeheartedly with the Wall Street Journal, in that this subject represents “the future of everything” for all neurosurgeons. KEY REFERENCES

Bakay, R. Brain-­computer interfacing prospects and technical aspects. In Quinones: Schmidek & Sweet Operative Neurosurgical Techniques, 7th ed. Gordon CR, Huang J, Brem H, et al. Neuroplastic surgery. J Craniofac Surg. 2018;29(1):1–2. Gordon CR, et al. Understanding cranioplasty. J Craniofac Surg. 2016;27(1):5. Gordon CR, et al. Immediate single-­ stage cranioplasty following calvarial resection for benign and malignant skull neoplasms using customized craniofacial implants. J Craniofac Surg. 2015;26(5):1456–1462. Gordon CR, Santiago GF, et al. First in-­human experience with complete integration of neuromodulation device within a customized cranial implant. Oper Neurosurg. 2018;15(1):39–45 Hochberg Leigh R, et al. Reach and grasp by people with tetraplegia using a neurally controlled robotic arm. Nature. 2012;485:372–375. Jackson A. Brain-­ controlled robot grabs attention. Nature. 2012;485:317–318. Mogilner AY, Benabid AL, Rezai AR. Chronic therapeutic brain stimulation: history, current clinical indications, and future prospects. In: Markov Marko, Rosch PJ, eds. Bioelectromagnetic Medicine. 2004. New York: Marcel Dekker; 2004. Wolff A, Santiago GS, Gordon CR, et al. Adult cranioplasty reconstruction with customized cranial implants: preferred technique, timing, and biomaterials. J Craniofac Surg. 2018;29:887–894.

Numbered references appear on Expert Consult.

REFERENCES

1. Bakay, R. Brain-­computer interfacing prospects and technical aspects. In Quinones: Schmidek & Sweet Operative Neurosurgical Techniques, 7th ed. 2. Youmans & Winn Neurological surgery. In Neuroprosthetics. 7th ed., Vol. 1. Philadelphia: Elsevier;2017:25–26. 3. Greenwald E, et al. Implantable neurotechnologies: bidirectional neural interfaces applications and VLSI circuit implementations. Med Biol Eng Comput. 2016;54:1–17. 4. Kian AN, et al. Implantable neurotechnologies: a review of integrated circuit neural amplifiers. Med Biol Eng Comput. 2016;54:45– 62. 5. Anoop C, Patil, et al. Implantable neurotechnologies: a review of micro and nanoelectrodes for neural recording. Med Biol Eng Comput. 2016;54:23–44. 6. Wall Street Journal newspaper advertisement. “Our reality is waiting” November. 2017;30. 7. Mims CA. Hardware Update for the Human Brain. Wall Street J.; 2017. 8. Wendelke S, et al. Restoration of motor control and proprioceptive and cutaneous sensation in humans with prior upper-­ limb amputation via multiple Utah Slanted Electrode Arrays (USEAs) implanted in residual peripheral arm nerves. J NeuroEngineering Rehab. 2017;14:121. 9. Ming Y, et al. Wireless Neurosensor for full-­spectrum Electrophysiology recordings during free Behavior. Neuron. 2014;84(6):1170– 1182. 10. Vidal JJ. Toward direct brain-­computer communication. Ann Rev Biophys Bioengineer. 1973;2(1):157–180. 11. Tyson A, et al. Decoding motor imagery from the posterior parietal cortex of a tetraplegic human. Science. 2015;348(6237):906–910. 12. Anderson RJ, Frye MA, Abulseoud OA, et al. Deep brain stimulation for treatment-­resistant depression: efficacy, safety and mechanisms of action. Neurosci Biobehav Rev. 2012;36(8):1920–1933. 13. Kringelbach ML, Jenkinson N, Owen SL, Aziz TZ. Translational principles of deep brain stimulation. Nat Rev Neurosci. 2007;8(8):623–635. 14. Volkmann J, Herzog J, Kopper F, Deuschl G. Introduction to the programming of deep brain stimulators. Mov Disord. 2002;17(suppl 3):S181–S187. 15. Young RF, Brechner T. Electrical stimulation of the brain for relief of intractable pain due to cancer. Cancer. 1986;15(6):1266–1272. 57. 16. Viswanathan A, et al. Deep brain stimulation for Tourette syndrome: target selection. Stereotact Funct Neurosurg. 2012;90(4):213– 224. 17. Krauss JK. Deep brain stimulation for dystonia in adults. Overview and developments. Stereotact Funct Neurosurg. 2002;78(3–4):168– 182. 18. Belzberg M, Ben-­Shalom N, Gordon CR, et al. Sonolucent cranial implants: cadaveric study and clinical findings supporting diagnostic and therapeutic Trans-­cranioplasty ultrasound. Operat Neurosurg. 2018. [submitted Nov 2018 -­currently under review]. 19. Quadri SA, et al. High-­intensity focused ultrasound: past, present, and future in neurosurgery. Neurosurg Focus. 2018;44(2):E16. 20. Bretsztajn, et al. Brain-­focussed ultrasound: what’s the “FUS” all about? A review of current and emerging neurological applications. Br J Radiol. 2018;91:81. 21. Robison A, et al. Surgery of the mind, Mood, and conscious state: an Idea in evolution. World Neurosurg. 2012;77(5–6):662–686. 22. Romanelli R, et al. A novel neural prosthesis providing long-­term electrocorticography recording and cortical stimulation for epilepsy and brain-­computer interface. J Neurosurg. 2018. 23. Monzurul A, et al. Brain-­machine interface facilitated neurorehabilitation via spinal stimulation after spinal cord injury: recent progress and future perspectives. Brain Res. 2016;1646:25–33. 24. Soekadar SR, et al. Brain–machine interfaces in neurorehabilitation of stroke. Neurobiol Dis. 2015;83:172–179. 25. Lee KH, et al. WINCS Harmoni: Closed-­loop dynamic neurochemical control of therapeutic interventions. Scientific Reports 7:46675 | DOI: 10.1038/srep46675 1 26. Gordon CR, et al. First in-­human experience with integration of a hydrocephalus device within a customized cranial implant. Operat Neurosurg. 2018. [Accepted—In Press].

27. Burgess, et al. Focused ultrasound-­mediated drug delivery through the blood-­brain barrier. Expert Rev Neurother. 2015;15(5):477–491. 28. Christian E, et al. Focused ultrasound: relevant history and prospects for the addition of mechanical Energy to the neurosurgical Armamentarium. World Neurosurg. 2014;82(3/4):354–355. 29. Bryden AM, Peljovich AE, Hoyen HA, Nemunaitis G, Kilgore KL, Keith MW. Surgical restoration of arm and hand function in people with tetraplegia. Spinal Cord Injury Rehabil. 2012;18(1):43–49. 30. Gordon CR, Huang J, Brem H, et al. Neuroplastic surgery. J Craniofac Surg. 2018;29(1):1–2. 31. Website accessed December 12, 2018. https://en.wikipedia.org/wi ki/Neuroplastic_surgery. 32. Murphy RJ, Wolfe KC, Gordon CR, et al. Computer-­ assisted single-­stage cranioplasty. Conf Proc IEEE Eng Med Biol Soc. 2015;2015:4910–4913. 33. Gordon CR, et al. Understanding cranioplasty. J Craniofac Surg. 2016;27(1):5. 34. Bakay R. Limits of brain–computer interface. Neurosurg Focus. 2006;20(5):e6. 35. Yanagisawa T, et al. Electrocorticographic control of a prosthetic arm in paralyzed patients. Ann Neurol. 2012;71(3):353–361. Epub 2011 Nov 2. 36. Boyden ES, et al. Scalable 3-­d microelectrode recording architectures for characterization of optogenetically modulated neural dynamics. Soc Neurosci. 2012. 610.06/FFF64. 37. Alvin Lucier. Website accessed December 12, 2018. https://et.wn .com/alvin_lucier/biography. 38. Benabid AL. What the future holds for deep brain stimulation. Expert Rev Med Devices. 2007;4:895–903. 39. Leigh RH, et al. Reach and grasp by people with tetraplegia using a neurally controlled robotic arm. Nature. 2012;485:372–375. 40. Jackson A. Brain-­ controlled robot grabs attention. Nature. 2012;485:317–318. 41. Mogilner AY, Benabid AL, Rezai AR. 2004. Chronic therapeutic brain stimulation: History, current clinical indications, and future prospects. In: Markov M, Rosch PJ, eds. Bioelectromagnetic Medicine. New York: Marcel Dekker; 2004. 42. Kim SP, Simeral JD, Hochberg LR, Donoghue JP, Black MJ. Neural control of computer cursor velocity by decoding motor cortical spiking activity in humans with tetraplegia. J Neural Eng. 2008;5(4):455–476. 43. Roche JP, et al. On the Horizon: cochlear implant technology. Otolaryngol Clin North Am. 2015;48(6):1097–1116. Epub 2015 Oct 9. 44. Bolu A, et al. Restoration of reaching and grasping movements through brain-­ controlled muscle stimulation in a person with tetraplegia: a proof-­ of-­ concept demonstration. Lancet. 2017;389(10082):1821–1830. 45. Sharlene N, Flesher, et al. Intracortical microstimulation of human somatosensory cortex. Sci Transl Med. 2016;8(361):141. 46. Youssef E, et al. Direct brain stimulation Modulates Encoding states and memory performance in humans. Curr Biol. 2017;27:1251– 1258. 47. Jonathan C, Kao, et al. Single-­ trial dynamics of motor cortex and their applications to brain-­machine interfaces. Nat Communi. 2015;6:7759. 48. Ison MJ, et al. Rapid Encoding of new Memories by individual neurons in the human brain. Neuron. 2015;87:220–230. 49. Kennedy PR, Bakay RA. Restoration of neural output from a paralyzed patient by a direct brain connection. Neuroreport. 1998;9(8):1707–1711. 50. Hochberg LR, Serruya MD, Friehs GM, et al. Neuronal ensemble control of prosthetic devices by a human with tetraplegia. Nature. 2006;442(7099):164–171. 51. Website accessed December 15, 2018. http://braingate.org. 52. Website accessed December 15, 2018. http://rippleneuro.com. 53. ALS Patients Communicate for the First Time in Years with New Device; 2018. Website accessed December 13. https://www.nbcnew s.com/health/health-­news/als-­patients-­communicate-­first-­time-­ years-­new-­device-­n715121. 54. Robotic Hand Exoskeletons Lets Quadriplegic People Use Cutlery. Vol 11. 2018. Website accessed Decmeber. https://www.ne wscientist.com/article/2115340-­robotic-­hand-­exoskeleton-­lets-­ quadriplegic-­people-­use-­cutlery/.

1282.e1

1282.e2References 55. Gordon C. “Low profile intercranial device (L.I.D.)”. U.S. Patent Application (WO2017039762 A1). Published March 9, 2017. 56. Gordon C, Christopher J. “Method for manufacturing a low profile intercranial device (L.I.D.) and the low profile intercranial device manufactured thereby. U.S. Patent Application (20180055640 A1). Published March 1, 2018. 57. Gordon CR, Santiago GF, et al. First in-­human experience with complete integration of neuromodulation device within a customized cranial implant. Oper Neurosurg. 2018;15(1):39–45. 58. Morrell MJ. RNS System in Epilepsy Study Group. Responsive corticalstimulation for the treatment of medically intractable partial epilepsy. Neurology. 2011;77(13):1295–1304. Epub 2011 Sep 14. 59. Heck CN, King-­Stephens D, Massey AD, et al. Two-­year seizure reduction in adults with medically intractable partial onset epilepsy treated with responsive neurostimulation: final results of the RNS System Pivotal trial. Epilepsia. 2014;55(3):432–441. Epub 2014 Feb 22. 60. Brindley GS, et al. The sensations produced by electrical stimulation of the visual cortex. J Physiol. 1968;196(2):479–493. 61. Markowitz M, et al. Rehabilitation of lost functional vision with the Argus II retinal prosthesis. Can J Ophthalmol. 2018;53(1):14–22. Epub 2018 Jan 12. 62. Robson JA, Davenport RJ. Neurotechnology: a new approach for treating brain disorders. R I Med J. 2014;97(5):18–21. 63. Yaremchuk, et al. Complications and Toxicities of implantable biomaterials used in facial reconstructive and aesthetic surgery: a Comprehensive review of the literature. Plast Recon Surg. 1997. 64. Wolff A, Santiago GS, Gordon CR, et al. Adult cranioplasty reconstruction with customized cranial implants: Preferred technique, timing, and biomaterials. J Craniofac Surg. 2018;29:887–894. 65. Gordon CR, et al. Immediate single-­ stage cranioplasty following calvarial resection for benign and malignant skull neoplasms using customized craniofacial implants. J Craniofac Surg. 2015;26(5):1456–1462. 66. Doshi PK. Long-­term surgical and hardware-­related complications of deep brain stimlation. Stereotact Funct Neurosurg. 2011;89(2):89– 95. 67. Lozano AM, et al. Long-­term hardware-­related complications of deep brain stimulation. Neurosurgery. 2002;50(6):1268–1274; discussion 1274-­6. 68. Boon P, et al. Deep brain and cortical stimulation for epilepsy. Cochrane Database Syst Rev. 2014;(6). Review. Update in: Cochrane Database Syst Rev. 2017;7:CD008497. 69. Boviatsis EJ, et al. Surgical and hardware complications of deep brain stimulation. A seven-­year experience and review of the literature. Acta Neurochir (Wien). 2010;152(12):2053–2062. Epub 2010 Jul 25. 70. Wei Z, Gordon CR, Bergey GK, et al. Implant site infection and bone Flap Osteomyelitis associated with the NeuroPace responsive neurostimulation system. World Neurosurg. 2016;4(10):e1–687. 71. Warwick K, et al. The application of implant technology for cybernetic systems. Arch Neurol. 2003;60(10):1369–1373.

72. Fakhoury M. Neural prostheses for restoring functions lost after spinal cord injury. Neural Regen Res. 2015;10(10):1594–1595. 73. Benedict Carey Chip, Implanted in Brain, Helps Paralyzed Man Regain Control of Hand. Website accessed December 14, 2018. https://www.nytimes.com/2016/04/14/health/paralysis-­l imb-­ reanimation-­brain-­chip.html. 74. Bouton, et al. Restoring cortical control of functional movement in a human with quadriplegia. Nature. 2016;533(7602):247–250. Epub 2016 Apr 13. 75. Website accessed December 19, 2018. “The Next Step in BCI Development”. https://www.wysscenter.ch/project/thought-­ controlled-­arm-­to-­help-­people-­with-­paralysis-­reach-­and-­grasp/. 76. liu X, et al. A fully integrated wireless compressed sensing neural signal acquisition system for chronic recording and brain machine interface. IEEE. 2016;10(4). 77. Harrison RR, et al. A low-­power integrated circuit for a wireless 100-­electrode neural recording system, IEEE. J Solid-­State. 42(1) 78. Website accessed December 19, 2018. https://www.brown.edu/aca demics/brain-­science/research/research-­projects/braingate. 79. Guger C, et al. Complete locked-­in and locked-­in patients: Command following Assessment and communication with Vibro-­ Tactile P300 and motor imagery brain-­computer interface tools. Front Neurosci. 2017;11:251. 80. Website accessed December 21, 2018. Dallon Adams, 8 Bold biohacks that blur the line between human and machine. May 20/2017 Digital trends. https://www.digitaltrends.com/cool-­tech/coolest-­ biohacking-­implants. 81.  Website accessed December 12, 2018. https://www.cnbc.co m/2018/09/07/elon-­m usk-­d iscusses-­n eurolink-­o n-­j oe-­r ogan-­ podcast.html. 82. Anderson WS, et al. Prediction of single neuron spikes in sensorimotor cortex may reflect generic properties of locally connected networks. BMC Neurosci. 2018;19(supp 2):65. published online 2018 Oct 29. 83. Website accessed December 20, 2018. https://www.braininitiative. nih.gov/. 84. Collinger JL, et al. Functional priorities, assistive technology, and brain-­computer interfaces after spinal cord injury. J Rehabil Res Dev. 2013;50(2):145–160. 85. Ireton JE, Unger JG, Rohrich RJ. The role of wound healing and its everyday application in plastic surgery: a practical perspective and systematic review. Plast Reconstr Surg Glob Open. 2013;1(1):e10– e19. 86. Meng, et al. Current and emerging brain applications of MR-­ guided focused ultrasound. J of Therapeutic Ultrasound. 2017;5:26. 87. Hersh, et al. Emerging applications of therapeutic ultrasound in neuro-­ oncology: moving beyond tumor Ablation. Neurosurgery. 2016;79:643–654. 88. Dasgupta, et al. Ultrasound-­mediated drug delivery to the brain: principles, progress and prospects. Drug Discovery Today: Technology. 2016;20:41–48.

CHAPTER 112

Thoracoscopic Sympathectomy for Hyperhidrosis JIAN GUAN  •  SUBU N. MAGGE Axillary and palmar hyperhidroses are relatively common disorders that together affect approximately 0.5% to 1% of the population, with possibly higher percentages in those of Asian descent.1 Hyperhidrosis is an idiopathic overactivation of sweat glands that results in secretion of sweat in excess of that needed for typical autonomically controlled thermoregulation. It is often overlooked or untreated and can cause significant distress that may lead to a negative impact on social and professional quality of life.2 Simple tasks such as handshaking, writing, and handling daily objects can become daunting problems. Hyperhidrosis can become so severe that sweat can drip off a person’s fingertips and can even require multiple changes of clothing daily. Individuals with untreated hyperhidrosis have an increased risk for cutaneous skin infection if the abnormal physiology is not adequately corrected; the overall odds ratio for infection of untreated hyperhidrosis is 3.2, for dermatophyte fungus is 9.8, and for bacteria is 2.6.3 Hyperhidrosis is also associated with a higher risk of psychiatric disorders such as anxiety and depression.4 Despite the significant impact of hyperhidrosis on the quality of life of individuals suffering from the condition, a large proportion them do not seek medical attention because they believe that it is not a medical condition or that no effective interventions exist.5 The diagnosis criteria for hyperhidrosis stratify its severity into four classes, according to the Hyperhidrosis Disease Severity Scale: never noticeable, tolerable but interferes, barely tolerable and frequently interferes, and intolerable and always interferes.6 Additional criteria include duration in the previous 6 months, bilateral with symmetry, onset before 25 years of age, family history, and asymptomatic during sleep.7 Treatment options include topical therapy with metal salts, anticholinergic agents, botulinum toxin therapy, iontophoresis, and surgical disruption of the upper thoracic sympathetic chain. After initial diagnosis, medical treatments should be pursued until deemed failed because of either persistence of symptoms despite adequate intensive therapy or intolerance to medical treatment. Only after all medical options are exhausted should surgical intervention be considered. Surgery consists of sectioning the second, third, and fourth ganglia of the sympathetic chain in the chest.

History Although the earliest surveys of the sympathetic nervous system were conducted by du Petit in 1727, the first report of surgical sympathectomy was at the level of the neck for treatment of epilepsy by Alexander in 1889.8,9 Since then, sympathectomy has been used for numerous clinical presentations, with limited success. For example, sympathectomy has been indicated in treatment of angina,10 Raynaud phenomenon,11 exophthalmic goiter,12 glaucoma,13 various pain conditions,14 and spastic paralysis of lower extremities.15 Bernard and Horner independently published a series of reports in the latter half of the 19th century describing sectioning of the sympathetic chain and associated clinical effects.16,17 Since the 1920s, when Kotzareff described anhidrosis with sectioning of the sympathetic chain,18 sympathectomy has been commonly used for hyperhidrosis. The adaptation of endoscopic surgery was introduced in the 1940s, when Hughes described an endoscopic approach for thoracic sympathectomy.19 Although endoscopic sympathectomy is the current standard surgical treatment for hyperhidrosis, a variety of other interventions have been attempted in the past. Weaver describes a series of patients treated for axillary hyperhidrosis through excision of skin and glandular tissue in the axillae.20 Other practitioners attempted less radical approaches, including the utilization of cryotherapy to damage the eccrine glands to achieve reduction in symptoms.21 Percutaneous sympathetic blocks under imaging guidance have also been used for hyperhidrosis treatment.22 

Anatomy and Physiology The eccrine glands function to release serous fluid to the skin to promote cooling by evaporation and are primarily innervated by autonomic, acetylcholinergic, sympathetic neurons. Eccrine glands are distributed throughout the skin surfaces, numbering between 2 million and 4 million per person, with the highest concentrations in the axilla, palms of the hands, and soles of the feet. The sweat response is under hypothalamic thermoregulatory control via the preoptic sweat area of the hypothalamus.23 Autonomic output to the eccrine glands arises both from input responding to thermoregulation and from

1283

1284

Section Six  •  FUNCTIONAL NEUROSURGERY

emotional state. Therefore heightened emotions trigger a sweat response, such as sweaty palms with anxiety or nervousness. Sympathetic pathways for eccrine sweat control originate in the preoptic sweat nucleus of the hypothalamus and travel through the nucleus raphe pallidus. In the spinal column, sympathetic fibers travel in the intermediolateral column in Rexed lamina VII. Sympathetic fibers pass out the ventral root and enter and synapse in the paravertebral sympathetic chain ganglia. Postganglionic fibers travel in peripheral nerves or arteries to their target organs, including the eccrine glands. Traditionally, the second and third sympathetic ganglia are thought to innervate sweat glands in the palms while the third and fourth ganglia innervate the axilla. Importantly, approximately 10% of the population carries the nerve of Kuntz, an additional aberrant division of the sympathetic chain arising from T1, T2, or T3.24 If present, the nerve of Kuntz must be sectioned to ensure that sympathectomy will be effective. Abnormalities in the pathways associated with eccrine gland function are thought to be the root cause of hyperhidrosis, and a strong hereditary component exists for the disease. One study estimated that an allele associated with palmar hyperhidrosis may be present in up to 5% of the population, with hyperhidrosis occurring in approximately a quarter of individuals who inherit two copies of this gene.25 Subsequent studies have located specific genetic loci for hyperhidrosis,26 although other candidate genes have also been found suggesting a more complex genetic picture.27

PATIENT SELECTION Careful patient selection is critical for success. Prior to consideration for surgery, patients should have completed a range of appropriate medical therapies unsuccessfully. The mainstay of medical therapy includes over-­the-­counter antiperspirants and topical 20% AlCl compounds; however, chronic use of such antiperspirants can be limited by skin irritation. Medications that block α-­adrenergic receptors such as phenoxybenzamine may also help symptoms. Often, these medications are poorly tolerated, as frequent side effects include hypotension and sexual dysfunction. Another, more invasive option consists of a series of topical injections of botulinum toxin A (Botox). For palmar hyperhidrosis, an average of 26 Botox injections were required for determination of success or failure.28 Typically, even successfully treated patients need repeated injections after several months. A more recently used medical therapy for hyperhidrosis is oxybutynin—an antimuscarinic agent more commonly prescribed for urologic conditions such as incontinence. Similar to other medical therapies, oxybutynin can lead to a variety of side effects including dry mouth and constipation, and the drug is not recommended for use during pregnancy.29 Iontophoresis treatments should also be tried prior to consideration of surgical treatment. Iontophoresis involves electrical stimulation, often with tap water, and can be conducted at home; however, it requires a significant daily time commitment. Another novel treatment modality involves microwave-­ based stimulation of eccrine glands, thereby reducing sweat production.30 Although this technology has been shown to be fairly safe and efficacious, significant complications with use have been reported, and its use is

A B

C FIGURE 112.1  Instruments used for thoracoscopic sympathectomy. (A) Threaded trocar for camera placement. (B) Cautery hook for sympathetic chain ablation. (C) A 5-­mm insufflation port for tool placement.

limited to cases of axillary hyperhidrosis.31 Lastly, in selected patients, imaging with computed tomography or magnetic resonance can be useful in excluding alternative pathologies, including infection, metabolic disorders, and neoplastic processes. If hyperhidrosis remains debilitating despite these interventions, surgery should be considered. 

Surgical Treatment ANESTHESIA Endoscopic thoracic sympathectomy typically requires placement of a double-­lumen endotracheal tube. This allows for deflation of the lung on the operative side while allowing for ventilation of the contralateral lung. Alternatively, a single-­lumen endotracheal tube may be used with positive pressure carbon dioxide insufflation.32 

INSTRUMENTS We typically use a 5-­mm rigid endoscope for thoracoscopic procedures. Lens angle depends upon surgeon preference. We typically prefer a 30-­degree angled scope. During the procedure, a dissection tool such as a cautery hook (Fig. 112.1) or scissors is necessary, as well as cotton pledgets and a suction irrigator. 

POSITIONING The patient should be positioned supine with the arms on arm boards perpendicular to the bed (Fig. 112.2). A reverse Trendelenburg position to approximately 40 degrees enables the deflated lung to fall away by gravity and minimizes the need for retraction. A footboard attached to the surgical table may be necessary to prevent the patient from sliding along the inclined bed. 

PROCEDURE In the multiport method, two 5-­mm thoracoscopic ports are placed in the third and fourth intercostal spaces (see Fig. 112.2). The endoscope is introduced through one, and the second serves as a working port for sectioning the sympathetic chain. Alternatively, the procedure may be performed through a single port.33 The sympathetic chain is identified using the rib heads as landmarks. The first rib is uniquely curved like a sickle (Fig. 112.3A). It is associated with a prominent fat pad containing

112  •  Thoracoscopic Sympathectomy for Hyperhidrosis

A

B

1285

FIGURE 112.2  Patient positioning and site selection. (A) The patient is placed supine with arms at 90 degrees. The head of bed may be elevated in a reverse Trendelenburg position to allow the lung to fall away from the sympathetic chain. (B) The T3– T4 region is prepared for trocar placement. In this figure, the two-­ port technique is used, allowing for a camera in one port and instruments in another.

G A D

B

A

C

F E

B

C

D

the first sympathetic ganglion, otherwise known as the stellate ganglion. The white sympathetic chain is seen coursing over each rib head, with the swelling of the ganglia close to the respective rib. After they have been adequately identified, the T2 to T4 portions of the sympathetic chain can be disconnected or clipped or excised. We prefer to disconnect the ganglia from the chain. A cotton pledget can be used to push the lung down and away from the upper thoracic spine if necessary. A cautery hook is then used to open the pleura on both sides of the ganglion. It is typically easiest to open the pleura directly over the bone of the rib (see Fig. 112.3B). The hook is dissected under the chain and used to elevate it into view. Cautery is then applied to cut the chain above and below the ganglion (see Fig. 112.3C). These steps are then repeated as many times

FIGURE 112.3  Operative images. (A) Intraoperative image allowing identification of the second through fourth rib heads. The image shows the (A) posterior mediastinum, (B) aortic arch, (C) second rib head, (D) second sympathetic ganglia, (E) third rib head, (F) third sympathetic ganglia, and (G) fat pad covering stellate ganglion. (B) A closer look at the second sympathetic ganglia; in this technique, ablation with cautery hook is undertaken. (C) The camera is shifted caudally, and the second through fourth sympathetic ganglia are ablated. (D) Finally, in this external view, a red rubber catheter is inserted through the port site, allowing air to efflux from the thorax.

as needed to disconnect the appropriate ganglia. Anecdotal evidence of the association of T2 with facial, T3 with palmar, and T4 with axillary hyperhidrosis has been observed34; however, contemporary practice includes sectioning the T2–T3 ganglia for palmar hyperhidrosis and T2–T4 ganglia for palmar and axillary hyperhidrosis. It is important to be sure any accessory fibers, including the nerve of Kuntz, if present, are disconnected or excised as well. Once the sympathectomy is completed, a red rubber catheter is inserted through one port site while the other port is removed and the wound is closed (see Fig. 112.3D). The catheter is submerged in saline while positive pressure ventilation by the anesthesiologist reexpands the lung. Bubbles of air can be seen in the saline as the lung inflates and air in the pleural space decreases. The red rubber catheter

1286

Section Six  •  FUNCTIONAL NEUROSURGERY

Complications

FIGURE 112.4  Postoperative image. Incision sites are closed with inverted, subcutaneous, absorbable suture and may be dressed as desired.

is removed when the lung is fully inflated, and incisions are closed with absorbable sutures and dressed with Steri-­Strips (Fig. 112.4). A postoperative chest x-­ray is obtained to confirm sufficient lung expansion (Video 112.1).

Outcomes Patients typically notice significant improvement almost immediately. This improvement remains fairly stable, as long-­term outcome studies show a range of efficacy of endoscopic sympathectomy for hyperhidrosis of 93.4% to 100% at 6 years.35,36 Moreover, surgery has been shown to result in a significant reduction in symptoms at both 6 and 12 months when compared with botulinum toxin injection.37 Myriad studies have investigated efficacy of treatment, comparing ablation level (T2–T4, T2, T3, or T4) and method (resection, electrocautery, transection, or clipping).38–42 Reduced incidence or severity of compensatory hyperhidrosis was noted in isolated T3 ablation compared with T2 or T2–T4.40 Ablation of T4 alone was found to have similar frequency of success but decreased incidence or severity of overdryness after surgery.43 One report advised complete excision of the sympathetic ganglia and rami with histologic confirmation for the best outcomes.44 A systemic review in 2008 concluded that there was no significant difference in outcome with respect to resection method, total ganglion resection, nerve transection, or ablation.39 The authors further concluded that inclusion of T2 and the adjacent sympathetic chain is important for success, in comparison with ablation of T3 or T4 alone, and may result in lower incidence of compensatory hyperhidrosis. In contrast, a subsequent meta-­analysis of randomized controlled trials of sympathectomy for palmar hyperhidrosis concluded that T4 sympathectomy allowed for lower incidence of compensatory hyperhidrosis in patients.45 Overall, the literature presents a mixed picture of which level or levels are necessary for resection to ensure success; thus further studies are warranted. 

Thoracoscopic sympathectomy is typically well tolerated; however, some adverse events are well-­known risks of surgery. Pneumothorax is among the most common complication, with incidence ranging from 7% to 17%.2,36 We routinely obtain a chest x-­ray while the patient is in the recovery room. If a substantial pneumothorax is seen, the patient remains in the hospital and another follow-­up film is obtained within 24 hours. In our experience, a chest tube is rarely needed and is reserved for symptomatic cases. Other centers prophylactically place a chest tube postoperatively and remove it shortly thereafter. Pleural effusion is attributed to a perioperative pleural tear during manipulation of the lung. Contemporary reports suggest the rate of occurrence of pleural effusion is nearly 7% of cases; however, the rate is likely lower when disconnection of the ganglia is performed rather than excision of the entire chain. Subcutaneous emphysema is caused by the collection of air in the subcutaneous tissues of the thorax and neck. Recent reports indicate that the rate of subcutaneous emphysema associated with thoracoscopic sympathectomy is approximately 2%.38,46 Horner syndrome can result from sympathectomy. This syndrome consists of miosis, ptosis, enophthalmos, hyperemia of the eye, and anhidrosis of half the face. It is the result of injury to the first cervical ganglion (stellate), and the incidence is reported to range from 0% to 24% in the initial postoperative period. When Horner syndrome occurs, symptoms typically resolve without further treatment. Studies suggest a 0% to 8% long-­term rate for persistent Horner syndrome.2 The incidence of this complication can be minimized by carefully avoiding direct injury to the stellate ganglion, excessive traction of sympathetic chain, or thermal injury to adjacent structures.47 Compensatory hyperhidrosis is an increase in perspiration occurring in areas other than the hands or axilla after a sympathectomy procedure. It is quite common in the initial few weeks after surgery and then typically subsides. The literature suggest compensatory hyperhidrosis can occur in 17% to 75% of patients after sympathectomy, and its occurrence has been related to both level and method of ablation.39,48–50 Fortunately, compensatory hyperhidrosis is severe in only approximately 5% to 10% of patients and tends to improve or resolve within 6 months after surgery. Severity, location, and prevalence of occurrence with respect to level of sympathectomy vary highly in reports, and no conclusive determination has been made. Reconstruction of the sympathetic chain as treatment has been described; however, substantiated claims have yet to be reported. Even successfully treated hyperhidrosis can recur over time. Freeman et al. suggested the recurrence rate of intolerable palmar hyperhidrosis ranges from 6.6% to 12.5% for thoracoscopic sympathomectomy.51 The success rate with reoperation was comparable to that with original surgery, with 95% experiencing improved symptoms in the reoperative group versus 98% in initial group, without significant increase in morbidity. However, compensatory sweating did significantly increase in those with a second procedure, 53% versus 31% (reoperation vs. initial, respectively). The authors did not comment on the ratio of patients with symptomatic recurrence to those who required reoperation. 

