Meningiomas E-Book

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Meningiomas, by M. Necmettin Pamir, MD, Peter M. Black, MD, PhD, and Rudolf Fahlbusch, MD, presents current and comprehensive guidance on this most common, yet clinically challenging type of brain tumor. Written and edited by the world’s most prominent brain tumor neurosurgeons, it helps you to not only determine the type and location of the tumor, but also the most ideal surgical approach to provide your patients with the best outcomes. An extensive collection of surgical photographs covers unique and original cases, while discussions of pre-surgical techniques and approaches emphasize decision making with the help of all imaging modalities and analysis of symptoms and patient history. Expert Consult functionality enhances your reference power with convenient online access to the complete text and illustrations from the book, along with videos that depict surgical techniques in real time.

  • Provides access to the complete text online—fully searchable, along with all of the illustrations downloadable for your personal presentations, and real-time surgical videos covering microscopic extended endonasal approach to suprasellar meningioma, and more, at expertconsult.com.
  • Covers today’s full range of management methods, including adjuvant therapies, providing you with the best strategies for obtaining optimal outcomes.
  • Features the work of the world’s most prominent brain tumor neurosurgeons—a completely international authorship—bringing you the best procedures globally.
  • Offers an in-depth section on surgical methods and approaches based upon tumor location, to help you in the decision-making process.
  • Includes coverage of spinal meningiomas including pre-diagnosis symptoms and outcomes.

Subjects

Books
Savoirs
Medicine
Vascular endothelial growth factor C
Surgical suture
Therapy
Benignity
Ascend
Biology
Diaphragma sellae
Sphenoid wing meningioma
Meningeal arteries
Ligation
Vitality
Perioperative
Superior sagittal sinus
Pulmonary valve stenosis
Neurofibromatosis type II
Biologic
Visual impairment
Neuro-ophthalmology
Neuropathology
Cell adhesion molecule
Microsurgery
Neoplasm
Craniotomy
Cadherin
Radiosurgery
Proton therapy
Traumatic brain injury
Meningioma
Platelet-derived growth factor
Vestibular schwannoma
Pituitary adenoma
Fractionation
Intracranial hemorrhage
Hypopituitarism
Biological agent
Subarachnoid hemorrhage
Melanoma
Anesthetic
Stroke
Optic Nerve
Daughter
Renal cell carcinoma
Meninges
Cerebral edema
Pleural effusion
Cauterization
Osteosarcoma
Wild Turkey
Medical imaging
Pulmonary embolism
Hydrocephalus
Natural history
Trepanning
Tinnitus
Cataract
Edema
Headache
Epidemiology
Angiogenesis
Neurofibromatosis
Ophthalmology
X-ray computed tomography
Multiple sclerosis
Philadelphia
Hearing impairment
Phenytoin
Brain tumor
Artery
Syringomyelia
Data storage device
Epileptic seizure
Radiation therapy
Paranasal sinuses
Positron emission tomography
Optic neuritis
Neurosurgery
Neurologist
Neurology
Mechanics
Molecule
Magnetic resonance imaging
Growth factor
Gene therapy
General surgery
Epilepsy
Major depressive disorder
Chemotherapy
Monitoring
Headache (EP)
Blindness
Keith Tucker
Pathology
Bypass
Multiple
Dindon sauvage
Gene
Turkey
Vascular endothelial growth factor
Genetics
Dissection
Intensive Care
Planning
Phénobarbital
Carbamazépine
Ablation
Fatigue
Electronic
Fossa
Syringomyélie
Vertigo
Acouphène
Philadelphie
Surface
Son
Boston
Copyright
Photon
Virus
thérapies
Factor de crecimiento endotelial vascular
Meleagris gallopavo
Derecho de autor
Vértigo (desambiguación)
Acúfeno
Angiogénesis
Múltiple
Turquía
Surgical incision
Oncology
Meningitis
Circulatory collapse
CDH1 (gene)
Vascular endothelial growth factor B