112  •  Thoracoscopic Sympathectomy for Hyperhidrosis

Conclusions Thoracoscopic sympathectomy remains a safe, well-­ tolerated, minimally invasive procedure with a low associated operative morbidity. In carefully selected patients with debilitating symptoms, surgery offers outstanding results with fairly rapid recovery. KEY REFERENCES

Ambrogi V, Campione E, Mineo D, et al. Bilateral thoracoscopic T2 to T3 sympathectomy versus botulinum injection in palmar hyperhidrosis. Ann Thorac Surg. 2009;88:238–245. Baumgartner FJ, Bertin S, Konecny J. Superiority of thoracoscopic sympathectomy over medical management for the palmoplantar subset of severe hyperhidrosis. Ann Vasc Surg. 2009;23:1–7. Chung IH, Oh CS, Koh KS, et al. Anatomic variations of the T2 nerve root (including the nerve of Kuntz) and their implications for sympathectomy. J Thorac Cardiovasc Surg. 2002;123:498–501. Doolabh N, Horswell S, Williams M, et al. Thoracoscopic sympathectomy for hyperhidrosis: indications and results. Ann Thorac Surg. 2004;77:410–414: discussion 414. Dumont P, Denoyer A, Robin P. Long-­term results of thoracoscopic sympathectomy for hyperhidrosis. Ann Thorac Surg. 2004;78:1801– 1807. Freeman RK, Van Woerkom JM, Vyverberg A, Ascioti AJ. Reoperative endoscopic sympathectomy for persistent or recurrent palmar hyperhidrosis. Ann Thorac Surg. 2009;88:412–416: discussion 416–417.

1287

Gossot D, Galetta D, Pascal A, et al. Long-­term results of endoscopic thoracic sympathectomy for upper limb hyperhidrosis. Ann Thorac Surg. 2003;75:1075–1079. Hornberger J, Grimes K, Naumann M, et al. Recognition, diagnosis, and treatment of primary focal hyperhidrosis. J Am Acad Dermatol. 2004;51:274–286. Kopelman D, Hashmonai M. The correlation between the method of sympathetic ablation for palmar hyperhidrosis and the occurrence of compensatory hyperhidrosis: a review. World J Surg. 2008;32:2343– 2356. Solish N, Bertucci V, Dansereau A, et al. A comprehensive approach to the recognition, diagnosis, and severity-­based treatment of focal hyperhidrosis: recommendations of the Canadian Hyperhidrosis Advisory Committee. Dermatol Surg. 2007;33:908–923. Solomon BA, Hayman R. Botulinum toxin type A therapy for palmar and digital hyperhidrosis. J Am Acad Dermatol. 2000;42:1026–1029. Vanaclocha V, Saiz-­Sapena N, Panta F. Uniportal endoscopic superior thoracic sympathectomy. Neurosurgery. 2000;46:924–928. Walling HW. Primary hyperhidrosis increases the risk of cutaneous infection: a case-­control study of 387 patients. J Am Acad Dermatol. 2009;61:242–246. Numbered references appear on Expert Consult.

REFERENCES

1. Baumgartner FJ, Bertin S, Konecny J. Superiority of thoracoscopic sympathectomy over medical management for the palmoplantar subset of severe hyperhidrosis. Ann Vasc Surg. 2009;23(1):1–7. 2. Adar R, Kurchin A, Zweig A, et al. Palmar hyperhidrosis and its surgical treatment: a report of 100 cases. Ann Surg. 1977;186(1): 34–41. 3. Walling HW. Primary hyperhidrosis increases the risk of cutaneous infection: a case-­control study of 387 patients. J Am Acad Dermatol. 2009;61(2):242–246. 4. Bahar R, Zhou P, Liu Y, et al. The prevalence of anxiety and depression in patients with or without hyperhidrosis (HH). J Am Acad Dermatol. 2016;75(6):1126–1133. 5. Doolittle J, Walker P, Mills T, et al. Hyperhidrosis: an update on prevalence and severity in the United States. Arch Dermatol Res. 2016;308(10):743–749. 6. Solish N, Bertucci V, Dansereau A, et al. A comprehensive approach to the recognition, diagnosis, and severity-­based treatment of focal hyperhidrosis: recommendations of the Canadian Hyperhidrosis Advisory Committee. Dermatol Surg. 2007;33(8):908–923. 7. Hornberger J, Grimes K, Naumann M, et al. Recognition, diagnosis, and treatment of primary focal hyperhidrosis. J Am Acad Dermatol. 2004;51(2):274–286. 8. Hashmonai M, Kopelman D. History of sympathetic surgery. Clin Auton Res. 2003;13(suppl 1):I6–9. 9. Alexander W. The Treatment of Epilepsy. Edinburgh: Pentland; 1889. 10. Jonnesco T. Angine de poitrine guérie par la résection du sympatique cervicothoracique. BUll Acad Med Paris. 1920;84:93–102. 11. Brüning F. Zur Technik der kombinierten Resektionsmethode sämtlicher sympathischen Nervenbahnen am Halse. Zentralbl Chir. 1923;5:1056–1059. 12. Jaboulay M. Chirurgie du Grand Sympathique et du Corps Thyroïde (Les Différents Goîtres). Articles Originaux Et Observations Réunis Et Publiés Par Le Dr. Etienne Martin. Paris: Lyon A. Storck & Cie; 1900. 13. François-­Franck M. Signification physiologique de la résection du sympathique dans la maladie de Basedow, l’épilepsie, l’idiotie et le glaucome. BUll Acad Med Paris. 1899;41:565–594. 14. Leriche R. The Surgery of Pain. London: Baillière, Tindall and Cox; 1939. 15. Royle N. A new operative procedure in the treatment of spastic paralysis and its experimental basis. Med J Aust. 1924;1:77–86. 16. Bernard C. Des phénomènes oculo-­ pupillaires produits par la section du nerf sympathique cervical: ils sont indépendants des phénomènes vasculaires calorifiques de la tête. C R Acad Sci Paris. 1852;55:381–388. 17. Horner J. Über eine Form von Ptosis. Klin Monbl Augenheilkd. 1869;7:193–198. 18. Kotzareff A. Resection partielle de trone sympathetique cervical droit pour hyperhidrose unilaterale. Rev Med Suisse Romande. 1920;40:111–113. 19. Hughes J. Endothoracic Sympathectomy. Proc R Soc Med. 1942;35(9):585–586. 20. Weaver PC. Axillary skin excision as a treatment for axillary hyperhidrosis. Postgrad Med J. 1970;46(537):422–424. 21. Ashby EC, Williams JL. Cryosurgery for axillary hyperhidrosis. Br Med J. 1976;2(6045):1173–1174. 22. Bale R. [Ganglion block. When and how?]. Radiologe. 2015;55(10):886–895. 23. Lowe N, Campanati A, Bodokh I, et al. The place of botulinum toxin type A in the treatment of focal hyperhidrosis. Br J Dermatol. 2004;151(6):1115–1122. 24. Chung IH, Oh CS, Koh KS, et al. Anatomic variations of the T2 nerve root (including the nerve of Kuntz) and their implications for sympathectomy. J Thorac Cardiovasc Surg. 2002;123(3):498–501. 25. Ro KM, Cantor RM, Lange KL, et al. Palmar hyperhidrosis: evidence of genetic transmission. J Vasc Surg. 2002;35(2):382–386. 26. Higashimoto I, Yoshiura K, Hirakawa N, et al. Primary palmar hyperhidrosis locus maps to 14q11.2-­ q13. Am J Med Genet A. 2006;140(6):567–572. 27. Chen J, Lin M, Chen X, et al. A novel locus for primary focal hyperhidrosis mapped on chromosome 2q31.1. Br J Dermatol. 2015;172(4):1150–1153.

28. Solomon BA, Hayman R. Botulinum toxin type A therapy for palmar and digital hyperhidrosis. J Am Acad Dermatol. 2000;42(6):1026– 1029. 29. Campanati A, Gregoriou S, Kontochristopoulos G, et al. Oxybutynin for the treatment of primary hyperhidrosis: current state of the art. Skin Appendage Disord. 2015;1(1):6–13. 30. Hong HC, Lupin M, O’Shaughnessy KF. Clinical evaluation of a microwave device for treating axillary hyperhidrosis. Dermatol Surg. 2012;38(5):728–735. 31. Chang CK, Chen CY, Hsu KF, et al. Brachial plexus injury after microwave-­based treatment for axillary hyperhidrosis and osmidrosis. J Cosmet Laser Ther. 2017;19(7):439–441. 32. Wong RY, Fung ST, Jawan B, et al. Use of a single lumen endotracheal tube and continuous CO2 insufflation in transthoracic endoscopic sympathectomy. Acta Anaesthesiol Sin. 1995;33(1):21–26. 33. Vanaclocha V, Saiz-­Sapena N, Panta F. Uniportal endoscopic superior thoracic sympathectomy. Neurosurgery. 2000;46(4):924–928. 34. Doolabh N, Horswell S, Williams M, et al. Thoracoscopic sympathectomy for hyperhidrosis: indications and results. Ann Thorac Surg. 2004;77(2):410–414; discussion 414. 35. Gossot D, Galetta D, Pascal A, et al. Long-­term results of endoscopic thoracic sympathectomy for upper limb hyperhidrosis. Ann Thorac Surg. 2003;75(4):1075–1079. 36. Dumont P, Denoyer A, Robin P. Long-­ term results of thoracoscopic sympathectomy for hyperhidrosis. Ann Thorac Surg. 2004;78(5):1801–1807. 37. Ambrogi V, Campione E, Mineo D, et al. Bilateral thoracoscopic T2 to T3 sympathectomy versus botulinum injection in palmar hyperhidrosis. Ann Thorac Surg. 2009;88(1):238–245. 38. Imhof M, Zacherl J, Plas EG, et al. Long-­term results of 45 thoracoscopic sympathicotomies for primary hyperhidrosis in children. J Pediatr Surg. 1999;34(12):1839–1842. 39. Kopelman D, Hashmonai M. The correlation between the method of sympathetic ablation for palmar hyperhidrosis and the occurrence of compensatory hyperhidrosis: a review. World J Surg. 2008;32(11):2343–2356. 40. Li X, Tu YR, Lin M, et al. Endoscopic thoracic sympathectomy for palmar hyperhidrosis: a randomized control trial comparing T3 and T2-­4 ablation. Ann Thorac Surg. 2008;85(5):1747–1751. 41. Walles T, Somuncuoglu G, Steger V, et al. Long-­term efficiency of endoscopic thoracic sympathicotomy: survey 10 years after surgery. Interact Cardiovasc Thorac Surg. 2009;8(1):54–57. 42. Weksler B, Pollice M, Souza ZB, et al. Comparison of ultrasonic scalpel to electrocautery in patients undergoing endoscopic thoracic sympathectomy. Ann Thorac Surg. 2009;88(4):1138–1141. 43. Chang YT, Li HP, Lee JY, et al. Treatment of palmar hyperhidrosis: T(4) level compared with T(3) and T(2). Ann Surg. 2007;246(2):330–336. 44. Rathinam S, Nanjaiah P, Sivalingam S, et al. Excision of sympathetic ganglia and the rami communicantes with histological confirmation offers better early and late outcomes in Video assisted thoracoscopic sympathectomy. J Cardiothorac Surg. 2008;3:50. 45. Zhang W, Yu D, Jiang H, et al. Video-­ assisted thoracoscopic sympathectomy for palmar hyperhidrosis: a meta-­analysis of randomized controlled trials. PLoS One. 2016;11(5):e0155184. 46. Zacherl J, Huber ER, Imhof M, et al. Long-­term results of 630 thoracoscopic sympathicotomies for primary hyperhidrosis: the Vienna experience. Eur J Surg. 1998;(suppl 580):43–46. 47. Singh B, Moodley J, Allopi L, et al. Horner syndrome after sympathectomy in the thoracoscopic era. Surg Laparosc Endosc Percutan Tech. 2006;16(4):222–225. 48. Lee KH, Hwang PY. Video endoscopic sympathectomy for palmar hyperhidrosis. J Neurosurg. 1996;84(3):484–486. 49. Shelley W, Florence R. Compensatory hyperhidrosis of sympathectomy. N J Med. 1960;263:1056–1058. 50. Shih CJ, Wang YC. Thoracic sympathectomy for palmar hyperhidrosis: report of 457 cases. Surg Neurol. 1978;10(5):291–296. 51. Freeman RK, Van Woerkom JM, Vyverberg A, et al. Reoperative endoscopic sympathectomy for persistent or recurrent palmar hyperhidrosis. Ann Thorac Surg. 2009;88(2):412–416; discussion 416–417.

1287.e1

CHAPTER 113

Surgery for Intractable Spasticity MARC SINDOU  •  GEORGE GEORGOULIS

Spasticity is defined as a velocity-­dependent resistance to passive movement of a joint and its associated musculature and is characterized by hyperexcitability of the stretch reflex. Disorders are related to the failure of descending supraspinal inhibition. Spasticity should not be treated just because it is present, as it may compensate for loss of motor power. Spasticity must be treated only when excess of tone leads to functional impairment, discomfort, pain, and deformities. Functional neurosurgery should be considered when the harmful components of spasticity cannot be controlled by physical therapy, medications, and botulinum toxin injections. The surgical procedures must be performed so that only excess of tone be reduced, without suppressing useful muscular tone or impairing the residual motor/sensory functions. In patients who retain some—often masked—­voluntary motility, surgery aims to improve—or restore—voluntary motor function. In patients with poor residual function, the aim is to stop the evolution of orthopedic deformities, reduce pain, and improve comfort. Neurosurgical methods are classified according to whether their impact is general or focal and whether the effects should be temporary or permanent (Fig. 113.1). Besides botulinum toxin, methods include intrathecal baclofen (ITB) therapy, as well as lesioning techniques directed to peripheral nerves, dorsal roots (DRs), the spinal cord, or the dorsal root entry zone (DREZ). Because spasticity features may differ from one patient to another, the first step is to define the objective(s) of the treatment for every patient, in other words what can be and what will not be obtained by surgery. These issues must be discussed within the frame of a multidisciplinary team and explained to the patient, relatives, and caregivers. The final decisions as well as the patient-­tailored preoperative chart have to be written down and signed in the informed consent form. The guidelines given in the present chapter have been developed based on personal surgical experience with more than 1300 adult or children patients operated over the last 30 years.1–5

Surgical Techniques INTRATHECAL BACLOFEN THERAPY ITB therapy consists in an intrathecal catheter connected to an implanted pump, which delivers medication in the

1288

cerebrospinal fluid (CSF) surrounding the spinal cord (Fig. 133.2). Baclofen is a γ-­aminobutyric acid B analogue, and direct delivery to the intrathecal CSF bypasses the blood– brain barrier.6,7 ITB can be preceded by a test to screen for adequate response to the medication. In the standard procedure the patient receives a bolus of 25 to 50 μg of baclofen via lumbar puncture or via a temporary lumbar catheter connected to a subcutaneous access reservoir. In the absence of a positive response, indicated by a two-­point reduction in the patient’s Ashworth score 4 to 8 hours following administration, the bolus dose is increased in 25-­μg increments up to a maximum bolus of 100 μg. Once a positive response is observed without unacceptable loss of function, the patient is considered to be a candidate for pump implantation. However, the “bolus method” can be misread as “false-­negative responses” in the sense that it may produce a brutal or exaggerated loss of motor power, which might be interpreted as a decrease in functional status. This holds especially true for the patients with the ability to walk. Therefore the bolus test should be replaced by a continuous infusion test, using an external automatic injection pump connected to a line implanted into a subcutaneous reservoir of the Ommaya-­type. The test should last several days so that functional capabilities can be reliably evaluated. Typically the initial starting dose is double the effective screening dose. The dose is then increased daily by 10% to 30% until the desired effect is achieved. The most useful criterion for dose adjustment is effective suppression of the hyperactive reflexes, such as tendon jerk, clonus, spasms, cramps, and decrease of muscle tone. For paraplegic or paraparetic patients with clinically typical hyperspasticity or those with handicapping mixed hypertonia in whom the spastic component is predominant, ITB will be effective on tone regulation. A preliminary bolus test of ITB would not be necessary to prove that such a patient will be a “responder.” The patient can undergo implantation directly and doses should be adjusted thereafter. In contrast to that situation, if the indication is not clear, that is, the diagnosis of spasticity is uncertain or involvement of the spastic component in the patient’s handicap is not established, a primary test of ITB should be considered. For patients for whom it is important to evaluate whether a reduction in spasticity will improve function, and to what degree, or on the contrary will weaken functionally useful hypertonia, a preliminary test prior to decision is mandatory. For such an

113  •  Surgery for Intractable Spasticity

evaluation a continuous infusion test for about one week is much preferable to the bolus method. Note that whatever the techniques used, lumbar puncture(s) or continuous infusions, CSF depletion or leak may provoke headaches, nausea, and vomiting that confound interpretation until those symptoms disappear. A programmable pump allowing cyclic dose adjustments makes it possible to provide levels that correlate with the daily variability of spastic symptoms. The SynchroMed pump (Medtronic, Minneapolis, MN) is the most frequently used device. According to the largest published series, the ITB dosage varies between 167 and 462 μg/day (average 298 μg/day), a mean Ashworth score decreasing from between 3 and 4 to between 0.5 and 1.8 (Fig. 113.3).8

FIGURE 113.1  Methods for controlling spasticity are based on whether the reduction of excess of tone should be focal or general and permanent or temporary. DREZ, Dorsal root entry zone.

A

C

1289

Adverse effects under continuous-­infusion mode are frequent but most often transient. They may include drowsiness, dizziness, mental confusion, light-­headedness, constipation, urinary retention. These side effects are reversed by decreasing the doses. Muscular hypotonia may also occur, leading to loss of muscular power and capacity to stand or walk in ambulatory patients. Adjusting the doses generally reverses hypotonia to the desirable level. Patients with multiple sclerosis or cerebral lesions are more inclined to present those adverse effects, especially fatigue and confusion. A potential serious risk of ITB is overdose, which could be irreversible because of lack of true baclofen antagonists. Fortunately, overdosing is infrequent. When it occurs it is rarely due to pump malfunctioning. It may rather be the consequence of inappropriate bolus dose, changes in drug concentration, or misprogramming the pump after reprogramming. Symptoms include weakness with rostral progression, blood pressure changes, respiratory depression, and alteration of consciousness: from somnolence to coma. There is no real antagonizing substance (antidote) of baclofen. However, physostigmine administered intravenously at a dose of 2 mg can reverse respiratory depression and lethargy. In the exceptional situation of respiratory distress, assisted ventilation should be performed on emergency. Baclofen withdrawal syndrome may happen if the pump is not refilled properly or at the scheduled intervals or in a case of pump or catheter malfunction. Symptoms include rebound motor spasticity and spasms, dysesthetic or itching sensations, headaches, drowsiness, confusion or even hallucinations, seizures, tachycardia, labile blood pressure,

B

D

FIGURE 113.2  Positioning of the patient for percutaneous insertion of the intrathecal catheter under fluoroscopy (A). Schematic representation of catheter and pump implantation (B). SynchroMed II programmable infusion pump manufactured by Medtronic incorporation (C). Radiographic control of the intrathecal catheter connected to the subcutaneously abdominal implanted pump (D). Arrowheads show the catheter, with tip (arrow) at level of the Th12 thoracic vertebra.

1290

Section Six  •  FUNCTIONAL NEUROSURGERY

generalized dystonia.10,11 The rationale for the use of IVB therapy is that for the treatment of dystonia the site of baclofen activity may be at the cortical level. As a matter of fact, intraventricular infusion results in a baclofen concentration over the cortex greater than that resulting from intrathecal infusion.12 When treating generalized dystonia, baclofen would act by inhibiting the stimulation of the premotor and supplementary motor cortex.13 

PERIPHERAL NEUROTOMIES Peripheral neurotomy (PN) was introduced as early as 1912 by Stoffel for the treatment of the spastic foot.14 Then PN was made more selective by using microsurgical dissection and mapping with electric stimulation to better identify the corresponding muscular “response functions” of individual nerve branches or fascicles.15–22 PN consists in partial sectioning of one or several motor fascicles corresponding to the muscle(s) harboring spasticity considered excessive, and acts by interrupting the segmental reflex arch at both its afferent and efferent pathways. PN must not involve sensory fibers, as even their partial sectioning could result in paresthesias and neuropathic pain. Empirically it is agreed upon that 50% to 80% of all motor fascicles to the targeted muscle(s) have to be sectioned for PN to be effective. PN aims not only to reduce spasticity but also to improve function by re-­equilibrating the tonic balance between agonist and antagonist muscles (Fig. 113.4). FIGURE 113.3  Clinical scores before (control) and under intrathecal baclofen (Baclofen) therapy in a series of patients affected with spastic paraplegia.8 Wilcoxon signed-­rank test showed a significant reduction in both hypertonia of lower limbs (Ashworth score) and frequency of spasms (***, P < .001). The lower and upper borders of the box represent the 25% and 75% quartiles of the distribution, while the line inside the box corresponds to the median value. The upper and lower whiskers stand for the 10th and 90th percentiles. The dots outside the whisker range are the observed values exceeding those percentiles.

and fever. Treatment is readministration of ITB. In life-­ threatening situations baclofen should be given by lumbar puncture or external catheter. To avoid a withdrawal syndrome even in a mild form, after ITB has been initiated, oral baclofen should be withdrawn gradually over a period of several weeks. Catheter problems and CSF leaks are the most common complications. Pump malfunction occurs rarely, the latter approximately at 1% per year. CSF leaks may happen; their appearance is more commonly observed in children than in adults, 12% versus 3%, respectively.9 Infection of the pump pocket and/or of the CSF may develop, in 3% of the patients. Clinical manifestations of infection may not become obvious until weeks or months after implantation. ITB is particularly indicated for patients with severe spasticity from a spinal cord origin, especially if painful contractions are present, as in advanced multiple sclerosis or after severe spinal cord injury. ITB can also be indicated for spastic quadriplegia due to brain-­stem lesions. ITB has also been included in the neurosurgical armamentarium for cerebral palsy (CP) patients. Recently several studies have reported the use of intraventricular baclofen (IVB) in refractory spasticity or dystonia: IVB may also be the first option in patients with

Principles General principles as follows (Fig. 113.5):

Preoperative Motor Blocks Before recommending PN, local nerve blocks with a long-­ lasting anesthetic (2 to 3 hours with bupivacaine) can be performed to evaluate the possible hidden motor power of the antagonist muscles and to determine whether the eventual articular limitations result from spasticity or musculotendinous contractures/articular ankyloses. Also b ­ otulinum toxin injections can be used as a “prolonged” test for ­several months, as they mimic the effect of corresponding neurotomy(ies). This strategy of using preoperative tests allows both the patients and their medical team to estimate the benefit that would follow the neurotomies. 

Anesthesia General anesthesia must also be induced without long-­ lasting myorelaxants so that the muscular responses to electric stimulation can be detected. Muscle relaxants must be avoided; nitrous oxide and propofol are contraindicated ­because they modify reflex excitability. 

Intraoperative Mapping Use of the operating microscope and individual mapping of branches/fascicles is required because of the frequent variations in the emergence and distribution of the nerve ­branches. Bipolar stimulation is preferred to monopolar stimulation to avoid spread of the electric current. Stimulation, such as using the Innopsys Nimbus I-­Care multifunctional neurostimulator (manufactured by Innopsys Parc d’Activités Activestre, Carbonne, France, www.innopsys.com), is performed using a frequency at 2 Hz at low intensity (currently 200 μA) to avoid electric diffusion and therefore incorrect

113  •  Surgery for Intractable Spasticity

A

1291

B

FIGURE 113.4  Gait analysis with poly-­electromyography. Preoperative polyEMG shows intense desynchronized activities in the triceps surae (A). After tibial neurotomy (B), note the reappearance of muscular activity in the tibialis anterior with normal alternation with triceps surae contractions, according to swing and stance phases. EMG, Electromyogram.

i­nterpretation. When fascicles are tightly apposed, a triple stimulation probe composed of an anode between two cathodes is the more accurate way of stimulating because of less current diffusion. The response to stimulation is visualized in the form of clinically observable muscular responses of the corresponding muscles by the surgeon. If considered useful, the surgeon may have recourse to electromyogram (EMG) recordings. Extreme care should be taken to recognize false-­ positive responses by diffusion of current to neighboring fascicles and false-­negative due to short circuits of current caused by serosities between contacts of stimulation probe. 

Sectioning Once all motor branches/fascicles have been identified, those considered to be targeted are marked separately with different-­colored threads. According to preoperative program variable proportions (50% to 80% depending on the degree of preoperative spasticity) of the selected motor branches/fascicles are cut. The effect of each interruption is then evaluated by comparing the intensity of the muscular responses to electric stimulation, proximally and then distally to the section. If the response after proximal stimulation is still intense, further sectioning is performed. 

Techniques Surgery at the Lower Limb Obturator Neurotomy for the Spastic Hip. Obturator neurotomy, which targets adductor muscles, can be proposed for diplegic children when walking is hampered by crossing of the lower limbs or for paraplegic patients to facilitate perineal toilet or self-­catheterization. The incision can be performed along the adductor longus at the proximal part of the thigh or transversely at the hip flexion fold

centered on the prominence of the adductor longus tendon. Both incisions allow adductor longus tenotomy if necessary (Fig. 113.6A). The dissection is conducted laterally to the adductor longus muscle body to locate the anterior branch of the obturator nerve, which is the target. The posterior branch, which is situated more deeply, should be spared to preserve the hip-­stabilizing muscles (see Fig. 113.6B).  Hamstring Neurotomy for the Spastic Knee. Hamstring neurotomy is indicated to counter flexion deformity of the knees. After skin incision performed at the gluteal fold centered on the groove between the ischium and the greater trochanter (Fig. 113.7A) and crossing the fibers of the gluteus maximus, the sciatic nerve is identified in the depth. Branches to the hamstring muscles are isolated at the medial border of the nerve, primarily based on responses of the semitendinosus muscle, which is the major muscle responsible for spasticity (see Fig. 113.7B). Tenotomy of the hamstring muscles can be associated to the neurotomy by performing additional incisions in the popliteal region.  Tibial Neurotomy for the Spastic Foot. Tibial neurotomy is indicated for the equinovarus spastic foot with or without dystonic claw of toes.17,19 It consists of exposing the motor branches of the tibial nerve at the popliteal fossa (i.e., the nerves to gastrocnemius and soleus, tibialis posterioris, flexor hallucis longus, and flexor digitorum longus).19 The incision can be bayonet-­shaped centered on the popliteal fossa or transverse. Both incisions allow gastrocnemius fascicles’ desinsertion if necessary (Fig. 113.8A). The most superficial nerve encountered is the (sensory) medial cutaneous nerve; it is situated adjacent to the saphenous vein and must be spared. More deeply, the tibial nerve trunk, from which the medial and lateral gastrocnemius

1292

Section Six  •  FUNCTIONAL NEUROSURGERY

cut. It is important to note that sectioning of these fascicles can be harmful if adjacent sensory fascicles are not clearly identified and preserved. As a matter of fact damages to sensory fascicles might lead to plantar sole hypoesthesia, allodynia, dysesthesias, and even plantar sores.  Anterior Tibial Neurotomy for Permanent ­Extension of the Extensor Hallucis. Anterior tibial neurotomy is indicated to treat the so-­called permanent Babinski sign, which makes it uncomfortable to wear shoes. A vertical incision is centered on the junction between the tibialis anterioris and the extensor hallucis at the middle third of the leg. The anterior tibial nerve is situated deeply between these two muscles, and the neurotomy is performed on the motor branch to the extensor hallucis. Sectioning of the corresponding tendon can be an alternative.  Femoral Neurotomy for the Spastic Quadriceps. When quadriceps muscle is spastic and interferes with gait by limiting knee flexion during the swing phase, its nerve can be targeted for neurotomy. Given its “strategic” importance in maintaining upright posture, a motor block is an essential part of the preoperative evaluation. Targets are the branches to the rectus femoris and the vastus intermedius muscles. After skin incision (Fig. 113.9A) the dissection passes medial to the sartorius muscle body and exposes the motor branches of the femoral nerve, first the nerve to the rectus femoris, then more deeply the nerve to the vastus intermedius (see Fig. 113.9B). Electrical stimulation is essential given the large number of sensory fascicles of the femoral nerve that must be spared. 

Surgery at the Upper Limb

FIGURE 113.5  General principles of peripheral neurotomy. Microsurgical views of steps of neurotomy—at level of the tibial nerve, for toes in claw, as an example. Upper view: distal trunk of the tibial nerve with fascicles enclosed in epineurium. Center: fascicles exposed after opening of epineurium, and individual stimulation with a (tripolar) electrical probe to identify the motor fascicles corresponding to the flexor digitorum muscles. Lower view: sectioning of a selected fascicle among several.

branches arise, is easily identifiable on the midline. Then progressing distally, the other branches can be identified by stimulation as they emerge from the tibial muscles, successively: the superior soleus and the inferior soleus (both responsible for equinism), the tibial posterioris (responsible for varus), and the flexor digitorum longus nerves (the later nerves just proximal to the soleus aponeurotic arch) (see Fig. 113.8B). The effect of a soleus/tibialis posterioris neurotomy can be confirmed by the immediate intraoperative disappearance of the ankle clonus. For (dystonic) claw of toes, flexor fascicles of toes can be targeted in the distal part of the tibial trunk at level of the soleus arcade. After epineurium has been longitudinally incised over about 1 cm and fascicles individualized by sharp interfascicular dissection, the exposed fascicles are individually stimulated with a thin bipolar or a tripolar probe. Those with muscular responses in flexors of toes are microsurgically

Pectoralis Major and Teres Major Neurotomies for the Spastic Shoulder. Neurotomies of collateral branches of the brachial plexus innervating the pectoralis major or the teres major are indicated for spasticity of the shoulder with internal rotation and adduction.20 For pectoralis major, the skin incision is made at the innermost part of the ­deltopectoral sulcus and curves along the clavicular axis. Then the clavipectoralis fascia is opened and the upper border of the pectoralis major muscle is reflected downward. Close to the thoracoacromialis artery, the ansa of the pectoralis muscle is identified with the aid of a nerve stimulator. For teres major, the skin incision follows the inner border of teres major, from the lower border of the deltoid muscle posterior head to the lower extremity of the scapula. The lower border of the long portion of brachii triceps constitutes the upper limit of the approach. The dissection goes deeply between teres minor and major muscles. In the vicinity of the subscapularis artery, the nerve ending on teres major is identified. The nerve is surrounded by thick fat when approaching the anterior facet of the muscle body, then identified by stimulation.  Musculocutaneous Neurotomy for the Spastic Elbow.  Spasticity of the elbow with flexion depends on the biceps brachii and the brachialis muscles. The skin incision is performed longitudinally, extending from the inferior edge of pectoralis major, medial to the biceps brachii, and down to 5 cm (Fig. 113.10A). The superficial fascia is opened between the biceps laterally and the brachialis medially. The dissection proceeds in this space where

113  •  Surgery for Intractable Spasticity

1293

2 PB AB

ON

1

1

2

AL

AB 3 G

4 5

A

B

FIGURE 113.6  Obturator neurotomy (right side). (A) Skin incision along the relief of adductor longus (1), or at the hip flexion fold centered on the prominence of the adductor longus tendon (2). In addition to its more aesthetic appearance, the latter incision facilitates tenotomy of adductor longus, if needed. (B) Dissection of the anterior branch of the obturator nerve (ON). The adductor longus (AL) is retracted laterally and the gracilis (G) medially. The nerve is anterior to the adductor brevis (AB). 1 and 2, Adductor brevis nerve; 3, adductor longus nerve; 4 and 5, gracilis nerve. The posterior branch (PB) which lies under the AB should be spared.

the musculocutaneous nerve lies anterior to the brachialis muscle (see Fig. 113.10B). Opening the epineurium allows the fascicles of the nerve to be dissected; the motor fascicles are distinguished from the sensitive ones by stimulation. 