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Published 25 January 2010
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EAN13 9781455708994
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Meningiomas
A Comprehensive Text
M. Necmettin Pamir, MD
Professor of Neurosurgery, Chairman, Department of
Neurosurgery, Acibadem University School of Medicine,
Istanbul, Turkey
Peter M. Black, MD, PhD, FACS
Franc D. Ingraham Professor of Neurosurgery, Harvard
Medical School
Founding Chair, Department of Neurosurgery, Brigham and
Women's Hospital, Chair Emeritus
Department of Neurosurgery, Children's Hospital Boston,
Boston, Massachusetts
Rudolf Fahlbusch, MD, PhD
Professor of Neurosurgery, Director, Endocrine Neurosurgery
and Intraoperative MRI, International Neuroscience Institute,
Hannover, Germany
S a u n d e r sFront matter
Meningiomas: A Comprehensive Text
M. Necmettin Pamir, MD
Professor of Neurosurgery, Chairman, Department of Neurosurgery,
Acibadem University School of Medicine, Istanbul, Turkey
Peter M. Black, MD, PhD, FACS
Franc D. Ingraham Professor of Neurosurgery, Harvard Medical School,
Founding Chair, Department of Neurosurgery, Brigham and Women’s
Hospital, Chair Emeritus, Department of Neurosurgery, Children’s Hospital
Boston, Boston, Massachusetts
Rudolf Fahlbusch, MD, PhD
Professor of Neurosurgery, Director, Endocrine Neurosurgery and
Intraoperative MRI, International Neuroscience Institute, Hannover,
Germany
Meningiomas: A Comprehensive Text@
@
Copyright
Saunders Elservier
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, Pennsylvania 19103-2899
MENINGIOMAS: A COMPREHENSIVE TEXT
ISBN: 978-1-4160-5654-6
Copyright © 2010 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
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copyright by the Publisher (other than as may be noted herein).
Notice
Knowledge and best practice in this eld 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
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be mindful of their own safety and the safety of others, including parties for
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With respect to any drug or pharmaceutical products identi ed, readers are
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To the fullest extent of the law, neither the Publisher nor the authors,
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contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Meningiomas: a comprehensive text/[edited by]
M. Necmettin Pamir, Peter Black, Rudolf Fahlbusch. - 1st ed.
p. ; cm.
Includes bibliographical references.
ISBN 978-1-4160-5654-6
1. Meningioma. I. Pamir, M. Necmettin. II. Black, Peter McL. III. Fahlbusch,
Rudolf.
[DNLM: 1. Meningioma. QZ 380 M5448 2009]
RC280.M4M46 2009
616.99′4--dc22
2009014345
Acquisitions Editor: Adrianne Brigido
Developmental Editor: Lisa Barnes
Design Direction: Ellen Zanolle
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1D e d i c a t i o n
To my mother, my wife and my daughter.
MNP
To my families: my wife Katharine and our wonderful children, and the family
of co-workers, students, and friends who have made academic life so fulfilling.
PMB
To my wonderful sons Fabian and Marius
RFContributors
John R. Adler, Jr., MD, Dorothy & TK Chan Professor of
Neurosurgery, Department of Neurosurgery & Radiation
Oncology, Stanford University School of Medicine,
Stanford, California
Linda S. Aglio, MD, MS, Director of Neuroanesthesia,
Department of Anesthesia, Perioperative and Pain
Medicine, Associate Director of Neurophysiologic
Monitoring, Brigham and Women's Hospital, Boston,
Massachusetts
Nejat Akalan, MD, PhD, Professor of Neurosurgery,
Department of Neurosurgery, Hacettepe University
School of Medicine, Ankara, Turkey
Serdar Baki Albayrak, MD, Assistant Professor of
Neurosurgery, Department of Neurosurgery, Suleyman
Demirel University, Medical Faculty Hospital, Isparta,
Turkey, Brain Tumor Fellow, Department of
Neurosurgery, Harvard Medical School, Brigham and
Women’s Hospital, Boston, Massachusetts
Ossama Al-Mefty, MD, Professor and Chairman,
Department of Neurosurgery, University of Arkansas for
Medical Sciences, Little Rock, Arkansas
Jorge E. Alvernia, MD, Senior Resident, Neurological
Surgery Department, Tulane University, New Orleans,
Louisiana
Danielle Baleriaux, MD, Neuroradiologist and
Department Head, Department of Neuroradiology,
Hôpital Erasme, Université Libre de Bruxelles, Brussels,
BelgiumFeyyaz Baltacioğlu, MD, Associate Professor of
Radiology, Department of Radiology, Marmara
University School of Medicine, Istanbul, Turkey
Hiriam Basiouni, MD, Department of Neurosurgery,
University of Essen, Essen, Germany
Muhittin Belirgen, MD, Clinical Fellow, Department of
Neurosurgery, University of Texas Southwestern
Children’s Medical Center, Dallas, Texas
Jacqueline A. Bello, MD, FACR, Professor of Clinical
Radiology, Department of Radiology, Albert Einstein
College of Medicine of Yeshiva University, Director of
Neuroradiology, Department of Radiology, Montefiore
Medical Center, Bronx, New York
Amaresh S. Bhaganagare, Mch, Department of
Neurosurgery, King Edward Memorial Hospital, Seth G.
S. Medical College, Parel, Mumbai, India
Peter M. Black, MD, PhD, FACS, Franc D. Ingraham
Professor of Neurosurgery, Harvard Medical School,
Founding Chair, Department of Neurosurgery, Brigham
and Women’s Hospital, Chair Emeritus, Department of
Neurosurgery, Children’s Hospital Boston, Boston,
Massachusetts
Alp Özgün Börcek, MD, Neurosurgeon, Department of
Neurosurgery, Division of Pediatric Neurosurgery, Gazi
University Faculty of Medicine, Ankara, Turkey
†John Borchers, III, MD , Neurosurgeon, Department of
Neurosurgery, Stanford University School of Medicine,
Stanford, California
Michael Brada, MB ChB, FRCR, FRCP, Professor of
Radiation Oncology, Academic Unit of Radiotherapy
and Oncology, The Institute of Cancer Research and
Neuro-oncology Unit The Royal Marsden NHS
Foundation Trust, Sutton, Surrey, United KingdomJacques Brotchi, MD, Emeritus Professor and Honorary
Chairman, Department of Neurosurgery, Hôpital
Erasme, Brussels, Belgium
Michael Bruneau, MD, Neurosurgeon, Université Libre
de Bruxelles, Associate Attending Neurosurgeon,
Department of Neuroradiology, Hôpital Erasme,
Brussels, Belgium
Lisa Calvocoressi, PhD, Associate Research Scientist,
Department of Epidemiology and Public Health, Yale
University School of Medicine, New Haven, Connecticuit
Giorgio Carrabba, MD, Neuro-oncology Fellow,
Department of Neurosurgery, Neurosurgery Fellow,
Department of Neurosurgery, Toronto Western Hospital,
Toronto, Ontario, Canada
Rona S. Carroll, PhD, Assistant Professor of Surgery,
Department of Surgery, Harvard Medical School,
Assistant Professor of Neurosurgery, Department of
Neurosurgery, Brigham and Women’s Hospital, Boston,
Massachusetts
Elizabeth B. Claus, MD, PhD, Professor of Epidemiology
and Public Health, Department of Epidemiology and
Public Health, Yale School of Medicine, New Haven,
Connecticut, Attending Neurosurgeon, Department of
Neurosurgery, Brigham and Women’s Hospital, Boston,
Massachusetts
V. Peter Collins, MD, PhD, Professor of Histopathology
and Morbid Anatomy, Pathology Division of Molecular
Histopathology, University of Cambridge, Honorary
Consultant Histopathologist, Department of
Histopathology, Addenbrooke’s Hospital, Cambridge,
United Kingdom, Foreign Adjunct Professor,
Histopathology, The Karolinska Institute, Stockholm,
Sweden
Jeroen R. Coppens, MD, Fellow, Department ofNeurosurgery, University of Utah, Salt Lake City, Utah
William T. Couldwell, MD, PhD, Professor and Joseph J.
Yager Chairman, Department of Neurosurgery,
Attending Physician, Department of Neurosurgery,
University of Utah, Salt Lake City, Utah
Chris Couser, MD, Department of Neurosurgery,
Brigham and Women’s Hospital, Boston, Massachusetts
Manoel A. de Paiva Neto, MD, Research Fellow, Division
of Neurosurgery, University of California at Los Angeles,
David Geffen School of Medicine, Los Angeles,
California, Clinical Instructor, Disciplina de
Neurocirurgia, Universidade Federal de Sao Paulo, Sao
Paulo, Brazil
Ketan I. Desai, Mch, Consultant Neurosurgeon,
Department of Neurosurgery, P.D. Hinduja National
Hospital and Medical Research Center, Mumbai,
Maharashtra, India
Alp Dinçer, MD, Assistant Professor of Radiology,
Department of Radiology, Acibadem University School
of Medicine, Istanbul, Turkey
Francesco Doglietto, MD, Clinical Fellow, Department of
Neurosurgery, Toronto Western Hospital, University
Health Network, Toronto, Ontario, Canada,
Neurosurgeon, Department of Neuroscience, Institute of
Neurosurgery, Catholic University School of Medicine,
Rome, Italy
Joshua R. Dusick, MD, Assistant Researcher, Division of
Neurosurgery, University of California at Los Angeles,
David Geffen School of Medicine, Los Angeles,
California
Canan Erzen, MD, Professor of Radiology, Department of
Radiology, Marmara University School of Medicine,
Istanbul, TurkeyRudolf Fahlbusch, MD, PhD, Professor of Neurosurgery,
Director, Endocrine Neurosurgery and Intraoperative
MRI, International Neuroscience Institute, Hannover,
Germany
Joaquim M. Farinhas, MD, Assistant Professor,
Department of Radiology, Albert Einstein College of
Medicine, Bronx, New York
Nasrin Fatemi, MD, Neuroendocrine Research Fellow,
Division of Neurosurgery, University of California at Los
Angeles, David Geffen School of Medicine, UCLA
Pituitary Tumor and Neuroendocrine Program, Los
Angeles, California
Shifra Fraifeld, MBA, Research Associate, Department of
Neurosurgery, Hadassah – Hebrew University Medical
Center, Jerusalem, Israel
Fred Gentili, MD, MSc, FRCSC, FACS, Professor, Deputy
Chief, Department of Surgery, Division of Neurosurgery,
University of Toronto, Professor, Department of
Otolaryngology and Head and Neck, Toronto Western
Hospital, University Health Network, Toronto, Ontario,
Canada
Venelin M. Gerganov, MD, PhD, Associate
Neurosurgeon, International Neuroscience Institute,
Hannover, Germany
Atul Goel, Mch, Professor and Head, Department of
Neurosurgery, King Edward Memorial Hospital, Seth G.
S. Medical College, Parel, Mumbai, India
Alexandra J. Golby, MD, Assistant Professor of Surgery,
Assistant Professor of Radiology, Harvard Medical
School, Associate Surgeon, Department of Neurosurgery,
Brigham and Women’s Hospital, Boston, Massachusetts
Menachem M. Gold, MD, Clinical Instructor, Department
of Radiology, Albert Einstein College of Medicine,Neuroradiology Fellow, Department of Radiology,
Montefiore Medical Center, Bronx, New York
William B. Gormley, MD, Director, Neurosurgical
Critical Care, Department of Neurosurgery, Harvard
Medical School, Boston, Massachusetts
Lance S. Governale, MD, Resident, Department of
Neurosurgery, Brigham and Women’s Hospital, Boston,
Massachusetts
Abhijit Guha, MD, Professor, Department of Surgery -
Neurosurgery, University of Toronto, Attending
Neurosurgeon, Department of Neurosurgery, Toronto
Western Hospital, Senior Scientist and Co-Director,
Brain Tumor Center, Department of Cell Biology,
Hospital for Sick Children Research Institute, Toronto,
Ontario, Canada
Wendy Hara, MD, Clinical Instructor, Department of
Radiation Oncology, Stanford University School of
Medicine, Stanford, California
Toshinori Hasegawa, MD, Chief Neurosurgeon,
Department of Neurosurgery, Komaki City Hospital,
Gamma Knife Center, Komaki, Japan
Werner Hassler, MD, PhD, Chief, Department of
Neurosurgery, Wedau Kliniken, Duisburg, Germany
Stanley Hoang, BS, Department of Neurosurgery,
Stanford University School of Medicine, Stanford,
California
Bernd M. Hofmann, MD, Neurosurgeon, Healthcare
Sector, Workflow & Solutions Division, Siemens AG,
Erlangen, Germany
Liz L. Holzemer, MA Journalism, Founder, Meningioma
Mammas, Highlands Ranch, ColoradoMark Hornyak, MD, Fellow, Department of
Neurosurgery, University of Utah, Salt Lake City, Utah
John A. Jayne, Jr., MD, PhD, FRCS(C), Assistant
Professor of Neurosurgery and Pediatrics, Department of
Neurosurgery, University of Virginia Health System,
Charlottesville, Virginia
Michel Kalamarides, MD, PhD, Professor of
Neurosurgery, Universite de Paris, Paris, France,
Department of Neurosurgery, Hospital Beaujon, AP-HP,
Clichy, France
Hideyuki Kano, MD, PhD, Research Assistant Professor,
Department of Neurological Surgery, University of
Pittsburgh, Pittsburgh, Pennsylvania
Tulay Kansu, MD, FAAN, Professor of Neurology,
Department of Neurology, Professor of
Neuroophthalmology, Department of
NeuroOphthalmology, Hacettepe University School of
Medicine, Ankara, Turkey
Takeshi Kawase, MD, Professor and Chairman,
Department of Neurosurgery, Keio University School of
Medicine, Tokyo, Japan
Dilaver Kaya, MD, Assistant Professor of Neurology,
Department of Neurology, Acibadem University School
of Medicine, >Attending Neurologist, Department of
Neurology, Adibadem Kozyatagi Hospital, Istanbul,
Turkey
Andrew H. Kaye, MBBS, MD, FRACS, James Stewart
Professor of Surgery, Head, Department of Surgery, The
University of Melbourne, Director, Department of
Neurosurgery, Director, The Melbourne Comprehensive
Cancer Centre, The Royal Melbourne Hospital,
Melbourne, Australia
Daniel F. Kelly, MD, Director, Brain Tumor Center, JohnWayne Cancer Institute at Saint John’s Health Center,
Santa Monica, California
Ron Kikinis, MD, Professor, Department of Radiology,
Harvard Medical School, Brigham and Women’s
Hospital, Boston, Massachusetts
Türker Kiliç, MD, Associate Professor of Neurosurgery,
Department of Neurosurgery, Marmara University
School of Medicine, Istanbul, Turkey
James A.J. King, MBBS, PhD, FRACS, Senior Lecturer,
Department of Surgery, University of Melbourne,
Neurosurgeon, Department of Neurosurgery, Royal
Melbourne Hospital, Melbourne, Australia
Saeed Kohan, MD, Clinical Fellow of Pediatric
Neurosurgery, Department of Neurosurgery, Marmara
University Medical Center, Istanbul, Turkey, Instructor,
Department of Neurosurgery, Concord Hospital,
University of Sydney, Sydney, Australia
Douglas Kondziolka, MD, FACS, FRCS, Peter J. Jannetta
Professor and Vice-Chairman of Neurological Surgery
and Radiation Oncology, Department of Neurosurgery,
University of Pittsburgh, Pittsburgh, Pennsylvania
Ender Konukoglu, PhD, PhD Candidate, Asclepios
Research Project, INRIA Sophia Antipolis, Sophia
Antipolis, France
Deniz Konya, MD, Assistant Professor, Department of
Neurosurgery, Marmara University School of Medicine,
Istanbul, Turkey
Niklaus Krayenbühl, MD, Neurosurgeon, Department of
Neurosurgery, University Hospital Zürich, Zürich,
Switzerland
Osami Kubo, MD, PhD, Professor, Department of
Neurosurgery, Institute of the Advanced BiomedicalSciences, Tokyo Women’s Medical University, Tokyo,
Japan
Edward R. Laws, Jr., MD, FACS, Director,
Pituitary/Neuroendocrine Center, Department of
Neurosurgery, Brigham and Women’s Hospital,
Neurosurgeon, Department of Neurosurgery, Children’s
Hospital Boston, Neurosurgeon, Dana-Farber Cancer
Institute, Boston, Massachusetts
Gordon Li, M.D., Resident, Department of Neurosurgery,
Stanford University School of Medicine, Stanford,
California
Jay S. Loeffler, MD, FACR, Herman and Joan Suit
Professor of Radiation Oncology, Harvard Medical
School, >Chief, Department of Radiation Oncology,
Massachusetts General Hospital, Boston, Massachusetts
L. Dade Lunsford, MD, FACS, Professor, Department of
Neurological Surgery, University of Pittsburgh Medical
Center, Pittsburgh, Pennsylvania
Dennis Malkasian, MD, PhD, Associate Clinical Professor
of Neurosurgery, Division of Neurosurgery, University of
California at Los Angeles, David Geffen School of
Medicine, UCLA Pituitary Tumor and Neuroendocrine
Program, Los Angeles, California
Carolina Martins, MD, PhD, Anatomy Professor, Medical
School of Pernambuco – IMIP, >Neurosurgeon, IMIP
Recife, Brazil, Visiting Professor, University of Florida,
Gainesville, Florida
Tiit Mathiesen, MD, Associate Professor, Department of
Neurosurgery, Karolinska University, Department of
Neurosurgery, Karolinska University Hospital Solna,
Stockholm, Sweden
Giuseppe Minniti, MD, PhD, Assistant Professor of
Radiation Oncology, Department of RadioterapiaOncologica, Ospedale Sant’Andrea, Rome, Italy
Debabrata Mukhopadhyay, MBBS, DNB (Neurosurgery),
Neuro-oncology Fellow, Department of Neurosurgery,
Neurosurgery Fellow, Department of Neurosurgery,
Toronto Western Hospital, Toronto, Ontario, Canada
Ajay Niranjan, MBBS, MS, MCh, Associate Professor,
Neurological Surgery, University of Pittsburgh,
Pittsburgh, Pennsylvania
Andrew D. Norden, MD, Instructor of Neurology,
Harvard Medical School, Associate Neurologist, Division
of Neuro-oncology, Department of Neurology, Brigham
and Women’s Hospital, Attending Neuro-oncologist,
Department of Medical Oncology, Center for
Neurooncology, Dana-Farber Cancer Institute, Boston,
Massachusetts
Y. Ono, MD, PhD, Professor, Department of
Neuroradiology, Tokyo Women’s Medical University,
Tokyo, Japan
Koray Özduman, MD, Assistant Professor of
Neurosurgery, Department of Neurosurgery, Acibadem
University School of Medicine, Attending Neurosurgeon,
Department of Neurosurgery, Acibadem Kozyatagi
Hospital, Istanbul, Turkey
M. Memet Özek, MD, Professor of Neurosurgery,
Chairman, Department of Neurosurgery, Marmara
University School of Medicine, >Chief, Division of
Pediatric Neurosurgery, Department of Neurosurgery,
Acibadem University, Istanbul, Turkey
Serdar Özgen, M.D., Associate Professor of
Neurosurgery, Department of Neurosurgery, Marmara
University School of Medicine, Istanbul, Turkey
Tuncalp Özgen, MD, Professor and Chairman,
Department of Neurosurgery, Hacettepe UniversitySchool of Medicine, Ankara, Turkey
M. Necmettin Pamir, MD, Professor of Neurosurgery,
Chairman, Department of Neurosurgery, Acibadem
University School of Medicine, Istanbul, Turkey
Chirag G. Patil, MD, MS, Chief Resident, Department of
Neurosurgery, Stanford University, Stanford, California
Selçuk Peker, MD, Associate Professor, Department of
Neurosurgery, Acibadem University School of Medicine,
Istanbul, Turkey
Annette M. Pham, MD, Private Practice, ENT Specialists
of Shady Grove, PC, Rockville, Maryland
Joseph M. Piepmeier, MD, Professor of Neurosurgery,
Department of Neurosurgery, Yale University School of
Medicine, New Haven, Connecticut
Killian M. Pohl, PhD, Research Associate, Computer
Science, Massachusetts Institute of Technology,
Cambridge, Massachusetts, Researcher, IBM Almaden,
San Jose, California
Ivan Radovanovic, MD, PhD, Clinical Fellow, Division of
Neurosurgery, Toronto Western Hospital, University of
Toronto, Toronto, Ontario, Canada
Naren Raj Ramakrishna, MD, PhD, Director, Neurologic
and Pediatric Oncology, MD Anderson Cancer Center,
Orlando, Florida
Albert L. Rhoton, Jr., MD, R.D. Keene Family Professor
and Chairman Emeritus, Department of Neurosurgery,
McKnight Brain Institute, University of Florida,
Gainesville, Florida
Guy Rosenthal, MD, Attending Neurosurgeon,
Department of Neurosurgery, Hadassah – Hebrew
University Medical Center, Jerusalem, Israel, AssistantAdjunct Professor, Department of Neurosurgery, San
Francisco General Hospital, University of California at
San Francisco, San Francisco, California
James T. Rutka, MD, PhD, FRCSC, FACS, FAAP, Chair,
Division of Neurosurgery, University of Toronto, The
Hospital for Sick Children, Department of
Otolaryngology, University of Toronto, University
Health Network, Toronto, Ontario, Canada
John A. Rutka, MD, FRCSC, Professor, Department of
Otolaryngology, University of Toronto, Staff
Neurotologist, Department of Otolaryngology,
University of Toronto, University Health Network,
Toronto, Ontario, Canada
Siegal Sadetzki, MD, MPH, Senior Lecturer, Department
of Epidemiology and Preventive Medicine, Sackler
School of Medicine, Tel-Aviv University, Tel Aviv, Israel,
Head, The Cancer & Radiation Epidemiology Unit, The
Gertner Institute for Epidemiology & Health Policy
Research, Chaim Sheba Medical Center, Tel Hashomer,
Israel
Gordon T. Sakamoto, MD, Chief Resident, Department of
Neurosurgery, Stanford University School of Medicine,
Stanford, California
Katsumi Sakata, MD, Associate Professor and Director,
Department of Neurosurgery, Yokohama City University
School of Medicine, Yokohama, Japan
Madjid Samii, MD, PhD, Professor of Neurosurgery,
International Neuroscience Institute, Hannover,
Germany
Aydin Sav, MD, Professor, Director, Department of
Pathology, Acibadem University, >Professor, Head,
Pathology Laboratory, Neuropathology Unit, Marmara
University Istanbul, TurkeyBernd Scheithauer, MD, Professor of Pathology,
Laboratory Medicine and Pathology, Mayo Clinic,
Rochester, Minnesota
Uta Schick, MD, PhD, Assistant Professor of the Clinic of
Neurosurgery, Department of Neurosurgery, University
of Heidelberg, Heidelberg, Germany
Johannes Schramm, MD, Professor and Chairman,
Department of Neurosurgery, Rheinische Friedrich
Wilhelms University, Bonn, Germany
Patrick Schweder, MD, Department of Neurosurgery, The
Royal Melbourne Hospital, Parkville, Victoria, Australia
Volker Seifert, MD, PhD, Professor and Chairman,
Department of Neurosurgery, >Director, Center of
Clinical Neurosciences, Johann Wolfgang Goethe
University, Frankfurt am Main, Germany
Askin Seker, MD, International Research Fellow,
Department of Neurosurgery, University of Florida,
Gainesville, Florida
Keivan Shifteh, MD, Assistant Professor of Radiology,
Department of Radiology, Albert Einstein College of
Medicine, Montefiore Hospital, Bronx, New York
Helen A. Shih, MD, MS, MPH, Assistant Professor,
Harvard Medical School, Radiation Oncologist,
Department of Radiation Oncology, Massachusetts
General Hospital, Boston, Massachusetts
Yigal Shoshan, MD, Associate Professor, Department of
Neurosurgery, Hebrew University – Hadassah School of
Medicine, Attending Neurosurgeon, Department of
Neurosurgery, Hadassah – Hebrew University Medical
Center, Jerusalem, Israel
Matthias Simon, MD, Assistant Professor of
Neurosurgery, Department of Neurosurgery, RheinischeFriedrich Wilhelms University, Bonn, Germany
Robert L. Simons, MD, FACS, Clinical Professor,
Department of Otolaryngology – Head and Neck
Surgery, Division of Facial Plastic and Reconstructive
Surgery, University of Miami, Medical Board Chairman,
The Miami Institute for Age Management and
Intervention, Miami, Florida
Marc P. Sindou, MD, PhD, Chairman, Professor of
Neurosurgery, Hospital Neurologique Pierre
Wertheimer, Universite de Lyon, Lyon, France
Sergey Spektor, MD, PhD, Clinical Senior Lecturer,
Department of Neurosurgery, Hebrew University –
Hadassah School of Medicine, Attending Neurosurgeon,
Department of Neurosurgery, Hadassah – Hebrew
University Medical Center, Jerusalem, Israel
K. Takakura, MD, Professor Emeritus, Department of
Neurosurgery, Institute of the Advanced Biomedical
Sciences, Tokyo Women’s Medical University, Tokyo,
Japan
Farzana Tariq, MD, Research Fellow, Department of
Neurosurgery, Harvard Medical School, Brigham and
Women’s Hospital, Boston, Massachusetts
A. Teramoto, MD, PhD, Professor of Neurosurgery,
Department of Neurosurgery, Tokyo Women’s Medical
University, Tokyo, Japan
Felix Umansky, MD, Chair, Department of Neurosurgery,
Hebrew University – Hadassah School of Medicine,
Chairman, Department of Neurosurgery, Hadassah –
Hebrew University Medical Center, Jerusalem, Israel,
Attending Neurosurgeon, Department of Neurosurgery,
Henry Ford Hospital, Detroit, Michigan
Onder Us, MD, Chairman and Professor, Department of
Neurology, Marmara University School of Medicine,Istanbul, Turkey
Marcus L. Ware, MD, PhD, Assistant Professor in
Neurosurgery, Department of Neurosurgery, Tulane
University School of Medicine, New Orleans, Louisiana
Damien C. Weber, MD, Vice Chairman, Radiation
Oncology Department, Geneva University Hospital
,Geneva, Switzerland
Patrick Y. Wen, MD, Clinical Director, The
DanaFarber/Brigham and Women’s Cancer Center, Associate
Professor of Neurology, Harvard Medical School, Boston,
Massachusetts
Guido Wollmann, MD, Associate Research Scientist,
Department of Neurosurgery, Yale University School of
Medicine, New Haven, Connecticut
Isao Yamamoto, MD, Professor and Chairman,
Department of Neurosurgery, Yokohama City University,
Yokahama, Japan
Jun Yoshida, MD, PhD, Professor and Chairman,
Department of Neurosurgery, Nagoya University
Graduate School of Medicine, Nagoya, Japan
Jacob Zauberman, MD, Trauma Unit, Chaim Sheba
Medical Center, Tel Hashomer, Israel
† Deceased.%
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Preface
M. Necmettin Pamir, Peter M. Black, Rudolf Fahlbusch
Meningiomas are fascinating tumors because of their surgical challenge, their
biological complexity, the possibility of achieving surgical remission and the
increasing recognition that they are very common. The classic monograph of
Cushing and Eisenhart on meningiomas was published in 1938; this monumental
book established the fundamental principles of meningioma treatment, and since
then there have been several other books devoted to them.
In the last decade, advances in the eld of molecular biology and other
experimental work have improved our understanding of the clinical behavior of
meningiomas. Progress in the eld of neurosurgery has also resulted in clinical
advances in meningioma treatment. These developments led us to the project of
collecting the new knowledge on scienti c and clinical progress in meningiomas
with a comprehensive book. The rst section on the “neurobiology of
meningiomas” is composed of ten chapters. In addition to the history, anatomy
and embryology, this section provides advanced knowledge on molecular biology
of meningiomas. The second section, in seven chapters, summarizes the classical
and advanced diagnosis of meningiomas including new imaging techniques and
the latest pathological classi cation. The third section is dedicated to general
issues on the surgical treatment of meningiomas. The fourth section covers the
surgical management of meningiomas by their site of origin. In this section, each
chapter is aimed to provide a detailed summary of surgical techniques, potential
pitfalls, and complication avoidance speci c to each location of meningioma.
Accompanying illustrative videos are also provided for some of the chapters. The
fth section focuses on adjuvant treatment alternatives including radiosurgical
and fractionated radiation treatment modality, chemotherapy and biological
treatment. The last section presents special topics on meningiomas. We also have
included a chapter on the patient’s point of view, which is quite uncommon in the
present literature. Each chapter is written by experts on each eld from all over
the world.
With such comprehensive content the book is intended not only to bring the
extensive understanding of each topic to the reader’s attention, but also to convey
each author’s personal experience. Repetitions were avoided but di erent points of%
view were encouraged. This comprehensive book is therefore intended for use by
neurosurgeons, neurologists and oncologists but also by physicians from other
disciplines, internists and nurses.
We hope that this book will boost the readers contemporary understanding of
meningiomas, promote re nement of meningioma treatment and contribute to the
care of meningioma patients.V i d e o s
1. Convexity Meningioma 339
Jacques Brotchi, MD, Michael Bruneau, MD, and Danielle Baleriaux, MD
CHAPTER 23
2. Falcine Meningioma 349
Jacques Brotchi, MD, Michael Bruneau, MD, and Danielle Baleriaux, MD
CHAPTER 24
3. Superior Sagittal Sinus Invasion and Its Repair 355
Marc P. Sindou, MD, PhD and Jorge E. Alvernia, MD
CHAPTER 25
4. Olfactory Groove Meningiomas 373
William T. Couldwell, MD, PhD and Jeroen R. Coppens, MD
CHAPTER 27
5. Anterior Clinoidal Meningioma 395
M. Necmettin Pamir, MD
CHAPTER 29
6. Suprasellar Meningioma 407
Edward R. Laws, Jr, MD, FACS,
Chirag G. Patil, MD, MS, and John A. Jayne, Jr, MD, PhD, FRCS(C)
CHAPTER 30
7. Suprasellar Meningioma 407
Edward R. Laws, Jr, MD, FACS,
Chirag G. Patil, MD, MS, and John A. Jayne, Jr, MD, PhD, FRCS(C)CHAPTER 30
8. Microscopic Extended Endonasal
Approach to Suprasellar Meningioma 413
Daniel F. Kelly, MD, Dennis Malkasian, MD, PhD,
Nasrin Fatemi, MD, Joshua R. Dusick, MD, and Manoel A. de Paiva Neto, MD
CHAPTER 31
9. Supra-Orbital Removal of an Olfactory
Groove Meningioma 413
Daniel F. Kelly, MD, Dennis Malkasian, MD, PhD,
Nasrin Fatemi, MD, Joshua R. Dusick, MD, and Manoel A. de Paiva Neto, MD
CHAPTER 31
10. Sylvian Meningioma 427
M. Necmettin Pamir, MD
CHAPTER 32
11. The Retrosigmoid Suprameatal
Approach in a Case of a Petroclival
Meningioma 503
Rudolf Fahlbusch, MD, PhD and Venelin M. Gerganov, MD, PhD
CHAPTER 39
12. Cerebello-Pontine Angle
Meningioma 529
Peter M. Black, MD, PhD, FACS and James A. J. King, MBBS, PhD, FRACS
CHAPTER 42
13. Cerebellopontine Angle Meningiomas 529M. Necmettin Pamir, MD
CHAPTER 42Table of Contents
Instructions for online access
Front matter
Copyright
Dedication
Contributors
Preface
Videos
Neurobiology of Meningiomas
Chapter 1: Meningioma: History of the Tumor and Its Management
Chapter 2: Meningeal Anatomy
Chapter 3: The Origin of Meningiomas
Chapter 4: Epidemiology and Natural History of Meningiomas
Chapter 5: Radiation-Induced Meningiomas
Chapter 6: Neuropathology of Meningiomas
Chapter 7: Biology of Meningiomas
Chapter 8: Molecular Biology and Genetics of Meningiomas
Chapter 9: Meningiomas and Brain Edema
Chapter 10: Angiogenesis in Meningiomas
Diagnosis of Meningiomas
Chapter 11: Clinical Presentation of Meningiomas
Chapter 12: Neuro-ophthalmology of Meningiomas
Chapter 13: CT Evaluation of Meningiomas
Chapter 14: MRI Evaluation of Meningiomas
Chapter 15: Advanced MRI and PET Imaging of Meningiomas
Chapter 16: Angiographic Evaluation of MeningiomasChapter 17: Automatic Tumor Growth Detection
Surgery of Meningiomas
Chapter 18: Decision Making in Meningiomas
Chapter 19: Perioperative Management of Patients with Meningiomas
Chapter 20: Anesthetic and Intensive Care Management of the Patient
with a Meningioma
Chapter 21: Indications and Technology of Neurophysiologic
Monitoring in Meningioma Surgery
Chapter 22: The Cerebral Venous System in Meningioma Surgery
Surgery of Meningiomas by Site of Origin
Chapter 23: Surgery of Convexity Meningiomas
Chapter 24: Parasagittal and Falx Meningiomas
Chapter 25: Dural Sinus Invasion in Meningiomas and Repair
Chapter 26: Management of Superior Sagittal Sinus Invasion in
Parasagittal Meningiomas: Resection Versus Irradiation
Chapter 27: Olfactory Groove Meningiomas
Chapter 28: Suprasellar Meningiomas
Chapter 29: Anterior Clinoidal Meningiomas
Chapter 30: Intrasellar and Diaphragma Sellae Meningiomas
Chapter 31: Minimally Invasive Approach to Frontal Fossa and
Suprasellar Meningiomas
Chapter 32: Sphenoid Wing Meningiomas
Chapter 33: Primary Optic Nerve Sheath Meningiomas
Chapter 34: Cavernous Sinus Meningiomas
Chapter 35: Middle Fossa Meningiomas
Chapter 36: Overview of Petroclival Meningiomas
Chapter 37: The Posterior Petrosal Approach for the Treatment of
Petroclival Meningiomas
Chapter 38: Petroclival Meningiomas: Middle Fossa Anterior
Transpetrosal Approach
Chapter 39: Petroclival Meningiomas: Suboccipital Retrosigmoid
ApproachChapter 40: Presigmoid Keyhole Approach for Petroclival Meningiomas
Chapter 41: Tentorial and Falcotentorial Meningiomas
Chapter 42: The Surgical Management of Cerebellopontine Angle
Meningiomas
Chapter 43: Cerebellar Convexity Meningiomas
Chapter 44: Foramen Magnum Meningiomas
Chapter 45: Intraventricular Meningiomas
Chapter 46: Spinal Meningiomas
Chapter 47: Pediatric Meningiomas
Chapter 48: Meningiomas and Neurofibromatosis Type 2
Chapter 49: Multiple Meningiomas
Radiation and Chemotherapy for Meningiomas
Chapter 50: Fractionated Radiation for Meningiomas
Chapter 51: Gamma Knife® Radiosurgery for Convexity and
Parasagittal Meningiomas
Chapter 52: Radiosurgery for Meningiomas (With Special Emphasis on
Skull-Base Meningiomas)
Chapter 53: LINAC-Based Stereotactic Radiosurgery and Stereotactic
Radiotherapy for Parasagittal, Skull-Base, and Convexity Meningiomas
Chapter 54: Proton Radiation Therapy for Meningiomas
Chapter 55: Cyberknife® Radiosurgical Ablation of Meningiomas
Chapter 56: Chemotherapy and Experimental Medical Therapies for
Meningiomas
Chapter 57: Gene Therapy for Meningiomas
Special Topics
Chapter 58: Recurrence of Meningiomas and Its Management
Chapter 59: Management of Atypical and Anaplastic Meningiomas
Chapter 60: Meningioma Metastasis
Chapter 61: Meningiomas: A Patient's View
Chapter 62: Emerging Surgical Techniques for the Treatment of
Meningiomas
Chapter 63: Experimental Meningioma ModelsChapter 64: Challenges and Opportunities in Future Meningioma
Research and Care
IndexNeurobiology of
MeningiomasCHAPTER 1
Meningioma
History of the Tumor and Its Management
Chirag G. Patil, Edward R. Laws, Jr.
Meningioma/s has attracted the attention of surgeons, anatomists, pathologists,
and physicians for many centuries. Given the tendency of these neoplasms to cause
thickening of the overlying calvarium, meningiomas have left an unmistakable
1-4mark on human skulls dated as far back as prehistoric times. Most of this
evidence has come from the well-preserved skulls of the Incas in the Peruvian
Andes that show classic hyperostosis indicating the presence of an underlying
meningioma (Fig. 1-1).
FIGURE 1-1 Prehistoric Peruvian skull, showing hyperostosis from an underlying
meningioma.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
Felix Plater (Fig. 1–2) was probably the ) rst to describe a meningioma in morerecent times. Born in 1536 in Sion, Switzerland, he was educated at Montpellier,
where he received his doctorate in 1557. Caspar Bonecurtius, a nobleman, was
Plater’s patient with a meningioma who presented with gradual physical and
mental deterioration. On autopsy, Plater described a round 4eshy tumor, like an
5,6acorn. It was as large as a medium-sized apple, hard and full of holes. It was
covered with a membrane and entwined with veins. Plater described it as having
no connections with the matter of the brain, so much so that when it was removed
by hand, it left behind a remarkable cavity. This ) rst clear description of a
7,8meningioma is most consistent with an encapsulated meningioma. Felix Plater
continued to practice as a distinguished Professor of Medicine at the University of
Basel and died in Basel at the age of 78.
FIGURE 1-2 Felix Plater (1536–1614) of Switzerland, the ) rst to describe a
meningioma.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
NOMENCLATURE
Harvey Cushing coined the term meningioma in 1922 to describe a benign
neoplasm of the meninges of the brain. However, many other surgeons and
pathologists described and named this neoplasm as well. In fact, naming of the
tumor likely represents one of the most frequently changed nomenclatures in thehistory of medicine. Antoine Louis, born in Metz, France, in 1723 into a family of
surgeons, developed an interest in surgery of dural tumors, which he named
9tumeurs fongueuses de la dure-mere or fungoid tumors of the dura mater. He
included their description in Memoire de l’Académie Royale de Chirurgie in 1774. In
1854, Sir James Paget named the neoplasm myeloid tumor (marrow like), based on
its gross appearance and less malignant behavior. In 1863, Virchow was the ) rst to
describe the granules in these tumors and named it psammoma (sand-like). As
Virchow was uncertain of the origin of these bodies, he gave the neoplasm a
descriptive name. Subsequently, he changed the nomenclature from psammoma to
2,10Sarkoma der dura mater to describe these tumors.
In the mid-1800s, Meyer, Bouchard, and Robin popularized the term epithelioma
2,10which was replaced later by the term endothelioma. Golgi believed that
because the tumor was of mesenchymal origin, endothelioma was a more suitable
term. Despite the myriad terminology, Virchow’s “sarcoma” and “psammoma” and
Golgi’s “endothelioma” came into general use in the late 1800s and early 1900s.
Harvey Cushing was troubled by the confusion that resulted from the diCerent
nomenclatures and thought that it would be desirable to place this tumor under a
single uni) ed designation. Cushing knew that since the cellular composition of the
tumor was in dispute, a histogenic name would not be universally accepted.
Further, because these tumors arose from many areas of the brain, a location-based
tumor name was not possible. Therefore, Cushing decided on a simple, suitable
“tissue name,” meningioma, that was “noncommittal and all-embracing.” In his
Cavendish lecture in 1922, Harvey Cushing used this designation to discuss 85
10patients with these tumors.
CLASSIFICATION
2In 1863, Virchow was the ) rst to attempt a classi) cation of meningiomas. This
was followed by classi) cation schemas by Engert (1900), Cushing (1920), Oberling
2,11(1922), Globus (1935), Russell and Rubinstein (1971), and others. The World
Health Organization (WHO) classi) cation is widely used today and has been
12revised regularly. It includes the recent concept of the “atypical meningioma” as
an aggressive variant. Table 1-1 lists the various classifications described.
TABLE 1-1 Classification of meningiomas.
Year Author Classification
1900 Engert Four types: (1) fibromatous; (2) cellular; (3)
sarcomatous; (4) angiomatous1920 Cushing Five types: (1) frontal; (2) paracentral; (3) parietal; (4)
occipital; (5) temporal
1922 Oberling; Three types: (1) type neuroepithelial; (2) type glial
later fusiforme; (3) type conjunctif
endorsed by
Roussy
1928 Cushing and Four types: (1) meningothelial; (2) fibroblastic; (3)
Bailey angioblastic; (4) osteoblastic
1930 Bailey and Nine types: (1) mesenchymatous; (2) angioblastic; (3)
Bucy meningotheliomatous; (4) psammomatous; (5)
osteoblastic; (6) fibroblastic; (7) melanoblastic; (8)
lipomatous; (9) generalized sarcomatosis of the
meninges.
1935 Globus Five types: (with emphasis on the tumor content of pial
vessels: (1) leptomeningioma; (2) pachymeningioma; (3)
meningioma omniforme; (4) meningioma
indifferentiale; (5) meningioma piale
1938 Cushing and Nine types with subvariants: (1) non-reticulin or
Eisenhardt collagen-forming meningothelial tumor; (2)
meningothelial tumor pattern with tendency to form
reticulin or collagen; (3) reticulin- or collagen-forming
fibroblastic tumors of benign type; (4) reticulin-forming
angioblastic tumors; (5) non–reticulin- or collagen
forming epithelioid tumors; (6) reticulin- or
collagenforming fibroblastic tumors of malignant type; (7)
osteoblastic meningiomas; (8) chondroblastic
meningiomas; (9) lipoblastic
1971 Russell and Five types: (1) syncytial; (2) transitional; (3)
Rubinstein fibroblastic; (4) angioblastic; (5) mixed type
2007 WHO (World (1) meningothelial: (2) fibrous (fibroblastic); (3)
Health transitional (mixed); (4) psammomatous; (5)
Organization) angiomatous; (6) microcystic; (7) secretory; (8)
lymphoplasmacyte-rich; (9) metaplastic; (10) chordoid;
(11) clear cell; (12) atypical; (13) papillary; (14)
rhabdoid; (15) anaplastic (malignant)
2Adapted from Al-Rodhan and Laws (1990).PATHOGENESIS
Antonius Pacchioni described arachnoidal granulations in 1705 as analogous to
13lymph glands. It was not until 1846, however, that Rainey suggested that these
14granulations were leptomeningeal in origin. Luschka, Ludwig Meyer, and Key
and Retzius supported this view but the association between the granulations and
meningeal tumors went unrecognized. In 1864, John Cleland, a Professor of
15Anatomy at Glasgow, described two dural tumors. One was an olfactory groove
tumor and the other was right frontal in origin. In the dissecting suite, Cleland was
able to separate the tumors from the dura, and hence appropriately described them
a s villous tumors of the arachnoid (Fig. 1-3). He suspected that they must have
originated from the pacchionian corpuscles and attributed to them an arachnoidal
origin. In 1902, Schmidt, after microscopic examinations of a series of meningeal
tumors concluded that the cellular structure of these tumors was similar to the cell
16clusters capping the arachnoid villi (Fig. 1-4). Many other competing theories on
the origin of these tumors were proposed by some of the leading physicians of the
17 18time, including Ribbert (connective tissue origin), Oberling (glial origin), and
19Roussy and Cornil (neuroepithelial origin). It was not until 1915, after Cushing
and Weed con) rmed that meningeal tumors arose from arachnoid cap cells, that
20Cleland’s theory gained widespread acceptance.
FIGURE 1-3 Cleland’s illustration of a villous tumor of the arachnoid.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)FIGURE 1-4 Schmidt’s illustration of cell clusters capping an arachnoid villus.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
ETIOLOGY
The association between head injury and meningioma development was ) rst
21proposed by Berlinghieri in 1813. In 1888, Keen published a series of three
surgical cases including a meningioma wherein he discussed the potential
connection between head injury and meningioma. Cushing agreed with this
2connection and wrote :
In so many cases in the series has a tumor been found at the exact situation
where a stunning blow had been received on the skull years before, that this
must represent something more than a mere coincidence. On the
circumstantial evidence it is tempting to assume that the injury has bruised
the meninges and caused an extravasation to aid in the absorption of which
the local cell-clusters have been incited into a state of morbid activity.
22In 1986, Barnett and colleagues concluded that the association between
meningioma and head trauma was largely anecdotal, but thought that trauma may
contribute in the development of meningiomas in some cases. This association was
22later refuted by a systematic epidemiological analysis.
Chronic irritation from abscess, hemorrhage, and tuberculosis were thought to
have possible connection with the development of meningioma. Cushing and
Eisenhardt, based on their experience in treating patients with von
Recklinghausen’s disease, implicated congenital factors in the etiology of
2meningioma. In 1981, Deen and Laws presented evidence supporting the irritation
theory by describing meningiomas that had developed contiguous to other primary
23brain tumors. Finally, cranial radiation has been shown to induce development24of meningioma.
RADIOGRAPHY
In 1897, Obici and Bollici were the ) rst to image the cranium, followed by
Oppenheim’s announcement in 1889 that imaging of the sella turcica was
2possible. In 1902, Mills and Pfahler were the ) rst to provide a radiologic account
25of a meningioma.
An exposure of four minutes made with a moderately hard vacuum. A
negative was obtained which showed good detail of all the structures. A
large shadow lying between the coronal suture and the posterior meningeal
artery corresponded to the area in which Dr. Mills located the tumor.
By 1920 may other reports of meningiomas were published and
stereoroentgenoscopy was in widespread use. The technology progressed through a series
of improvements such as replacement of the old glass plates with more sensitive
7) lms, thus shortening exposure time. However, the largest improvement in the
visualization of brain tumors (including meningiomas) came with Dandy’s seminal
26paper on the use of ventriculograpy in 1918. Later as the utility of
ventriculograpy became more apparent, Cushing and Eisenhardt described it as
“one of the most dependable contributions to tumor localization and diagnosis ever
2made.”
SURGICAL RESECTION
In 1743, Heister in Helmstead, Germany was the ) rst to treat a meningioma
2surgically. His patient was a 34-year-old Peruvian soldier who developed a
postoperative infection and died after Heister had applied a caustic lime to the
tumor. At autopsy, Heister termed the tumor de tumore capitis fungoso. Olaf Acrel
(Fig. 1-5A), the father of Swedish surgery, operated on a brain tumor in a
30-year2old patient with a history of head injury 18 months earlier (Fig. 1-5B). The patient
was found to have a pulsatile tumor that was explored by insertion of a ) nger.
Severe bleeding and convulsions ensued and the patient died a few days later.
FIGURE 1-5 A, Olaf Acrel, the father of Swedish surgery (1717–1806). B,
Illustration of Olaf Acrel’s case of meningioma in 1768.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
In 1847, Zanobi Pecchioli of Italy performed the ) rst successful meningioma
27removal. He was a professor of operative medicine and surgery at Siena
University and published a series of 1524 operations, 16 of which were
neurosurgical procedures. One of his cases involved a large meningioma of the
right sinciput. He removed the tumor through a triangular 4ap made by drilling
three widely spaced burr holes. The operative site was covered with sweet almond
oil–soaked cambric. The patient survived for more than 30 months, and in 1840,
the description of this operation was chosen for the competition for the chair of
surgery at the University of Paris.In 1879, Sir William McEwen carried out a successful meningioma removal in
Glasgow, the ) rst in northern Europe (Fig. 1-6). In the 19th century, the most
celebrated and well known neurosurgical operation was performed by Franceso
21,28Durante (Fig. 1-7) of Italy on June 1, 1885. His patient was a 35-year-old
woman with a left olfactory grove meningioma. Durante completely resected the
lobular apple size tumor, which weighed 70 grams, in 1 hour. He left a drainage
tube that came down to the left nasal fossa through the opening made in the
ethmoid sinus by the tumor. On postoperative day 7 the tube was removed and the
patient was discharged home. The patient did very well and required a reoperation
11 years later for a recurrence. As a result of the favorable outcome of the patient,
this case was published in Lancet in 1887 and presented at the International
28Medical Congress in Washington, DC, in September of the same year.
FIGURE 1-6 Sir William McEwen.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)FIGURE 1-7 Francesco Durante (1844–1934).
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
William W. Keen (Fig. 1-8), one of America’s pioneer neurosurgeons, was the ) rst
to successfully remove a meningioma in the United States on December 15, 1887.
Keen was chair of surgery at the JeCerson Medical College in his home town of
Philadelphia. His meningioma patient was a 26-year-old carriage maker with
headaches, seizures, and partial blindness (Fig. 1-9). The patient reported a history
of head injury as a child and Keen documented an aphasia and a right hemiparesis
on physical examination. The operation was performed after intricate antiseptic
measures such as removal of the carpet from the operating theater and cleaning of
the walls and ceiling. The operation commenced at 1 P.M. to maximize natural
light and lasted 2 hours. The tumor, weighing 88 grams, was completely removed
via a frontotemporal craniotomy. Although the procedure was complicated by
cerebrospinal 4uid leakage and poor wound healing for 5 weeks, the patient
recovered and was discharged on postoperative day 84. In gratitude, the patient
promised Keen his brain for study. Keen, nearly 30 years older than the patient,
outlived him. The patient died 30 years and 44 days after the operation, and the
7,29promise was kept on January 29, 1918.FIGURE 1-8 William W. Keen (1837–1932) of Philadelphia, Pennsylvania.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
FIGURE 1-9 Keen’s early case of a meningioma.
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
Harvey Cushing’s contributions to the surgical resection of meningioma are
unequaled. Born in Cleveland, Ohio, Harvey Cushing (Fig. 1-10) graduated
Harvard Medical School in 1895 and joined Halsted’s surgical service at the Johns
Hopkins Hospital in Baltimore. In 1912, he became Professor of Surgery at Harvard
and Surgeon-in-Chief at the Peter Bent Brigham Hospital. Cushing’s most famousmeningioma patient was General Leonard Wood, a military surgeon, Chief of StaC
of the United States Army. In 1909, he presented to Cushing with frequent
leftsided jacksonian attacks. The next year, Cushing, in a two-stage operation, 4 days
apart, resected his right parasagittal meningioma. General Wood was discharged in
good health and went on to be the Republican favorite to succeed President
Woodrow Wilson. He re-consulted Cushing in 1927, complaining of severe left
sided spasticity. Unfortunately, hours after this reoperation, Wood suCered an
2intraventricular hemorrhage and died.
FIGURE 1-10 Harvey Cushing (1869–1939).
(From al-Rodhan NR, Laws ER Jr. Meningiomas: a historical study of the tumor and its
surgical management. Neurosurgery 1990:26(5):832–46; discussion 846–7.)
COMMENTARY
The improvement in neurosurgical outcomes at the turn of the 20th century was a
result of more re) ned surgical technique, application of Lister’s antiseptic
4,7principles, and more precise localization of tumor. Cushing’s contributions were
crucial to the advancement of intracranial surgery for meningioma and for that
matter, all of neurosurgery in general. In 1922, Cushing concluded his Cavendish
10lecture by saying :
There is today nothing in the whole realm of surgery more gratifying thanthe successful removal of a meningioma with subsequent perfect functional
recovery, especially should a correct pathological diagnosis have been
previously made. The diL culties are admittedly great, sometimes
insurmountable and though the disappointments still are many, another
generation of neurological surgeons will unquestionably see them largely
overcome.
MacCarty, considering the role of meningioma in neurosurgical history, thought
that it had the most prominent role on the development of surgery of the central
30nervous system :
The road toward understanding and managing meningiomas has been long
and eventful. Although many problems remain unsolved, the cumulative
contributions of many generations of anatomists, pathologists,
neurosurgeons, engineers, and, most of all patients have made the most
diL cult and inaccessible meningiomas within the safe reach of the modern
neurosurgeon.
References
[1] Abbott K.H., Courville C.B. Historical notes on the meningiomas. I. A study of
hyperostosis in prehistoric skulls. Bull Los Angeles Neurol Soc. 1939;4:101-113.
[2] Cushing H., Eisenhardt L. Meningiomas: Their Classification, Regional Behaviour,
Life History and Surgical End Results. Springfield, IL: Charles C Thomas, 1938.
[3] Moodie R.L. Studies inR. XVIII. Tumors of the head among pre-Columbian
Peruvians. Ann Med Hist. 1926;8:394-412.
[4] Wang H., Lanzino G., Laws E.R.J. Meningioma: the soul of neurosurgery: historical
review. Sem Neurosurg. 2003;14:163-168.
[5] Netsky M.G. The first account of a meningioma. Bull Hist Med. 1956;30:465-468.
[6] Plater F. Observationum in hominis affectibus plerisque, corpori et animo,
functionum laesione, dolore, aliave molestia et vitio incommodantibus, libri tres.
Basileae: Impensis Ludovici Konig, 1614.
[7] Al-Rodhan N.R., Laws E.R.Jr. Meningioma: a historical study of the tumor and its
surgical management. Neurosurgery. 1990;26:832-846. discussion 846–837
[8] Al-Rodhan N.R., Laws E.R.Jr. Meningioma: a historical study of the tumor and its
surgical management. In: Al-Mefty O., editor. Meningioma. New York: Raven
Press; 1991:1-8.
[9] Louis A. Mémoire sur les Tumeuers Fongueuses de la Dure-mère. Mem Acad R Chir
Paris. 1774;5:1-59.
[10] Cushing H. The meningiomas (dural endotheliomas): their source, and favored
seats of origin. Brain. 1922;45:282-316.
[11] Russell D.S., Rubenstein L.J. Pathology of Tumors of the Nervous System. London:Edward Arnold, 1971.
[12] Louis D.N., Ohgaki H., Wiestler O.D., Cavanee W.K. WHO Classification of
Tumours of the Central Nervous System. Geneva: WHO Press, 2007.
[13] Pacchioni A. Dissertatio epistolaris de gladulis conglobatis durae meningis
humanae, 1705. Rome
[14] Rainey G. On the ganglionic character of the arachnoid membrane of the brain
and spinal marrow. Med Chir Trans. 1846;29:85-102.
[15] Cleland J. Description of two tumors adherent to the deep surface of the dura
mater. Glasgow Med J. 1864;11:148-159.
[16] Schmidt M. Ueber die pachioniischen Granulationen u. ihr Verhaltniss zu den
Sarcomen u. Psammomen der Dura Mater. Virchows Arch. 1902;170:429-469.
[17] Ribbert M.W. Uber das Endotheliom der Dura. Virchows Arch. 1910;200:141-151.
[18] Oberling C. Les tumeurs des meninges. Bull Assoc Franc Cancer. 1922;11:365-394.
[19] Learmonth J.R. On leptomeningiomas (edotheliomas) of the spinal cord. Br J
Surg. 1927;14:396-476.
[20] Cushing H., Weed L.H. Studies on the cerebrospinal fluid and its pathway. IX.
Calcarious and osseous deposits in the arachnoidea. Johns Hopkins Hosp Bull.
1915;26:367-372.
[21] Guidetti B., Giuffre R., Valente V. Italian contribution to the origin of
neurosurgery. Surg Neurol. 1983;20:335-346.
[22] Barnett G.H., Chou S.M., Bay J.W. Posttraumatic intracranial meningioma: a case
report and review of the literature. Neurosurgery. 1986;18:75-78.
[23] Deen H.G., Laws E.R. Multiple primary brain tumors of different cell types.
Neurosurgery. 1981;8:20-25.
[24] Waga S., Handa H. Radiation-induced meningioma: with review of literature.
Surg Neurol. 1976;5:215-219.
[25] Mills C.K., Pfaher G.E. Tumors of the brain localized clinically and by roentgen
rays, with some observations relating to the use of the roentgen rays in the
diagnosis of lesions of the brain. Phil Med J. 1902;9:268-273.
[26] Dandy W.E. Ventriculography following the injection of air into the cerebral
ventricles. Ann Surg. 1918;68:5-11.
[27] Giuffre R. Successful radical removal of an intracranial meningioma in 1835 by
Professor Pecchioli of Siena. J Neurosurg. 1984;60:47-51.
[28] Durante F. Contribution to endocranial surgery. Lancet. 1887;2:654-655.
[29] Keen W.W., Ellis A.G. Removal of a brain tumor, report of a case in which the
patient survived for more than thirty years. JAMA. 1918;70:1905-1909.
[30] MacCarty C.S. The Surgical Treatment of Intracranial Meningiomas. Springfield,
IL: Charles C Thomas, 1961.
'

CHAPTER 2
Meningeal Anatomy
Askin Seker, Carolina Martins, Albert L. Rhoton, Jr.
THE MENINGEAL COVERINGS
The brain and spinal cord are covered by layers of connective tissue called meninges,
from the Greek word meninx, which means membrane. In shes, only a single layer, the
primitive meninx, is present. Amphibians and reptiles have two meningeal layers, the
outer dura mater (meaning “hard mother”) and an inner, thin layer the secondary
meninx. In mammals and birds, three meningeal layers are present. The pia mater
(meaning “tender mother”) is thin, vascular, and closest to the brain. The arachnoid
membrane, which has a spider web–like appearance, is the middle, avascular layer. The
space between the pia mater and arachnoid is the subarachnoid space. The outermost
layer is the dura mater, composed of two layers. Therefore, the meningeal coverings
consist of three membranous layers, composed primarily of broblasts, varying amounts
of extracellular connective tissue and one well-organized uid-containing space. The
membranes are the dura mater (pachymeninx) and the leptomeninges (arachnoid and
pia mater). The use of the word mater (“mother”) to describe these membranes comes
from the ancient notion that they were the origin, or mother, of all membranes in the
1body.
THE LEPTOMENINGES
Leptomeninx is the term used when the pia mater and arachnoid are considered together
as a functional unit and contraposed to pachymeninx (from the Greek packys, meaning
2thick), designates the finer meningeal coverings.
The arachnoid is attached to the overlying dura mater. It consists of several layers of
translucent cells that follow with the dura and a contingent of cells that form spindly
trabeculae that bridge the subjacent space and attach to the pia mater on the surface of
the brain. The subarachnoid space is bordered outside by the layer of arachnoid cells
attached to the dura and on the inside by pial cells on the surface of the neural tissue.
These structural relationships form the basis for the occurrence of the subarachnoid
cisterns, which are dilations of the subarachnoid space containing arteries, veins, and
neural structures (see Table 2-1 later).
TABLE 2-1 Classification of subarachnoid cisterns.'