Median Neurotomy for Spastic Wrist and Fingers Neurotomy of the median nerve is indicated for spasticity of (1) the forearm with pronation, depending on the pronator teres and quadratus muscle; (2) the wrist with flexion, depending on the flexor carpi radialis and palmaris longus muscles; and/or (3) the fingers with flexion, depending on the flexor digitorum superficialis (for flexion of the metacarpophalangeal and the proximal interphalangeal joints) and on the flexor digitorum profundus (for flexion of the distal interphalangeal joints).20–22 Swan-­neck deformation of the fingers, which depends on the lumbrical and interosseous muscles, can be limited by a combined median/ulnar neurotomy. With regard to the thumb, neurotomy of the median

nerve is indicated for spasticity with flexion and adduction/ flexion (thumb-­in-­palm deformity), depending on the flexor pollicis longus. The skin incision begins 2 to 3 cm above the flexion line of the elbow, medial to the biceps brachii tendon; it passes through elbow line and curves toward the junction of the upper and middle thirds of the anterior aspect of the forearm (Fig. 113.11A). The nerve is identified medially to the brachial artery, deeply under the lacertus fibrosus, which is cut, and its branches dissected. The pronator teres belly with its two heads is retracted medially and distally so that its muscular branches can be inspected. Then this muscle is retracted up and laterally while the flexor carpi radialis is pulled down and medially. The muscular branches to the flexor carpi radialis and to the flexor digitorum superficialis can then be seen. Finally the latter is retracted medially, uncovering the branches to the flexor digitorum profundus, the flexor pollicis longus, and the pronator quadratus. These latter muscular branches may be individualized as separate

1294

Section Six  •  FUNCTIONAL NEUROSURGERY

P

1

GM

GT IT

2 GM

SN IGN IGA

HF

A

B

FIGURE 113.7  Hamstring neurotomy (right side). (A) The skin incision is located on the midline between the ischial tuberosity (IT) and the greater trochanter (GT) (1). A transverse incision can also be made in the gluteal fold (2) for better cosmetics. (B) Dissection of the sciatic nerve (SN) under the piriformis muscle (P) is performed after passing through the fibers of the gluteus maximus (GM). The epineurium of the nerve is opened and fascicles for the hamstring muscles (HF), located at the medial part of the nerve trunk, are identified using electrical stimulation. IGA, Inferior gluteal artery; IGN, inferior gluteal nerve.

branches or remain together in the distal trunk of the anterior interosseous nerve. It may be useful to divide the fibrous arch of the flexor digitorum superficialis muscle to make dissection easier (see Fig. 113.11B). As an alternative to this approach, a minimal approach can be performed with dissection of the different fascicles in the trunk of the median nerve just medial to the brachial artery. This more limited, cosmetic, approach has the inconvenience of a nerve exposure less suitable for identifying the various motor branches and those sensory whose damages would entail the risk of sensory complications, namely allodynia and/or a complex regional pain syndrome. 

Ulnar Neurotomy for Spastic Wrist and Fingers Neurotomy of the ulnar nerve is also indicated for spasticity of (1) the wrist with flexion and ulnar deviation, both depending on the flexor carpi ulnaris; (2) the fingers with flexion, depending on the flexor digitorum profundus, which is partly innervated by the ulnar nerve; and/or (3) the thumb for spasticity with adduction/flexion, depending on

the adductor pollicis.20,22 Ulnar neurotomy can also be performed in combination with median neurotomy for swan-­ neck deformation of the fingers. To expose the ulnar nerve, a skin incision is made at the level of the epitrochleo-­olecranean region of the elbow (Fig. 113.12) where the nerve enters between the two heads of the flexor carpi ulnaris. There the motor branches to this latter muscle and more distally the branches to the medial half of the flexor digitorum profundus are identified. 

Complications and Recurrences Sensory disturbances such as paresthesias or dysesthesias, complex regional pain syndromes, or even deafferentation pain may be observed if section would inappropriately include sensory fascicles.4 This might be particularly severe and disabling with neurotomy of the median nerve or the tibial nerve. Hypoesthesia of the anterior part of the forearm or of the lateral aspect of the foot might also happen due to inadvertent damage to the subcutaneous sensory nerves during approach.

1295

113  •  Surgery for Intractable Spasticity

FIGURE 113.8  Tibial neurotomy (right side). (A) A vertical bayonet skin incision is made at the right popliteal fossa (1), or a transverse incision at the popliteal fold (2) for better aesthetic result, the latter allowing desinsertion of the gastrocnemius fascias at the end of the procedure, if necessary. (B) Dorsal view of the right popliteal region after dissection of the tibial nerve. 1, Tibial nerve; 2, peroneal nerve. The sensory sural nerve (3), which lies superficially as a satellite of the saphenous vein just beneath the subcutaneous aponeurosis between the two gastrocnemius muscles, should be spared. The medial and lateral gastrocnemius nerves (4) may arise either separately from the sides of the tibial trunk or posteriorly from a common origin sometimes including the sensory sural nerve. Each gastrocnemius nerve usually divides into two distal branches on approaching muscle. One or two soleus nerves, separately (5), may arise from the tibial nerve. The posterior tibialis nerve (6)—like the soleus nerve—originates from the ventrolateral aspect of the tibial nerve, but more distally just above the level of the soleus arch (S). Sometimes the posterior tibialis nerve may originate from a common trunk with the inferior branch of the soleus nerve. The distal trunk of the tibial nerve (7) contains five to eight fascicles averaging 1 mm in diameter each; two-­thirds of them are motor fascicles with a third being sensory fascicles. LG, Lateral gastrocnemius; MG, medial gastrocnemius.

A

B

Patients rarely complain of decreased muscle strength after neurotomy because no single muscle solely ensures the movement of a body segment. However, paresis of the flexors of wrist and/or fingers, with deficit in the prehension, or deformity in talus in the foot may occur secondary to excessive motor fascicle sectioning. Recurrence of spasticity can be observed when the amount of sectioning is insufficient. In such cases reoperation can be offered after a new blocking test. 

In 1951, Bischof described longitudinal myelotomy with the aim of interrupting the spinal reflex arch between the dorsal and ventral horns by a vertical coronal incision performed laterally from one side of the spinal cord to the other from L1 to S1 segments. Indications were totally paraplegic patients with triple flexion and sphincter deficits.26 Intrathecal chemical rhizotomies, originally introduced for the treatment of pain associated with cancerous lesions, were then used for the treatment of severe spasticity in bed-­ ridden patients. Alcohol was the first chemical agent used, followed by phenol, a hyperbaric solution.27 Percutaneous radiofrequency rhizotomies, also developed for chronic pain, were then applied to certain forms of spasticity, especially to treat neurogenic detrusor hyperreflexia for which the target is the sacral roots, or hip spasticity in flexion–adduction at lumbar roots L2 to L3 level.28 To reduce the harmful effects of dorsal rhizotomy on postural tone in ambulatory patients, Gros and pupils introduced topographic selection of the roots by electrical stimulation to preserve the innervation of muscles responsible for useful tone (the quadriceps and abdominal and gluteal muscles in particular). This technique was termed sectorial posterior rhizotomy.29,30

Surgery in the Spinal Roots and Spinal Cord Based on Sherrington’s experiments, Foerster performed— and reported in 1913—the first dorsal rhizotomies for lower-­limb spasticity in CP patients.23,24 As a general rule he recommended to resect the DRs from L2 to S2 with the exception of the fourth lumbar root since the root “generally guarantees the extensor reflex of the knee so very necessary for standing and walking.” In 1945, to treat irreducible spasticities with severe spasms, as seen after anoxia, Munro suggested sectioning the lumbar ventral roots (VRs), on the rationale that such phenomena are associated with spontaneous hyperactivity of the motor neurons and that in such cases sectioning DRs is ineffective, whereas sectioning VR abolishes spasms.25

D M

o

a

w

y

n

l 0

o 6

a

,

d

e 2

d 0

2

f

1

o

.

r

F

j

o

u

r

l

i

p

a

e

r

s

s

p

o

a

n

r

a

r

l

o

w

1296

Section Six  •  FUNCTIONAL NEUROSURGERY

FN 2

FA

FA FV

P

1

S

A

B

FIGURE 113.9  Femoral neurotomy (right side). (A) Skin incision below the inguinal ligament, lateral to the femoral artery (1) or horizontal at the hip flexion fold (2). (B) Dissection of the femoral nerve (FN) and its branches after opening the anterior fascia of the psoas muscle (P). Bipolar stimulation allows identification of the two or three branches to the sartorius muscle (S) and the three or four branches to the rectus femoris muscle, which produces flexion of the hip. The nerve to the vastus intermedius can be found more deeply. FA, Femoral artery; FV, femoral vein.

Apart from effects on the lower limbs Gros observed in his CP patients a decrease in spasticity of the upper limbs and improvement in speech and swallowing.16 In 1977, Fraioli and Guidetti proposed the partial dorsal rhizotomy, which consisted of incising the most dorsal part of each rootlet a few millimeters before entry into the dorsolateral sulcus in an attempt to spare some sensation.31 In 1976, Fasano developed the functional posterior rhizotomy, a technique based on stimulation of the DR/ rootlets with corresponding EMG recordings.32 Exaggeration of the duration or of extent of the muscular responses indicated the particular roots that must be surgically sectioned. Contrary to what was developed for lower limbs spasticity, very few dorsal rhizotomies were attempted at the cervical level for upper-­limb spasticity. From an experience of 23 patients with spastic paralysis of the upper limb

treated by resection of the DRs from C4 to Th2 (with the exception of C6), Foerster concluded that “in the majority the result is not good; therefore we do not recommend dorsal rhizotomy as a valuable procedure for spasticity of the upper limb.”33 In 1972, Sindou observed that his technique of microsurgical lesioning of the ventrolateral region of the DREZ, for treating pain, led to marked hypotonia in the muscles corresponding to the operated spinal cord segments.34–38 Subsequently, his technique was applied to treat hyperspasticity in severely affected paraplegic patients and also to treat excess of spasticity in the upper limb of hemiplegic patients. The potent effect of the Microsurgical DREZotomy procedure (MDT) is presumably due not only to the interruption of the (tonigenic) dorsal afferent fibers, but also to the lesioning of the dorsal horn gray matter—which contains a quantity of interneurons that convey “tonigenic” input to motor

113  •  Surgery for Intractable Spasticity

1297

CB

BB

H

MC

1

4

2 B 3

A

B

FIGURE 113.10  Musculocutaneous neurotomy (right side). (A) Skin incision along the medial aspect of the biceps brachii (BB) below the inferior edge of the pectoralis major muscle. (B) Dissection of the musculocutaneous nerve (MC) in the space between the BB laterally, and the coracobrachialis (CB) medially. The brachialis (B) is found posteriorly. Branches to B (1, 2, and 3) and to BB (4) are recognized by stimulation giving elbow flexion. The humeral artery (H) and the median nerve are situated medially, and not dissected.

neurons of the ventral horn. Of note, if MDT is performed deeply down into the base of the ventral horn, the procedure is able to alleviate the focal dystonia component.39

Dorsal Rhizotomies The surgical approach for dorsal rhizotomy varies significantly from one team to another (Fig. 113.13). The up-­to-­ now most currently used technique—described by F ­ asano et al., and popularized by Peacock and Arens then by A ­ bbott et al.—is as follows.25,40,41 One-­piece laminotomy is performed from L1 to S1, using a power saw, which a­llows repositioning at end of the procedure. This approach gives exposure to the entire cauda equina. Electric stimulation of the sensory roots combined with multichannel EMG ­recordings is carried out, in addition to palpation of the contractions of the leg muscles by a physiotherapist. Roots that, when stimulated, cause either activity lasting after cessation of the stimulus or muscle responses outside their myotome are deemed abnormal, and accordingly cut. For some teams stimulation is at level of rootlets after DRs have been separated into their rootlets. The rootlets are in turn individually stimulated, and the same criteria are used to judge their normality. Abnormally responsive rootlets are candidates to be cut. Changes in excitability due to long exposure and extensive manipulation of the rootlets are major drawbacks of the method. To limit the extent of the approach, we and others, especially Park, performed a limited laminotomy at end of conus medullaris, from T11 to L1.42,43 Through such approach, L2 and L3 ventral (and corresponding dorsal) roots can be identified by their muscular responses to electric stimulation performed intradurally inner to their

respective dural sheaths. Then their dorsal rootlets from L4 to all sacral segments are identified at their entry into the dorsolateral sulcus of the conus medullaris and stimulated. In 2001, to further reduce the invasiveness of the laminotomies, and to access the roots to be targeted—­individually— at their exit from/entry to the intradural space, we developed a modality that we termed “Keyhole Interlaminar Dorsal rhizotomy—KIDr” (Fig. 113.14).44 In this technique, the interlaminar spaces to be approached (one, two, or more often three, according to patient’s clinical presentation) are determined on the basis of the preoperative chart. The L1–S2 lumbosacral spine is approached posteriorly. After resecting the flavum ligament, the chosen interlaminar spaces are enlarged as maximally as possible by resecting the lower two-­thirds of the upper lamina and the upper three-­ fourths of the lower lamina. The spinous processes and their interspinous ligaments are respected. Through the obtained fenestration(s) dura and arachnoid are incised on the midline for a height of approximately 2 cm. The L2 and L3 roots can be reached through a L1–L2 opening, L4 and L5 through a L3–L4 opening, and S1 and S2 through a L5–S1 opening. The microsurgical steps are then conducted following the principles of keyhole surgery. Microscope is installed with an oblique trajectory at approximately 45 degrees so that the surgeon’s view passes underneath the (respected) interspinous ligament. Goal is to access—intradurally—the contralateral root, with its ventral and dorsal components, at exit to/entry from corresponding dural sheath. At exit from dural sheath, VR is easily identified on its ventral position. The dorsal rootlets (on average five per root) are also easily identified; they are grouped posteriorly to the VR,

1298

Section Six  •  FUNCTIONAL NEUROSURGERY

2 1

A

FDS

FCR

2

1

MN

HA

PT

3

1

2

3 FPL

FDS

PT

FDP

B FIGURE 113.11  Median neurotomy (right side). (A) Skin incision from the medial aspect of the biceps brachii at level of the elbow, longitudinally along the bicipital crest (1). The incision can eventually be continued distally toward the midline above the wrist for better access to distal branches (2). (B) Dissection of the median nerve (MN) in two stages. In the first stage (upper view), the pronator teres (PT) is retracted upward and laterally and the flexor carpi radialis (FCR) is retracted medially. Branches from the MN before it passes under the fibrous arch of the flexor digitorum superficialis (FDS) are dissected: a branch to the pronator teres (1) and (2) nerve trunks to the flexor carpi radialis, palmaris longus and flexor digitorum superficialis (2 and 3). In the second stage (lower figure), the fibrous arch of the FDS is divided to allow a more distal dissection of the MN. The FDS is retracted medially and branches from the median nerve identified: (1) branch to the flexor pollicis longus (FPL), (2) branch to the flexor digitorum profundus (FDP), and the interosseous nerve with its proper branches to these muscles (3). Humeral artery (HA).

113  •  Surgery for Intractable Spasticity

1299

2 1 FIGURE 113.12  Ulnar neurotomy (right side). The skin incision is either a longitudinal incision posteriorly to the medial epicondyle and medially to the olecranon at the elbow (1) or distally a transverse medial incision at the wrist fold (2), depending on the spastic muscles to be targeted.

FIGURE 113.13  Main modalities of lumbosacral dorsal rhizotomies for spastic diplegic (quadriplegic) children affected with cerebral palsy. Left: Extended approach: Laminotomy is performed from L1 to S1, giving exposure to the entire cauda equina. This allows easy identification of radicular levels on exit to (for ventral roots) and entry from (for dorsal roots) their corresponding dural sheath. Center: Limited approach: Limited laminotomy of one to three laminae, from Th11 to L1, to expose the end of conus medullaris. L2 and L3 dorsal and ventral roots are identified on reaching corresponding dural sheaths. Dorsal rootlets from L4 to all sacral segments are targeted at their entry into the dorsolateral sulcus of the exposed conus medullaris. Right: Keyhole interlaminar dorsal rhizotomy (KIDr) approach. The L2 and L3 roots can be—individually— targeted at the L1–L2 interlaminar (IL) space, the L4 and L5 roots at the L3–L4 IL space, and the S1 and S2 (S3,S4) roots at the L5–S1 IL space. A (maximally) enlarged fenestration, on midline, allows access to two roots—on each side—through each IL opening.

often separated from the latter by an arachnoid fold. At each level muscle responses to stimulation, using a bipolar electrode to avoid spreading of current, are tested first for the VR, then for the DR. VR is stimulated first, to identify its innervation territory and thereby confirm topographical

level; this phase is anatomical mapping. Stimulation is at 2 Hz with an intensity of 200 μΑ (to 500 μA), i.e., slightly above threshold. To be noted, a muscle response by DR stimulation would require a three to five times higher intensity. Then the DR undergoes physiological testing to

1300

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 113.14  Keyhole interlaminar dorsal rhizotomy: A: Exposure of L1–S1 laminae on both sides, with L1–L2, L3–L4, and L5–S1 interlaminar (IL) fenestrations. At each level to be fenestrated, the inferior two-­thirds of upper lamina and the superior three-­fourths of the lower lamina are resected on midline and flavum ligament removed so that dura and arachnoid can be opened (on midline) over 20 to 30 mm in height. Note that the spinous processes and interspinous ligaments are respected. B: Surgeon’s view is an (±45 degrees) oblique trajectory, which passes underneath the arch formed by the (respected) interspinous ligament, so that the contralateral roots can be accessed at exit to (for ventral root)/ entry from (for dorsal root) corresponding dural sheaths. Two radicular levels can be reached per IL fenestration, one upward and the other downward. C to E: Microsurgical steps per radicular level are as follows. Stimulation of ventral root, at 2 Hz and 200 µA (C), stimulation of dorsal root (DR) at 50 Hz and 1 mA (D). According to preoperative chart and adjustments from monitoring, sectioning of DR is performed (in this case: two-­thirds of the dorsal rootlets of this root).

evaluate excitability of its contained circuitry. Stimulation is a train of 1 second at frequency of 50 Hz and with an intensity of 1 mA. Excitability is considered excessive when stimulation elicits an “exaggerated,” i.e., a sustained and/or spreading, response according to Fasano’s classification.45 This testing is to confirm or modify the percentage of the dorsal rootlets previously specified in the pre­operative chart to be cut. The amount cut generally ranges between one-­ third and four-­fifths of a root’s constituting rootlets. The intraoperative mapping and monitoring followed by the microsurgical sectioning is successively performed at each targeted radicular level, on one side first, then on the other side after turning the microscope 180 degrees. At the end, each dural incision is sutured in a watertight fashion and the dural suture line covered with fat harvested subcutaneously and biological glue if necessary. To be effective, there is a general (empirical) consensus that an overall amount of 60% of all the DRs targeted should be cut, of course with a different proportion of cutting according to the level and function of the roots involved and their implication in the “conveying” of the harmful components of the spasticity.44,45 

SURGERY IN THE DORSAL ROOT ENTRY ZONE MDT34–38 aims to preferentially interrupt both the small-­ caliber (nociceptive) and the large-­caliber (myotatic) fibers of the DRs both tonigenic—respectively situated laterally

and in middle of the DREZ—and also must partially, if not totally, preserve the medially located bundle of large-­ caliber fibers that reaches the dorsal column. The surgical target should also include most of the dorsal horn, where the fibers and neurons that activate the segmental circuitry are located (Fig. 113.15). The technique for the cervical and the lumbosacral cord segments are detailed in Figs. 113.16 and 113.17, respectively. Briefly the procedure consists of a 3-­mm-­deep microsurgical incision—at level of the dorsolateral sulcus—with an obliquity of 35-­degree angle at the cervical and 45-­degree angle at the lumbosacral regions. It is important to be strictly in the axis of the dorsal horn at respective levels. Bipolar coagulations are then performed— under direct magnified vision inside the dorsolateral incision, in a dotted fashion, ventrolaterally at the very entry of the rootlets into the sulcus. Those coagulations must penetrate approximately 5 mm inside the gray matter of the dorsal horn, along all the spinal cord segments selected for lesioning. The lesion-­maker is a fine bipolar microcoagulation forceps, graduated every millimeter over 6 uninsulated millimeters. Intensity starts at the minimum of the bipolar coagulator and remains at a low value. Duration of each microcoagulation is 1 to 3 seconds. By principle, degree and extent of the coagulation are controlled by direct vision. For performing MDT, special instruments have been designed by the senior author (GmbH & Co KG; Stryker-­Leibinger, Freiburg, Germany). 

113  •  Surgery for Intractable Spasticity

A

1301

B

FIGURE 113.15  Schematic representation of the dorsal root entry zone (DREZ) and the target of the microsurgical DREZotomy (MDT) with Rexed lamination of the dorsal and ventral horns. (A) Transverse hemisection of the spinal cord (at a lower cervical level) with myelin stained by Luxol– fuchsin, showing the myelinated rootlet afferents that reach the dorsal column (DC). The small arrow designates the so-­called pial ring (PR) of the dorsal rootlet (diameter = 1 mm), which is the junction between the central and the peripheral portions of the spinal rootlet. The two large arrows indicate entry of the incision for opening the dorsolateral sulcus (DLS) to perform the MDT. P, Pyramidal tract; tl, Tract of Lissauer. (B) Upper part: Each rootlet can be divided into a peripheral (Schwannian) and a central (glial) segment, the transition of which (PR) is located approximately 1 to 2 mm outside the rootlet penetration into the DLS. Peripherally the fibers are mixed together. As they reach the PR, the fine fibers (considered nociceptive) move toward the rootlet surface. In the central segment they re-­group in the ventrolateral part of the DREZ to enter the dorsal horn (DH) through the tl. The large myotatic fibers (myot.) are located in the middle of the DREZ, whereas the large lemniscal fibers are located dorsomedially. Lower part: Schematic simplified representation of the DH circuitry. Note the monosynaptic excitatory arc reflex of the myotatic fibers on the motoneurons (MN) and the inhibitory influence on a DH cell and an interneuron (IN) from the collaterals of the large myelinated fibers (=gate control). Note also the excitatory input of the fine fibers onto the DH cells and the IN. Note the origin of the anterolateral pathways (ALP) (=spinoreticulothalamic) in layers I and IV to VII. The MDT (large arrowhead) interrupts the fine and the myotatic fibers and also enters the medial (excitatory) part of the LT and the DH. Target preserves at least part of the fibers going to the DC. (C) Postoperative MRI after cervical MDT (performed from C5 to Th1) in a hemiplegic patient affected with severe spasticity and handicapping focal dystonia in upper limb. Axial view of T2-­weighted sequence with multi-­echo image combination shows a conic-­shaped lesion that occupies the entire DH and reaches the base of the ventral horn (to a depth of 6 mm in this case with dystonia associated to spasticity). (B, From Sindou M, Quoex C, Baleydier C. Fiber organization at the posterior spinal cord–rootlet junction in man. J Comp Neurol. 1974;153:14–26.)

ORTHOPEDIC SURGERY Orthopedic surgical procedures may reduce spasticity by means of muscle relaxation especially when multi-­site release of the musculotendinous apparatus and/or lengthening of tendons are performed. The techniques currently available for correcting shortness of the muscle-­ tendon assembly are muscle disinsertion, aponevrotomy, myotomy, tenotomy, or lengthening tenotomy. Tendon transfer has a different goal: to normalize articular orientation when disturbed by muscular imbalance. Transfer of spastic muscles must be avoided; suppression of spasticity should be achieved first by botulinum toxin injections or neurosurgical procedures. Osteotomies aim to correct bone deformity caused by pathology of growth or at treating stiffened joints. Articular surgery is indicated when deformities cannot be corrected by osteotomy or tendon surgery alone. Arthrodesis must not be used in children until growth is complete. 

Decision-Making in Adults Generally patients do not complain about spasticity; they are more likely to be aware of stiffness, deformity, and

limitations in functional abilities. Over time patients have a mixture of spasticity and muscle shortening with contracture. Consensus on terminology is important in recognizing two principal components of muscle stiffness. The first is “dynamic” shortening of muscles caused by spasticity; such patients exhibit hyperreflexia, clonus, and velocity-­dependent resistance to passive joint motion. The second is “fixed” shortening of muscles, i.e., contracture, which is much less velocity dependent and remains present under local anesthetic blocks or anesthesia. Spasticity should not be treated just because it is present; it should be treated because it is harmful to the patient. Spasticity may be useful for functional activities. An extension pattern in lower limb(s) may aid in standing transfers. In this scenario, “effective” spasticity management, if measured by reduction in tone and improved range of motion, might reduce rather than enhance function. Guidelines for treating spasticity are shown in Fig. 113.18. 1. ITB therapy is particularly indicated for patients with spasticity from a spinal cord origin, especially when ­painful

1302

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 113.16  Illustration of the microsurgical DREZotomy technique at the cervical level (right side, C6, as an example). Exposure of the right dorsolateral aspect of the cervical cord through right hemilaminectomy with preservation of the spinous processes. Upper view: The dorsal rootlets are displaced dorsally and medially for access to the ventrolateral border of the dorsolateral sulcus. A 2-­to 3-­mm-­deep incision at an angle of 35 degrees ventrally and medially in the dorsal horn (DH) axis is made with a microknife of the ophthalmic type. Lower view: Microcoagulations are performed 5 mm into the DH gray matter (for spasticity) and down to 6 mm intently including the base of the ventral horn (for associated focal dystonia), with a sharp bipolar microforceps (graduated every mm over the 6 uninsulated mm). Each microcoagulation is performed under direct vision with high magnification of the microscope, for a short duration (1 to 3 seconds), with low-­intensity coagulation. Lesioning is made in a dotted manner every millimeter inside the gray matter, along the dorsolateral sulcotomy of all selected roots according to patient’s clinical presentation.

spasms are present—such as in advanced multiple sclerosis or after severe spinal cord injury, when physical ­therapy has not succeeded in preventing “harmful” spasticity to appear. ITB is also indicated for hyperspasticity/­rigidity after brain stem lesions. ITB therapy has also ­entered the neurosurgical armamentarium to treat patients with CP, especially the ones at an adult age. In patients with the capacity to walk, adequate doses, i.e., ones effective on the excess of tone that do not produce motor weakness, are difficult to find. 2. Peripheral neurotomies (PN) are indicated when spasticity is focal, i.e., localized to only a few muscular groups, supplied by one single or a few peripheral nerves. Focal spasticity must be first treated with b ­ otulinum

toxin injections. Only after these should surgical procedures be considered. To decide PN, a local anesthetic block of the nerve is useful to give the patient and caregivers an idea of what to expect. Botulinum toxin injections may also act as a “prolonged” test. Tibial neurotomy for the spastic foot and obturator neurotomy for spastic flexion–adduction of the hip are the most common. PN can also be indicated for spasticity in the upper limb: PN of the musculocutaneous nerve for elbow in flexion, PN of the median (and ulnar) nerve(s) for flexion of the wrist and fingers—the aim is to open the hand and improve prehension. Basically PN are able not only to reduce excess of spasticity and prevent deformity, but also to improve motor function by re-­equilibrating the tonic balance between agonist and antagonist muscles. This is especially true for the spastic foot with equinovarus deformity, as shown in Fig. 113.4. With regard to the spastic hand, which is a more difficult problem to deal with, a functional benefit in prehension can only be achieved if patients retain some residual motor function in the extensor muscles together with sensory capacity. If these conditions are not present, only better comfort and cosmetic aspect can be achieved. 3. Surgery in the DREZ is preferred when s­ pasticity is severe and affects the entire limb at the point to render it functionally useless. For patients with paraplegia, the L2–S5 segments are approached through a T11–L2 laminectomy. For patients with a hemiplegic upper limb, a C4–C7 hemilaminectomy with conservation of the spinous processes is sufficient to reach the C5–T1 segments. MDT is indicated in paraplegic patients, especially when they are bedridden and ITB not indicated or has failed. In hemiplegic patients, MDT is indicated when the upper limb is affected with irreducible and/or painful hyperspasticity. In severely affected patients harboring an intense spasticity and focal dystonia, MDT can be effective on the dystonic component if done deeply inside the spinal cord. Lesioning should be performed through the dorsal horn, down to the ventral horn, as deep as 6 mm for dystonia.39 MDT also can be applied to treat patients affected with disabling neurogenic bladder, i.e., with uninhibited detrusor contractions resulting in voiding around the catheter and having loss of genito-­sphincterian functions. Guidelines for surgical indications are summarized in Fig. 113.15. Because features and consequences of spasticity largely differ from one patient to another, and objectives are different according to the severity affecting each patient, the general rule is to tailor individual treatments. 

Decision-Making in Children Most indications are for children with CP. The choice among the various therapeutic options is difficult at the pediatric age because children are continuously developing and the evolution of spasticity and dystonia, which are frequently associated, has dynamic characteristics. Dorsal rhizotomies improve spasticity but not dystonia, whereas ITB can improve to a certain extent both spasticity and dystonia.46 As in adults, spasticity in children can be either useful for function or detrimental. Efficient treatments are

113  •  Surgery for Intractable Spasticity

A

B

C FIGURE 113.17  Illustration of the microsurgical DREZotomy technique at the lumbosacral level (on the left side, as an example). (A) Schematic drawing of the approach of the conus medullaris through a T11 to L1 laminectomy with exposure of the dorsolateral sulcus on the left side in this example (B): The dorsal rootlets of the selected roots are retracted dorsally and medially to obtain proper access to the ventrolateral aspect of the dorsolateral sulcus. After the main arteries running ventrally along the dorsolateral sulcus are dissected (and preserved), while the smaller ones are coagulated with a sharp bipolar microforceps (not shown), a continuous incision is performed using a microknife, at a 45-­degree angle. (C): Then the surgical lesion is completed by doing microcoagulations under direct magnified vision, at a low intensity—in a dotted manner every millimeter, for a short duration (1 to 3 seconds) each, through the dorsolateral sulcomyelotomy, 5 mm in depth inside the grey matter of the dorsal horn. These microcoagulations are made all along the segments of the cord selected to be operated on, by means of the special sharp bipolar forceps, insulated except at the tip over 6 mm and graduated every millimeter (bipolar coagulation forceps, from Stryker-­Leibinger).