The arachnoid granulations or villi are specialized segments of the arachnoid and
subarachnoid space that invaginate along the dura mater of the sinus and are involved on
cerebral spinal uid resorption. Although present in any major dural sinuses, they are
most concentrated along the superior sagittal sinus, where they enter into the sinus cul de
sacs (lacunae lateralis). These large arachnoid granulations leave indentations, called the
granular fovea, in the inner table of the skull, parallel to the superior sagittal sinus
groove.
Pial cells form a delicate membrane intimately attached to the neural surface,
surrounding vessels located in the subarachnoid space and interconnecting with the
arachnoid trabecular cells. Spinal pial cells contribute to the formation of the denticulate
ligaments, located on the lateral surface of the cord, halfway between the dorsal and
ventral roots and extending laterally to the inner surface of the spinal dura. In likewise
manner, the lum terminale arises from the conus medullaris, has a core of pial cells and
an arachnoid cells covering, and transverses the subarachnoid space of the lumbar cistern
to attach to the inner surface of the caudal extreme of the dural sac.
GENERAL STRUCTURE OF THE DURA MATER: ENDOSTEAL AND
MENINGEAL LAYERS
The cranial dura mater is a thick, collagenous sheath that lines the cranial cavity and is
continuous with the spinal dura at the foramen magnum. The dura is adherent to the
surrounding bones, especially at the sutures, cranial base, and around the foramen
magnum. With increasing age, the dura becomes less pliable and more rmly adherent to
the inner surface of the skull, particularly at the calvaria.
The dura is composed of an endosteal layer that faces the bone and a meningeal layer
3that faces the brain. These layers are distinguished as separate sheaths at the venous'
'
sinuses, foramen magnum, and optic canal. The meningeal layer is continuous with the
dural covering of the spinal cord and optic nerves, providing tubular sheaths for the
cranial nerves as they pass through the cranial foramina. These sheaths fuse with the
epineurium as the cranial nerves emerge from the skull, except at the optic nerve, where
the dural sheath blends into the sclera. At the vascular foramina, the meningeal layer
fuses with the adventitia of the vessel. The meningeal layer folds inwards to form the falx
cerebri, the tentorium cerebelli, the falx cerebelli, and the diaphragm sellae, which
partially divide the cranial cavity into freely communicating spaces. The endosteal layer
of dura is continuous through the cranial sutures and foramina with the pericranium and
3through the superior orbital fissure and optic canal with the periorbita.
The walls of the cavernous sinus are formed by the dura lining the internal surface of
the calvaria. In the lateral portion of the middle cranial fossa, the meningeal and
endosteal layers are tightly adherent, but at the lateral aspect of the trigeminal nerve they
are separated into two layers. At the upper border of the maxillary nerve, which is the
most inferior limit of the cavernous sinus, the meningeal layer extends upward to form
the outer part of the lateral wall of the cavernous sinus, and it wraps around the anterior
petroclinoid fold, extending medially to form the roof of the cavernous sinus and the
upper layer of the diaphragm sellae. The endosteal layer, at the upper border of the
maxillary nerve and the lower margin of the carotid sulcus, divides into two layers. One
layer adheres to the sphenoid bone, covering the carotid sulcus and the oor of the sella,
and the other layer extends upward to constitute the internal layer of the lateral wall and
roof of the cavernous sinus and diaphragm sellae. The endosteal layer invests the cranial
nerves coursing in the lateral wall of the cavernous sinus. The thin layer in the sellar part
of the medial wall of the cavernous sinus is thought to represent a continuation of the
meningeal dural layer that faces the brain. Thus, two layers line the sellar oor and the
lower surface of the pituitary gland, one that is adherent to the sphenoid bone and the
other that comes from the diaphragm and wraps around the pituitary gland. Therefore,
with the exception of the paired lateral aspects of the sella and pituitary gland that are
covered by one layer, two layers cover the other sellar surfaces. The meningeal and
endosteal layers of the lateral wall and cavernous sinus roof and diaphragm sellae
continue anteriorly to line the anterior cranial fossa and posteriorly as the covering of the
dorsum sellae and clivus. The meningeal layer also continues anteriorly to form the upper
(distal) dural ring around the carotid artery and the optic sheath, whereas the endosteal
layer continues anteriorly and medially to form the lower (proximal) dural ring around
4the carotid artery.
VASCULAR ORGANIZATION OF DURA
The origin of the membranes of the skull starts when the embryo has a crown-to-rump
length of 12 to 20 mm, at which time di4erentiation of the skull, dura mater, arachnoid,
and pial membranes begins. The gradual cleavage of the vascular system into external,
dural, and cerebral layers also takes place at this stage, which has been referred to as the
5third stage of cerebrovascular development. As the membranes covering the brain
di4erentiate, the anastomosing channels that connect the deep capillary plexus with the