1303

available, including botulinum toxin injections, ITB, dorsal rhizotomies, and neurotomies. These treatments can be used in isolation or in combination with orthopedic surgery. To formulate a treatment plan one must project into the future by extrapolating the extent and severity of musculoskeletal contractures and their harmful consequences, as well as the positive effects of spontaneous psychomotor development. The first step is to observe the child clinically to understand the child’s function and disability. The second step is to measure range of motion to detect contractures that will not respond to neurosurgical treatment alone. The third step is to quantify the spasticity by using scales. The final step is to grade the child on the Gross Motor Function Classification System (GMF-­CS) and to observe the evolution of the Gross Motor Function Measurement (GMFM) with time (Fig. 113.19). For diffuse spasticity of the lower limbs, dorsal rhizotomy or ITB administration may be considered. Dorsal rhizotomy is generally preferred in younger patients as the size of the implanted pump poses an obstacle in young children. ­Dorsal rhizotomy is proposed when definitive action targeted to certain muscle groups is preferred.47–50 For focal spasticity / dystonia, botulinum toxin injections permit delaying surgery until a surgical decision is taken. In children with spastic diplegia having the “scheme of Little,” the target is to improve quality of walking and decrease amount of assistance (use of canes, crutches, walkers) required for ambulation. In children with spastic quadriplegia the aim is to improve ease of caretaking, facilitate function in sitting position, decrease pain, and obtain favorable distant effects on upper limbs. In children with dominant hemiplegic disorders, if spasticity involves the shoulder, elbow, wrist, and fingers together, multiple neurotomies or a cervical MDT can be indicated. In cases with severe focal dystonia in upper limb, the dystonia component can be favorably influenced if the cervical MDT is performed deeply into the ventral horn at the corresponding segmental levels. It is important to note that because expectations of both the child and the family can be quite different from what can be achieved, the realistic goals should be clearly explored and written down in the informed patient consent form. 

Conclusion The goals of surgery for spasticity are well defined. They are to decrease “harmful spasticity,” respect “useful spasticity,” preserve residual motor/sensory functions, reveal eventually masked capabilities, and improve functional ability. Because of its complexity, neurosurgical management of spasticity requires a multidisciplinary approach.

1304

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 113.18  Decision-­making for treating disabling hyperspasticity in paraplegic and hemiplegic adult patients.

113  •  Surgery for Intractable Spasticity

1305

FIGURE 113.19  Indication for dorsal rhizotomy in cerebral palsy children affected with spastic diplegia. We advise that the decision should be taken essentially based on the evolution of the Gross Motor Function Measure (GMFM) scale. In this example, D.Rh. was indicated after botulinum toxin injections and revealed insufficient. Note that the score significantly improved after D.Rh. was performed.

KEY REFERENCES

Decq P, Mertens P, et al. La Neurochirurgie de la Spasticité. Neurochirurgie. 2003;49:135–416. Fasano VA, Barolat-­Romana G, Ivaldi A, Squazzi A. La radicotomie postérieure fonctionnelle dans le traitement de la spasticité cérébrale. Neurochirurgie. 1976;22:23–34. Foerster O. On the indications and results of the excision of posterior spinal nerve roots in men. Surg Gynecol Obstet. 1913;16:463–474. Georgoulis G, Brinzeu A, Sindou M. Dorsal rhizotomy for children with spastic diplegia of cerebral palsy origin: usefulness of intraoperative monitoring. J Neurosurg Pediatr. 2018:1–13. Gros C. Spasticity—clinical classification and surgical treatment. In: Krayenbühl, ed. Advances and Technical Standards in Neurosurgery. Advances and Technical Standards in Neurosurgery. Vol 6. Wien, New York: Springer-­Verlag; 1979:55–97.

Park TS, Gaffney PE, Kaufman BA, Molleston MC. Selective lumbosacral dorsal rhizotomy immediately caudal to the conus medullaris for cerebral palsy spasticity. Neurosurgery. 1993;33:929–933. Penn RD, Kroin JS. Intrathecal baclofen alleviates spinal cord spasticity. Lancet. 1984;1:1078. Sindou M, Georgoulis G, Mertens: neurosurgical treatment for spasticity. In A Practical Guide for Children and Adults. Vienna: Spinger; 2014. Sindou M, Georgoulis G. Keyhole interlaminar dorsal rhizotomiey for spastic diplegia in cerebral palsy. Acta Neurochir (Wien). 2015;157:1187–1196. Sindou M, Quoex C, Baleydier C. Fiber organization at the posterior spinal cord–rootlet junction in man. J Comp Neurol. 1974;153(a):14–26. Numbered references appear on Expert Consult.

REFERENCES

1. Sindou M, Abbott A, Keravel Y. Neurosurgery for Spasticity: A Multidisciplinary Approach. Wien, New York: Springer-­Verlag; 1991:218. 2. Mertens P, Sindou M. Surgical management of spasticity. In: Barnes MP, Johnson GR, eds. Clinical Management of Spasticity. Cambridge: Cambridge University Press; 2001:239–265. 3. Decq P, Mertens P, et al. La neurochirurgie de la Spasticité. Neurochirurgie. 2003;49:135–416. 4. Sindou M. Neurosurgical management of disabling spasticity. In: Spetzler RF, ed. Operative Techniques in Neurosurgery. Operative Techniques in Neurosurgery. Vol. 7. Philadelphia: Elsevier; 2004:95– 174. 5. Sindou M, Georgoulis G, Mertens: neurosurgical treatment for spasticity. In A Practical Guide for Children and Adults. Vienna: Spinger; 2014. 6. Penn RD, Kroin JS. Intrathecal baclofen alleviates spinal cord spasticity. Lancet. 1984;1:1078. 7. Penn RD. Intrathecal baclofen therapy. Operat Tech Neurosurg. 2004;7:124–127. 8. Parise M, Garcia-­Larrea, Mertens P, Sindou M, Mauguière F. Clinical use of polysynaptic flexion reflexes in the management of spasticity with intrathecal baclofen. Electroengephalogr Clin Neurophysiol. 1997;105(2):141–148. 9. Albright AL, Turner M, Pattisapu JV. Best-­ practice surgical techniques for intrathecal baclofen therapy. J Neurosurg. 2006; ­ 104(suppl 4):233–239. 10. Albright AL, Ferson SS. Intraventricular baclofen for dystonia: techniques and outcomes. Clinical article. J Neurosurg Pediatr. 2009;3:11–14. 11. Turner M, Nguyen HS, Cohen-­ Gadol AA. Intraventricular baclofen as an alternative to intrathecal baclofen for intractable spasticity or dystonia: outcomes and technical considerations. J Neurosurg Pediatr. 2012;10:315–319. 12. Albright AL. Long-­term intraventricular baclofen infusion in beagles. J Neurosurg. 2007;107(suppl 3):225–227. 13. Siebner HR, Dressnandt J, Auer C, Conrad B. Muscle Nerve 21:1209–1212Stoffel A. The treatment of spastic contractures. Am J Orthop Surg. 1998;10:611–644. 1912. 14. Stoffel SA. The treatment of spastic contractures. Am J Orthop Surg. 1912;10:611–644. 15. Gros C. La chirurgie de la spasticité. Neurochirurgie. 1972;23:316– 388. 16. Gros C. Spasticity—clinical classification and surgical treatment. In: Krayenbühl, ed. Advances and Technical Standards in Neurosurgery. Advances and Technical Standards in Neurosurgery. Vol. 6. Wien, New York: Springer-­Verlag; 1979:55–97. 17. Sindou M, Mertens P. Selective neurotomy of the tibial nerve for the treatment of the spastic foot. Neurosurgery. 1988;23:738–744. 18. Mertens P, Sindou M. Selective peripheral neurotomies for the treatment of spasticity. In: Sindou M, Abbott R, Keravel Y, eds. Neurosurgery for Spasticity. A Multidisciplinary Approach. Wien, New York: Springer-­Verlag; 1991:119–132. 19. Decq P, Cuny E, Filipetti P, Keravel Y. Role of soleus muscle in spastic equinus foot. Lancet. 1998;11:118. 20. Decq P, Filipetti P, Feve A, et al. Peripheral selective neurotomies of the brachial plexus branches for the spastic shoulder. Anatomical study and clinical results in 5 patients. J Neurosurg. 1997;86:648– 653. 21. Brunelli G, Brunelli F. Selective microsurgical denervation in spastic paralysis. Ann Chir Main. 1983;2:277–280. 22. Maarrawi J, Mertens P, Luaute J, et al. Long-­ term functional results of selective peripheral neurotomy for the treatment of spastic upper limb: prospective study in 31 patients. J Neurosurg. 2006;104:215–225. 23. Sherrington CS. Decerebrate rigidity and reflex coordination of movements. J Physiol. 1898;22:319–332. 24. Foerster O. On the indications and results of the excision of posterior spinal nerve roots in men. Surg Gynecol Obstet. 1913;16:463– 474. 25. Munro D. The rehabilitation of patients totally paralysed below waist: anterior rhizotomy for spastic paraplegia. Engl J Med. 1945;233:456–461.

26. Bischof W. Die longitudinal myelotomie. Zbl Neurochir. 1951;11: 79–88. 27. Nathan PW. Intrathecal phenol to relieve spasticity in paraplegia. Lancet. 1959:1099–1102:ii. 28. Segnarbieux F, Frerebeau P. The different (open surgical, percutaneous thermal, and intrathecal chemical) rhizotomies for the treatment of spasticity. In: Sindou M, Abbott R, Keravel Y, eds. Neurosurgery for Spasticity: A Multidisciplinary Approach. Wien, New York: Springer-­Verlag; 1991:133–139. 29. Gros C, Ouaknine G, Vlahovitch B, Frerebeau PH. La radicotomie sélective postérieure dans le traitement neurochirurgical de l’hypertonie pyramidale. Neurochirurgie. 1967;13:505–518. 30. Privat JM, Benezech J, Frerebeau P, Gros C. Sectorial posterior rhizotomy, a new technique of surgical treatment for spasticity. Acta Neurochir. 1976;35:181–195. 31. Fraioli B, Guidetti B. Posterior partial rootlet section in the treatment of spasticity. J Neurosurg. 1977;46:618–626. 32. Fasano VA, Barolat-­Romana G, Ivaldi A, Squazzi A. La radicotomie postérieure fonctionnelle dans le traitement de la spasticité ­cérébrale. Neurochirurgie. 1976;22:23–34. 33. Foerster O. On the indications and results of the excision of posterior spinal nerve roots in men. Surg Gynecol Obstet. 1913;16: 463–474. 34. Sindou M. Anatomical study of the dorsal root entry zone (DREZ). In: Surgery in the DREZ for Pain. MD Thesis: University of Lyon; 1972:182. 35. Sindou M, Quoex C, Baleydier C. Fiber organization at the posterior spinal cord–rootlet junction in man. J Comp Neurol. 1974;153(a):14–26. 36. Sindou M, Fischer G, Goutelle A, Mansuy L. La radicellotomie postérieure sélective. Premiers résultats dans la chirurgie de la douleur. Neurochirurgie. 1974;20(b):391–408. 37. Sindou M, Jeanmonod D. Microsurgical DREZotomy for the treatment of spasticity and pain in the lower limbs. Neurosurgery. 1989;24:655–670. 38. Sindou M, Mifsud JJ, Boisson D, Goutelle A. Selective posterior rhizotomy in the dorsal root entry zone for treatment of hyperspasticity and pain in the hemiplegic upper limb. Neurosurgery. 1986;18:587–595. 39. Sindou M, Georgoulis G. Focal dystonia in hemiplegic upper limb: favorable effect of cervical microsurgical DREZotomy involving the ventral horn—a report of 3 patients. Sterotactic Funct Neurosurg. 2016;94(3):140–146. 40. Peacock WJ, Arens LJ. Selective posterior rhizotomy for the relief of spasticity in cerebral palsy. S Afr Med J. 1982;62:119–124. 41. Abbott A, Forem SL, Johann M. Selective posterior rhizotomy for the treatment of spasticity. Childs Nerv Syst. 1989;5:337–346. 42. Sindou M. Radicotomies dorsales chez l’enfant. Neurochirurgie. 2003;49:312–323. 43. Park TS, Gaffney PE, Kaufman BA, Molleston MC. Selective lumbosacral dorsal rhizotomy immediately caudal to the conus medullaris for cerebral palsy spasticity. Neurosurgery. 1993;33:929–933, 35. 44. Sindou M, Georgoulis G. Keyhole interlaminar dorsal rhizotomiey for spastic diplegia in cerebral palsy. Acta Neurochir (Wien). 2015;157:1187–1196. 45. Georgoulis G, Brinzeu A, Sindou M. Dorsal rhizotomy for children with spastic diplegia of cerebral palsy origin: usefulness of intraoperative monitoring. J Neurosurg Pediatr. 2018:1–13. 46. Steinbok P. Selective dorsal rhizotomy for spastic cerebral palsy: a revew. Childs Nerv Syst. 2007;23:981–990. 47. Sindou M, Mertens P. Decision-­making for neurosurgical treatment of disabling spasticity in adults. Operat Tech Neurosurg. 2004;7:113–118. 48. Hodgkinson I, Berard C. Assessment of spasticity in pediatric patients. Operat Tech Neurosurg. 2004;7:109–111. 49. Hodgkinson I, Sindou M. Decision-­making for treatment of disabling spasticity in children. Operat Tech Neurosurg. 2004;7:120–123. 50. Sindou M, Simon F, Mertens P, Decq P. Selective peripheral neurotomy for spasticity in childhood. Childs Nerv Syst. 2007;23:957– 970 (contains 30 references for SNP).

1305.e1

SURGICAL MANAGEMENT OF INTRACTABLE PAIN CHAPTER 114

Retrogasserian Glycerol Rhizolysis in Trigeminal Neuralgia GÖRAN ERLAND LIND  •  BENGT LINDEROTH Many patients with trigeminal neuralgia (TN) are elderly, often with concurrent diseases; therefore there is a constant search for appropriate therapeutic methods with low surgical risk, little impact on facial sensibility, and the ability to perform such methods under local anesthesia. Glycerol rhizolysis, the procedure described in this chapter, is one such. The availability of a method that can be used even in medically infirm patients may also broaden the indications for surgical treatment, because the usual regimen with carbamazepine, other anticonvulsants, or baclofen is known to cause severe side effects in many patients. These problems apply particularly to patients with paroxysmal facial pain associated with multiple sclerosis (MS).

History The discovery of the beneficial effects of glycerol in patients with TN was purely accidental. During the course of development of a procedure for producing lesions in the gasserian ganglion in patients with TN in the 1970s, in which the Leksell gamma knife in Stockholm was to be used, x-­ray contrast medium (metrizamide) and glycerol were tried as vehicles for a radiopaque metal dust (tantalum powder). The tantalum powder was to be introduced into the retroganglionic cistern as a permanent marker to constitute a visible target for subsequent stereotactic calculations.1,2 Glycerol was chosen as the vehicle because, being the base for triglyceride formation in the body, it was presumed to be harmless, and its viscosity would ensure that the tantalum suspension was maintained long enough for the powder to be deposited in the trigeminal cistern. In fact, glycerol had been used earlier in the treatment of TN as a vehicle for the highly neurolytic phenol,3 which was used for percutaneous treatment of TN at that time. It was noted that merely injecting the glycerol and tantalum dust mixture in patients abolished paroxysmal pain before the gamma knife procedure was performed. On the basis of these observations, Håkanson developed the technique for treating TN by glycerol injection into the trigeminal cistern. A report on the first series of patients was presented in 1981,4 after which the method was rapidly adopted in many neurosurgical centers. Over the years, many series of patients treated using Håkanson’s procedure or some variation of the original method have been reported. The results from different series have been highly variable. In many centers the

outcome has been quite satisfactory,5–9 and glycerol rhizolysis has continued to be the method of choice, particularly for elderly and infirm patients. In other series, the results have been so discouraging (Siegfried, 1985, and Rhoton, 1985, unpublished results, both cited in Sweet10); Price, 1985, unpublished results, cited in Sweet11 and Fujimaki and colleagues12) that some neurosurgeons have entirely abandoned the procedure. In this chapter, beginning with a description of the mechanisms behind the beneficial effects of glycerol, the possible reasons for these discrepancies are examined and a standard procedure to ensure maximum efficacy and safety is described. 

Probable Mechanisms of Action of Glycerol The etiology of TN is likely multifactorial, but degradation of the myelin sheath due to advancing age, neurovascular conflicts with compression of the nerve root by an arterial branch in the posterior fossa or demyelination and formation of plaques in MS seem to constitute a common denominator. In many instances, however, the etiology remains obscure. We find no satisfactory animal models of TN in the literature, and it is difficult to obtain relevant histologic data from patients. However, TN presents with such idiosyncratic signs and symptoms and responds to so distinctive a set of therapeutic modalities that scientific deduction can be used to generate likely hypotheses. The “ignition hypothesis” of TN13–15 is based on advances in the understanding of abnormal electrical activation of injured sensory neurons16; this is supported by histopathologic examinations of biopsy specimens from patients with TN who are undergoing microvascular decompression (MVD) of the trigeminal root in the posterior fossa.14 According to this hypothesis, TN results from specific abnormal activation of trigeminal afferent neurons in the trigeminal root or ganglion. Injury renders both axons and axotomized somata hyperexcitable. The hyperexcitable afferents, in turn, induce pain paroxysms as a result of synchronized postdischarge activity. The ignition hypothesis accounts for the major positive and negative signs and symptoms of TN, for its pathogenesis, and for the efficacy of treatment modalities (for discussion, see Devor et al.13 and Rappaport and Devor15).

1307

1308

Section Six  •  FUNCTIONAL NEUROSURGERY

The only therapeutic method currently in use for tic doloureux directed onto one of the mentioned etiologic factors is MVD, where the surgeon resolves a neurovascular conflict if found during posterior fossa exploration. The other surgical approaches all include graded lesioning of the trigeminal nerve (i.e., postganglionic root fibers or proximal root) using minimally invasive approaches chemically, heat, physical compression, or radiation (gamma knife treatment). The attained spectrum of fibers in the nerve seems to differ between the methods but the clinical objective is similar—that is, relief from the pain paroxysms with no or only slight side effects. However, in experienced hands, glycerol rhizotomy, as will be demonstrated further on, is probably the most lenient method for the patient. Retrogasserian glycerol rhizolysis is thus a purely empiric method, the beneficial effects of glycerol having been discovered accidentally. There has been much debate about the putative mechanisms behind the effects of glycerol on paroxysmal pain. It is evident from the side effects reported (e.g., hypesthesia) that the substance is neurolytic in the concentrations and volumes used for injection. An important issue is whether the neurolytic effect is selective for a certain fiber spectrum. From clinical observations, it is clear that the trigger mechanism for the pain paroxysms is activated by tactile stimulation and impulse propagation in large myelinated fibers.

MORPHOLOGIC EFFECTS OF GLYCEROL Glycerol is a trivalent alcohol normally present in human tissue, where it forms the skeleton of the triglycerides, among other functions.17,18 Glycerol readily penetrates cell membranes and seems to possess distinct cryoprotective properties beneficial to cells. Its toxicity is low; comparatively high doses must be injected systemically or intrathecally to induce toxic effects.19,20 Glycerol’s neurolytic action is thought to be due to its hypertonicity, a condition known to injure nerve fibers, especially thin, unmyelinated and myelinated fibers.21 Although the myelin sheath of the coarse fibers gives some transitory protection from this effect, length of exposure, neuron type, and the presence of previous demyelination may be important determinants of the vulnerability of individual fibers. For example, with longer exposures, Robertson22 and Pal and colleagues23 observed that myelinated fibers were particularly vulnerable, and the degree of damage correlated positively with fiber diameter. Studies on isolated animal nerve fibers show morphologic changes after exposure to glycerol. These consist of disruption of the tight junction between the Schwann cells and the axolemma without damage to the axon proper.24 Bathing the fibers in glycerol initially causes the axons to shrink, with a return to basal volume after equilibration of the substance over the cell membranes. With transfer to iso-­ osmotic conditions, the fibers swell markedly before returning to their normal volume. Thus marked structural changes are observed with glycerol administration, but the conduction properties of the treated nerve axons remain intact.24 After intraneural and perineural injection of glycerol, Håkanson25 and Rengachary and associates26 observed axolysis with marked myelin sheath swelling. The coarse myelinated fibers sustained the most severe damage, whereas the small-­diameter myelinated and unmyelinated fibers are relatively well preserved.23 In contrast, Bremerich and Reisert27 found only slight histomorphologic changes after glycerol

injection in the region of the foramen ovale in the rat in their long-­term (180 days) comparative study of axonal damage after the injection of glycerol, phenol-­glycerol, and saline. A more recent study in dogs submitted to glycerol injection in a single trigeminal ganglion28 demonstrated axonolysis both in myelinated as well as in nonmyelinated fibers. The damage following glycerol injection into a cavity with isotonic body fluid is probably considerably less severe than that following perineural deposition. However, Lunsford and associates8 observed extensive areas of myelin degradation and axonal swelling in cats subjected to retrogasserian glycerol injections 4 to 6 weeks earlier. The site of glycerol effects has been specifically studied by Stajcic,29 who injected 3H-­labeled glycerol into peripheral branches of the maxillary nerve and in the infraorbital canal of rats. The amount of radioactivity detected in the nerve distal to the foramen rotundum as well as in the ipsilateral and contralateral gasserian ganglion was less than 0.1% in all specimens. The author concluded that a retrograde transport mechanism behind the effect is improbable and that the beneficial effect of glycerol occurs at the site of injection. There is as yet no publication of an autopsy series of patients with TN treated by retrogasserian glycerol rhizolysis. Sweet11 provides an anecdotal description of a patient undergoing a retrogasserian glycerol injection of the extreme volume of 1.5 mL, with subsequent development of anesthesia dolorosa. At a posterior fossa craniotomy “many months” later, the trigeminal rootlets were found to be markedly atrophic. 

NEUROPHYSIOLOGIC CHANGES AFTER GLYCEROL APPLICATION It is likely that the change in osmolarity causes the damage to nerve axons, and the morphologic changes seem to be minimized by a gradual alteration in the osmolarity (e.g., by slowly instilling and removing glycerol from the compartment housing the axons). The functional consequences of glycerol application to normal and damaged nervous tissue are known only fragmentarily, but there are a few observations that might apply to the clinical use of the substance. Burchiel and Russel30 studied the effect of glycerol on normal and damaged nerves in a rat neuroma model. The neuromas, produced by sectioning of the saphenous nerve, were mechanosensitive and discharged both spontaneously and in response to light manipulation. These researchers found evidence supporting the view that glycerol exerts its major action on the large-­diameter fibers. Exposure of the injured nerve to glycerol induced a short episode of increased spontaneous firing in the nerve, a response shown to originate from the myelinated fibers. The observation by Rappaport and associates31 that glycerol injected into neuromas was more effective than alcohol in decreasing autotomy in rats suggests that autotomy may be related to unpleasant “tic-­like” paresthesias. The therapeutic mechanism, according to these investigators, could be suppression of ectopic impulse barrage from the neuroma. Sweet and coworkers32 found that glycerol injected into the trigeminal cistern of patients abolished the late components (corresponding to A-­delta and C fibers) of trigeminal root potentials recorded with electrical stimulation of the surface of the cheek. These recordings were made only minutes after the injection and therefore do not permit conclusions concerning long-­term effects.

114  •  Retrogasserian Glycerol Rhizolysis in Trigeminal Neuralgia

Hellstrand and colleagues (unpublished data; see Håkanson25) studied the effects of glycerol both on isolated frog nerve and on trigeminal root fibers after cisternal injection in the cat. They observed a severe reduction of the evoked potentials with glycerol but a nearly total restoration after rinsing the compartment with saline. This recoverability probably has a bearing on clinical effects and must be taken into account when interpreting the short-­ term observations of Sweet and associates32 referred to previously. Based on knowledge that glycerol requires at least 30 minutes to equilibrate across a membrane of a living cell and according to the aforementioned experimental observations, evacuation of the glycerol from the cistern after a short time (e.g., 5 to 20 minutes10,33,34) might induce more severe damage, especially to fine fiber systems, than a slow unloading by diffusion into the subarachnoid space. Longer-­term observations of trigeminal evoked potentials have been reported by Bennett and Lunsford,35 who investigated patients before and 6 weeks after trigeminal glycerol rhizolysis. They confirmed the earlier findings of Bennett and Jannetta36 that thresholds were elevated and evoked potentials had a markedly increased latency on the affected side compared with the healthy one. An additional, unexpected finding was that these aberrations were “normalized” after glycerol rhizolysis. Because partially demyelinated fibers are known to conduct with a slower velocity and at a lower rate,37,38 they interpreted this finding to indicate that glycerol selectively attacked partially damaged trigeminal axons; after their elimination, the evoked trigeminal potentials appeared “normalized.” Further long-­term observations were supplied by Lunsford and colleagues,8 who noted the most marked changes in trigeminal evoked potentials in cats in the large-­diameter myelinated fibers, with additional changes noted as late as 6 weeks after the injection. Quantitative sensory testing using von Frey hairs, mechanical pulses, and the Marstock technique39 also corroborates the notion that glycerol acts mainly on the large myelinated fiber spectrum.40 Eide and Stubhaug4,41 examined thresholds for tactile and temperature stimuli in patients with TN before and after glycerol rhizolysis. They found evidence that pain relief after glycerol treatment involved normalization of previously abnormal temporal summation phenomena with little accompanying sensory loss. Kumar and associates42 found postinjection quantitative abnormalities of the blink reflex that correlated with sensory impairment. Thus experimental and clinical observations indicate that the effects of glycerol may be due to its hyperosmolarity and that the rate of alteration of osmolarity is critical for the effect. Furthermore, there are indications that the major part of the effect is exerted through actions on large myelinated fibers, notably those with previous damage to the myelin sheath, thereby possibly affecting the “trigger mechanism” for pain paroxysm. Glycerol has also been reported to downregulate central neuronal hyperexcitability, often without signs of significant additional nerve damage.41 

Indications The main indication for glycerol rhizolysis remains classic idiopathic TN. Common reasons for progressing to surgical

1309

treatment include deficient control of paroxysms in spite of an adequate pharmaceutical regimen, severe medication side effects, development of drug allergy or intolerance, or signs of hepatic malfunction ascribed to medication. Paroxysmal facial pain in MS is another prime indication. The initial outcome in this group of patients is as satisfactory as for idiopathic TN, but the long-­term results are, as with other available methods, less encouraging. This is discussed further next. Patients with signs of deafferentation should, in principle, not be submitted to a neurolytic procedure. However, many patients with TN previously treated by other methods display signs of neural damage, such as hypesthesia, allodynia, hyperalgesia, and some degree of continuous deafferentation pain. Such patients should be accepted for treatment only if a paroxysmal pain component is dominant and after careful evaluation of sensory deficits. If such patients are accepted for glycerol rhizolysis, the procedure should be carried out with the utmost care, using a reduced amount of glycerol. The same considerations also apply to the use of glycerol rhizolysis in atypical facial pain/painful trigeminal neuropathy. In general, the method is not indicated in these cases. Only when a dominant paroxysmal component is present, and the signs of deafferentation are slight, may the method be considered. Both neurosurgeon and patient should be aware that the procedure might aggravate the deafferentation and therefore the constant neuropathic pain.

PREOPERATIVE EVALUATION The preoperative evaluation should focus on the presence of typical signs of TN, previous treatments, the pharmaceutical regimen, the presence of sensory deficits, constant pain components, and ipsilateral hearing loss. Because we recommend the use of contrast medium injection in all cases, intolerance to iodine and previous adverse reactions to contrast medium should be determined. A magnetic resonance imaging study with a sequence optimized for the detection of possible neurovascular conflicts or at least a computed tomography (CT) scan with and without contrast injection should be performed before surgery. The surgeon must evaluate the patient before the procedure to individualize premedication and describe the details of the procedure to the patient to ensure good cooperation during its performance. Most patients tolerate the procedure well in local anesthesia with adequate premedication and with only slight sedation (see “Technique,” next), but very anxious patients may require general anesthesia. 

Technique The original technique of Håkanson has been subject to many modifications by various neurosurgeons. These variations encompass the type of anesthesia selected, general or local; patient position and fluoroscopic projection; whether cisternography is performed; other modes of localization of the needle tip (electrical stimulation; reactions to drop-­by-­ drop injection of glycerol, local anesthetic injection43); the dose of glycerol used; instillation of glycerol in one step or as minute volumes in an incremental fashion, with intermittent sensory testing; trials to empty the cistern after attaining a satisfactory effect according to perioperative testing; and how long the patient is kept sitting with the head flexed after completion of the procedure.

1310

Section Six  •  FUNCTIONAL NEUROSURGERY

POSITIONING V1

The Trigeminal Cistern

V2

V3 Arachnoid Cannula FIGURE 114.1  Schematic picture illustrating the contents of the Meckel cave: the Gasserian ganglion, the retroganglionic root fibers in the cerebrospinal fluid–filled cistern, and the meningeal coverings. A needle is penetrating the ganglion, entering the cistern. (Modified from Håkanson S. Trigeminal Neuralgia Treated by Retrogasserian Injection of Glycerol. Stockholm: Karolinska Institute; 1982.)

Some of these modifications have resulted in less satisfactory results.10,12,34,44 We consider retrogasserian glycerol rhizolysis to be an anatomically based method aimed at graded lesioning of fibers in a certain locus. Thus the localization procedure should also be anatomic and the treatment should be meticulously performed, using the smallest possible volume of pure sterile glycerol considered to be effective in each case. The procedure as it is currently performed at the Department of Neurosurgery, Karolinska University Hospital, Stockholm, is described in this section.

ANESTHESIA AND SEDATION Until the late 1990s, retrogasserian glycerol rhizolysis was performed in a radiographic suite with the patient awake and premedicated approximately 45 minutes before the start of the session with 5 to 10 mg of subcutaneous morphine hydrochloride-­ scopolamine and 2.5 mg of intramuscular droperidol. The doses were adjusted according to the age and condition of the patient. In some cases, 0.5 mg of atropine was given intravenously immediately before the procedure to prevent bradycardia during needle insertion. An intravenous line with slow infusion of Ringer solution is maintained during the session and for some hours thereafter. Our current protocol involves sedation with intravenous propofol using a syringe pump. No intubation is required and oxygen is supplied via a nasal catheter. In anxious patients a low oral dose of benzodiazepine is given 1 hour preoperatively. The legs are wrapped or compression stockings applied to counteract blood pressure decrease in the semisitting position. General anesthesia and endotracheal intubation are used only in particularly anxious patients. If used, it is important that the anesthesia be terminated with the patient in the sitting position with the head flexed according to the surgeon’s instructions. The skin at the point of needle insertion and the underlying soft tissue are infiltrated with local lidocaine 0.5%. 

Since the mid-­1990s, a modified dentist’s operating chair has been used in the surgical theater in conjunction with a standard C-­arm fluoroscopic image intensifier with image-­ storing capacity, which provides sufficient picture quality for the clinical procedure. In most cases, fluoroscopy with lateral projection is used when the cistern is punctured. Further guidance is obtained by switching to the anteroposterior projection. In difficult cases in which entering the proper part of the oval foramen is a problem, the patient’s head may be extended and rotated 15 to 20 degrees from the affected side and the fluoroscopy arm tilted to give an axial-­oblique projection of the skull base including the foramen ovale. With some older equipment, it might be difficult to readily identify the proper foramen on the fluoroscopy monitor. If one needle has already penetrated the foramen, identification should be easy, and a new needle can readily be inserted in the desired (often medial) part of the foramen. 