super cial vessels close, thus separating the vessels surrounding the brain from those
5,6belonging to the skull and its coverings. The major meningeal arteries originating from
this cleavage give rise to a rich anastomotic network that may enlarge after various
7insults and play a role in the genesis of dural arteriovenous malformations. This
anastomotic network divides progressively into primary, secondary, and penetrating
vessels.
The primary anastomotic vessels change little in diameter as they course over the dural
surface and anastomose frequently with each other. They cross the superior sagittal sinus,
connecting the dura over the paired cerebral hemispheres into a single vascular unit.
Crossing vessels are particularly large when one middle meningeal artery is hypoplastic.
The primary anastomotic arteries have a straight course and measure 100 to 300 m in
diameter, whereas the main meningeal feeders have a diameter of 400 to 800 m. The
primary anastomotic arteries give rise to arteries to the skull, secondary anastomotic
8arteries, penetrating dural vessels, and arteriovenous shunts.
Secondary anastomotic arteries also lie on the outer dural surface. They measure 20 to
40 microns in diameter, are short, and their anastomotic pattern form a regular
8polygonal network. Penetrating vessels arise from primary and secondary anastomotic
arteries, leave the dural surface and extend to within 5 to 15 m of inner and
juxtaarachnoid surface of dura, to end in the capillary network. Capillaries, 8 to 12 m in
diameter, are present throughout dura, including the falx and tentorium, and are
especially rich parasagittally, where they may form several layers. The capillary bed is
located on the inner or cerebral surface of dura and is separated from arachnoid by only
8a few microns.
The arteries to the skull originated from the primary anastomotic vessels. They are well
seen when the dura is stripped from the skull and many small arteries are torn out of the
diploe, revealing their tiny foramina on the inner table of the skull. They measure 40 to
80 microns and supply the metabolic needs of the skull and diploic contents. These
vessels, which are often enlarged in dural arteriovenous malformations, can be a source
of copious bleeding during elevation of the bone flap, during craniotomy.
Overview of Dural Supply
The dural arteries arise from the internal and external carotid, vertebral, and basilar
arteries (Table 2-1) and may be the site of formation of saccular aneurysms,
pseudoaneurysms, and arteriovenous stulas and the source of traumatic and
spontaneous hemorrhage into the epidural, subdural, and intraparenchymal area, in
addition to the well known role in the vascularization of meningiomas, other tumors, and
parenchymal arteriovenous malformations (AVMs).
The pattern of arterial supply of the dura covering the skull base is more complex than
over the convexity. The internal carotid system supplies the midline dura of the anterior
and middle fossae and the anterior limit of posterior fossa; the external carotid system
supplies the lateral segment of the three cerebral fossae; and the vertebrobasilar system
supplies the midline structures of the posterior fossa and the area of the foramen'
'