Anatomic Landmarks and Important Structures The trigeminal cistern is punctured by the anterior percutaneous route through the foramen ovale, as described by Härtel (Fig. 114.1).45 After local anesthesia, a 22-­ gauge lumbar cannula (outer diameter 0.7 mm; length 90 mm) is inserted from a point approximately 3 to 4 cm lateral to the corner of the mouth. The trajectory is aimed at a point that lies, in the lateral view, approximately 0.5 cm anterior to the anterior margin of the mandibular joint, and in the anteroposterior view toward the medial margin of the pupil with the eyeball in the neutral position. There are several landmarks that may be used for reaching the foramen ovale,46,47 but in most cases these two coordinates are sufficient. In Fig. 114.2, CT scans from a patient with tantalum dust in the trigeminal cistern are provided to show the relationship of the oval foramen and the trigeminal cistern to these structures (see Fig. 114.2A through D). It is often wise to direct the needle to touch the medial wall of the foramen. When bone contact is experienced, the needle is withdrawn a short distance, redirected a few millimeters more laterally, and introduced through the medial part of the foramen. Intermittent fluoroscopy is used during these maneuvers. When the needle penetrates the foramen, the patient may experience a brief episode of pain due to penetration of V3 and the semilunar ganglion. As a rule, the cannula should not reach beyond the clival contour as seen on the orthogonal lateral projection. When the tip of the cannula is located inside the arachnoid of the trigeminal cistern, there should be a spontaneous exit of cerebrospinal fluid (CSF), especially at the first treatment. Because the location of the trigeminal ganglion and cistern can vary in relation to the landmarks of the skull base, a contrast injection must be performed to ascertain the correct site for glycerol injection. However, spontaneous CSF drainage is not sufficient for accepting the location as intracisternal, as CSF may originate from other locations; in fact, a brisk flow of CSF often indicates a subtemporal tip location.

114  •  Retrogasserian Glycerol Rhizolysis in Trigeminal Neuralgia

8 mm

9 mm

A

C

1311

B

D

TRIGEMINAL CISTERNOGRAPHY The technique we use is essentially the same as that described by Håkanson,48 although estimation of the cisternal volume is of less importance for deciding what volume of glycerol to inject. The contrast medium must be water soluble, with high radiographic attenuation and low toxicity, and it must have a higher specific gravity than CSF. The contrast medium used since 1986 is iohexol (300 mg iodine/ mL).49 Approximately 0.3 to 0.6 mL is injected with the patient sitting with his or her head slightly flexed to retain as much of the medium in the cistern as possible. If intermittent fluoroscopy is used during injection, the position of the needle tip may be estimated immediately, but it should always be confirmed by radiography in both the lateral and

FIGURE 114.2  Consecutive axial computed tomography scan images of a patient with intracisternal tantalum dust.  The anteroposterior distance from the anterior portion of the oval foramen to the anterior portion of the mandible is measured. The relationship of the oval foramen and the trigeminal cistern in laterality to the eye is also worth noting. However, there is a certain variation partly depending on the skull shape.

anteroposterior projections. The typical appearance of the trigeminal cistern is illustrated in Fig. 114.3. Ideally, the sensory root filaments (and sometimes the motor portion) should be visualized by lateral cisternography, leaving no doubt about the intracisternal position of the tip. The typical 45-­degree medial tilt of the cistern should be seen from the anteroposterior view (see Fig. 114.3B). The appearance of the cistern may vary considerably between patients, and it is essential that the surgeon be familiar with this anatomy. Furthermore, there is a subdural-­ extracisternal compartment in the Meckel cave that may be injected with contrast medium (Fig. 114.4). This usually happens when contrast medium is injected without prior spontaneous CSF drainage or if the needle is dislodged from the intracisternal position during injection. 

1312

Section Six  •  FUNCTIONAL NEUROSURGERY

B

A

C FIGURE 114.3  The typical appearance of the trigeminal cistern filled with contrast medium in the lateral (A) and anteroposterior projections (B). Note the root fibers (A) that give the cistern its striped texture. In the lateral projection (C), there is also sparing of contrast, which indicates the position of the trigeminal motor root (arrow).

SPECIFIC DIFFICULTIES Spontaneous CSF drainage from the needle does not guarantee an intracisternal tip location. In fact, if the cannula is placed a few millimeters too lateral, the tip may be located in the subtemporal subarachnoid space, and a flow of CSF will still be produced. Subsequent cisternography solves this problem. Fig. 114.5A shows the proximity of the cisternal and subtemporal subarachnoid compartments in the anteroposterior projection. Fig. 114.5B and C illustrate a pure subtemporal contrast injection. Our strategy in this case is to leave the first needle in place and to introduce a second needle using the first for guidance (Fig. 114.6A and B). It cannot be overemphasized that spontaneous CSF drainage is required before contrast injection. If, in such a case, the contrast medium is injected without fulfilling this requirement,

the glycerol may be deposited in the extra-­arachnoid subdural compartment, as shown above (see Fig. 114.4). Another problem may arise if the patient’s head is not adequately tilted forward during the injection because the contrast medium then flows out the porus trigemini and escapes to the posterior fossa, with insufficient cisternal filling to confirm the correct position of the needle tip (Fig. 114.7). This situation may also result in underestimation of the cisternal volume. 

CONTRAST EVACUATION When the intracisternal position of the tip has been confirmed, the syringe is gently removed from the cannula and the contrast medium permitted to flow out of it in a drop-­ by-­drop fashion. We usually evacuate the cistern by tilting

114  •  Retrogasserian Glycerol Rhizolysis in Trigeminal Neuralgia

1313

the patient to the supine position. If it is difficult to evacuate all contrast medium from the bottom of the cistern to permit the glycerol to reach the lowest root fibers (see later), the patient can be placed in the Trendelenburg position for a few minutes, a maneuver that permits the contrast medium to drain to the posterior fossa. Furthermore, the cistern may be flushed with 2 to 3 mL of sterile saline until the control radiograph indicates that the cistern is properly rinsed from contrast. Some of the less satisfactory results are probably due to failure to empty the cistern properly.12,44 An extracisternal needle-­tip position precludes a subsequent glycerol injection and must lead to repositioning or abortion of the procedure. 

V1 V2

V3

FIGURE 114.4  Schematic picture of the different compartments in the Meckel cave.  The arachnoid is drawn with a wavy line. Note the sites (*) where extracisternal deposits of contrast medium and glycerol may be placed. (From Pauser G, Gerstenbrand F, Gross D, eds. Gesichtsschmerz, Schmerzstudien Z. New York: Verlag; 1979, with permission.)

GLYCEROL INJECTION Glycerol injection should always be performed with the patient in the sitting position to minimize extracisternal spillover. The glycerol should be anhydrous (greater than 99.5%) and sterile and should be injected slowly from a 1-­mL syringe. In general, 0.18 to 0.30 mL is sufficient; the usual dose ranges from 0.18 to 0.28 mL (present average, 0.25 mL). When the neuralgia encompasses all three branches

A B

C FIGURE 114.5  This anteroposterior roentgenogram (A), with both the trigeminal cistern and the subtemporal space injected with contrast medium, illustrates the proximity of these two compartments. Medially, the contrast-­filled cistern (arrow) is seen barely pierced in its lateral margin by one of the needles. Injection of contrast medium through the lateral needle yielded filling of the subtemporal space (arrow) instead. The lateral roentgenogram (B) shows a pure subtemporal contrast injection. (C) Subtemporal outflow of contrast medium in the anteroposterior projection is shown. No contrast filling of the cistern was obtained, although exit of cerebrospinal fluid from the needle was noted.

1314

Section Six  •  FUNCTIONAL NEUROSURGERY

A

B

FIGURE 114.6  This schematic figure (A) illustrates that because the foramen ovale is a fulcrum point, the needle entry site determines the intracranial destination of the needle tip. A puncture site that is too lateral produces a medial tip position. An entry site that is too medial results in placement of the needle lateral to the trigeminal cistern (c). A puncture site that is too lateral produces a medial tip position (a). Adequate entry is shown by the track (b). (From Jho HD, Lunsford LD. Percutaneous retrogasserian glycerol rhizotomy. Neurosurg Clin North Am. 1997;8:63–74, with permission.) (B) The anteroposterior roentgenogram demonstrates the penetration of the foramen with three needles. Contrast injection via the most medial, only, produces cistern filling.

with multiple trigger points, a somewhat larger volume is used. Injection exceeding 0.35 mL is discouraged because of the risk for postoperative sensory deficits. Furthermore, inability to demonstrate an adequate intracisternal needle-­ tip position precludes glycerol injection. 

BRANCH SELECTIVITY

FIGURE 114.7  During contrast injection, the patient’s head should be tilted forward to prevent immediate contrast flow to the posterior fossa. In this case, the positioning of the head was not adequate, and some contrast escaped to the posterior fossa, which is the reason why the filling of the cistern was only partial.

If it is desired to inject glycerol selectively into one or more trigeminal branches, one of the following four maneuvers can be used. First, the volume of glycerol can be varied to fill more or less of the cistern. When the trigeminal cistern has been entirely emptied after contrast injection, the amount of glycerol injected partly determines which branches will be influenced. With the patient’s head only slightly flexed, a small volume of glycerol (i.e., 0.15 to 0.2 mL) is deposited at the bottom of the cistern and mainly affects the fibers of the third and second branches. Increasing the amount of glycerol causes additional rhizolysis in the two upper portions. Second, contrast medium may be left at the bottom of the cistern to protect the third branch. Both contrast agents have a specific gravity exceeding that of pure glycerol (with 300 mg iodine/mL, iohexol =1.345 g/L; compared with glycerol =1.242 g/L and CSF =1.007 g/L). This implies that these substances, when deposited in the same compartment, replace the original CSF contents and are layered with the contrast medium at the bottom and the glycerol on top of it. With the patient’s head slightly flexed and a little contrast medium remaining at the bottom of the cistern, thus

114  •  Retrogasserian Glycerol Rhizolysis in Trigeminal Neuralgia

FIGURE 114.8  The trigeminal cistern on the patient’s left side is permanently marked by tantalum dust, which lines the arachnoid of the bottom and walls of the cistern (anteroposterior view). The right cistern has been punctured and injected with contrast medium. After marking of the cistern with tantalum, the puncture and glycerol injection may be carried out without the intervening cisternography.

protecting the fibers of the third branch, glycerol may be gently injected to form a layer floating on the contrast medium. Rhizolysis will then engage mainly the upper two branches. When a patient with third-­ branch neuralgia is being treated, no contrast medium should be allowed to remain in the cistern for the glycerol injection. Third, the position of the needle tip is partly indicative of which branch will be most affected. The tip of the cannula should preferentially be positioned in the part of the cistern traversed by the root fibers to be treated. This means that for treatment of third branch neuralgia, the optimal position is in the lower part of the cistern, whereas a first-­or second-­branch neuralgia is best treated using a tip site in the upper portion. This seems especially important at repeat treatments when some degree of intracisternal fibrosis may be present (see later). During or immediately after the injection of glycerol, the patient will experience short bouts (usually 74a >95a >67a >91a >76a >80a >90a >73a >80a >90a >92a >84a >93a >97a >90a >95a

>75 >66 >95 >72 >85 >17 >53 >78 >74 >26 >50 >71 >59 >50 >76 >55 50

30 100 98 79 1174 152

100 0 100 100 100 100

b

66 71 50 60 60 57 (12 months)

aMost bNot

90 73 80 90 71

failures previously treated by destructive method; otherwise 96%.

reported.

Outcomes of 18 major studies. Number of patients, use of cisternography for ascertaining intracisternal injection, percentage of patients with initial pain relief after first injection, and percentage of patients pain free (including reinjections) at follow-­up are given.

of first-­branch neuralgia; and yet in others it was used only when there was no spontaneous CSF outflow through the cannula.57 The extent to which cisternography is used in the series reviewed here is shown in Table 114.1. In our experience, there is a relationship between the quality of the cisternography, adequacy of needle placement, and treatment outcome. A very important factor is the amount of glycerol used. Sometimes the range of volumes is not explicit, and in several series it far exceeds the original recommendations.9,12,58,59 This must be taken into account in interpreting the data (ranges of volumes of glycerol used are given later; see Table 114.3). A third factor of major importance for the outcome is whether the patient has been subjected to some other destructive procedure before (or after) the glycerol rhizolysis and if information about this is given in the reports. This is of critical importance with regard to the estimation of sensory disturbances after the procedure, and it also has an impact on deciding the volume of glycerol to use in a specific case. In some series, patients with diagnoses other than classic TN are included. It is often impossible to determine this from the reports. This, of course, is most important in judging the outcome, because the results, as described later, in other facial pain conditions are often inferior to those in classic tic. 

SHORT-­AND LONG-­TERM RESULTS The outcomes in 23 major series with long-­term follow-­up periods encompassing more than 2700 patients are given in Table 114.1. Cisternography was used routinely for all patients in only 17 of the series.6,12,44,46,53,54,57,58,60–68 The percentage of patients experiencing relief from paroxysmal facial pain within 2 weeks varies in the different series from 67% to 97%. There is no clear association between the mere use of cisternography and success rates for either immediate or long-­term outcomes. This finding may seem remarkable in light of the current authors’ experience, but it may also point to large differences in the accuracy of the cisternographic procedure. The follow-­up periods in these series range from a few months to more than 10 years. The recurrence rates are difficult to estimate correctly because of the differences in techniques of reporting, statistics, and so forth. Kaplan-­Meier analysis has been used by several researchers,44,55,57,58,68 facilitating the interpretation of recurrences. The recurrence rate in relation to length of follow-­up is reviewed in Table 114.2. Within roughly 2 years of treatment, between 2% and 60% of patients with a successful initial outcome experience recurrent pain. This large variation obviously casts doubt on both the technical performance of the procedure and the follow-­up methodology. It is difficult to evaluate how many of the patients have been reinjected and to determine whether these cases are included in the final results.

1318

Section Six  •  FUNCTIONAL NEUROSURGERY

TABLE 114.2  Pain Recurrence after Glycerol Rhizolysis Authors

No. of Patients/Procedures

Early Recurrence (2 Years, %)

Range of Follow-­up

Håkanson54 Lunsford53 Arias5 Beck et al.72 Dieckmann et al.6 Saini56 Burchiel44 Young9 Waltz et al.83 Fujimaki et al.12 North et al.55 Ischia et al.58 Steiger57 Slettebo et al.67 Bergenheim and Hariz60 Jho and Lunsford46 Blomstedt and Bergenheim61 Febles et al.62 Jagia et al.64 Pollock66 Henson et al.63 Kondziolka and Lunsford65 Noorani et al.68

100 62 100 58 252 550 46 162 200 122 85 112 122 60 99 523 139

∼26 ∼21 ∼2 ∼11 ∼11 ∼41 ∼47 ∼11 ∼23 ∼45 ∼40 −20 ∼30 ∼27 ∼33 (1 year) ∼13 ∼35

∼43 ∼a ∼10a ∼a ∼37a ∼92a ∼75a ∼34a ∼25a −72a ∼55a ∼26a ∼41a ∼55a ∼a ∼a ∼45

5–10 years 3–28 months 2–3 years 2–40 months 2–5 years 1–6 years 3–44 months 6–67 months 25–64 months 38–54 months 6–54 months 1–5 years 1–96 months 4.5–9 years 12 months 11 years Up to 11 years

30 100 98 79 — 152

a

— 20 25 — 62

33 — 36 25 — 85

Median 33.5 months 6–36 months 3–52 months 4–100 months Up to 11 years 4–180 months

aNot

reported.

Percentage of patients in each series with early recurrence (within 2 years) after treatment and late (cumulative) recurrence (after 2 years). Follow-­up range is also indicated.

The original Stockholm series of 100 patients was followed between 5 and 10 years (mean, 5 years, 4 months). At the last follow-­up, 53% were still pain free after the first injection. Twenty-­two patients had at that time been reinjected with glycerol and 75% of those from the entire series were pain free. An additional 23% had only mild pain easily controlled by a pharmaceutical regimen.40 The average volume of glycerol injected in this series was 0.21 mL. The average risk of recurrence within 2 years is approximately 20%, and the rate of late reappearance of symptoms (within 5 to 10 years) approaches 50%. Nevertheless, because injection can be repeated and carries little risk for the patient, most of the patients (more than 75%) may be maintained pain free by a small number of reinjections (see Table 114.1). By comparison, Jannetta69 found an 80% rate of permanent pain relief in most series of MVD, 10% with some pain, and a 10% failure rate. Two reports of major series of patients with TN treated by glycerol rhizolysis have been presented by Spaziante and colleagues70 and Lunsford and Duma.71 The two series comprise 191 and 480 patients, respectively. The follow-­up periods were as long as 10 years. The percentage of patients pain free immediately after treatment was 93% in the series of Spaziante and associates70; long-­term follow-­up showed that 77%70 and 75%71 were pain free. No patients with anesthesia dolorosa were observed, but mild hypesthesia was found in 46% and 20%, respectively. Both teams of researchers concluded that glycerol rhizolysis is a mildly neurodestructive procedure indicated as the first choice70 in elderly patients, those with MS, and in patients in whom other procedures, including MVD, have been unsuccessful.71

A 1997 report of the Pittsburgh series by Jho and Lunsford46 showed that of their large group of 523 patients, 90% were immediately pain free and 55% stayed pain free at follow-­up (which extended to more than 10 years). The highest figures for patients initially pain free are those of Håkanson4 (96%) and Bergenheim and Hariz60 (97%). 

SIDE EFFECTS AND COMPLICATIONS Glycerol rhizolysis in the hands of an experienced and careful neurosurgeon should not result in serious complications. Only one fatal myocardial infarction has been reported46,71,72 in the recovery room after the procedure. Despite the fact that glycerol rhizolysis is used in patients of advanced age and sometimes with severe disabilities, the number of severe complications is remarkably low. Other serious complications relate to the attempts to penetrate the foramen ovale with a needle (e.g., intracranial hemorrhage) rather than glycerol instillation per se.11 The most feared consequence of neurolytic procedures, postoperative anesthesia dolorosa, is rarely observed after glycerol rhizolysis. An exception to this is the rather heterogeneous series of 552 cases by Saini,56 in which rhizolysis was performed without cisternography or some other technique to confirm the localization of the needle tip before glycerol injection. In this series, the number of patients with anesthesia dolorosa was 26 (5%). Furthermore, six patients (3%) had signs of disturbance of third-­ branch motor function. This malfunction resolved within 3 to 4 months after injection. Transient masseter weakness has also been described by others.58,59 Otherwise, only

114  •  Retrogasserian Glycerol Rhizolysis in Trigeminal Neuralgia

1319

TABLE 114.3  Sensory Complications After Glycerol Rhizolysis Authors Håkanson54 Lunsford53 Arias5 Beck et al.72 Dieckmann et al.6 Saini56 Burchiel44 Young9 Waltz et al.83 Fujimaki et al.12 North et al.55 Ischia et al.58 Steiger57 Slettebø et al.67 Bergenheim and Hariz60 Jho and Lunsford46 Blomstedt and Bergenheim61 Febles et al.62 Jagia et al.64 Pollock66 Henson et al.63 Kondziolka and Lunsford65 Noorani et al.68 aMany bAfter cNot

No. of Patients/ Procedures

Volume of Glycerol (mL)

100 62 100 58 252 550 46 162 200 122 85 112 122 60 99

0.2–0.3 0.15–0.25a 0.1–0.4 0.2–0.4 0.15–0.4 0.2–0.3 0.15–? 0.15–0.55 0.2–0.6 0.3–0.5 0.3–0.4 0.4–0.5 0.2–0.35a 0.15–0.70 0.20–0.35

523 139

0.20–0.50 0.13–0.35

30 100 98 79 1174

c

152

Slight Hypesthesia (%)

Severe Hypesthesia (%)

Dysesthesia (%)

60 21a 13 17 20

0 0 0 2 1 5d 7 12 7 29 2e 0 3d 6

0 3b 0 0 2 11 13 3 2 26 4e 3 13 13 5

32 47.3

6a 45.5

2 22.7

53 — 45 52 —

13 — — 34 —

c

0.1–0.3 0.8–0.45 ≈0.3 — 0.36

64

—

9

c

72 72 37 63 4 32 53a 35d 42

c

40 8 5 —

with previous or additional destructive procedures. herpes reactivation.

reported.

dOnly

cases with previous destructive procedures.

eTransient.

Percentage of different types of sensory disturbance in each series. Range of glycerol volumes used is also indicated. In several series, it cannot readily be judged in sensory disturbances recorded after glycerol treatment were already present before the procedure. Furthermore, other destructive procedures may have been used subsequently without specific notice.

single cases with transitory cranial nerve dysfunction after glycerol rhizolysis have been reported. Some of these are reviewed by Sweet.10 A review of 260 consecutive procedures performed in 139 patients between 1986 and 1987 reported a fairly high frequency of perioperative side effects.61 In this series, a variety of intraoperative technical obstacles, severe vasovagal responses, and even cardiac arrest occurred. In total, complications or side effects occurred in 67.3% of procedures. This series evidently encompasses learning curves for several surgeons. Penetration of the foramina of Vesalius (0.8%) and spinosum (0.4%) occurred, as did buccal penetration (1.5%). Actually, three patients (1.2%) reported a postoperative ipsilateral decrease of hearing ability. Arterial bleeding occurred in 0.4%, while venous blood from the needle occurred in 3.5%. The side effects and complications are detailed in Tables 114.3 and 114.4.

Postoperative Facial Sensory Disturbance A disturbance of facial sensibility is not uncommon after the procedure but usually lasts for only a few hours to 1 to 2

weeks. This is not tabulated as a side effect. The following discussion focuses on persistent alterations in sensory function or perception in the trigeminal area: (1) postoperative hypesthesia, slight or severe; and (2) the presence of dysesthesia or allodynia. Paresthesias that are not unpleasant are not included. 

Hypesthesia Serious sensory disturbance (e.g., anesthesia dolorosa) is rare after glycerol rhizolysis. However, transitory facial hypesthesia is a common phenomenon (up to 70%) after the procedure. The complaints usually vanish 3 to 6 months after the operation.5,9,40,59 The frequency of slight hypesthesia persisting for longer periods is variable between different series (see Table 114.3). In some series, only a small percentage of patients experience this,5,55 but in others more than two thirds present with hypesthesia at follow-­up.9,44 More severe hypesthesia and anesthesia is rare (see Table 114.3). There is only one series with a figure approaching 30%.9,12,44 This is of course unacceptable, and the clinicians

1320

Section Six  •  FUNCTIONAL NEUROSURGERY

TABLE 114.4  Infectious Complications After Glycerol Rhizolysis Authors

No. of Patients/Procedures

Herpes Reactivation (%)

Aseptic Meningitis (%)

Bacterial Meningitis (%)

Håkanson54

100 62 100 58 252 550 46 162 200 122 85 112 122 60 99 523 139

50 13 10 9 77 3 5 38

0 3 2 4 1

0 0 0 0 1

Lunsford53 Arias5 Beck et al.72 Dieckmann et al.6 Saini56 Burchiel44 Young9 Waltz et al.83 Fujimaki et al.12 North et al.55 Ischia et al.58 Steiger57 Slettebø et al.67 Bergenheim and Hariz60 Jho and Lunsford46 Blomstedt and Bergenheim61 Febles et al.62 Jagia et al.64 Pollock66 Henson et al.63 Kondziolka and Lunsford65 Noorani et al.68 aNot

30 100 98 79 1174 152

a

a

2 0 7

2 1 1

a

a

a

a

a

a

a

a

a

a

0 1.6

a

a

0 a

a

a

a

37 3.8

0.6 1.5

a

a

a

a

3.6 12 — “Common” 19

0 1 -­b 0.2 —

0.7 0 8b — —

1.5

reported.

bThree

patients reported with meningitis; aseptic or bacterial was not specified.

Percentage of cases in each series with herpes simplex reactivation, aseptic meningitis, and bacterial meningitis.

consequently abandoned the procedure. The figures from the series of Saini,56 Burchiel,44 Young,9 Waltz and associates,59 Bergenheim and Hariz,60 and Jho and Lunsford46 must also be considered high (5% to 12%). There are at least four possible explanations for this outcome: (1) some of these patients may have had other previous or subsequent destructive procedures, (2) there may have been technical difficulties during the procedure, (3) the volume of glycerol injected may have been too large, and (4) previous procedures may have produced cistern obliteration by fibrosis.46,52,53 Sweet10 described a case in which 1.5 mL of glycerol was injected in 0.1-­mL increments, resulting in anesthesia dolorosa. When properly performed with a reasonable volume of glycerol, the incidence of severe sensory disturbances with glycerol rhizolysis should be low (3

89 75

NR NR

3 1

3 8

0.2 0.1

0.2 0.1

0 0

111

1–7

80

6.3

2

NR

0

0

0

1000 702 124 1070 265

9 5.5 3.7 9 3.8

78 63 67 73 71

6.5 9 6 6.5 8

17 9 2 3.5 9

10 65 3 26 NR

0.5 0.4 4 0.2 NR

0.5 0.5 NR 0.5 NR

0 0 NR 0.2 0

1200

9

79

4

6

16

1

1.3

0

185

51

4

NR

NR

NR

NR

NR

Spendel et al.26 Mathews and Scrivani27 Kanpolat et al.28 Tronnier et al.29

182 258

95 74

NR 8

NR 2.3

NR 28.8

NR 0

NR 0

NR 0

1600

1–16 (avg 8) 0.5–10 1–6.5 (avg 3) 1–5

75

1.8

5.7

4.1

0.13

1.6

0

316

14

25

0.9

0

NR

0.8

NR

0.8

Series

Printed with permission from the Mayfield Clinic.

corneal sensation). Based on our experience, a dense hypalgesic lesion is associated with a 25% risk of pain recurrence over 15 years and a 15% risk of dysesthesia, which is usually minor and does not require treatment (see Table 115.2).15 A review of the literature from 1989 to 2003 focused on series that included more than 100 patients, percutaneous radiofrequency rhizotomy was effective in controlling trigeminal neuralgia pain, had minimal morbidity, and demonstrated acceptable rates of recurrence (Table 115.4).16–29 Furthermore, the radiofrequency rhizotomy procedure can easily be repeated with neither higher complication rates nor reduction in efficacy. 

CONSIDERATIONS FOR OTHER APPROACHES Alternative percutaneous techniques, such as glycerol injection or balloon compression, have not been detailed as thoroughly in the literature. Glycerol injection is appealing because it appears to anatomically preserve the sensory rootlets. Theoretically, it is a mechanism to relieve pain without major sensory loss or dysesthesias while preserving the corneal reflex. However, data suggest that this technique is destructive and requires sensory denervation to avoid a high rate of recurrence.30 In many series, recurrence rates are prohibitively high, and dysesthesia still constitutes a major complication. In addition, unique to this procedure, chemical meningitis occasionally constitutes a major perioperative morbidity. Table 115.5 summarizes the results of several large series of patients treated with glycerol injection.30–41 Percutaneous balloon compression has been demonstrated to preserve most small myelinated and unmyelinated fibers. Theoretically it should preserve light touch. Some advocate for this procedure because the patient’s cooperation is not required and general anesthesia can be used.

Recurrence rates remain high and occur after a short period of time. Table 115.6 summarizes the results of several large series of patients treated with this procedure.16,17,42–49 Balloon compression is a destructive procedure that can cause dysesthesia, facial numbness, and other complications such as carotid-­ cavernous fistula formation,43 transient blindness,50 and death.45 Some advocate that balloon compression may have a role in treating patients with pain of the first trigeminal division (V1) who require preservation of the corneal reflex. Among the open intracranial procedures for trigeminal neuralgia, posterior fossa MVD and open partial rhizotomy are usually performed. MVD has a high rate of immediate trigeminal neuralgia pain relief and boasts a recurrence rate equal to or better than percutaneous rhizotomy.51–58 In the most comprehensive study of MVD, Barker et al. demonstrated a 30% recurrence rate over a 20-­year period (median follow-­up, 6.2 years) in 1155 patients.55 Importantly, most postoperative recurrences occurred within the first 2 years after surgery and were less than 1% per year at 10 years after the procedure. Because of these and similar results reported in the literature and the avoidance of troublesome numbness, most advocate MVD as the procedure of choice, especially in young patients. However, patient selection remains important because posterior fossa exploration is associated with higher mortality and morbidity rates than any percutaneous technique. Posterior fossa exploration should be considered with caution in patients who have significant risk factors for craniotomy (e.g., cardiac disease, absolute need for anticoagulation, adverse reaction to general anesthesia, etc.). Although a physiologic age over 65 was previously a contraindication for surgery, recent evidence suggests that with careful patient selection, age alone does not increase morbidity or mortality

115  •  Percutaneous Stereotactic Rhizotomy in the Treatment of Intractable Facial Pain

1331

Table 115.5  Results of Glycerol Rhizotomy in Series of ≥∼100 Patients Since 1989 (%) Series Bergenheim et al.30 Young31 Waltz et al.32 Fujimaki et al.33 Ischia et al.34 De La Porte et al.35 Steiger36 Cappabianca et al.37 Jho and Lunsford38 Hakanson and Linderoth39 Jho and Lunsford40 Erdem and Alkan41

No. of Patients (n)

Follow-­Up (year)

Long-­Term Pain Relief

Significant Dysesthesia

Corneal Analgesia

Trigeminal Motor Weakness

Cranial Nerve Palsy

PO Morbidity

Severe PO Morbidity or Mortality

99

1

64

7

5

0

0

0

0

162 200 122 112 120

0.5–5.5 — 4.5 3.5 —

63 55 22 73 NR

3 2 13 3 0

2 NR 0 8 2.5

0 NR 0 0 0

0 0 0 0 NR

0.6 NR 0 0 0

0 NR 0 0 0

122 191

5 1–7

41 70

13 0

16 10

4 6

0 0

0 6

0.8 NR

523

0.5–11

46

2

0

0

0

0

0

100

5.4

57

0

0

0

0

0

0

365

11

77

2

0

NR

NR

1

157

4

62

8.9

NR

NR

NR

0.6 (aseptic meningitis) NR

NR

Printed with permission from the Mayfield Clinic.

Table 115.6  Results of Balloon Compression in Reported Series With ≥100 Patients (%) Series et al.16

Fraioli Frank and Fabrizi17 Lichtor and Mullan43 Lobato et al.44 Abdennebi et al.45 Brown and Gouda46 Correa and Teixeira47 Skirving and Dan48 Chen and Lee49

No. of Patients (n)

Follow-­Up (year)

Long-­Term Pain Relief

Significant Dysesthesia

Corneal Analgesia

Trigeminal Motor Weakness

Cranial Nerve Palsy

PO Morbidity

Severe Morbidity or Mortality

159 212

3.5 face tingling, warmth

Periaqueductal gray

Lateral spinothalamic tract

Medial lemniscus

Monopolar L face, arm cool vibration

Mesencephalic reticular area

Midline

A

Monopolar L face warmth Monopolar L face warmth

0

5

7 8 9 mm

FIGURE 118.1  Schematic diagram of the midbrain at the level of the superior colliculus, demonstrating the anatomic location and the somatotopic organization of the lateral spinothalamic tract. Note also the anatomic location of the usually elicited responses during electrophysiological stimulation.