magnum. Dural territories often have overlapping supply from several sources. Areas
supplied from several overlapping sources are the parasellar dura, tentorium, and falx.
The tentorium and falx also receive a contribution from the cerebral arteries, making
these structures an anastomotic pathway between dural and parenchymal arteries. A
reciprocal relationship, in which the territories of one artery expand if the adjacent
arteries are small, is common.
The dura covering the anterior fossa oor draws its supply from the anterior and
posterior ethmoidal arteries, the super cial recurrent ophthalmic artery, and the middle
meningeal artery (Fig. 2-1). The middle meningeal artery will not contribute to the
supply of the dura lining the oor of anterior fossa if the artery or its anterior branch
arises from the ophthalmic arterial system. The territory of the anterior convexity and
parasagittal area is supplied by both the anterior branch of the middle meningeal artery
and the anterior meningeal branch from the ophthalmic artery (Fig. 2-2).
'
FIGURE 2-1 Superior view of the skull base showing the area of supply of the individual
meningeal arteries. Dural branches from the internal carotid arterial system are
highlighted in shades of green, external carotid system in shades of blue, and the
vertebrobasilar system in shades of red. A, Internal carotid system. The dura covering the
medial part of the anterior fossa oor is supplied by the anterior and posterior ethmoidal
arteries, the super cial recurrent ophthalmic artery, and olfactory branches of the
anterior cerebral artery. The internal carotid system, through its inferolateral trunk and
dorsal meningeal artery, supplies most of the parasellar dura and part of the anterior
wall of the posterior fossa and the sellar dura through its paired capsular, inferior
hypophyseal, medial clival, and dorsal meningeal arteries. B, External carotid system. The
anterior and posterior divisions of the middle meningeal artery and its petrosal branch
supply the dura covering the lateral skull base. The territories of the anterior and
posterior branches of the middle meningeal artery extend toward the supra- and
infratentorial convexity dura and medially over the falx and tentorium. The accessorymeningeal and the ascending pharyngeal artery branches contribute to the supply of the
area between the internal carotid and middle meningeal territories on the middle and
posterior fossae. The jugular and hypoglossal branches of the ascending pharyngeal
arteries supply the inferior portion of the posterior surface of the petrous bone, lateral
cerebellar dura, the midclivus, and anterolateral foramen magnum. The mastoid branch of
the occipital artery constitutes the main supply to the lateral part of the cerebellar fossae.
C, Vertebrobasilar system. The anterior and posterior meningeal branches of the vertebral
artery supply the foramen magnum dura. The posterior meningeal artery provides the
major supply to the paramedial and medial portions of the dura covering the cerebellar
convexity. The subarcuate artery, a branch of the anterior inferior cerebellar artery,
supplies the dura of the posterior surface of the petrous bone and adjacent part of the
internal acoustic meatus, as well as the bone in the region of the superior semicircular
canal. D, Overview. A., artery; Access., accessory; Ant., anterior; Asc., ascending; Br.,
branch; Brs., branches; Caps., capsular; Car., carotid; Cer., cerebral; Cliv., clival; Div.,
division; Dors., dorsal; Eth., ethmoidal; For., foramen; Hypogl., hypoglossal; Inf., inferior;
Jug., jugular; Lac., lacrimal; Lat., lateral; Med., medial; Men., meningeal; Mid., middle;
Occip., occipital; Olf., olfactory; Ophth., ophthalmic; Pharyng., pharyngeal; Pet.,
petrosal; Post., posterior; Rec., recurrent; Subarc., subarcuate; Tr., trunk.FIGURE 2-2 Superior view of the convexity showing the area of supply of the individual
meningeal arteries. Dural branches from the internal carotid arterial system are
highlighted in shades of green, the external carotid system meningeal branches in shades
of blue, and vertebrobasilar system in red. A, Internal carotid system. The anterior
ethmoidal artery has also been called the anterior meningeal artery, when its territory
extends to the dura of the frontal convexity. It gives origin to the anterior falcine artery,
also called the artery of the falx cerebri, which supplies the anterior portion of the falx
cerebri and adjacent dura covering the frontal pole. B, External carotid system. The
convexity dura is supplied predominantly by branches of the middle meningeal arteries,
which supply the dura of frontal, temporal, and parietal convexity and the adjacent walls
of the transverse and sigmoid sinus. C, Vertebrobasilar system. The posterior meningeal
artery may reach the dura of the posterior convexity in the area above the torcula. D,
Overview. The dura over the frontal convexity is supplied by the anterior meningeal
branch of the anterior ethmoidal artery and branches of the anterior division of the
middle meningeal artery that also reach the dura in the anterior parietal region. Theparieto-occipital and petrosquamosal branches of the posterior division of the middle
meningeal artery supply the dura over the posterior convexity. A., artery; Access.,
accessory; A., artery; Ant., anterior; Div., division; Men., meningeal; Mid., middle; Post.,
posterior.
The supply to middle fossa and paracavernous dura derives laterally from the middle
meningeal, accessory meningeal, and ascending pharyngeal arteries. In an anterior to
posterior direction, it receives contributions from the recurrent branches of the
ophthalmic and lacrimal arteries, as well as from the medial tentorial artery (Figs. 2-1
and 2-3). Medially those arteries anastomose with the cavernous branches of the internal
carotid artery. In this system, dominance of a particular vessel can lead to unusual
anatomic variants. The sellar dura has a bilateral supply from the paired capsular,
inferior hypophyseal, medial clival, and dorsal meningeal arteries that anastomose across
9,10the midline in front and behind the dorsum sellae (Figs. 2-1, 2-3, and 2-4). The
inferior hypophyseal artery can supply pituitary adenomas and tumors of the sphenoid
11-13sinus.
FIGURE 2-3 Superior view of the tentorium showing the area of supply of the individual
meningeal arteries. Dural branches from the internal carotid arterial system are
highlighted in shades of green, external carotid in shades of blue, and the vertebrobasilar
system in shades of red. A, Internal carotid system. From medial to lateral, the dorsal
meningeal, the medial and lateral tentorial arteries supply the tentorium at its petrosal
attachment. B, External carotid system. The branches of the posterior division of the
middle meningeal artery contribute to the supply of the anterolateral tentorium and
extend superiorly to supply the falcotentorial junction and falx. The posterior branch of
the middle meningeal artery gives rise to the petrosquamosal branch at the junction of the
skull base and convexity and supplies the insertion of the tentorium along the petrous
ridge and groove for the transverse sinus; the dura of the torcula; and the junction of the
sigmoid, transverse and superior petrosal sinuses. A., artery; Ant., anterior; Br., branch;Div., division; Dors., dorsal; Lat., lateral; Med., medial; Men., meningeal; Mid., middle;
P.C.A., posterior cerebral artery; Post., posterior; Tent., tentorial.
FIGURE 2-4 Enlarged superior view showing the supply of the parasellar area. Dural
branches from the internal carotid arterial system have been highlighted in shades of
green, the external carotid system meningeal branches in shades of blue, and the
vertebrobasilar system in shades of red. A, Internal carotid system. In an anterior to
posterior direction, the parasellar dura receives contributions from the recurrent branches
of the ophthalmic artery and the meningolacrimal, medial tentorial, medial clival, and
dorsal meningeal arteries. The medial clival and dorsal meningeal arteries supply the
dura over the posterior roof of the cavernous sinus and posterior diaphragma sellae and
anastomoses laterally, with the branches of the inferolateral trunk, the main supplier of
the lateral wall of the cavernous sinus. B, External carotid system. The supply to
parasellar part of the middle fossa arises from the main divisions of the middle meningeal
artery. The accessory meningeal and ascending pharyngeal arteries may provide an
alternative supply of the lateral portion of the parasellar area in their reciprocal
relationship with the branches of the internal carotid artery that supply the same area. C,
Vertebrobasilar system. There are no branches of the vertebrobasilar system to the
parasellar dura. The anterior meningeal artery from the vertebral artery supplies the
anterolateral portion of the posterior fossa and foramen magnum. D, Overview. The
intracavernous carotid branches provide the major supply to the roof and posterior and
lateral walls of the cavernous sinus. These branches border laterally with the ascending
pharyngeal and accessory meningeal branches. The main divisions of middle meningeal
artery supply the middle fossa dura. The branches of the internal carotid artery supplying
the posterior wall of the cavernous sinus may anastomose with the branches of the
ascending pharyngeal and vertebral artery to supply the clival dura. A., artery; Access.,
accessory; Ant., anterior; Asc., ascending; Br., branch; Car., carotid; Cliv., clival; Div.,
division; Dors., dorsal; Eth., ethmoidal; Inf., inferior; Lac., lacrimal; Lat., lateral; Med.,
medial; Men., meningeal, meningo; Mid., middle; Ophth., ophthalmic; Pharyng.,pharyngeal; Post., posterior; Rec., recurrent; Tent., tentorial; Tr., trunk.
The convexity dura is supplied predominantly by branches of the middle meningeal
arteries. These branches course toward the superior sagittal sinus, where they are
distributed to the sinus walls and give o4 descending branches to the adjacent falx
cerebri. The scalp arteries, through the emissary foramina, also send branches to the
convexity dura. The dura over the frontal convexity is supplied by the anterior meningeal
branch of the anterior ethmoidal artery and branches of the anterior division of the
middle meningeal artery that also distributes to the dura in the anterior parietal region.
The dura over the posterior convexity is supplied by the parieto-occipital an
9,10petrosquamosal branches of the posterior division of the middle meningeal artery.
This area also receives a contribution from the posterior meningeal branch of the
14vertebral artery, when this vessel extends above the torcular (see Fig. 2-2).
The falx cerebri, falx cerebelli, and tentorium are supplied by basal and convexity
branches of the meningeal arteries and receive a contribution from the cerebral arteries,
making these structures an anastomotic pathway between dural and parenchymal
arteries. Most of the vascular supply of the falx cerebri comes through its insertion on the
vault, with the anterior basal insertion, the falcotentorial angle, and the free margin
15receiving independent contributions (Figs. 2-3 and 2-5). The dural walls of the superior
sagittal sinus, the site of insertion of the falx on the dura of the convexity, are supplied by
the middle meningeal arteries, which form two paramedial arcades, and are reinforced
anteriorly, at the level of the insertion of the falx on the crista galli, by the anterior
falcine arteries (see Fig. 2-5).
FIGURE 2-5 Lateral view showing the supply of the tentorium and falx. The dural
branches from the internal carotid arterial system are highlighted in shades of green, theexternal carotid system in shades of blue, and the vertebrobasilar system in shades of red.
A, Internal carotid system. The anterior falcine artery, the distal continuation of the
anterior ethmoidal artery, enters the falx at the cribriform plate and supplies the anterior
portion of the falx cerebri and adjacent dura covering the frontal pole. The free border of
the falx and the walls of the inferior sagittal sinus receive branches from the pericallosal
arteries anteriorly and the medial tentorial artery posteriorly. B, External carotid system.
The anterior and posterior divisions of the middle meningeal artery supply the walls of
the superior sagittal sinus and give rise to descending branches that are the main supply
to the falx and the falcotentorial junction. C, Vertebrobasilar system. The posterior
meningeal arteries reach the falcotentorial junction and posterior third of the falx cerebri.
D, Overview. A., artery; Ant., anterior; Br., branch; Brs., branches; Div., division; Falc.,
falcine; Lat., lateral; Med., medial; Men., meningeal; Mid., middle; P.C.A., posterior
cerebral artery; Perical., pericallosal; Post., posterior; Tent., tentorial.
Posteriorly, at the falcotentorial junction, the paramedial arcades are reinforced from
three sources: the posterior meningeal artery from the vertebral artery, medial tentorial
artery from the cavernous carotid, and an occasional branch of the posterior cerebral
artery. The posterior meningeal artery, the major contributor, extends along the insertion
of the falx cerebri after coursing into the insertion of the falx cerebelli. The medial
tentorial artery, which supplies the medial third of the tentorium, reaches the straight
9,10sinus and torcular and may ascend in the posterior portion of the falx cerebri (see
Fig. 2-5). The pericallosal branches of the anterior cerebral artery may also pierce the
falx at or near its free edge to reinforce the arterial network along the deep edge of the
falx.
The tentorium receives supratentorial and infratentorial contributions (Figs. 2-3, 2-5,
26). The supratentorial sources are the marginal and lateral tentorial branches of the
cavernous carotid medially and the branches of the middle meningeal artery
anterolaterally. The infratentorial components are the superior extensions of the jugular
branch of the ascending pharyngeal artery and the tentorial branch of the posterior
cerebral artery medially, the occipital artery laterally, and the posterior meningeal artery
posteriorly (see Fig. 2-3). The lateral two thirds of the tentorium and its edge along the
transverse sinus derive their supply mainly from two arterial arcades, petrosal and
occipital. The petrosal arcade follows the superior petrosal sinus and is composed of the
lateral tentorial artery, branches from the petrous and petrosquamosal trunk of the
middle meningeal artery, and the lateral branch of the dorsal meningeal artery. The
occipital arcade is composed above the tentorium by the petrosquamosal trunk and
occipital branchs of the middle meningeal artery, and the occipital and posterior
9,10meningeal arteries form its infratentorial limb (see Fig. 2-6). The medial third of the
tentorium is supplied by the medial tentorial artery from the internal carotid artery. This
artery may receive a contribution from the posterior cerebral artery through the artery of
Davidoff and Schechter (see Figs. 2-3 and 2-6).FIGURE 2-6 Posterior fossa and tentorial dura. The view is directed from medially into
the left half of a posterior fossa in which the cerebellum was removed. The clivus in on
the right and the transverse sinus on the left. Dural branches from the internal carotid
arterial system have been highlighted in shades of green, the external carotid system in
shades of blue, and the vertebrobasilar system in shades of red. A, Internal carotid system.
The medial tentorial artery supplies the medial third of the tentorium and the dorsal
meningeal and the lateral tentorial artery contribute to the arcade that supply the
attachment of the tentorium to the petrous ridge. The medial clival and dorsal meningeal
arteries supplies the dorsum sellae and upper clivus. B, External carotid system. The
hypoglossal and jugular branches of the ascending pharyngeal artery and the branches of
the occipital artery supply the dura of the lateral part of the cerebellar fossa and the
inferior portion of the posterior surface of the petrous temporal bone. The mastoid branch
of the occipital artery constitutes the main supply of the lateral part of the cerebellar
fossae and has a role on the supply of the lateral tentorial attachment. C, Vertebrobasilar
system. The subarcuate artery, a branch of the anterior inferior cerebellar artery, supplies
the posterior surface of the petrous bone above the internal acoustic meatus and
surrounding the subarcuate fossa. The anterior and posterior meningeal arteries branches
of the vertebral artery supply the foramen magnum dura. The posterior meningeal artery
supplies the medial and intermediate portions of the cerebellar fossae dura. The
vertebrobasilar system may also infrequently supply the medial edge of the tentorium
through a branch of the posterior cerebral artery. D, Overview. Branches derived from all
three arterial systems supply the dura covering the posterior surface of the petrous bone
and clivus. A., artery; Ac., acoustic; Asc., ascending; Ant., anterior; Br., branch; Brs.,
branches; Cliv., clival; Dors., dorsal; For., foramen; Hypogl., hypoglossal; Int., internal;
Jug., jugular; Lat., lateral; Med., medial; Men., meningeal; Occip., occipital; P.C.A.,
posterior cerebral artery; Pharyng., pharyngeal; Post., posterior; Sig., sigmoid; Subarc.,
subarcuate; Tent., tentorial; Transv., transverse.
The clival area derives its supply from the medial clival and dorsal meningeal,branches of the internal carotid artery, the anterior meningeal branch of the vertebral
artery, and branches of the ascending pharyngeal artery. The dura over the posterior
surface of the petrous bone is supplied by the dorsal meningeal and subarcuate arteries
and branches of the middle meningeal, occipital, and ascending pharyngeal arteries (see
Figs. 2-1 and 2-6). The dura of the lateral portion of the cerebellar fossa receives its
supply from the ascending pharyngeal, occipital, and vertebral arteries. The posterior
meningeal artery is the major supplier of the paramedial and medial portions of the
cerebellar dura, but this area also receives contributions from the middle meningeal and
occipital branches to the region of the torcular (Fig. 2-7).
FIGURE 2-7 Posterior view of the dura covering the cerebellum and foramen magnum.
A suboccipital craniectomy and C2 laminectomy has been performed while preserving the
posterior arch of C1. Dural branches from the external carotid system are highlighted in
shades of blue and the vertebrobasilar system in shades of red. No branches of the internal
carotid system supply the dura covering the posterior cerebellar surface. A, External
carotid system. The mastoid branches of the occipital artery constitute the main supply to
the lateral part of the cerebellar fossae. The posteromedial division of the mastoid branch
anastomoses with the petrosquamous branch of the middle meningeal artery above and
below with the hypoglossal branch of the ascending pharyngeal artery. B, Vertebrobasilar
system. The posterior meningeal artery supplies the medial and paramedial cerebellar
fossae between the transverse sinus and torcula above, and the posterior edge of the


foramen magnum below. C, Overview. The dura of the lateral portion of the cerebellar
fossa receives its supply from the middle meningeal, occipital, ascending pharyngeal, and
vertebral arteries. The walls of the falx cerebelli and enclosed occipital sinus are supplied
mainly by the branches of the posterior meningeal artery. The posterior meningeal artery
is also the major supplier of the paramedial and medial portions of the cerebellar dura,
with lesser contributions from the middle meningeal and occipital arteries. A., artery;
Asc., ascending; Br., branch; Brs., branches; Div., division; Hypogl., hypoglossal; Men.,
meningeal; Mid., middle; Occip., occipital; Pharyng., pharyngeal; Post., posterior.
In this discussion, the dura of the posterior fossa has been subdivided into several
areas. The clival dura extends from the dorsum sellae to the anterior border of foramen
magnum and is limited laterally by the petroclival ssure. The posterior petrous dura
extends from the petroclival ssure to the sigmoid and superior petrosal sinuses. The
cerebellar fossa dura is limited laterally by the sigmoid sinuses and extends over the
cerebellar surface from the transverse sinus to the foramen magnum. The dura on each
side of the midline has been further subdivided into a medial region, adjacent to the falx
cerebelli; a lateral region, adjacent to the sigmoid sinus; and a paramedial region
between the two. At the level of the foramen magnum, the dural supply arises
16predominantly from the external carotid and vertebral arteries (see Fig. 2-6). The
anterior and posterior meningeal arteries, branches of the vertebral artery, anastomose
with the jugular and hypoglossal branches of the ascending pharyngeal artery and the
mastoid branch of the occipital artery. The cavernous carotid may also contribute
12through the clival branches of the dorsal meningeal arteries. The dural branches of the
vertebral artery are usually small but may enlarge to supply dura-based lesions.
Enlargement of the anterior meningeal artery is seen with meningiomas, glomus jugulare
17tumors, recurrent hemangioblastomas, and metastatic tumors.
Dural territories often have overlapping supply from several sources. A reciprocal
relationship between the territories of adjacent arteries is common so that when the area
supplied from one source is small another artery enlarges to supply the area. This
reinforces the need to see all possible sources of supply to a lesion before any surgical or
endovascular treatment. Areas supplied from several overlapping sources are the
tentorium and adjacent falx, the walls of the cavernous sinus, and the dura around the
18gasserian ganglion.
Dural Arteries
External carotid artery branches
Three posteriorly directed branches of the external carotid artery—the ascending
pharyngeal, occipital, and maxillary arteries—give rise to dural branches. The super cial
temporal or posterior auricular arteries, or both, or connections over the convexity that
pass through the emissary foramina, may occasionally contribute to the dural supply
when one of the three external carotid branches is small.
Ascending pharyngeal arteryThe ascending pharyngeal artery, the smallest branch of the external carotid artery,
usually arises from the proximal portion of the external carotid artery. It has an
ascending vertical course, along the posterolateral wall of pharynx, anterior to the longus
capitis muscle, and medial to the styloglossus and stylopharyngeus muscles (Fig. 2-8A, B).
This initial segment of the artery can be seen, in the lateral angiogram, in front of the
vertebral column, and medial to the main external carotid trunk on the anteroposterior
view.
FIGURE 2-8 A, Lateral view of the left parapharyngeal space and the ascending
pharyngeal artery origin and course. The ascending pharyngeal artery makes a sharp
anterior turn at the base of the skull, running downward and forward, following the
upper border of the superior pharyngeal constrictor muscle to supply the pharynx and
auditory tube. B, The segment of the internal carotid artery below the carotid canal has
been removed and the stump retracted posteriorly to expose the anterior and posterior
divisions of the ascending pharyngeal artery. The anterior division gives o4 the
pharyngeal rami and the posterior, or neuromeningeal division, sends branches to the
posterior fossa dura. The ascending ramus of the anterior branch, also called Eustachian
branch, supplies the Eustachian tube and gives o4 a carotid branch, which accompanies
the internal carotid artery within the carotid canal, supplying the periosteum, the
sympathetic network around the vessel, and the arterial walls. The jugular branches of the
ascending pharyngeal and occipital arteries send branches to cranial nerves IX, X, and XI.
C, Intracranial view of the left jugular foramen. The jugular branch descends below the
jugular foramen. D, Lateral view of a left mastoidectomy. The mastoid air cells have been
removed to expose the superior, posterior, and lateral semicircular canals, facial nerve,
sigmoid sinus, and jugular bulb. The lateral division of the jugular branch of the
ascending pharyngeal artery ascends along the anterior edge of the sigmoid sinus and
anastomoses medially with the meningeal branches of the internal carotid artery,
superiorly with the subarcuate artery, and laterally with the mastoid branches of the
occipital artery. E, Posterior view of the left lower cranial nerves. The cerebellum and
accessory nerve have been elevated to expose the hypoglossal nerve. The hypoglossal
branch of the ascending pharyngeal artery passes through the hypoglossal canal with the
hypoglossal nerve and enters the dura. F, Posterior view of a hypoglossal canal that has
been opened to expose the hypoglossal nerve and the hypoglossal branch of the ascending
pharyngeal artery. The hypoglossal branch supplies the dura of the lateral portion of the
foramen magnum and inferolateral cerebellar fossa. The posterior inferior cerebellar
artery arises from the extradural segment of the vertebral artery. G, The right cerebellar
tonsil has been elevated to expose a meningeal artery that arises from intradural
vertebral artery and supplies the dura on the lateral edge of the lateral foramen magnum.
A., artery; Ant., anterior; Asc., ascending; Br., branch; Cap., capitis; Car., carotid; CN,cranial nerve; Constr., constrictor; Div., division; Ext., external; For., foramen; Hypogl.,
hypoglossal; Int., internal; Jug., jugular; Lat., lateral; Long., longus; M., muscle; Men.,
meningeal; Occip., occipital; P.I.C.A., Posterior inferior cerebellar artery; Palat., palatini;
Pharyng., pharyngeal; Post., posterior; Proc., process; Semicirc., semicircular; Sig.,
sigmoid; Sup., superior; Tens., tensor; Vert., vertebral.
The meningeal contribution of the ascending pharyngeal artery is via three branches:
hypoglossal, jugular, and carotid (see Fig. 2-8A). The hypoglossal and jugular branches,
10the more constant, originate from the posterior division, and the carotid branch from
the anterior division (Fig. 2-8C–G). The hypoglossal branch accompanies the hypoglossal
nerve and enters the skull through the hypoglossal (anterior condylar) canal, to be
distributed to the dura surrounding the foramen magnum and clivus, where it
anastomoses with the branches arising from the ipsilateral cavernous carotid and
vertebral arteries, and its mate from the opposite side. The hypoglossal artery may also
arise from the vertebral artery (see Fig. 2-8G). The area of supply of the hypoglossal
branch (see Figs. 2-1, 2-6, and 2-7) may extend to the dura of the lateral portion of the
cerebellar fossae, where it borders and has a reciprocal relationship with the territory
supplied by the mastoid branch of the occipital artery and the posterior meningeal artery
of the vertebral artery. In the clival area it may anastomose superiorly with the medial
clival branch of the inferior hypophyseal artery and the dorsal meningeal artery and
9,10inferiorly with the anterior meningeal artery of the vertebral artery.
The jugular branch enters the jugular foramen with cranial nerves IX, X, and XI, where
it divides into medial and lateral branches. The lateral branch courses along the dural
wall of the sigmoid sinus (see Fig. 2-8D), where it anastomoses with the jugular branch of
the occipital artery (Fig. 2-9). The medial branch courses along and supplies the dura
bordering the inferior petrosal sinus. Its territory (see Figs. 2-1, 2-6, and 2-7) borders the
area supplied by the dorsal meningeal artery and medial clival artery from the cavernous
carotid. Superiorly, it anastomoses with the subarcuate artery and the petrosquamosal
branch of the middle meningeal artery and laterally with the mastoid branches of the
occipital artery. The jugular branch distal to the jugular foramen supplies the dura facing
9,10the inferior part of the cerebellopontine angle (see Fig. 2-6). The hypoglossal and
jugular branches also supply of the adjacent segments of cranial nerves IX through
10,19,20XII. On lateral angiograms, the posterior division of the ascending pharyngeal
artery ascends besides and overlaps the foramen magnum. On anteroposterior views, the
hypoglossal is the most medial of the terminal branches of the posterior division.
FIGURE 2-9 A, Lateral view of a left occipital artery in the area below the mastoid
process. The occipital artery originates from the posterior surface of the external carotid
artery, courses posteriorly and upward, and passes deep to the posterior belly of digastric
muscle in the occipital groove of the temporal bone. B, Posterior view of the
retroauricular area. The occipital artery passes between the longissimus capitis and
semispinalis capitis muscle and gives rise to a mastoid branch that passes through the
mastoid foramen to reach the dura in the area of the junction of sigmoid and transverse
sinus. C, A descending branch of the occipital artery arises as the artery passes above the
superior oblique muscle and gives rise to deep rami that anastomose with the vertebral
artery. D, Enlarged view of C. The mastoid branch of occipital artery enters the cranium,
by passing through the mastoid foramina and anastomoses over the junction of sigmoid
and transverse sinus with the branches of the middle meningeal artery. E and F, Left (E)
and right (F) retromastoid areas. E, When the occipital artery’s course is low, no occipital
groove is present and the artery passes super cial to the longissimus capitis muscle. F, If