The central gray of the mesencephalon represents a complex anatomical structure. It surrounds the sylvian aqueduct, and contains several nuclei and a mixture of myelinated and unmyelinated fibers.1 It is well known that the central gray is implicated in pain conduction. Enkephalin, a neuropeptide associated with pain alleviation, has been identified in large quantities in the central gray. It has been postulated that stimulation of ventro-­lateral regions of the central gray produces enkephalins, which subsequently act on serotonergic neurons in the medulla oblongata, which in turn project on afferent axons (concerned with pain) in the dorsal horn of the spinal cord to produce analgesia. Contrariwise, stimulation of the lateral and rostral areas of the central gray facilitates pain conduction. Furthermore, the production of several other neuropeptides by different areas of the central gray, such as neurotensin, substance P, cholecystokinin, serotonin, somatostatin, and dynorphin has been demonstrated in numerous studies.1 The central gray has also been involved in the vocalization process, the modulation of medullary respiratory centers, the vertical gaze, the presence of aggressive behavior, and the control of reproductive behavior. 

HISTORICAL EVOLUTION The first open mesencephalic tractotomy for managing medically intractable pain was performed by Dogliotti in 1938.2 Although he described his surgical procedure as a

surgical section of the “lemniscus lateralis” at the level of the rostral pons, it should be considered certain that the level of the incision was at the lower mesencephalon (inferior colliculi).2,3 His surgical methodology consisted of surgical exposure of the lower part of the midbrain, and introduction of an electric coagulator into the lateral sulcus.2 His initial series included four patients with medically refractory pain.2 He reported pain abolishment postoperatively in two of them, while there was significant pain reduction in one patient, and the other patient died immediately after surgery.2 In all his reported cases, there was some degree of hemihypoalgesia associated with paresthesia postoperatively.2 Bailey and his coworkers described their experience from performing an open mesencephalic tractotomy for managing medically intractable pain.3 They performed their tractotomy by making an incision, approximately 8 mm in length and 4 mm in depth, extending from the lateral sulcus of the midbrain to the posterior edge of the inferior colliculus, on a plane between the superior cerebellar artery and the trochlear nerve.3 They reported excellent pain control postoperatively, while they observed some transient postoperative drowsiness and aphasia in one of their cases, most probably due to surgical manipulation of the dominant hemisphere of their patient.3 Similarly, Drake and McKenzie reported their experience from a series of six patients, undergoing mesencephalic tractotomy for drug-­ resistant upper extremity or facial

1350

A

Section Six  •  FUNCTIONAL NEUROSURGERY

B

C pain.4 In all their cases, the patient was placed in a sitting position, while the incision was made through a small occipital bone flap, placed between the sagittal sinus medially and the transverse sinus inferiorly. The overlying occipital lobe was gently retracted in superior and lateral direction, and the tentorium was incised along the straight sinus. The posterolateral aspect of the midbrain was exposed after opening the arachnoid, overlying the cisterna ambiens. A tractotomy incision was placed by using a cordotomy knife. The incision usually extended from the lateral sulcus to the lower pole of the superior colliculus, and it was 5 mm deep. They reported that all their patients had postoperatively no pain and temperature sensation in the contralateral half of their body. However, all their patients developed progressively quite bothersome dysesthesias after surgery, while one patient developed postoperatively severe, burning, dysesthetic pain. Interestingly, the touch, the vibration, and the position sensations remained unaffected after surgery in all their cases. They observed in five sixths5 of their cases temporary complete homonymous hemianopsia postoperatively, apparently due to the retraction of the occipital lobe, and/or the sacrifice of the cortical occipital veins. The observed hemianopsia was spontaneously resolved with no further sequelae.4 Stereotactic mesencephalotomy for pain management was introduced by Spiegel and Wycis in 1947.5,6 In their first attempts, they combined this procedure with thalamotomy for treating patients with chronic, medically refractory pain of noncancerous origin, which showed no response to any previous surgical procedures, such as retrogasserian

FIGURE 118.2  (A) Axial T2 weighted image of the midbrain at the level of the superior colliculi demonstrating the major nuclei groups. (B) Axial fractional anisotropy image at the level of the midbrain showing the major ascending and descending tracts. Note the circled area, which represents the ascending spinothalamic tracts. (C) Tractography (diffusion tensor imaging, DTI) depicting the ascending spinothalamic tracts bilaterally.

rhizotomy, sympathectomy, and cordotomy.5,6 In their initial cases, they aimed not only at the spinothalamic and the quintothalamic tracts, lateral to the sylvian aqueduct, but also at the tegmentum adjacent areas, dorsally to the red nucleus.5 Pneumoencephalography was routinely employed for their surgical planning. Both patients in their initial report demonstrated satisfactory long-­term pain relief.5,6 In a later study, they described their modified technique, in which the entry point was through a burr hole, placed on a paramedian plane (7.5 mm lateral to the midline) at the interaural level, and the trajectory was inclining 34 degrees posteriorly, passing through the posterior commissure, which was serving as a reference point.7 A lesion, approximately 5.5 to 9.5 mm in dorso-­ventral diameter, was placed 2 to 3 mm posterior and 0 to 3.5 mm inferior to the posterior commissure, thus destroying the spinothalamic and the reticulothalamic tracts at this level, after applying anodal direct electrical current for 60 seconds. Intraoperative electrical stimulation was usually employed in order to physiologically verify the anatomical target, and thus to minimize the possibility of any procedure-­related complications. They reported immediate, complete pain relief in 72.2% (39/54 patients), partial relief in 31%, while 20.3% of their patients demonstrated no response.7 In the case of proximity of the inserted electrode to the deeply seated oculomotor fibers, ipsilateral ocular movements were observed, while tinnitus could occur due to stimulation of the adjacent lateral geniculate body in cases of a laterally placed electrode. Their indications included atypical or postherpetic facial pain, pain

118  •  Mesencephalic Tractotomy and Anterolateral Cordotomy for Intractable Pain

secondary to tabes dorsalis, chronic pain secondary to spinal cord and/or spinal roots trauma, cancer-­related pain, thalamic and phantom-­limb pain.7 They reported a 7.4% (4/54 patients) mortality rate, limited to patients with thalamic or cancerous pain. They also reported 14.8% permanent postoperative dysesthesia, while ocular disturbances occurred in 3.7%, and permanent motor deficits in 1.8%.7 Torvik reported Leksell’s experience with stereotactic mesencephalic tractotomy (SMT).8 They performed their procedures under local anesthesia, while the Leksell stereotactic apparatus was used.8 A small burr hole was placed in the parieto-­occipital region, and an electrode was stereotactically inserted by utilizing the sylvian aqueduct and the posterior commissure as reference points.8 An electrical stimulation study was routinely performed for verifying the anatomical target, and subsequently a spherical lesion was placed via a bipolar coagulation (lesioning temperature 52°C to 60°C), extending from the level of the posterior commissure to the rostral level of the trochlear nucleus, in a rostro-­ caudal direction. A microscopic examination of the lesioned midbrain area in a postmortem autopsy study in their patients, showed a sharply circumscribed cavity filled with debris and macrophages, surrounded by a thin and sparse gliotic rim, with no evidence of retrograde or anterograde corticospinal fiber degeneration. Interestingly, the ipsilateral medial lemniscus and the spinothalamic tract were completely destroyed; the adjacent reticulothalamic tract was massively damaged, while the superior colliculus and the red nucleus were partially destroyed. Torvic reported in his article that despite the extensive lesioning of the reticulothalamic and the spinothalamic tracts at the midbrain, there was still postoperatively some residual pain sensation. He postulated that tracts other than the reticulothalamic and the spinothalamic might be involved in pain propagation.8 Orthner and Roeder9 reported their surgical technique in stereotactic mesencephalic tractotomy in managing patients with trigeminal, postherpetic, phantom-­limb, and Dejerine-­ Roussy syndrome pain. Their anatomical target was at the level of the posterior commissure, 7.5 mm lateral to the midsagittal plane.9 They routinely employed an electrode and a radiofrequency generator at 30 mA for 30 seconds for making a lesion. In their report, they emphasized the importance of partially destroying the spinoreticular along with the spinothalamic tract, in order to maximize the pain relief effect.9 Mazars et al.10 reported their experience with a different, and more accurate approach (through a transcortical posterior parietal lobe trajectory) for SMT. The proposal of a more precise anatomical target in their clinical series had equally good pain relief rates as a consequence, along with significantly reduced morbidity.10 The occurrence of postoperative dysesthesia and anesthesia dolorosa was significantly diminished; on the other hand, the occurrence of oculomotor palsies was increased due to the passage of the lesioning electrode through the quadrigeminal plate.10 At approximately the same time Amano et al.11 reported their technique and their results from treating medically intractable pain of cancerous origin with SMT. They performed their procedures under local anesthesia by utilizing either the Sano’s or the Todd-­Wells’ stereotactic frame.11 The surgical planning was based on pneumoencephalography and the Schaltenbrand-­Bailey stereotactic atlas.11 The dorsal portion of mesencephalic tegmentum near the central

1351

gray, at the level of the rostral end of the superior colliculus, was used as their anatomical target. The stereotactic coordinates for their selected target was P 14, H –5 to –8, and L 5 to 8, while the laterality of the target was measured from the midline of the sylvian aqueduct.11 They emphasized that the usage of a frontal entry point could minimize the incidence of postoperative Parinaud syndrome. A radiofrequency lesion was made after electrophysiological confirmation of the target. They reported significant information regarding the electrophysiological profile of the mesencephalic reticular formation, by routinely employing detailed microelectrode recordings.11 Nashold and his coworkers employed a slightly different surgical technique for performing SMT.12-­15 The surgical planning was based on a contrast ventriculography for visualizing the sylvian aqueduct, and the anterior commissure (AC) and posterior commissure (PC). The procedure was routinely performed under local anesthesia. A burr hole was placed 1 cm anterior to the coronal suture, and 1.5 cm from the midsagittal plane. Nashold et al. had developed a mesencephalon stereotactic atlas, which could be used for this anterior approach.12-­15 After accurate recognition of the rostral end of the sylvian aqueduct and the AC-­PC line, an electrode was inserted in a trajectory crossing the AC-­PC line at a 65-­to 70-­degree angle. The latero-­medial angulation of the electrode was 2 to 4 degrees off the midsagittal plane. Electrical stimulation could be performed for verifying the anatomical target, and for identifying the fine somatotopic organization of the spinothalamic and the reticulothalamic tracts. A radiofrequency generator was used for 30 seconds for placing a spherical lesion. Nashold et al. initially in their series utilized a target located at the level of the PC, 3 mm posterior to this (“superior colliculus target”), while later on they utilized a target located 5 mm posterior, inferior, and lateral to the PC (“inferior colliculus target”).12-­15 In their reports they greatly emphasized the importance of intraoperative stimulation for verifying the anatomical target in order to maximize their physiologic effect.12-­15 

Current Indications for Stereotactic Mesencephalic Tractotomy The recent advances in neuropharmacology, the development of multidisciplinary pain management strategies, and the emerging of novel neuromodulative surgical techniques have limited the role of SMT, making it a valid treatment option only for those patients with medically refractory pain due to extensive carcinoma involving the head, neck, and/or arm, with likely survival time in the order of 6 (±3) months. Several previous reports have confirmed the achievement of pain relief, and the diminishing of pain-­associated anxiety after performing SMT and lesioning of the spinoreticular along with the spinothalamic tracts, in cases of extensive head and neck cancer.9,12 Moreover, the performance of SMT carries the advantage of reducing the patient’s emotional reaction to pain. It has been reported that the postoperative calming effect of the patient’s fear and anxiety after an SMT closely resembles that of a bilateral cingulotomy.12 In cases of unilateral facial, neck, and/or arm medically intractable pain of cancerous origin, an SMT on the opposite side should be performed. In cases of bilateral pain, the

1352

Section Six  •  FUNCTIONAL NEUROSURGERY

side of the greatest involvement should be managed. However, it has to be mentioned that Whisler and Voris reported no serious postoperative side effects from placing bilateral SMT lesions in patients with bilateral pain.12,13 Patients suffering from phantom-­ limb pain following avulsion of the brachial plexus, post-­cordotomy dysesthesia, or central pain secondary to thalamic syndrome, who failed medical or other surgical treatment, may be candidates for SMT. Although the analgesic effect of SMT wears off in the vast majority of the reported cases, there are a few reports of long-­lasting pain relief.9 Relative contraindications for SMT are patient’s advanced age (≥70 years), poor general medical condition, short life expectancy, and pre-­existing altered level of consciousness. 

Surgical Technique PREOPERATIVE PREPARATION The surgical procedure is carefully explained to the patient. The importance of the patient’s cooperation cannot be overemphasized. The patient remains fasted for a minimum of 8 hours before the procedure. The required dose of analgesics is parenterally administered. Antibiotics are intravenously begun on the morning of surgery and are continued for 24 hours after surgery. Midazolam is intravenously given for preoperative sedation. The procedure is routinely performed with neuroleptanalgesia using intravenous alfentanil and propofol. The whole procedure is performed under noninvasive blood pressure and electrocardiogram (ECG) monitoring, as well as pulse oximetry. The area of the burr hole is clipped and saved. The skin is thoroughly prepped and appropriately draped in a standard sterile fashion. A field block of the scalp is performed, by injecting a mixture of

20 mL of 0.25% bupivacaine hydrochloride with epinephrine, 20 mL of 0.5% lidocaine with epinephrine, and 4 mL of sodium bicarbonate 8.4% is used.16 The bicarbonate neutralizes acidity and considerably reduces the discomfort of the block. 

OPERATIVE PROCEDURE The magnetic resonance imaging (MRI)/computed tomography (CT)-­compatible Leksell base ring and localizer (Elektra, Stockholm, Sweden) are fixed to the patient’s skull.16 Carbon fiber posts and MRI/CT-­compatible pins are used. The MRI scan consists of a contrast-enhanced T-­1–weighted volume acquisition and MPRAGE pulse sequences, using axial 1.3-­mm slices with zero slice gap. This is followed by a whole head CT scan, using 3-­mm slices, with zero slice gap. The two data sets are imported over the local network to the computer workstation. After fusing the MRI to the CT data, the targets and trajectories are defined. If an automatic fusion software program is not available, a visual anatomic point-­to-­point matching between CT and MRI studies may be performed for ruling out any magnetic-­field-­generated distortion. A probe-­view algorithm is used to maximize the distance between any surface cortical veins and the cortical entry points. After defining the AC, the PC, and the AC-­PC line, the mesencephalic target is set 5 mm inferior to the AC-­ PC line, and 5 to 8 mm lateral to the midsagittal plane, at the level of the superior colliculus (Fig. 118.3).16 The entry point and a transcortical trajectory are selected, and a frontal stab incision is appropriately made. A 7/64-­inch twist– drill hole is usually placed, approximately 1 cm anterior to the coronal suture and 1.5 cm lateral to the midsagittal plane. The underlying dura and pia are carefully cauterized with a monopolar cautery. A 1.1-­mm diameter bipolar

FIGURE 118.3 Preoperative planning (spoiled-­gradient-­echo magnetic resonance images) demonstrating the anatomic target of the lateral spinothalamic tract at the midbrain, the anterior commissure (AC) and the posterior commissure (PC) commissures, the AC-­PC line, and the selected entry point.

118  •  Mesencephalic Tractotomy and Anterolateral Cordotomy for Intractable Pain

FIGURE 118.4  The utilized 2-­× 4-­mm straight monopolar (top), 1.1-­ mm straight bipolar (middle), and the side-­extruding (bottom) thermo-­ coupled stimulation-­lesioning electrodes (F.L. Fischer, Freiburg, Germany.)

straight stimulation-­ lesioning thermo-­ coupled electrode (F.L. Fischer, Freiburg, Germany) (Fig. 118.4) is inserted, and its proper positioning is confirmed with intraoperative fluoroscopy. Neuroleptanalgesia must be reversed as much as possible, at this point, in order to maximize the patient’s cooperation. Stimulation studies may be performed at this point for electrophysiological verification of the anatomic target (see Fig. 118.1). The topographic distribution of the thermal or pain response, and/or the observation of any side effects may require repositioning of the electrode, and redefining of the target. Tinnitus would indicate that the inserted electrode is too laterally placed within or adjacent to the inferior quadrigeminal brachium. Limb paresthesias would indicate too anterior placement of the electrode in the medial lemniscus. Ipsilateral ocular movement would also indicate that the inserted electrode is too medially and inferiorly placed. It has been demonstrated that physiological responses are best produced by bipolar electrical stimulation with a square wave generator, using various pulse widths (1 or 0.5 millisecond), and pulse frequencies (5, 15, 30, 60, 120, 300 Hz).12 It is apparent that electrophysiological stimulation requires an awake, cooperative patient with minimal pain medication. Initially Spiegel and Wycis,6 and later Nashold and co-­workers,13 showed that a definite topographical organization of the observed paresthesia existed, and noted painful paresthesias and ocular and auditory phenomena occurring during mesencephalic stimulation. It has to be emphasized that the observed response of the patient to the employed intraoperative electrical stimulation is related not only to the anatomical location of the tip of the inserted electrode, but also to the electrical parameters of the employed stimulation. A detailed description of the observed responses after intraoperative mesencephalic electric stimulation may be found in the work of previous investigators.11,12 A side-­searching, extruding electrode may also be used for more extensive electrophysiologic mapping.16 This is a monopolar electrode, the outer diameter of which is 2 mm, while the extruding noninsulated tip has a 0.5-­ mm diameter.16 The lateral-­extruding searching tip of the electrode can extrude up to a maximum of 8.5 mm, under a 30-­degree angle. A millimetric Vernier scale at the proximal end of the electrode controls the lateral extrusion of the side-­searching electrode (see Fig. 118.4). We have been

1353

using the searching electrode for electrophysiological mapping and target localization in order to minimize the passages of straight electrodes for stimulation, with subsequent minimalization of the passage-­associated trauma to the brain parenchyma. It has to be emphasized that the avoidance of even the slightest rotary movement of the side-­searching electrode when its tip is extruding, is of paramount importance for avoiding any shear injuries. The usual stimulation parameters include monopolar stimulation, frequency of 60 Hz, duration of 0.5 milliseconds, and amplitude range between 0.1 and 0.4 V. A millimetric Vernier scale is used and the lateral extrusion of the side-­searching electrode is plotted. When the target has been adequately verified and thorough electrophysiological stimulation has confirmed the absence of any serious ocular side effects, then the 1.1-­mm straight bipolar electrode (F.L. Fischer, Freiburg, Germany) is introduced, and lesioning is begun at 70°C for 90 seconds (to ensure thermal equilibrium). Additional lesioning may be done at 5°C increments up to 90°C, until satisfactory thermanalgesia has been achieved. If thermanalgesia is inadequate, the lesion may be enlarged by employing 2-­× 4-­mm, straight monopolar electrode (F.L. Fischer, Freiburg, Germany) at 70°C for 90 seconds. If the pain involves head, neck, and upper extremity or thorax, both a medial and a lateral lesion will be required, placed at 5 and 8 mm lateral to the midline, respectively. In such cases, the lateral lesion should be made first because the medial lesion will cause temporary confusion, making testing of analgesia quite difficult. Once adequate thermanalgesia is obtained, we recommend waiting for approximately 20 minutes before removing the lesioning electrode, in order to minimize the chance of an early return of pain sensation. At the completion of the procedure, the previously inserted electrode is carefully withdrawn. The surgical wound is thoroughly irrigated with antibiotic irrigation and is closed with a single 3/0 nylon suture. A sterile dressing is applied, and the patient remains in the postanesthesia care unit for approximately 1 hour, and then is transferred to the ward for further observation and treatment. A postoperative MRI study is usually obtained for verifying the accurate location of the lesion (Fig. 118.5). 

Results and Complications Satisfactory pain relief has been reported in the vast majority of cases with various recurrence rates.2,17 Shieff and Nashold reported 66.7% long-­term relief in their series (27 patients suffering medically intractable thalamic pain).14,15 They noted that 77.8% of their patients were pain free at their discharge from the hospital; however, pain progressively recurred in 11.1% of them.14,15 Amano et al.11 reported excellent pain control in both their cases for 12 months, with no ocular or other complications. Similarly, Frank et al.18 reported their experience from treating a large series of 202 patients with pharmaco-­resistant pain of cancerous origin. The vast majority of their cases suffered face or upper body pain.18 They observed pain recurrence during the first postoperative month in 15% of their patients, while late (4 to 14 postoperative months) pain recurrence occurred in 4.2%.18 Their immediate transient postoperative complications included gaze palsy (9%), dysesthesia (5%), and anesthesia

1354

Section Six  •  FUNCTIONAL NEUROSURGERY

FIGURE 118.5 Postoperative magnetic resonance images (spoiled-­gradient-­echo) demonstrating the placed lesion of the lateral spinothalamic tract after a stereotactic mesencephalic tractotomy.

dolorosa (1%), while their permanent complications were limited to dysesthesias (6%) and gaze palsy (3%).18 The potential SMT-­ associated complications have to be thoroughly discussed preoperatively with the patient. Various complications such as postoperative altered mental status, dysphasia, dysarthria, paresis, or paralysis of the contralateral lower extremity, dysesthesias and/or painful dysesthesias of the affected area, paralysis of the vertical gaze, ocular convergence defects, divergent paralysis, skew deviation, and miotic pupils have been reported in the literature.12 The occurrence of contralateral leg weakness has been significantly diminished with the evolution of the SMT, while the incidence of postoperative dysesthesia seemed to be diminishing, with the employment of smaller size mesencephalic lesions. The postoperative ocular motility changes may be transient, resolving within a short period of time, or permanent. Most of the observed ocular complications are temporary and result in no significant disability. The vertical gaze paralysis is usually permanent; however, this does not cause any significant disability. 

Percutaneous Anterolateral Cordotomy ANATOMIC BACKGROUND It is well known that pain and temperature as well as tactile information are conveyed by the ascending lateral spinothalamic tract (LST), which is located in the anterolateral part of the spinal cord.1 It has been demonstrated that the LST is organized in such a way that superficial pain is conveyed in the outer part of the tract, temperature is more inward, and deep pain is even more central.1 In addition, LST is characterized by somatotopic organization with fibers from the upper extremities and upper body located antero-­medially, while fibers from the lower extremities and the lower body

are located posterolaterally.1 The sensory segmentation and the somatotopic organization of the LST allow its selective destruction, thus providing us with a surgical treatment option for patients suffering localized, medically intractable pain. Sectioning of the LST produces loss of pain and thermal sense on the opposite side of the body, beginning approximately one dermatome level below the sectioning level.1 The reticulospinal tract is located antero-­medially to the LST and its accidental lesioning, due to its close relationship, may be responsible for the observed respiratory complications in cases of bilateral cordotomy.1 Likewise, the anterior spinocerebellar tract is located laterally to the LST and its accidental injury may cause ataxia. The rest of the ascending and descending spinal tracts are usually not in close proximity to the LST. However, it has to be emphasized, that there is much variation in the size and the location of the spinal tracts (particularly of the anterior corticospinal tract), and there have been much fewer anatomic stereotactic atlas measurements of the spinal cord than that of the brain. It needs to be mentioned at this point that the continuously increasing clinical employment of diffusion tensor imaging in the cervical spinal cord may provide in the near future, more detailed knowledge of the variation of the tract topography on each patient 

HISTORICAL EVOLUTION Interruption of the LST in the anterolateral spinal cord is known as cordotomy. The introduction of this term has to be credited to Schuller, while the first open cordotomy was performed by Martin.19-­21 There are reports of open anterior cordotomies performed by Collis in 1963 and Cloward in 1964.22,23 At approximately the same time, Mullan et al. performed the first radioisotope percutaneous cervical cordotomy, which was the first stereotactic spinal

118  •  Mesencephalic Tractotomy and Anterolateral Cordotomy for Intractable Pain

procedure.24,25 In their technique, a strontium needle was introduced postero-­laterally under fluoroscopic guidance to the subarachnoid space of the anterior lateral quadrant of the cervical spinal cord, between the posterior arch of C1 and the lamina of C2.24 The radioisotope was left in place, and a lesion was gradually developed affecting the underlying LST, thus producing analgesia and pain relief.24 This first stereotactic cordotomy carried several disadvantages: the lesioning could not be controlled, the effect was gradual, and there was radiation exposure for both the patient and the performing surgeon.24 All these limitations led to the development of a radiofrequency-­ lesioning percutaneous cordotomy by Rosomoff et al. in 1965.26 They performed their procedures under local anesthesia with the patient awake. They introduced a 3-­inch lumbar puncture stylet into the anterolateral quadrant of the cervical spinal cord under fluoroscopic guidance. Then, a radiofrequency electrode was inserted through the stylet, and a lesion was placed in a fractionated manner, guided by the patient’s physiologic response.26 The occurrence of respiratory impairment as a complication in cases of percutaneous cervical cordotomies due to the accidental lesioning of the descending respiratory fibers of the adjacent reticulospinal tract,27,28 led to the development of a lower cervical cordotomy technique by Lin et al. in 1966.29 In their technique, the 3-­inch stylet was introduced diagonally through the disc, at a lower cervical level, for avoiding the upper cervical pulmonary fibers, and thus minimizing the chance of postoperative respiratory impairment.29 The procedure was performed with the patient awake, in a supine position, and under dual fluoroscopic guidance (antero-­posterior and lateral views).29 They used the lowermost cervical disc that could be seen on the lateral fluoroscopic view, and the stylet was introduced so that its tip lies in the intervertebral disc near the midline.29 Hitchcock reported his stereotactic technique for performing percutaneous cordotomies in 1972.30 He used his own stereotactic frame with the patient awake in a sitting position. Lateral and AP x-­rays were routinely obtained for verifying the midline, and a needle was inserted into the subarachnoid space through the C1–C2 interspace. Then, a small amount of emulsified Pantopaque was injected through the needle, for identifying the dentate ligament and the obex under fluoroscopy. A sharpened 0.015-­inch, insulated, stainless-­steel, electrode (with a noninsulated 2-­mm tip) was introduced through the needle into the spinal cord. Electrical stimulation studies were performed for physiologically identifying the LST (tingling sensation). After appropriately identifying the LST, a radiofrequency lesion was placed.30 Todd and his coworkers employed a similar stereotactic technique for performing percutaneous cervical cordotomies.31,32 The only modifications were that the patient was in a prone position, and the stereotactic apparatus was the Todd-­Wells frame.31,32 They routinely employed electrophysiologic stimulation studies for verifying their anatomical target before making the radiofrequency lesions.31,32 The wide application of CT imaging allowed better visualization of the spinal cord, and led to the development of CT-­guided percutaneous stereotactic cordotomy (PSC) by Kanpolat and his team in 1986.33,34 They approached their anatomic target, the LST, through a C1–C2 approach.33,34 With their technique, the obtaining of coronal and sagittal

1355

spinal cord diameter measurements was possible, while high-­ resolution cord imaging could be accomplished, giving a new dimension to cordotomy practice and making stereotactic cordotomy a valid treatment option for medically intractable pain management, which still continues to this day. 

Current Indications for Stereotactic Percutaneous Cordotomy Despite the recent advances in neurostimulation procedures and implantable neuropharmacologic delivery systems, stereotactic percutaneous cordotomy (SPC) still remains a considerable management option for patients suffering terminal cancer, pharmaco-­resistant pain.35 Ideal candidates for SPC are patients with unilateral localized intractable cancer pain, or severe localized pain of noncancerous origin.34-­37 Patients with medically intractable pain due to chest wall mesothelioma, Pancoast tumors, pulmonary malignancies, gastrointestinal malignancies, or terminal lower extremity carcinoma may be relieved by an SPC.35 Even patients with bilateral lower extremity pain of cancerous origin may be offered the option of SPC for pain relief.35 In contrast, the performance of SPC in patients with bilateral upper body pain is not advocated, mainly due to the associated high complication risk.35 The presence of severe pulmonary dysfunction, preoperative oxygen saturation of 80% or less, life expectancy less than 3 months, advanced patient age, and poor general medical condition are considered contraindications for performing SPC.35 Additionally, a patient’s neuropsychological condition (especially in patients receiving long-­term opiate alkaloid analgesics), or the existence of another dysfunctional patient-­family relationship may be relative contraindications.35 Furthermore, SPC requires an awake, emotionally stable patient who can cooperate during the procedure.35 The issue of performing SPC before or after initiating morphine therapy for pain management remains controversial.35 There is a general consensus that SPC should be considered after morphine treatment failure.38 However, Kanpolat et al. consider that SPC may be offered in good candidates even before initiating any morphine treatment.35 We prefer to consider a neuroablative procedure such as SPC only in those cases where any acceptable medical treatment has been adequately employed but has failed. 

Surgical Technique The surgical technique that we recommend is the one described and widely employed by Kanpolat and his asso­ciates.33,37,39-­43

PREOPERATIVE PREPARATION The patient remains fasted for a minimum of 8 hours before the procedure. The required dose of analgesics is parenterally administered. Antibiotics are intravenously begun on the morning of surgery, and are continued for 24 hours after surgery. Midazolam is given intravenously for preoperative sedation. The procedure is routinely performed with neuroleptanalgesia using intravenous alfentanil and propofol. The whole procedure is performed under noninvasive blood pressure and ECG monitoring, as well as pulse oximetry.

1356

Section Six  •  FUNCTIONAL NEUROSURGERY

The surgical procedure is carefully explained to the patient. The importance of the patient’s cooperation cannot be overemphasized. The patient is positioned prone on a rotating table, and the lower lumbar area is prepped and draped in the standard sterile fashion. Iohexol is administered to the patient by a lumbar puncture, and the table is repositioned to Trendelenburg position in order to adequately visualize the cervical spinal cord. If a lumbar puncture cannot be performed, contrast material may be injected through a C1–C2 puncture. 

OPERATIVE PROCEDURE After the contrast administration, the patient is transported to the CT unit where the procedure is performed under direct CT guidance. After positioning the patient on the CT table in a supine position, the head is positioned on the headrest and is flexed and fixed with a Velcro band. An upper cervical spine CT scan is obtained, covering the C1–C2 area with 1-­mm thick, gapless slices. The sagittal and the transverse diameters of the cervical cord are measured, as well as the distance between the overlying skin and the dura. Based on the obtained measurements, a cordotomy needle is inserted after infiltrating the skin with local anesthetic, and is propagated until puncturing the dura. The dura may be very thick and fibrotic, especially in cancer patients with previous radiotherapy.35 A new CT study is obtained for exactly localizing the tip of the inserted needle. The ideal position for the tip of the inserted needle is 1 mm anterior to the dentate ligament when the lumbosacral fibers of the LST are the target, or 2 to 3 mm anterior to the dentate ligament when the thoracic or cervical fibers are the target.35 After verifying the proper position of the inserted needle with a new CT scan, a straight electrode is inserted through the needle. Electrical impedance studies may be performed for verifying the exact position of the inserted electrode. The impedance measurements are approximately 100 Ω when the tip is in the cerebrospinal fluid, 300 to 400 Ω when the tip is against the cord surface, and more than 700 Ω when it is inside the cord.35 Stimulation electrophysiologic studies may also be performed for verifying the position of the electrode, although the obtained CT provides accurate localization of the inserted electrode (Fig. 118.6). The process of stimulation is begun. When little or no motor response is obtained at low frequency, and stimulation at 50 to 100 Hz produces a warm or cool thermal sensation, or less likely, pain or paresthesias on the contralateral body side, this indicates proper electrode position. The observation of sensory responses, which involve the entire contralateral body below the neck level or the hand, suggest that satisfactory analgesia below C5 dermatome will be obtained. After reaching the target point and verifying the ideal position, a radiofrequency lesion is placed by applying 60°C for 30 seconds. The patient is monitored during the whole process, and motor function, pain perception, and temperature sensation are meticulously examined. A final lesion is then placed by applying 80°C for 60 seconds, and the physiologic result is tested again. If the obtained level of analgesia is not satisfactory, a second or rarely a third lesion may be necessary.35 At the completion of the procedure, the previously inserted electrode is carefully withdrawn. The puncture site

is covered with a sterile dressing, and the patient is transported to the postanesthesia care unit, where he/she remains for approximately 1 hour and then is transferred to the ward for further observation and treatment. 