the artery courses below the skull base in an occipital groove it passes deep to the
longissimus capitis muscle. G, Posterior view of the left occipitomastoid area. The mastoid
foramen transmits the mastoid emissary vein and the mastoid branch of the occipital
artery. H, A meningeal branch of this segment courses toward the midline and passes
through the parietal foramen. I, Posterior view of the sagittal and lambdoid sutures. The
parietal foramen, which transmits an emissary vein and a meningeal branch of the
terminal segment of the occipital artery, is located near the midline, 3–5 cm above the
lambda. J, Lateral view. The stylomastoid artery arises from the posterior surface of the
external carotid artery and passes through the stylomastoid foramen to reach the facial
canal, where it supplies the mastoid portion of the facial nerve and walls of the tympanic
cavity. K, The posterior belly of digastric has been removed to expose the jugular branch
of the occipital artery, which ascends behind the carotid sheath to supply the dura around
the jugular foramen and cranial nerves IX, X, and XI. A., artery; Br., branch; Brs.,
branches; Cap., capitis; Car., carotid; CN, cranial nerve; Desc., descending; Digast.,
digastric; Ext., external; For., foramen; Gr., greater; Inf., inferior; Int., internal; Jug.,
jugular; Longiss., longissimus; M., muscle; Men., meningeal; Mid., middle; N., nerve; Obl.,
oblique; Occip., occipital; Occipitomast., Occipitomastoid; Par., parietal; Petrosquam.,
petrosquamosal; Post., posterior; Proc., process; Sag., sagittal; Sup., superior; Superf.,
superficial; Temp., temporal; Transv., transverse; V., vein; Vert., vertebral.
The carotid ramus originates from the anterior branch of the ascending pharyngeal
artery. It courses in the periosteal lining of the carotid canal and anastomoses, at the level
9,10of the foramen lacerum, with branches arising from the carotid siphon to form the
recurrent artery of the foramen lacerum. This recurrent artery also anastomoses at the
lower edge of the trigeminal ganglion with the posterior branch of the inferolateral trunk
and the cavernous branch of the middle meningeal artery. The carotid branch usually
does not extend to the dura of clivus and cerebellopontine angle as do the other dural
9,10branches of the ascending pharyngeal artery. The recurrent artery of foramen
lacerum may be involved in the supply of angiomas, lymphoid tumors, angio bromas of
9,10the nasopharynx, and tumors of the cavernous sinus and caroticocavernous fistulas.
Occipital artery
The occipital artery originates from the posterior surface of the external carotid artery, at
the level of the angle of the mandible, and courses posteriorly and upward, being crossed
super cially by the hypoglossal nerve. It passes deep to the posterior belly of the digastric
muscle and lateral to the internal jugular vein, vagus nerve, internal carotid artery, and
accessory nerve (see Fig. 2-9A). At the level of a vertical plane crossing the posterior
border of the external auditory canal, the occipital artery can be found in a tunnel
formed above by the occipital groove of the temporal bone—a prominent sulcus on the
undersurface of the temporal bone, medial to the digastric groove—medially by the
attachment of the superior oblique muscle on the transverse process of atlas, and laterally
by the cranial insertion of the posterior belly of the digastric muscle in the digastric
groove (see Fig. 2-9B–F). The presence of the occipital groove is dependent on whether
the artery courses super cial or deep the longissimus capitis muscle. The groove is
present if the artery courses deep to the longissimus capitis muscle along the lower


surface of the skull base and is absent if the artery courses inferior to the skull base or
12lateral to the longissimus capitis muscle (see Fig. 2-9E–G).
The occipital artery at the level of the posterior border of the upper insertion of the
longissimus capitis muscle courses in the upper part of the space between the occipital
bone and C1 and lateral to the rectus capitis posterior major and semispinalis capitis
muscle. It is covered by a deeper layer formed by the splenius capitis muscle and a more
super cial layer formed, from lateral to medial, by the sternocleidomastoid and
trapezius. The occipital artery pierces the fascia between the trapezius and
sternocleidomastoid, near the superior nuchal line and ascends in the super cial fascia of
the scalp, where it is accompanied by the greater occipital nerve (see Fig. 2-9H).
The occipital artery gives rise to the auricular branch, which anastomoses with the
posterior auricular artery behind the ear; the stylomastoid artery, muscular branches to
the sternocleidomastoid, digastric, stylohyoid, splenius, and longissimus capitis muscles;
and meningeal branches to the posterior fossa that enter the skull through the jugular
foramen and condylar canal and to inconstant branches that runs through the mastoid
foramen (see Fig. 2-9B, D, G).
The occipital artery is divided into three portions: (1) ascending cervical, (2)
cervico21occipital or horizontal, and (3) ascending occipital (see Fig. 2-9A). The meningeal
branches most frequently originate from the second and third arterial segments.
21The mastoid branch, present in about one half of specimens (see Fig. 2-9B, D, G),
3,9,10also called the transmastoid branch or the artery of the mastoid foramen, originates
from the second segment of occipital artery, at the level of the insertion of the
semispinalis capitis muscle, midway between the inferior and superior nuchal lines. From
its origin, the mastoid branch courses between the splenius capitis muscle and the
junction of the mastoid and occipital bones. It enters the cranial cavity at the level of the
superior nuchal line, by passing through the mastoid foramen. Intracranially, the superior
nuchal line corresponds to the level of the transverse sinus. The mastoid branch emerges
intracranially at the posterior border of the upper end of the sigmoid sinus and divides
21into three groups of branches: descending, ascending, and posteromedial. The
descending branches are directed toward the jugular foramen and border the dural
territory supplied by the jugular branch of the ascending pharyngeal artery (see Fig.
28D). The posteromedial branches anastomose with the petrosquamous branch of the
middle meningeal artery and constitute the main supply to the lateral part of the
cerebellar fossae that borders the territory of the hypoglossal branch of the ascending
pharyngeal artery or the posterior meningeal branch of the vertebral artery, or both. The
ascending branches, which are directed to the dura covering the superior part of the
posterior surface of the temporal bone that faces the cerebellopontine angle, anastomoses
with the subarcuate branch of the anterior inferior cerebellar artery (see Figs. 2-1 and
26), and can supply acoustic neurinomas, meningiomas, and arteriovenous stulas. The
22mastoid branches also supply the endolymphatic duct and sac.
The third or ascending occipital portion gives rise to the terminal branches of the
occipital artery, which supply the musculocutaneous structures of the posterior portion of
the cranial vault, and anastomoses with the branches of the super cial temporal artery
(see Fig. 2-9H). The parietal foramen (see Fig. 2-9J), which is an inconstant opening
3located near the sagittal suture, about 3 to 5 cm in front of the lambda, transmits a
21meningeal branch of the ascending occipital segment and a small emissary vein.
Variations of the stylomastoid artery and the mastoid branch include their origin from
the ascending pharyngeal artery or from the posterior auricular artery. Alternatively,
other meningeal arteries that commonly have other sites of origin, like the posterior
meningeal and the branch to the falx cerebelli from the posterior meningeal artery, may
also arise from the occipital artery.
Maxillary artery
The maxillary artery, through its middle meningeal and accessory meningeal arteries
(Figs. 2-10 and 2-11), provides almost all of the supply to the dura over the convexity
and important contributions to the supply of the basal dura (see Figs. 2-1,2-3, and 2-4).


'
FIGURE 2-10 A, Lateral view of the left mandible and infratemporal area. The
super cial temporal artery arises from the external carotid artery and courses behind the
condylar process of the mandible and the temporomandibular joint. B, The maxillary
artery is divided into mandibular, pterygoid, and pterygopalatine segments. The
mandibular segment courses deep to the neck of the mandible. The pterygoid segment
courses between the temporalis and pterygoid muscles and gives rise to the deep temporal
and pterygoid arteries. The pterygopalatine segment passes through the pterygomaxillary
ssure to enter the pterygopalatine fossa. The deep temporal arteries and nerves enter
the deep surface of the temporalis muscle. C, The middle meningeal veins accompany the
divisions of the artery and communicate above with the superior sagittal sinus through the
venous lacunae. D, Middle meningeal artery, which arises from the mandibular segment
of the maxillary artery, passes upward between the roots of the auriculotemporal nerve
and the foramen spinosum to reach the middle fossa dura. E, Enlarged view. The
pterygoid venous plexus has been removed to expose the middle meningeal artery arising
from the maxillary artery and coursing between the roots of the auriculotemporal nerve.
F, The dura has been elevated from the oor of the left middle fossa to expose the
bifurcation of the middle meningeal artery into anterior and posterior divisions lateral to
the foramen spinosum. The medial branch of the anterior division courses near the
sphenoid ridge and anastomoses with the meningolacrimal or sphenoidal branches of the
ophthalmic system, or both. The lateral branch ascends toward the superior sagittal sinus.
G, The middle meningeal artery gives rise to cavernous and petrous branches before
splitting into anterior and posterior divisions just anterior and lateral to the foramen
spinosum. H, Enlarged view of G. Immediately after entering the cranial cavity, the
middle meningeal artery gives o4 a short vessel, which divides into the petrosal artery
laterally and a cavernous branch to the trigeminal ganglion medially. The cavernous
branch anastomoses with the posterior branch of the inferolateral trunk. The

petrosquamosal branch arises from the posterior trunk at the junction of the skull base
and convexity; supplies the insertion of the tentorium to the petrous ridge, the dura of the
torcula, and the junction of the sigmoid, transverse, and superior petrosal sinuses; and
extends to the dura of the posterior fossa bordering the area supplied by the external
carotid branches. I, Lateral view of the anterior division of the left middle meningeal
artery in another specimen. A branch of the anterior division ascends grooving the
parietal bone approximately 1.5 cm behind the coronal suture. In this case, the segment
encased in a bony canal was removed in elevating the bone. The petrosquamosal branch,
described in H, arises from the middle meningeal artery at the junction of the skull base
and convexity. J, Posterolateral view of the dura over the right transverse sinus and
torcula. The petrosquamosal branch of the middle meningeal artery supplies the insertion
of the tentorium; the dura of the torcula; and the junction of the sigmoid, transverse, and
superior petrosal sinus and extends to the dura of the posterior fossa bordering the area
supplied by the external carotid branches. K, Superior view of the convexity dura. The
middle meningeal arteries give rise to a rich anastomotic layer of vessels referred to as
the primary anastomotic arteries. These arteries change little in diameter as they course
and anastomose over the dural surface. They cross the superior sagittal sinus, connecting
the dura over the paired cerebral hemispheres into a single vascular unit. L, Enlarged
view of the area of the superior sagittal sinus. Each middle meningeal artery forms a
paramedian arcade just lateral to the superior sagittal sinus. The arcades anastomose
across the midline connecting the dural arterial network in a single vascular unit. M,
Enlarged view of the sagittal sinus. The middle meningeal branches reach and participate
in the supply of the walls of the superior sagittal sinus, where they give o4 descending
branches to the adjacent falx cerebri and anastomoses with the other falcine arteries. N,
The superior sagittal sinus has been opened and its walls hold laterally with pins to
expose the branching pattern of the middle meningeal arteries along the sinus walls. A.,
artery; Alv., alveolar; Ant., anterior; Auriculotemp., auriculotemporal; Br., branch; Car.,
carotid; Clin., clinoid; CN, cranial nerve; Div., division; Ext., external; Fiss., ssure; For.,
foramen; Gr., greater; Inf., inferior; Int., internal; Lat., lateral; M., muscle; Mandib.,
mandibular; Med., medial; Men., meningeal; Mid., middle; N., nerve; Parieto-Occip.,
parieto-occipital; Palat., palatini; Pet., petrosal; Petrosquam., petrosquamosal; Plex.,
plexus; Post., posterior; Proc., process; Pteryg., pterygoid; Pterygomax., pterygomaxillary;
Sag., sagittal; Sup., superior; Superf., super cial; Temp., temporal, temporalis; Tens.,
tensor; Transv., transverse; Tymp., tympani; V., vein; Ven., venous; Zygo., zygomatic.
FIGURE 2-11 A, Inferolateral view of the right foramina ovale and spinosum and the
middle and accessory meningeal arteries passing through the skull base. The accessory
middle meningeal artery arises from the maxillary artery, and passes through the foramen
ovale in this case. B, Anterior view of the right foramen ovale exposing the sharp lateral
curve of the middle meningeal artery above foramen spinosum. The intracranial territory
of the accessory meningeal artery includes the gasserian ganglion and adjacent middle
fossa dura, where it anastomoses with the meningeal branches from the ophthalmic and
middle meningeal arteries and the carotid siphon. C, Endocranial surface of the sella and
middle fossa. The sphenoidal emissary foramen is present in approximately 40% of the
skulls. It is located medial to the foramen ovale. D, The deep temporal nerves and arteries
pierce the deep surface of the temporalis muscle. The middle meningeal artery arises from
the mandibular segment of the maxillary artery and gives rise to the accessory meningeal
artery. E, Enlarged view of D. In this specimen, the accessory meningeal artery ascends
super cial to lingual and inferior alveolar nerves. F, The upper segment of the ascending