Results and Complications Sanders and Zuurmond reported their results from a series of 80 patients with medically intractable pain of malignant etiology, for which they underwent unilateral (62 patients) and bilateral (18 patients) fluoroscopically guided PSC.44 They reported initial complete pain relief in 87.1%, partial pain response in 9.7%, and no response in 3.2% of their unilateral cases. The respective percentages for the bilateral PSC group were 50%, 33.3%, and 16.7%. The observed permanent complications in the unilateral group were hemiparesis occurring in 8.1%, urinary retention in 6.5%, and new postoperative mirror-­image pain in 6.5%. The observed permanent complications in the bilateral group were hemiparesis occurring in 11.1%, urinary retention in 11.1%, and new postoperative mirror-­image pain in 5.6%. They concluded that unilateral PSC was a safe and efficacious surgical procedure for patients with intractable malignant pain, while bilateral PSC had a high complication rate in their series.44 Crul et al. presented their results after performing unilateral fluoroscopically guided PSC in 43 terminally ill cancer patients.45 They reported 95% initial good results, while satisfactory pain control was maintained until death in 69% of these patients. A quantitative measurement of the pain relief was performed by employing the Numeric Rating Scale (NRS), showing that there was an initial postoperative mean decrease from 7.2 to 1.1.45 At the end of life in their patients, the mean NRS score was 2.9. They observed transient postoperative new mirror-­image pain in 16.3%, transient muscle weakness in 4.6%, transient short-­lasting apnea in 2.3%, transient bladder dysfunction in 2.3%, and permanent ipsilateral leg paresis in 2.3% of their patients.45 Kanpolat reported his 20-­year experience in performing CT-­guided PSC in a series of 207 patients (232 procedures).35,46 The vast majority of these patients (93.2%) suffered medically intractable pain of cancerous etiology, while the remaining 6.7% had chronic, pharmaco-­resistant pain of benign etiology. The reported initial success rate was as high as 95%, while this rate was even higher among patients with cancerous pain. There was a subgroup of 12 patients in this series, who underwent bilateral PSC with great pain relief rates. In the cases of bilateral PSC, the procedures were performed at different settings 1 week apart from each other to minimize the chance of postoperative respiratory impairment (night sleep apnea), which constitutes the most serious complication. It has to be emphasized that all the reported bilateral cases suffered lower body pain. There was no mortality in this series; however, there was a 2.4% incidence of temporary motor deficits, and 2.4% occurrence of temporary ataxia.35,46 These symptoms were completely resolved within 3 weeks postoperatively, with no further consequences. Permanent dysesthesia was postoperatively developed in 1.9% of the reported cases. In the group of bilateral PSC, there was no respiratory impairment; however, there was postoperative temporary hypotension in 1.4%, and temporary urinary retention in 0.9%.35,46

118  •  Mesencephalic Tractotomy and Anterolateral Cordotomy for Intractable Pain

Dura mater

1357

Subarachnoid space Pia mater

Dentate ligament Insulation of lesioning electrode Guide needle Automatic respiratory pathway

Electrode tip

P 100 Ω

Autonomic bowel and bladder pathways

300–400 Ω

>700 Ω

Foot

nd

Ha

A FIGURE 118.6  Schematic diagram of the high cervical spinal cord, demonstrating the anatomic location, and the somatotopic organization of the lateral spinothalamic tract. Note also the exact location of the applied electrical impedances. A, Anterior; P, posterior.

Kanpolat et al. reported another series of five patients suffering intractable bilateral lower trunk and extremity pain for which they underwent bilateral CT-­guided PSC.47 Their reported success rate was 100%; however, the only observed complications were transient Horner syndrome in one of five patients (20%), and transient urinary retention in one of five patients (20%).47 Raslan reported his results from a series of 41 terminal cancer patients undergoing unilateral CT-­guided PSC.48 The initial postoperative pain relief rate was 98%, and at 6 months was 80%. Furthermore, the mean preoperative Karnofsky Performance Scale score was 55.5±6.7, while the mean postoperative score was 76.9±7.6. Similarly, the mean preoperative Visual Analog Scale score was 8.5±0.8, while the immediate postoperative was 1.2±1.0, increasing to 1.7±1.2 at 1 month after the procedure, 1.8±1.1 at 3 months, and 2.3±0.6 at 6 months. The preoperative mean sleeping time in this series

was 3.2 during a 24-­hour period, and the immediate postoperative mean increased to 7 hours, then progressively decreased to 4.8 hours 6 months after the procedure. Raslan concluded that CT-­guided PSC remains a valuable and safe surgical option for managing patients with cancer pharmaco-­resistant pain.48 In a systematic review of the pertinent literature, Raslan et al. identified 47 published papers employing percutaneous cordotomy via various surgical techniques in approximately 3600 patients, suffering from medically intractable pain of cancerous or noncancerous origin.49 In the vast majority of cases there was satisfactory pain relief after the procedure, which—especially for pain of cancerous origin—was relatively long lasting. In contrast, the cordotomy effect was shorter among patients with pain of non-­ cancerous origin, while in this group of patients cordotomy was also more frequently associated with bothersome postoperative dysesthesias.49

1358

Section Six  •  FUNCTIONAL NEUROSURGERY

In a recent study, Fonoff et al. reported a micro-­ endoscope assisted surgical technique for performing radiofrequency (RF) percutaneous cordotomies.50 They employed two trocars under fluoroscopic guidance, one for inserting a 0.9 mm micro-­endoscope, and the other for inserting the RF lesioning electrode. In this way they were able to identify the adjacent dentate ligament and the nerve entry zone while inserting the electrode into the spinal cord under direct vision, thus avoiding any surface cord vessels. They presented their results from a prospective series of 24 patients suffering from thorax or lower body pain of cancerous origin. They found that all their patients responded to the performed percutaneous cordotomy, obtaining satisfactory pain control. They did not encounter any complications in their series.50 

Future of Neuroablative Stereotactic Pain Procedures The introduction of high-­magnetic-­field MRI units in the daily neurosurgical practice (3 or 7 Tesla) allow better visualization and delineation of the mesencephalic and high cervical cord anatomy, the identification of the ascending and descending neuronal pathways, and more accurate, sub-­ millimetric definition of their anatomic relationships. Moreover, the emergence of newer MRI techniques, such as diffusion tensor imaging, may provide better visualization of the lateral spinothalamic, corticospinal, and reticulospinal tracts.51 These recent imaging advances, along with the designing and manufacturing of more precise frame-­based or frame-­less stereotactic devices, may further increase the accuracy, efficacy, and safety of SMT and PSC. 

Conclusions Despite the advances of analgesic pharmacology and the wide application of neurostimulation and implantable analgesic medication delivery systems, SMT and PSC remain valid treatment options for cancer patients with intractable pain. The high efficacy and the low incidence of procedure-­ associated complications, as depicted in the results of the newer clinical series, make SMT or PSC the treatment of choice for carefully selected patients with severe pain of malignant etiology for whom any other medical or even surgical treatment has failed. The employment of newer high-­ resolution MRI techniques, and the performance of these stereotactic pain procedures in specialized centers with expertise in stereotactic and functional neurosurgery, may further increase their efficacy and safety, and may strengthen their role in the management of end-­stage cancer patients with medically refractory pain. ACKNOWLEDGMENTS The authors wish to thank Mr. Mike Jensen for his valuable assistance with the medical illustrations of this chapter. KEY REFERENCES

Afifi AK, Bergman RA. Functional Neuroanatomy. New York: Lange Medical Books/McGraw-­Hill; 2005.

Amano K, Kitamura K, Sano K, Sekino H. Relief of intractable pain for neurosurgical point of view with reference to present limits and clinical indications. A review of 100 cases. Neurol Med Chir. 1976;16:141–153. Bailey RA, Glees P, Oppenheimer DR. Midbrain tractotomy: a surgical and clinical report, with observations an ascending and descending tract degeneration. Eur Neurol. 1954;127:316–335. Crul BJP, Blok LM, Egmond JV, et al. The present role of percutaneous cervical cordotomy for the treatment of cancer pain. J Headache Pain. 2005;6:24–29. Dogliotti M. First surgical sections, in man, of the lemniscus lateralis (pain-­temperature path) at the brain stem, for the treatment of diffuse rebellious pain. Curr Res Anesth. 1938;17:143–145. Drake CG, McKenzie KG. Mesencephalic tractotomy for pain. Experience with six cases. J Neurosurg. 1953;10:457–462. Fonoff ET, Lopez WO, de Oliveira YS, Teixeira MJ. Micro-­endoscopy guided percutaneous cordotomy for intractable pain: a case series of 24 patients. J Neurosurg. 2016;124:389–396. Fountas KN, Lane FJ, Jenkins PD, Smith JR. MR-­based stereotactic mesencephalic tractotomy. Stereotact Funct Neurosurg. 2004;82:230–234. Frank F, Fabrizi AP, Gaist G. Tractotomy in the treatment of chronic cancer pain. Acta Neurochir. 1989;99:38–40. Gildenberg PL. Spinal stereotaxic procedures. In: Schaltenbrand G, Walker AE, eds. Stereotaxy of the Human Brain. Stuttgart: Verlag; 1982:469–474. Kanpolat Y, Akyar S, Caglar S. Diametral measurements of the upper spinal cord for Stereotactic pain procedures; experimental and clinical study. Surg Neurol. 1995;43:478–483. Kanpolat Y, CaglarUgur H, Ayten M, et al. Computed tomography-­ guided percutaneous cordotomy for intractable pain in malignancy. Neurosurgery. 2009;64:187–194. Kanpolat Y, Deda H, Akyar S, et al. CT-­guided percutaneous cordotomy. Acta Neurochir Suppl (Wien). 1989;46:67–68. Kanpolat Y, Savas A, Caglar S, et al. Computerized tomography-­ guided percutaneous bilateral selective cordotomy. Neurosurg Focus. 1997;15(2):e4. Kanpolat Y. Percutaneous destructive pain procedures on the upper spinal cord and brain stem in cancer pain: CT-­guided techniques, indications and results. Adv Tech Stand Neurosurg. 2007;32:147–173. Kanpolat Y. The surgical treatment of chronic pain: destructive therapies in the spinal cord. Neurosurg Clin North Am. 2004;15:307–317. Lin PM, Gildenberg PL, Polakoff PP. An anterior approach to percutaneous lower cervical cordotomy. J Neurosurg. 1966;25:553–560. Nashold BS. Brainstem stereotaxic procedures. In: Schaltenbrand G, Walker AE, eds. Stereotaxy of the Human Brain. Stuttgart: Verlag; 1982:475–483. Orthner H, Roeder F. Further clinical and anatomical experiences with stereotactic operations for relief of pain. Confin Neurol. 1966;27:418–430. Raslan A. Percutaneous computed tomography-­guided radiofrequency ablation of upper spinal cord pain pathways for cancer-­related pain. Neurosurgery. 2008;62:226–234. Raslan AM, Cetas JS, McCartney S, Burchiel KJ. Destructive procedures foe control of cancer pain: the case for cordotomy. J Neurosurg. 2011;114:155–170. Sanders M, Zuurmond W. Safety of unilateral and bilateral percutaneous cervical cordotomy in 80 terminally ill cancer patients. J Clin Oncol. 1995;13:1509–1512. Shieff C, Nashold BS. Stereotactic mesencephalic tractotomy for thalamic pain. Neurol Res. 1987;9:101–104. Shieff C, Nashold BS. Thalamic pain and stereotactic mesencephalotomy. Acta Neurochir Suppl. 1988;42:239–242. Spiegel EA, Wycis HT. Mesencephalothalamotomy for Relief of Pain: in Anniversary Volume of O. Petzl. Vienna: Wagner; 1948:437–443. Torvik A. Sensory, motor, and reflex changes in two cases of intractable pain after stereotactic mesencephalic tractotomy. J Neurol Neurosurg Psychiatry. 1959;22:299–305. Wycis HT, Spiegel EA. Long-­range results in the treatment of intractable pain by stereotaxic midbrain surgery. J Neurosurg. 1962;9:101–107. Numbered references appear on Expert Consult.

REFERENCES

1. Afifi AK, Bergman RA. Functional Neuroanat. New York: Lange Medical Books/McGraw-­Hill; 2005. 2. Dogliotti M. First surgical sections, in man, of the lemniscus lateralis (pain-­temperature path) at the brain stem, for the treatment of diffuse rebellious pain. Curr Res Anesth. 1938;17:143–145. 3. Bailey RA, Glees P, Oppenheimer DR. Midbrain tractotomy: a surgical and clinical report, with observations an ascending and descending tract degeneration. Eur Neurol. 1954;127:316–335. 4. Drake CG, McKenzie KG. Mesencephalic tractotomy for pain. Experience with six cases. J Neurosurg. 1953;10:457–462. 5. Wycis HT, Spiegel EA. Long-­ range results in the treatment of intractable pain by stereotaxic midbrain surgery. J Neurosurg. 1962;9:101–107. 6. Spiegel EA, Wycis HT. Pain: mesencephalotomy and mecencephalo-­ thalamotomy. In: Spiegel EA, Wycis HT, eds. Stereoencephalotomy. Vol. 2. New York: Grune and Stratton; 1962:205–244. 7. Spiegel EA, Wycis HT. Mesencephalothalamotomy for Relief of Pain. Anniversary Volume of O. Petzl. Vienna: Wagner; 1948:437–443. 8. Torvik A. Sensory, motor, and reflex changes in two cases of intractable pain after stereotactic mesencephalic tractotomy. J Neurol Neurosurg Psychiatry. 1959;22:299–305. 9. Orthner H, Roeder F. Further clinical and anatomical experiences with stereotactic operations for relief of pain. Confin Neurol. 1966;27:418–430. 10. Mazars G, Merienne L, Cioloca C. Etatactuel de la chirurgie de la douler. Neurochirurgie. 1976;22:53–61. 11. Amano K, Kitamura K, Sano K, Sekino H. Relief of intractable pain for neurosurgical point of view with reference to present limits and clinical indications. A review of 100 cases. Neurol Med Chir. 1976;16:141–153. 12. Nashold BS. Brainstem stereotaxic procedures. In: Schaltenbrand G, Walker AE, eds. Stereotaxy of the Human Brain. Stuttgart: Verlag; 1982:475–483. 13. Nashold BS, Wilson WP, Slaughter DG. Sensations evoked by stimulation in the midbrain of man. J Neurosurg. 1969;3:14–24. 14. Shieff C, Nashold BS. Stereotactic mesencephalic tractotomy for thalamic pain. Neurol Res. 1987;9:101–104. 15. Shieff C, Nashold BS. Thalamic pain and stereotactic mesencephalotomy. Acta Neurochir Suppl. 1988;42:239–242. 16. Fountas KN, Lane FJ, Jenkins PD, Smith JR. MR-­based stereotactic mesencephalic tractotomy. Stereotact Funct Neurosurg. 2004;82:230– 234. 17. Whisler WW, Voris HC. Mesencephalotomy for intractable pain due to malignant disease. Appl Neurophysiol. 1978;41:52–56. 18. Frank F, Fabrizi AP, Gaist G. Tractotomy in the treatment of chronic cancer pain. Acta Neurochir (Wien). 1989;99:38–40. 19. Kanpolat Y. The surgical treatment of chronic pain: destructive therapies in the spinal cord. Neurosurg Clin North Am. 2004;15:307– 317. 20. Schuller A. Uber operative Durchtrennung der ruckenmarksstrange (Chordotomie). Wien Med Wschr. 1910;60:2291. 21. Spiller WG, Martin E. The treatment of persistent pain of organic origin in the lower part of the body by division of the antero-­lateral column of the spinal cord. JAMA. 1912;58:1489–1490. 22. Collis Jr JS. Anterolateral cordotomy by an anterior approach: report of a case. J Neurosurg. 1963;20:445–446. 23. Cloward RB. Cervical cordotomy by an anterior approach: report of a case. J Neurosurg. 1925;21:1964. 24. Mullan S. Percutaneous cordotomy. J Neurosurg. 1971;35:360. 25. Gildenberg PL. Spinal stereotaxic procedures. In: Schaltenbrand G, Walker AE, eds. Stereotaxy of the Human Brain. Stuttgart: Verlag; 1982:469–474. 26. Rosomoff HL, Carroll F, Brown J, et al. Percutaneous radiofrequency cervical cordotomy technique. J Neurosurg. 1965;23:639– 644. 27. Fox JL. Localization of the respiratory motor pathway in the upper cervical spinal cord following percutaneous cordotomy. Neurology. 1969;19:1115–1118.

28. Rosomoff HL, Kringer AJ, Kupman AS. Effects of percutaneous cervical cordotomy on pulmonary function. J Neurosurg. 1969;31:620–627. 29. Lin PM, Gildenberg PL, Polakoff PP. An anterior approach to percutaneous lower cervical cordotomy. J Neurosurg. 1966;25:553– 560. 30. Hitchcock ER. Stereotaxis of the spinal cord. Confin Neurol. 1972;34:299–310. 31. Crue BL, Todd EM, Carregal EJA. Posterior approach for high cervical percutaneous radiofrequency cordotomy. Confin Neurol. 1968;30:41–52. 32. Todd EM, Crue BL, Carregal EJA. Posterior percutaneous tractotomy and cordotomy. Confin Neurol. 1969;31:106–115. 33. Kanpolat Y, Atalag M, Deda H, et al. CT-­guided extralemniscal myelotomy. Acta Neurochir (Wien). 1988;91:151–152. 34. Kanpolat Y, Deda H, Akyar S, et al. CT-­guided percutaneous cordotomy. Acta Neurochir Suppl (Wien). 1989;46:67–68. 35. Kanpolat Y. Percutaneous destructive pain procedures on the upper spinal cord and brain stem in cancer pain: CT-­guided techniques, indications and results. Adv Tech Stand Neurosurg. 2007;32:147– 173. 36. Kanpolat Y, Caglar S, Akyar S, et al. CT-­ guided pain procedures for intractable pain in malignancy. Acta Neurochir Suppl. 1995;64:88–91. 37. Kanpolat Y. Cordotomy for pain. In: Schulder M, ed. Handbook of Stereotactic and Functional Neurosurgery. New York: Markel & Dekker; 2003:459–472. 38. Gybels LM. Indications for the use of neurosurgical techniques in pain control. In: Bond MR, Charlton LE, Wolf J, eds. Proceedings of the Sixth World Congress on Pain. Amsterdam: Elsevier; 1995:475. 39. Kanpolat Y, Deda H, Akyar S, et al. CT-­guided trigeminal tractotomy. Acta Neurochir (Wien). 1989;100:112–114. 40. Kanpolat Y. Percutaneous cordotomy, tractotomy and midline myelotomy, minimally invasive stereotactic pain procedures. SeminNeurosurg. 2004;2/3:203–220. 41. Kanpolat Y. Percutaneous stereotactic pain procedures: percutaneous cordotomy, extralemniscal myelotomy, trigeminal tractotomy-­ nucleotomy. In: Burchiel K, ed. Surgical Management of Pain. Stuttgart: Thieme; 2002:745–762. 42. Kanpolat Y. Percutaneous cervical cordotomy for persistent pain. In: Gildenberg PL, Tasker RR, eds. Textbook of Stereotactic and Functional Neurosurgery. New York: McGraw-­ Hill; 1998:1485– 1490. 43. Kanpolat Y, Akyar S, Caglar S. Diametral measurements of the upper spinal cord for Stereotactic pain procedures; experimental and clinical study. Surg Neurol. 1995;43:478–483. 44. Sanders M, Zuurmond W. Safety of unilateral and bilateral percutaneous cervical cordotomy in 80 terminally ill cancer patients. J Clin Oncol. 1995;13:1509–1512. 45. Crul BJP, Blok LM, Egmond JV, et al. The present role of percutaneous cervical cordotomy for the treatment of cancer pain. J Headache Pain. 2005;6:24–29. 46. Kanpolat Y, CaglarUgur H, Ayten M, et al. Computed tomography–guided percutaneous cordotomy for intractable pain in malignancy. Neurosurgery. 2009;64:187–194. 47. Kanpolat Y, Savas A, Caglar S, et al. Computerized tomography-­ guided percutaneous bilateral selective cordotomy. Neurosurg Focus. 1997;15(2):e4. 48. Raslan A. Percutaneous computed tomography-­guided radiofrequency ablation of upper spinal cord pain pathways for cancer-­ related pain. Neurosurgery. 2008;62:226–234. 49. Raslan AM, Cetas JS, McCartney S, Burchiel KJ. Destructive procedures foe control of cancer pain: the case for cordotomy. J Neurosurg. 2011;114:155–170. 50. Fonoff ET, Lopez WO, de Oliveira YS, Teixeira MJ. Micro-­ endoscopy guided percutaneous cordotomy for intractable pain: a case series of 24 patients. J Neurosurg. 2016;124:389–396. 51. Ciccarelli O, Toosy AT, Parker GJ, et al. Diffusion tractography based group mapping of major white-­matter pathways in the human brain. Neuroimage. 2003;19:1545–1555.

1358.e1

CHAPTER 119

Spinal Cord Stimulation for Chronic Pain RICHARD B. NORTH  •  BENGT LINDEROTH

A theory of pain transmission published in 19651 inspired researchers to develop a reversible, nondestructive pain therapy that relied on equipment adapted from cardiac pacemaker technology to deliver electrical stimulation to the spinal cord. The initial results of this therapy, now known as spinal cord stimulation (SCS), were inconsistent, but many patients benefited dramatically. During the intervening decades, refinements in SCS techniques, stimulation patterns, equipment, and patient selection criteria as well as new targets (Table 119.1) have led to clinical results that continue to improve.

Background: The Gate Control Concept Melzack and Wall’s gate control theory provided a theoretical rationale for the use of electrical stimulation in the management of pain.1 The theory proposes that a neuronal “gate” controls the transmission of pain signals from the dorsal horn of the spinal cord to the brain. An excess of small-­fiber afferent input opens the gate, and a dominance of large-­fiber afferent activity closes it. The gate concept is, in some aspects, a bit similar to Head and Holmes’ 1911 proposal that parallel “epicritic and protopathic” input systems govern sensory influx.2 This hypothesis provided the physiologic basis for Gabriel Mazars’ therapeutic trials with sensory thalamic stimulation in Paris beginning in the 1960s, which were the first modern attempts to treat severe neuropathic pain with electric stimulation.3,4 Because large fibers are more susceptible than small fibers to electrical depolarization, it seemed reasonable to attempt to close the gate and stop pain transmission with low-­ amplitude stimulation that would selectively recruit large-­fiber activity in a mixed population of nerves. Electrical stimulation of mixed peripheral nerves can achieve this effect,5 but stimulation of peripheral nerves at an amplitude close to that required for a therapeutic effect can cause unwanted motor effects. In addition, pain generally involves multiple peripheral nerves. Therefore, investigators decided to apply electrical stimulation to the spinal cord, where they could recruit large fiber primary afferents from multiple segments conveniently isolated in the posterior columns. As expected, antidromic activation of these primary afferents, whose collateral processes extend into the dorsal horn, yielded a wide area of paresthesia with, in successful cases, ensuing pain relief. The electrical stimulation techniques

that grew out of the gate control theory has been succeeded, but the theory itself remains controversial. One reason is that activation of peripheral large fibers can result in increased pain (hyperalgesia or allodynia) in some pathologic circumstances.6 Thus, peripheral nerve stimulation or SCS might relieve pain by blocking the conduction of primary afferents at the branch points of dorsal column fibers and their collaterals.6 The mechanism of action of SCS, however, cannot depend solely on blocking conduction (e.g., by impulse collision) because electrical stimulation does not inhibit all types of pain,7 and therapeutic SCS does not normally evoke the pain that would occur if SCS also activated small-­diameter, high-­threshold fibers in the spinothalamic tracts. Dorsal column activation is more successful than ventral stimulation, which is closer to the spinothalamic tracts.8 Until the first decade of the 21st century, SCS was generally applied with frequencies between 30 and 100 Hz; pulse widths between 150 and 500 μs, and an amplitude to produce comfortable paresthesia covering the painful area (conventional SCS) (Fig. 119.1). In clinical application for chronic pain, a major technical goal was to place the electrodes over a “sweet spot” where stimulation-­induced paresthesia covered the area(s) of pain well below the discomfort threshold. Notwithstanding predictions from the gate theory, conventional SCS has proved to be less effective for treating acute nociceptive pain conditions than for treating chronic neuropathic pain of peripheral origin, which has become its principal indication.35 As the 20th century drew to a close, we learned that SCS could also alleviate certain types of ischemic pain states, such as peripheral arterial occlusive disease (PAOD), vasospastic conditions, and therapy-­resistant angina pectoris (Fig. 119.2). We now understand that mechanisms of pain relief with SCS differ fundamentally between neuropathic and ischemic/vasculopathic pain conditions (e.g., in ischemic pain, the primary effect of SCS appears to be alleviation of tissue ischemia, and pain reduction is a secondary effect).

NEW SPINAL CORD STIMULATION ALGORITHMS During the past decade, new SCS approaches that are not based on the gate control theory have been launched: high-­ frequency stimulation (HF SCS): with frequencies up to 10,000 Hz (10 KHz) (75–86) and burst SCS: with bursts of five pulses (internal frequency 500 Hz) applied with a frequency of 40 Hz (89–95) (see Fig. 119.1). At the same time,

1359

1360

Section Six  •  FUNCTIONAL NEUROSURGERY

TABLE 119.1  Chronic Pain Patient Selection Criteria 1. An objective basis for the patient’s pain (with a specific diagnosis). The results of physical examinations and diagnostic imaging studies in patients with failed back surgery syndrome, for example, should be consistent with the reported distribution of radiating pain, and these findings should predominate over functional, nonphysiologic signs.268 2. Spinal cord stimulation (SCS) should be a late resort. Reasonable alternative treatments should be exhausted or comparatively unacceptable (e.g., repeated reconstructive spine surgery). 3. A multidisciplinary evaluation, with specific attention to psychological issues, rules out any unresolved major psychiatric problem or personality disorder, significant issues of secondary gain, or major drug habituation problem. 4. The technical feasibility of overlapping pain with paresthesia and the resulting relief of pain is demonstrated through a screening trial. 5. No coagulopathy (that cannot be reversed during implantation), ulcers close to implantation sites, or chronic septicemia. 6. The patient must be able to control the device. 7. Patients with on-­demand pacemaker, defibrillators, or the need for magnetic resonance imaging (MRI) require special attention. MRI in patients with an SCS system is feasible for some “MRI contingent” systems, some areas of imaging (e.g., brain) and some MRI field strengths.

Tonic

A Burst

B HF 10

C

From Pope, Falowski & Deer 2015

FIGURE 119.1  During the past decade, new spinal cord stimulation (SCS) waveforms have been introduced, supplementing or replacing conventional tonic stimulation (A). Among them are Burst SCS: with groups of five pulses (internal frequency 500 Hz) applied with a frequency of 40 Hz (B) and high-­frequency stimulation (HF SCS): with frequencies up to 10,000 Hz (10 KHz) (C). (From Pope JE, Falowski S, Deer TR. Advanced waveforms and frequency with spinal cord stimulation: burst and high-­frequency energy delivery. Expert Rev Med Devices. 2015;12[4]:431–437.)

additional peripheral targets have been identified: not only discrete peripheral nerves, but also “nerve field” stimulation and stimulation of the dorsal root ganglia. These targets outside the spinal cord per se will not be discussed in this chapter. At present much less is known about the physiological mechanisms underlying the effects of these new techniques as compared with conventional SCS. HF SCS and burst SCS are said to provide effective treatment for nociceptive as well as neuropathic components of pain; for example, the

low back pain that occurs in patients with failed back surgery syndrome (FBSS), which is one of the most common indications for conventional SCS therapy. In the following sections we will discuss (1) conventional SCS (with the electric parameters commonly used 1970 to 2010), (2) high-­frequency SCS, (3) burst SCS, and (4) SCS with slightly moderated parameters to increase transmission of the electric charge from the lead to the neural tissue without side effects. 

MECHANISMS OF ACTION Conventional Spinal Cord Stimulation for Neuropathic Pain In neuropathic pain states, activation of peripheral nerve fibers increases the sensitivity and activity of wide dynamic range neurons in the superficial laminae of the corresponding dorsal horns, which in turn causes hyperalgesia (increased sensitivity to pain) and/or allodynia (normally nonpainful stimuli cause pain). In rat models of neuropathy that employ stimulation parameters similar to those used in humans, SCS effectively suppresses this heightened activity and relieves tactile hypersensitivity as reflected by responses to innocuous stimuli (similar to clinical allodynia).9 In a study that sought to determine if SCS suppresses long-­term potentiation of wide dynamic range dorsal horn neurons, SCS gradually reduced the C-­fiber response to the baseline level. Aβ-­fibers, on the other hand, were not potentiated by the conditioning stimulus or affected by SCS.10 This indication that SCS affects C-­fiber responses is noteworthy because the findings of previous studies supported the view that SCS primarily influences Aβ-­fibers. Investigators have used finite-­ element computer techniques to model the electrical fields produced in the spinal cord by SCS.11–13 These models reveal distributions of current and voltage that agree with measurements in cadaver and primate spinal cords.14 The models and measurements predict that an electrode’s longitudinal position is the most important factor in achieving the desired segmental effect (fibers decrease in diameter as they ascend the fasciculus gracilis),15 that bipolar stimulation with contacts 6 to 8 mm apart provide the greatest selectivity for longitudinal midline fibers, and that the electrical field between two cathodes that bracket the midline does not sum constructively in the midline. Clinical experience confirms that the correct position and spacing of SCS electrodes is essential and that instead of expanding the area of paresthesia, positioning electrodes more cephalad than the target area commonly elicits unwanted local segmental effects.16 Psychophysical studies have found that stimulation induces a subtle loss of normal sensation in SCS patients but does not affect acute pain sensibility to an extent that could lead to undesirable side effects, such as Charcot joints.17,18 Side effects increase with increases in stimulation amplitude and in recruitment of nerve fibers; psychophysical studies in individual patients document this with quantitative measures of stimulation adjusted over the range of amplitudes from perception to motor threshold.19 To explain the sustained pain relief (often lasting from 1 to 3 hours) that patients experience following a 30-­minute period of SCS, investigators hypothesized that SCS affects the release of neurotransmitters in the dorsal horn and brain.20

119  •  Spinal Cord Stimulation for Chronic Pain

1361

Effect of SCS related to stimulation site along neuro-axis

SCS Cervical

Target Organ C2

1

1. Bronchodilation

2

2. Peripheral vasodilation

3 High Thoracic

3. Stabilization of ICNS Reduction of Ischemia and Pain Decreased Infarct Size

T1

4

Middle Thoracic Low Thoracic

Organ Response

5

4. Decreased Colonic Spasms Pain Reduction 5. Peripheral vasodilation lower limbs

L1

6 6. Decreased Bladder Spasticity Increased volume tolerance

Sacral S1

FIGURE 119.2  This figure illustrates how SCS applied to different regions of the spinal cord, besides the effect on neuropathic pain, also induces changes in the function of different target organs via local autonomic activity changes, dorsal root reflexes and viscero-somatic reflexes. The numbers on the lightning bolts refer to numbers on the organ responses to the right of the figure. (Adapted from Linderoth, Foreman, Meyerson, Chapter 138, in Lozano AM, et al., Textbook of sterotactic and functional neurosurgery, Ed 2. Springer, 2009.)

This led to several lines of investigation, which revealed that SCS changes the concentration of neurotransmitters and their metabolites in cerebrospinal fluid8,21; administration of high doses of opioid antagonists, such as naloxone, does not affect the relief of pain achieved by SCS22,23; and both SCS and administration of γ-­aminobutyric acid (GABA) agonists to neuropathic rats suppresses the allodynia that occurs from peripheral nerve lesions.24,25 SCS induces GABA release in the dorsal horn,26 and the pain-­relieving effect of SCS depends on activation of the GABA-­B receptor.24,25 In fact, for a period of time SCS inhibits the pathologic response properties of dorsal horn neurons often observed in allodynic rats after peripheral nerve injury (e.g., elevated firing frequency of wide dynamic range neurons, presence of after-­ discharge),9 conceivably because of an electrically induced increase in GABAergic activity.27 SCS likely prompts the release of a multitude of as-­yet-­ unidentified transmitters and neuromodulators in the dorsal horn as well as supraspinally.7,26,28,29 In addition to GABA, animal and human studies indicate that SCS releases substance P, serotonin, glycine, adenosine, and noradrenaline in the dorsal horn.20,21,25 The resultant beneficial effect likely depends on a complicated interaction among several substances.30 Studies also indicate that the cholinergic system is involved in the SCS effect in painful neuropathy via activation of the muscarinic M4 receptors.31,32 Descending inhibition via a brain stem loop was proposed in the 1980s as the principal mechanism by some research groups.38 Our early studies indicated that only a minor part

(800 Hz) SCS might result in uncomfortable experiences as soon as the amplitude is beyond the sensory (paresthetic) threshold.104 The pulse widths used, both in the clinic and in animal studies, are necessarily very short (around 24 to 30 microseconds), and the amplitude is set so low that the patient does not feel anything. With such current parameters, one critical factor might be the amount of electric charge transmitted per unit time to the nervous tissue. Studies comparing monophasic and biphasic SCS with different pulse widths82 indicate this. Preclinical studies as yet published only as conference abstracts83,84 focusing on dorsal horn modulation with high-­frequency SCS (2 to 10 kHz) have yielded interesting results. Application of 10 kHz SCS at a low amplitude (20% of motor threshold) in the rat through conductive agar from needle electrodes directly over the L5 segment demonstrated no evidence of either DC fiber conduction block or activation. Stimulation for several hours did not induce asynchronous firing in myelinated primary sensory neurons. In different pain models, as much as 135 minutes of SCS at very low amplitudes: 20% of motor threshold, which was verified to be subthreshold for activation of A-­β projection neurons, induced late inhibition of A-­δ and C-­fibers, which occurred after 45 to 90 minutes both in superficial and in deeper laminae (lam. IV to V).85 The critical issues here seem to be the very low amplitude, high frequency: 10 kHz, very short pulse width resulting in the marked latency for the appearance of the effects. It is expected that more data from these experiments will be published in the near future.83,85 Based on the few published basic studies available so far and the demonstration of some effect both with mono and biphasic SCS pulses77,78 and the absence of numbness in clinical cases (Van Buyten and others; personal comm.) as well as the demonstration of no effect on the impulse traffic in the DCs,77 the putative mechanisms so far are considered

to be most likely segmental. This is also supported by the McMahon et al. observations discussed above. Thus, while the definitive mechanisms of high-­ frequency SCS are not yet known, the direct effect of the low intensity, kHz electrical field applied to the dorsal surface of the SC acting at a population of neurons in the DH might be responsible for the beneficial effects of 10 kHz paresthesia-­free SCS with a considerable latency, as observed clinically. Several reviews86 summarize both hypotheses about HF mechanisms and the clinical studies up to 2018. 

Burst Spinal Cord Stimulation for Neuropathic/Nociceptive Pain The principle of burst stimulation advanced by De Ridder is based upon his work with cortical stimulation. The concept is not new; in the 1970s, burst transcutaneous electrical nerve stimulation (TENS) was launched as a variant to steady-­frequency TENS.87 At that time, hypotheses about the mechanisms for burst and high-­frequency TENS were discussed; burst TENS was generally applied for nociceptive pain, and mediation by release of endogenous opioids was inferred as a possible mechanism, notwithstanding evidence to the contrary.22,23 Recent animal studies indicate that the antinociceptive effect of low-­frequency stimulation (SCS) might depend on opioid mechanisms.88 Burst SCS was presented as a stimulation mode that would be effective for axial lumbosacral pain as well as for neuropathic pain.89,90 De Ridder argues that bursting or irregular firing is more like normal nerve activity than is tonic stimulation, as delivered in conventional SCS. Burst stimulation is said to require less temporal integration to activate neurons and to be more effective as “a wake-­up call to the brain.”91 De Ridder et al. have, on the basis of “source localized EEG” investigations of patients with burst SCS, advanced the idea that burst SCS could activate cortical areas (the dorsal anterior cingulate and the dorsolateral prefrontal cortex) involved in the modulation of pain perception (Fig.119.5).90 A study by Tang et al.92 demonstrates that there is no activation of the dorsal column Aβ fibers (as measured by recordings from the gracile nucleus in the brain stem) with burst SCS, whereas conventional SCS produces a powerful increase in firing. Another finding is that the efficacy of burst stimulation seems to relate to the electric charge per burst—at least in a rat model of neuropathic pain.93 Other studies report that burst SCS increases GABA levels in peripheral blood of the rat and does not rely on activation of GABA-­B receptors,94 as has been claimed for traditional SCS (e.g.,95–97; Ultenius et al. 2012). De Ridder and Vanneste presented data from five patients undergoing tonic, burst, and sham stimulation.199 In a source-­ localized electroencephalogram subtraction and conjunction analysis they showed that burst and tonic stimulation share activation of some cortical areas such as the pregenual anterior cingulate cortex, while only burst SCS reduces the connectivity between the dorsal anterior cingulate and the parahippocampal cortices. They hypothesize that burst stimulation must modulate the medial pain pathway directly by actions onto C-­fibers ending in lamina 1 connecting to the dorsomedial nucleus of the thalamus and hence to the dorsal

119  •  Spinal Cord Stimulation for Chronic Pain

anterior cingulum (see Fig 119.5). A further hypothesis presented here—linking it to the high-­frequency tonic stimulation hypotheses—is that burst stimulation could disrupt synchronous firing of high threshold fibers, thus inhibiting activation directly related to pain perception. A functional magnetic resonance imaging study98 demonstrated that conventional SCS predominantly modulates lateral pain pathways as shown by changes in blood oxygen levels in the somatosensory cortices; however, research on eventual participation of supraspinal circuitry in burst SCS is ongoing, and the stimulation paradigm itself might be subject to change in the near future. 

Moderate Adaptation of Spinal Cord Stimulation Parameters Most modern pulse generators can generate stimulation frequencies up to, if not above, 1000 Hz and pulse widths up to 1000 microseconds. Higher frequencies than typically used for SCS have been available for many years but have used infrequently; for example, as high cervical SCS for torticollis.203 A common denominator of the new SCS algorithms is that they are applied with a relatively low amplitude and/or pulse width, so that the subject does not experience paresthesia or other cue as to whether active stimulation or placebo SCS is delivered. This admits the possibility of blinded, controlled trials. A few studies show that conventional tonic SCS with subparesthetic amplitude might also be effective,99–101 but so far it has not convincingly been demonstrated that the outcomes of this type of SCS are equal to those of conventional paresthetic stimulation.

1365

By increasing the frequency and/or the pulse width but keeping the amplitude so low that stimulation is not felt, larger amounts of electric charge can be delivered to neural tissue without discomfort or damage (Fig. 119.6).102 It has been demonstrated convincingly in rodent experiments that subsensory SCS can exert clear effects on models of neuropathic pain.77,82 These studies also demonstrate that moderately increased frequencies (e.g., 1000 Hz) can be as effective at the subsensory level as 10 kHz SCS. Such changes in SCS parameters have been labeled “High-­Density Stimulation” (HD) referring to the fact that pulse density (i.e., the duty cycle) can be increased from 1% to 2% up to 20% to 25% while remaining below the sensory threshold (Fig. 119.7). Overall electric charge transfer is comparable to that of HF SCS and burst SCS. In fact, an electrophysiological animal study103 demonstrated that compared with typical clinical SCS parameters (200 microseconds/50 Hz), 1 kHz SCS suppressed responses of more spinal neurons and/or demonstrated longer persisting suppressive effects. Thus SCS at 1 kHz might equal or exceed 10 kHz in effectiveness, as was reported by Shechter et al. in 2013 and Thomson et al. in 2018. High-­frequency SCS at amplitudes above sensory threshold (beginning above 800 Hz) generates an uncomfortable sensation rather than pleasant “tingling” paresthesia.104

SPINAL CORD STIMULATION DEVICES Electrode Placement and Design The first applications of SCS involved high thoracic electrode placement in an attempt to treat pain in all caudal segments105; however, this strategy commonly caused excessive, uncomfortable radicular effects before the desired segments could be recruited. When it became apparent that

FIGURE 119.5  Present “working hypotheses” for mechanisms behind effects of burst stimulation of the spinal cord (presented by De Ridder & Vanneste in several articles e.g., Neuromodulation Nov 2015) during the last decade: Burst SCS is hypothesized to especially modulate the activation of the medial (affective/attentional) pathway (in the middle of the figure (encircled). On the contrary the anterior spinothalamic pathway mainly activates the lateral (sensory) pathway (left part of figure). The right figure illustrates some of the descending pathways via the PAG and the RVM. (Adapted from Linderoth & Foreman 2017.)

1366

Section Six  •  FUNCTIONAL NEUROSURGERY

stimulation paresthesia should overlap the distribution of pain, clinicians adjusted the placement of electrodes to achieve this effect.106 For example, low thoracic electrode placement (T9 to T12) is most effective in the treatment of persistent low back and lower extremity pain following spine surgery (FBSS).107 In the late 1960s and early 1970s, SCS electrodes were two-­dimensional and required a laminectomy or laminotomy for introduction into the epidural, endodural, or subarachnoid space.108–110 Use of these electrodes was problematic because clinicians had no way of determining the ideal spinal level for electrode placement in any given patient and because laminotomy under local anesthesia limits longitudinal access. Furthermore, even when electrodes are placed so that paresthesia overlaps the area of pain, not all patients report pain relief. For these reasons, test stimulation with a temporary electrode is desirable. Accordingly, in the 1970s, investigators111–114 developed percutaneous techniques using a Tuohy needle to insert temporary catheter-­ type electrodes for a screening trial to establish the best level for electrode placement and to determine if SCS had the desired analgesic effect. Clinicians soon applied these percutaneous techniques to the implantation of electrodes for chronic use, thus avoiding the need for laminectomy.115,116 However, the use of a percutaneous technique to place multiple individual electrodes and achieve bipolar stimulation increased the likelihood of electrode migration, compromising stimulation, thus reducing or eliminating pain relief, and requiring surgical revision. In the early 1980s, in response to this problem, electrode manufacturers introduced percutaneous electrodes with arrays of contacts. If such an electrode migrates slightly, its implanted pulse generator (IPG) can be reprogrammed with a different selection of stimulating anodes and cathodes to reestablish appropriate paresthesia. This noninvasive postoperative adjustment can be made with the patient in the upright or supine position (in which the device is ordinarily used, as opposed to the prone position in which it is usually implanted). Multicontact programmable systems rarely require surgical revision, and this development has led to significantly improved long-­term clinical results.117–119 New electrode designs based on computer models of SCS have facilitated steering paresthesia to cover the painful area.120 Clinicians are also improving results by refining the method of anchoring percutaneous electrodes.121 Despite these improvements in the use of percutaneous electrodes, properly placed laminectomy electrodes offer advantages. For example, a prospective randomized, controlled technical comparison involving 24 patients—half of whom received a four-­contact percutaneous electrode and half a four-­ contact insulated laminectomy electrode122— yielded significantly superior results with the laminectomy electrode for paresthesia coverage of pain, at the same time reducing power requirements sufficiently to double battery life. Fig. 119.8 shows a sample of percutaneous and laminectomy electrodes as well as the oblique-­lateral approach used to place a percutaneous electrode and a small laminotomy opening for a laminectomy electrode. The percutaneous electrode is inserted under local anesthesia, which does not interfere with the clinician’s ability to monitor paresthesia

Adjusting SCS to increase electric charge transfer frequency

Increase pulse rate

Pulse width

frequency

Increase pulse width

Increase pulse rate

Pulse width

Increase pulse width

FIGURE 119.6  Illustrates how merely increasing stimulation frequency and/or pulse duration can increase the amount or electric charge transmitted. There are at present several protocols proposed by different manufacturers how to enable transfer of larger electric charges without disturbing sensory effects to the patient. Most often the amplitude is below sensory threshold and the stimulation periods allowed to be longer than with older paradigms. (Adapted from Linderoth & Foreman 2017.)

during test stimulation. The laminectomy electrode can be implanted with local anesthesia alone, using regional anesthesia (with paresthesia achieved at a slightly higher than normal stimulation threshold to guide electrode positioning) or even with spinal anesthesia to a degree allowing intraoperative paresthesia testing.123,124 Implantation of laminectomy electrodes under general anesthesia, using evoked potentials, has been refined and reportedly can improve outcomes.125 New waveforms described above are delivered using the same electrode designs, targets, and methods of placement as those used with traditional waveforms. It has been suggested that paresthesia mapping in each patient is not necessary to optimize placement for high-­frequency (HF10) paresthesia-­free stimulation and that fluoroscopic guidance alone (spanning levels identified in populations of patients by paresthesia mapping) is sufficient; but affirmative evidence of this is lacking.126 Most studies of new waveforms have begun with electrode implantation using conventional stimulation and paresthesia mapping.127 –129) If an electrode is ever to be used for conventional paresthesia-­based stimulation (e.g., when a patient fails HF SCS), then implantation using paresthesia mapping (or evoked potentials as a surrogate) remains appropriate. 

Pulse Generators The prototype SCS generator, used exclusively during the first decade of experience, was a passive implant powered to deliver stimulation pulses by an external radiofrequency transmitter. Although the implant contained no life-­limiting components and thus avoided the expense and potential morbidity of eventual replacement, this system was cumbersome. An IPG powered by an internal battery was subsequently developed from pacemaker technology. Patients

119  •  Spinal Cord Stimulation for Chronic Pain

High-Density Programming Examples Pulse

1367

Pulse Density (% active stim. or duty cycle)

1.6%

Conventional SCS (eg. 40 Hz 400µs)

200 Hz 1000 µs

20% 25%

500 Hz 500 µs

1200 Hz 200 µs

24% Maximal rate for conventional IPG:s

FIGURE 119.7  Illustrates how increases of the stimulation frequency result in higher pulse densities. It is evident that the conventional SCS settings produce a low pulse density while the lower parts of the picture with settings of 500 Hz/500 μsec or 1200 Hz and 200 μsec can produce pulse densities between 2425% even with subparestetic amplitudes. This opens a set of new stimulation routines for many patients. (Adapted from Linderoth & Foreman 2017.)

compound action potentials.131 Some evidence has been reported that SCS is safe in patients with cardiac pacemakers or cardioverter defibrillators132 if the devices are managed appropriately.133 

Computerized Methods

FIGURE 119.8  Spinal cord stimulation electrodes are arrays with multiple contacts (up to 32). Some require a limited laminectomy, and others may be inserted percutaneously through a modified Tuohy needle.

operate these systems and control the amplitude within preset limits with an external magnet or handheld remote control. The first IPGs were powered by nonrechargeable lithium cells that required replacement approximately every 4 years. To avoid such frequent surgical replacement of the battery, with attendant expense and risk, SCS device manufacturers developed IPGs with rechargeable batteries. This, of course, increases initial cost, and comparative cost effectiveness remains to be established by long-­term study. The less expensive radiofrequency systems remain in use, and miniaturization of circuitry and new antenna designs have allowed development of a system that can be inserted in its entirely through a needle.130 Additional IPG technical improvements include automated amplitude adjustment to compensate for postural changes, which is based upon accelerometer data or

The development of programmable multicontact SCS electrodes has improved the technical (overlap of pain by paresthesia) and clinical results of SCS and immensely increased the number of possible anode and cathode assignments. However, achieving the best results still requires testing various electrode combinations over a range of pulse parameters (especially various amplitudes). By scaling the amplitude from perception of pain and paresthesia overlap to stimulation of discomfort, we can compare the results of various electrode configurations and stimulation parameters at identical subjective stimulus intensities.134 Systematic quantitative assessment of these effects generates a large volume of data that would be prohibitively difficult to analyze without a computer.135,136 These data can be entered by a skilled operator working with the patient or, given a suitable means of control, by the patient alone. Fig. 119.9 illustrates a computer system that presents the patient with a prespecified series of contact combination and pulse parameters. The patient adjusts the stimulation amplitude and draws the area of paresthesia for comparison with drawings of the painful area. Optimal settings are derived from analysis of these results. In a randomized controlled trial involving 44 patients from two centers, the computerized system produced significantly better technical results at a significantly faster rate than did the manual adjustment method. This occurred regardless of practitioner experience, but results improved with patient experience.137 Use of the computerized system also allowed identification of new settings that improved expected battery life for 95% of the patients.138 With an assumed battery use of 24 hours per day, the average battery life predicted after manual settings was 25.4 ± 49.5 months versus 55.0 ± 71.7 months for the computerized settings. For 72% of the patients, the settings that extended battery life led to equivalent or improved technical results.

1368

Section Six  •  FUNCTIONAL NEUROSURGERY

Computerized systems that directly control the implanted stimulator also facilitate the investigation of novel modulation schemes and pulse sequences. 

Screening Protocols Percutaneous placement of a temporary epidural electrode for an SCS screening trial is a straightforward procedure that can take place in a fluoroscopy suite instead of an operating room and facilitates testing of electrode positions and contact combinations for optimal therapeutic effect. Indeed, most third-­party payers in the United States and in some European countries require that patients complete a successful screening trial before undergoing implantation of an SCS system for chronic use. A brief period of intraoperative stimulation immediately before permanent implantation technically meets this requirement,139 but an extended trial allows the patient to assess stimulation effects while engaging in everyday activities. The role of SCS trials was assessed critically in a retrospective comparison of 15-­minute versus 5-­day trials in 54 patients, in which the positive predictive value was equivalent

for predicting SCS outcome.140 However, the trial success rate was an extraordinarily high 47 of 52 at 5 days, and the number of patients who failed the prolonged trial (5) was significantly greater than the number who failed the on-­table trial (1); thus, despite the equivalent predictive value of each trial, the prolonged trial identified more patients who would fail long-­term therapy. Furthermore, if all clinicians obtained such a high trial success rate for patients with chronic low back pain and/or lower extremity pain, the trials would not be necessary. In fact, a lower trial success rate is likely to result in a higher long-­term success rate, and some reports note that as few as 40% of patients undergoing temporary electrode placement proceed to permanent implantation.141 Whereas some clinicians go in the other direction and extend the SCS screening trial for as long as 2 months142 (indeed, some European health authorities require 30-­day trials), the potential morbidity of infection and epidural scarring (which can compromise permanent device implantation) and the expense of such intensive follow-­up must be balanced against potential yield.

Stimulation drawing

Usage threshold

More Please outline the areas where you feel stimulation.

Increase the power until you feel stimulation over the largest area that STILL FEELS COMFORTABLE.

To start over, press Erase. When finished, press Done.

When finished, press Done.

Less STIM OFF

Done

A

Done

Erase

STIM OFF

B

Stimlation overlap rating Please rate how much of your pain is being covered or overlapped by stimulation by marking the line below. When finished, press Done.

1 2 3 4 5 6 7 8 9 No overlap

Complete overlap Done

STIM OFF

C FIGURE 119.9  A computer graphics interface used by patients to control radiofrequency-­coupled spinal cord stimulation systems. The controls of the device allow greater ease of operation than do the controls of standard radiofrequency transmitters or programming units. (A) For each new setting, the patient adjusts amplitude with a “thermometer.” (B) The patient uses the graphics tablet to enter “pain drawings,” distribution of paresthesia drawings, and ratings on a standard 100-­mm visual analog scale to control amplitude and to answer Yes–No questions for psychophysical studies. The computer fills in the area of paresthesia outlined by the patient. (C) Overlap of pain by stimulation paresthesia is readily calculated from these graphic data, and settings are easily ranked for everyday use by the patient. (Reprinted with permission from North RB, Brigham DD, Khalessi A, et al. Spinal cord stimulator adjustment to maximize implanted battery longevity: a randomized, controlled trial using a computerized, patient-­interactive programmer. Neuromodulation. 2004;7:13–25.)

119  •  Spinal Cord Stimulation for Chronic Pain

A screening trial percutaneous electrode can be secured with a simple skin suture at the point where the lead emerges from the Tuohy needle tract. Alternatively, an incision can be made and a subcutaneous anchor placed, and then a pocket and tunnel can be made for a connector and percutaneous extension cable. The latter allows the original electrode to be preserved and connected to a chronic system, if the trial is successful, and this avoids the expense of replacing it, but the former is preferable for the following reasons: Anchoring and removing an anchored electrode (if the trial fails) must take place in an operating room instead of a fluoroscopy suite. This increases the cost. Anchoring a temporary electrode implies a commitment on the part of the patient and the physician to proceed to internalization, which partly defeats the purpose of the trial. The physician cannot adjust the position of an anchored electrode at the bedside as the patient gains experience with the system. In contrast, if the physician places a temporary percutaneous array at the most cephalad position that shows promise during preliminary testing of the naive patient, the electrode can be incrementally withdrawn at the bedside (instead of in an operating room or fluoroscopy suite) for testing at more caudal positions. Plain radiographs can document successful repositioning. Pain from the anchoring incision might confound the results of the therapeutic trial. Placing a percutaneous extension and staging the implant increases the risk of infection.143,144 The criteria used for proceeding from a trial to a system implanted for chronic use have varied from 30%145 to 75% reported pain relief.146–148 The first author (RBN) has historically conducted 7-­to 9-­day trials, shortening or extending them as appropriate, with patients proceeding to implantation for chronic use after achieving at least 50% reported relief of pain with stable or improved levels of activity and analgesic use. However, new wireless technology makes it possible to place a “trial” system with no physical percutaneous extension, mitigating the risk of infection with a prolonged trial.130 Not only may the “trial” with such a system continue indefinitely, allowing multiple waveforms to be assessed, the “trial” system may also be left in place and become “permanent” without the need for a secondary procedure. Assessment of the potential benefits and cost savings is ongoing.149 

Indications for Spinal Cord Stimulation for Pain NEUROPATHIC PAIN Failed Back Surgery Syndrome Persistent pain after spinal surgery (FBSS)—often with an axial component—is the most common indication for SCS in the United States, especially when patients’ symptoms have not been alleviated by a repeat operation (a repeat operation is indicated in cases of gross instability or significant neurologic deficit caused by neural compression). When FBSS causes a chief complaint of axial low back pain, achieving pain overlap by paresthesia is technically difficult and might require the use of complex electrode arrays (and/ or the addition of subcutaneous electrodes).150,151 In addition, mechanical or nociceptive axial low back pain does not respond as well to conventional SCS as does neuropathic pain.28,152 

1369

PERIPHERAL NERVE INJURY SCS is also used to treat pain from peripheral nerve injury (e.g., postherpetic neuralgia and CRPS) with or without signs of disturbed sympathetic function. For CRPS, appropriate SCS electrode placement in the cervical or lumbar regions yields statistically equivalent results.153 SCS is used to treat both stump neuroma pain and phantom limb pain (the latter requiring that the phantom limb be covered with paresthesia). However, pain from pressure applied directly onto a stump neuroma (e.g., from a prosthesis) does not respond adequately to SCS.154 This might be due to the technical difficulty of covering an entire phantom limb with paresthesia or to the degeneration of dorsal column fibers as a consequence of nerve damage. 

ISCHEMIC PAIN Peripheral Arterial Occlusive Disease Clinicians have used SCS to treat pain arising from PAOD since Cook and associates published their report in 1976.155 When several investigators presented encouraging results from confirmatory studies,156–161 the use of SCS for ischemic pain spread rapidly in Europe. However, despite fairly wide acceptance of the therapy during the late 1980s and early 1990s, ill-­ defined patient selection resulted in poor long-­term outcomes. This situation, combined with a lack of knowledge about the mechanism underlying the beneficial effect of SCS, likely hindered the use and further development of SCS for PAOD. During the same period, advances in vascular surgery enabled physicians to perform increasingly complicated bypass grafting procedures, endovascular interventions, and so forth. Thus, only extremely fragile patients are deemed unable to benefit from surgery. These patients—often elderly and suffering from advanced arteriosclerosis with concurrent disease (e.g., coronary ischemia, diabetes)—generally progress rapidly toward critical, limb-­threatening ischemia. Arterial vasospastic diseases, such as Raynaud syndrome, respond extremely well to stimulation if the underlying disease is not progressing rapidly. Thus, in many countries, the use of SCS for PAOD decreased considerably. During 1994, for example, Swedish neurosurgeons implanted only 13 SCS systems for PAOD.47 However, the fact that most PAOD patients have a satisfactory outcome and more than half achieve good pain control has helped the application of SCS for PAOD to survive in a few centers, which follow strict patient selection criteria (Table 119.2). SCS alleviates ischemic pain (and this effect is immediate for vasospastic conditions and angina pectoris). Typical ischemia (e.g., of the foot) might induce ischemic, neuropathic, and nociceptive pain from ischemic ulcers and from the border of gangrenous zones.162,163 Clinicians who used SCS to treat ischemic pain conducted prospective randomized studies to determine the impact of SCS on tissue salvage164 and found statistically significant limb-­ saving effects of SCS only in subgroups of their subjects (see later section on Ischemic Pain under Clinical Results here you can also give).146–149 However, despite a recommendation that clinicians should not offer SCS therapy to patients with major tissue loss,165 patients who reach stage IV on the Fontaine Classification System for Peripheral Artery Disease (tissue loss or ulceration) might benefit from SCS therapy, and patients with diabetes can do as well as those without this condition.166

1370

Section Six  •  FUNCTIONAL NEUROSURGERY

TABLE 119.2  Additional Peripheral Vascular Disease Patient Selection Criteria 1. Severe pain at rest, with or without defined tissue loss (Fontaine grade III) 2. Reconstructive vascular surgery is impossible or contraindicated. 3. Life expectancy is more than 3 months. 4. Any ischemic ulcer is less than 3 cm in diameter. 5. If arrest of tissue loss, or use of spinal cord stimulation (SCS) as an adjunct in ulcer healing, is the primary goal, it should be evaluated objectively. 6. Any gangrene should be dry, and when patients have gangrene, SCS is regarded as a means of obtaining a more distal amputation site. 7. Appropriate preoperative transcutaneous oxygen pressure (TcPo2) is used, measured apically on the diseased extremity,269 compared with the patient in supine versus seated position,270 or change is assessed while the patient breathes pure oxygen.271 8. During a screening trial, the patient should report a significant decrease in the ischemic component of the pain on a visual analog scale and/or demonstrate a clear increase in TcPo2 or in some other objective indicator of microflow concurrent with the therapy. 9. The patient should be able to understand that SCS can alleviate ischemic pain but not nociceptive pain from ulcers and gangrene.

Initial case reports indicate that a patient undergoing SCS for PAOD can later receive a cardiac pacemaker or a dual-­chamber cardioconverter-­defibrillator capable of delivering tiered therapies in both the atrium and ventricle with no adverse effect on either therapy,167 given proper programming of the devices (see earlier). 

Angina Pectoris Angina pectoris is often refractory to standard treatment (administration of appropriate pharmaceuticals and revascularization) and is a major reason for hospitalization. As more and more patients live longer with coronary artery disease, the number with refractory angina will increase. Many patients suffering from disabling angina (New York Heart Association [NYHA] class III to IV) are elderly or have a comorbidity that makes them unsuitable candidates for invasive first-­line treatment. Other patients have typical symptoms of angina but no signs of obstruction in cardiac circulation and are said to suffer from syndrome X, which has its physiologic basis in small vessel disease, vasospasm, or some other undetected anomaly.168 In the 1980s, TENS became the first stimulation technique used to treat otherwise refractory angina pectoris,169,170 and the outcome was so promising that clinicians who were already using SCS to treat ischemic pain in the lower extremities began to position the electrode at the T1 to T2 level so they could induce paresthesia that would also overlap the pain of otherwise refractory angina.171,172 The initial use of SCS for angina caused concern that paresthesia would conceal the warning signs of a myocardial infarction, but paresthesia has neither this effect nor an adverse impact on arrhythmia.173,174 That thoracic SCS can be safely used in angina patients being treated concurrently with a pacemaker was demonstrated by researchers who conducted electrocardiographic monitoring in 18 subjects while increasing the pacemaker setting and SCS intensity to the maximum tolerated. The investigators also asked the subjects for information on any

interference during long-­term treatment. Nothing indicated an adverse reaction to this combination treatment, but the investigators recommended individual patient assessment and proposed a safety testing procedure.133 The first report of SCS to treat angina in a patient with a cardioverter-­defibrillator appeared in 2007175 and was followed the next year by a report from the same investigators of a study demonstrating a time-­dependent positive effect of SCS on the arrhythmic substrate in three such patients.176 Although thousands of SCS systems have been implanted for angina and the success rate is greater than 80%,177 the US Food and Drug Administration has not approved the use of SCS specifically for this indication; however, long-­ standing approval for intractable pain of the trunk and limbs might apply. Table 119.3 lists additional selection criteria for patients with angina who are being considered for SCS therapy. 

CLINICAL RESULTS WITH CONVENTIONAL SPINAL CORD STIMULATION THERAPY Neuropathic Pain The clinical results of SCS for neuropathic pain vary considerably, and investigators often express these results in terms of the number of systems implanted for chronic use instead of the number of screening trials. When the rate of implantation for chronic use versus screening trials is as low as 40%, adjustment for this factor is more important than when the implantation rate exceeds 75%. Patient-­rated pain relief is the most common outcome criterion, and the most commonly used definition of “success” is a minimum 50% reported relief. However, this definition arbitrarily emphasizes only one of many outcome measures for successful pain management, which include consumption of health care resources, including medication; ability to engage in productive activity or work; and changes in neurologic function. The source of this information is another important consideration. For example, data collected by a disinterested third-­party interviewer can differ from those gleaned from a review of physicians’ office records and hospital charts. Because this difference likely means that use of the disinterested interviewer reduces bias, many investigators have adopted this technique. For a comprehensive bibliography of the studies that report the use of SCS to treat neuropathic pain, see www.WIKISTIM.org. 

FAILED BACK SURGERY SYNDROME After retrospective studies indicated that SCS can produce better results with fewer risks than those associated with reoperation in FBSS patients,178,179 the first author’s (RBN’s) research group conducted the first randomized controlled trial in subjects whose FBSS caused unrelieved leg pain with or without low back pain. All subjects were eligible for a specific operation to relieve nerve compression and were randomized either to SCS or to the proposed reoperation. Subjects with unsatisfactory results could request crossover to the other treatment, and the frequency of this crossover was a primary outcome measure. Among 45 subjects (90%) available for a mean follow-­up of 3 years, SCS was successful in 9 of 19 randomized to this arm, whereas reoperation was successful in only 3 of 26. Subjects

119  •  Spinal Cord Stimulation for Chronic Pain

TABLE 119.3  Additional Angina Patient Selection Criteria 1. Severe handicapping angina pectoris (New York Heart Association Class III or IV) 2. Significant coronary artery disease or syndrome X refractory to conventional treatment. 3. Further revascularization therapy not immediately applicable. 4. Demonstrated reversible myocardial ischemia. 5. Pain alleviation with transcutaneous electrical nerve stimulation (not an absolute criterion). 6. No recent (