pharyngeal artery makes a sharp anterior turn, super cial to constrictor pharynx muscle
and gives rise to a well developed carotid branch that follows the carotid artery into the
carotid canal. A., artery; Access., accessory; Alv., alveolar; Ant., anterior; Asc., ascending;
Auriculotemp., auriculotemporal; Br., branch; Cap., capitis; Car., carotid, Clin., clinoid;
CN, cranial nerve; Emiss., emissary; For., foramen; Inf., inferior; Int., internal; Jug.,
jugular; Long., longus; M., muscle; Men., meningeal; Mid., middle; N., nerve; Occip.,
occipital; Pharyng., pharyngeal; Post., posterior; Sphen., sphenoidal; Temp., temporal;
Superf., superficial; V., vein.
Middle meningeal artery
The middle meningeal artery normally arises from the rst or mandibular segment of the
maxillary artery, just behind the condylar process of the mandible, and enters the skull
through the foramen spinosum (see Fig. 2-10A–H). After passing through the foramen
spinosum, the main stem courses laterally, grooving the greater sphenoid wing, where it
divides in its anterior and posterior divisions, which supply the dura of frontal, temporal,
and parietal convexity; the upper surface of the temporal bone; and the adjacent walls of
the transverse and sigmoid sinus as well as the middle fossa dura adjacent to the
cavernous sinus (see Fig. 2-10F–N). In its path between the anterosuperior angle of the
greater sphenoid wing and the sphenoid angle of the parietal bone, the anterior division,
and sometimes the sphenoparietal sinus, can be encased in a bony canal that varies in
23extension from 1 to greater than 30 mm. The anterior division is usually single but may
be composed of two branches (duplicated) in 0.8%, or absent in 0.7% of cases, while the
23posterior division is duplicated in 8.1%. At the level of the superior sagittal sinus the
middle meningeal artery anastomoses with the anterior falcine branch of the ophthalmic
artery to supply the dural layers of the falx (see Fig. 2-5).
The middle meningeal artery, and the osseous groove in which it courses, begins at the
foramen spinosum and divide into anterior and posterior divisions 15 to 30 mm
anterolateral to foramen spinosum (see Fig. 2-10F–I). The anterior division and its groove
divide behind the lateral part of the greater wing into a lateral branch, which passes
across the pterion to reach the dura of the lateral convexity, and a medial branch, which
courses medially along the lower surface of the sphenoid ridge where it anastomoses with
the recurrent branch of the lacrimal artery. In 9 out of 10 orbits dissected, Liu and
24Rhoton reported the presence of anastomotic connections between the recurrent
meningeal branch of the lacrimal artery and the medial branch of the anterior division of
the middle meningeal artery. Occasionally, the recurrent meningeal branch of the
lacrimal artery gives rise to the anterior segment of the middle meningeal artery or more
rarely, the ophthalmic artery can give rise to the main stem of the middle meningeal
artery itself. In these cases, with an ophthalmic or lacrimal origin of the middle
meningeal artery, the grooves marking the course of the main stem of the middle
25meningeal artery will originate at the lateral edge of the superior orbital ssure and the
26foramen spinosum will be hypoplastic or absent. Another, less frequent, site of origin of
the middle meningeal artery is from the petrous portion of the internal carotid artery,
referred to as a stapedial-middle meningeal artery, an anomaly that results from failure'


of the embryonic stapedial branch of the internal carotid artery to regress and allow the
26middle meningeal artery to become connected to the external carotid artery.
Angiographically, in the anterior view, the middle meningeal artery is easily recognized
by a sharp turn along the oor of the middle fossa after passing through the foramen
spinosum. Its course along the inner table is characterized by smooth curves, in contrast
with the sinuous course of the overlapping super cial temporal artery. This initial
intracranial portion of the middle meningeal artery can be elevated and stretched by
lesions arising at the skull base (see Fig. 2-5B). Radiographically, the grooves for the
meningeal branches can become tortuous and the foramen spinosum can enlarge in
27,28meningiomas and vascular malformations.
Immediately adjacent to the foramen spinosum the middle meningeal artery gives o4 a
short branch, which divides into the petrosal artery laterally and a branch to the
trigeminal ganglion medially (see Fig. 2-10G, H). The trigeminal branch has been
referred to as the cavernous branch of the middle meningeal artery. The petrosal branch
runs with the greater petrosal nerve and penetrates the temporal bone by passing through
29,30the facial hiatus and supplies the facial nerve and walls of the tympanic cavity.
Damage to the petrosal branch occurring as the dura is elevated in a subtemporal
extradural approach to the trigeminal nerve, cavernous sinus, or internal acoustic meatus
may result in a facial nerve de cit. Bleeding at this site should be controlled by a method
other than coagulation in order to avoid damaging the facial nerve, which may be
25,30exposed in the floor of the middle fossa at the level of the hiatus fallopii.
The posterior branch of the middle meningeal artery gives rise to the petrosquamosal
branch at the junction of the skull base and convexity (see Fig. 2-10I, J). It supplies the
insertion of the tentorium along the petrous ridge and groove for the transverse sinus; the
dura of the torcular; and the junction of the sigmoid, transverse, and superior petrosal
sinuses, and extends to the dura of the posterior fossa bordering the area supplied by the
31other branches of the external carotid artery (see Fig. 2-7). The petrosquamosal artery
may infrequently supply almost all the posterior fossa dura, including the cerebellar fossa
31and tentorium cerebelli. The parieto-occipital branch of the middle meningeal artery
supplies the dura over the posterior convexity (see Fig. 2-10J).
The middle meningeal artery in the middle fossa has anastomotic connections with the
ophthalmic system and the meningeal branches of the cavernous carotid artery (see Fig.
2-1). The middle meningeal artery may contribute to the supply of the second and third
19trigeminal divisions in addition to the facial nerve. It may supply most of the tentorium
when giving rise to a medial tentorial branch. The medial tentorial artery may arise from
either the main divisions of the middle meningeal artery or from the accessory meningeal
31artery, described in the next section.
The middle meningeal artery anastomoses over the upper clivus and adjacent posterior
surface of the temporal bone with the dorsal meningeal artery and the subarcuate artery.
The distal part of the petrosquamosal branch anastomoses, at the level of the junction of
the sigmoid, transverse, and superior petrosal sinuses, with the branches of the occipital
artery that passes through the mastoid foramen and the meningeal branches of the
ascending pharyngeal and vertebral arteries.
The middle meningeal artery may also anastomose with a branch of the basilar
32,33artery.
Accessory meningeal artery
34,35The accessory meningeal artery, also called the lesser or small meningeal artery (see
Table 2-1), may arise from either the maxillary or middle meningeal artery depending on
10,34the relationship of the maxillary artery to the pterygoid muscles. It arises from the
maxillary artery if the maxillary artery courses deep to the pterygoid muscles and from
the middle meningeal artery if the maxillary artery passes super cial to the pterygoid
muscle. In the cases in which the middle meningeal artery arises from the ophthalmic,
internal carotid or basilar artery, the accessory meningeal artery will arise directly from
36the trunk of the maxillary artery. The caliber of the accessory middle meningeal artery
is about one third to one half of the middle meningeal artery (see Fig. 2-11A, B, D–F) and
34,35in 30% to 45% of the cases it is formed by of multiple small arteries, especially if it
34arises from the maxillary artery.
From its origin, the accessory meningeal artery courses toward the angle between the
posterosuperior edge of the lateral pterygoid plate and the infratemporal surface of the
34sphenoid bone. It usually passes posterior to the inferior alveolar and lingual nerves
(see Fig. 2-11A, E). In 78% of the cases, the accessory meningeal artery enters the
cranium through the foramen ovale. In the remaining 22%, it passes through the emissary
sphenoid foramen (foramen of Vesalius), an opening occasionally found 2 to 3 mm
medial to the anterior edge of foramen ovale that also transmits an emissary vein linking
34,36the pterygoid plexus and the cavernous sinus (see Fig. 2-11C).
The extracranial segment of the accessory meningeal artery has anastomoses with the
9,10,36ascending pharyngeal artery and pterygopalatine arteries (see Fig. 2-11A, F). It
supplies the membranous portion of the Eustachian tube and external acoustic meatus,
the lateral pharyngeal wall and medial pterygoid muscle, the mandibular nerve below
the foramen ovale, and sphenoid periosteum. It has been suggested that it be called the
pterygomeningeal artery because the extracranial structures receive the predominance of
36its flow while the intracranial branch receives only 10%.
The intracranial territory of the accessory meningeal artery includes the gasserian
ganglion and adjacent middle fossa dura, where it anastomoses with the meningeal
branches from the ophthalmic and middle meningeal arteries and the carotid siphon. The
accessory meningeal artery has a reciprocal relationship with the inferolateral trunk of
the internal carotid artery in the supply of the mandibular nerve and the dura adjacent to
the cavernous sinus. It has prominent anastomoses with the posterolateral branch of the
36inferolateral trunk (see Fig. 2-1). Lasjaunias and Theron found that the accessory
meningeal artery was small in 25% of the cases that it anastomoses with the inferolateral
trunk of the cavernous carotid artery, had a size similar to the inferolateral trunk in 59%,
and that it was the only supply to the cavernous sinus area in 16%. In the latter case, the


diameter of this accessory meningeal artery approaches that of the middle meningeal
9,36artery. Occlusion of this artery during endovascular procedures may result in cranial
nerve de cits because of its supply to the oculomotor, trochlear, trigeminal, abducens
10,36and facial nerves.
35Dilenge and Geraud found that the artery could be identi ed in lateral angiograms
throughout its extracranial course in 60% of 100 selective angiographies, but was
recognizable intracranially in only six cases because of its small size. It was more easily
identi ed when it was part of an anastomotic network between the carotid siphon and
the internal maxillary artery. On the anteroposterior angiographic view, the accessory
meningeal artery slants medially, above the skull base, toward the cavernous sinus at the
point of arborization of the inferolateral trunk. It may contribute to the vascular pedicle
35of meningiomas and schwannomas of the gasserian ganglion, and can be involved in
paracavernous arteriovenous malformations.
Internal carotid artery branches
Cavernous segment
The cavernous portion of the internal carotid artery gives rise to branches that supply the
walls and enclosed structures of sella, cavernous sinus, and the tentorium (see Figs. 2-3
and 2-4). The branches can be divided based on the direction of their course into a
medial group that includes the inferior hypophyseal, medial clival, and capsular arteries;
a lateral group that includes the inferolateral trunk, also called artery of the inferior
cavernous sinus, and its branches and the lateral tentorial artery; and a posterior group
that includes the dorsal meningeal artery and medial tentorial artery (Fig. 2-12A–L). The
medial branches, including the inferior hypophyseal and medial clival artery, derive from
the primitive maxillary artery, while the dorsal meningeal artery is the adult remnant of
the primitive trigeminal artery. When these two embryonic vessels originate in a single
trunk, the meningeal, hypophyseal, and neural branches will arise from a single source,
9,10referred to as the meningohypophyseal trunk.

FIGURE 2-12 A, Superior view of the sella and roof of the cavernous sinus. The right
anterior clinoid has been removed. The medial clival artery, usually a branch of the
inferior hypophyseal artery and less commonly of the cavernous carotid artery, runs in
the dura of the sinus roof and is distributed to the dura over the posterior clinoid and
upper dorsum. B, Superolateral view of the left cavernous sinus. The meningohypophyseal
trunk gives origin to the dorsal meningeal, medial clival, and tentorial arteries. C,
Superolateral view after opening the lateral sinus wall. The rst division of the trigeminal
nerve has been retracted laterally to expose the inferolateral trunk, which arises from the
lateral side of the midportion of the horizontal segment of the cavernous carotid, passes
above the abducens nerve, and deep to the rst trigeminal segment, supplies the dura of
the inferolateral wall of the cavernous sinus and adjacent middle fossa, and anastomoses
with the recurrent artery of the foramen lacerum. The dorsal meningeal artery passes
posteriorly with the abducens nerve and is distributed to the dura over the dorsum sellae
and clivus and anastomoses with its mate from the opposite side. Its territory has a
reciprocal relationship with that of the medial clival artery. The medial clival artery arises
from the meningohypophyseal trunk in this specimen. Its initial course is anterior to the
posterior clinoid, but it also reaches to the dura over the posterior surface of dorsum
sellae. The tentorial arteries pass laterally to reach the tentorium. D, Lateral view. The'


'

medial edge of the petrolingual ligament marks the beginning of the intracavernous
segment of the carotid. E, Enlarged view of D. The meningohypophyseal trunk arises near
the apex of the posterior bend of the intracavernous carotid on the medial side of the
trochlear nerve. The tentorial artery arises as a branch of the meningohypophyseal trunk
and divides into the medial and lateral tentorial arteries at the level of the petrous ridge.
The medial tentorial artery supplies the medial edge and medial one third of the
tentorium, reaching the area around the straight sinus and posterior attachment of falx.
The lateral tentorial artery supplies the lateral two thirds of the tentorium and the
attachment of the tentorium to the petrous ridge and anastomoses with the petrosal and
petrosquamosal branches of the middle meningeal artery, the lateral branch of the dorsal
meningeal artery, and the mastoid branch of the occipital artery. The dorsal meningeal
artery runs posteriorly and passes through Dorello’s canal located below the
petrosphenoidal ligament. F, The posterior bend of the intracavernous carotid artery has
been retracted laterally to expose the inferior hypophyseal artery passing medially across
the cavernous sinus to reach the lateral surface of the posterior lobe and capsule of the
pituitary gland.G, Lateral view of the posterior part of a right cavernous sinus. The
tentorial, inferior hypophyseal, and dorsal meningeal arteries arise from the
meningohypophyseal trunk. The petrosphenoidal ligament has been excised to expose the
passage of the dorsal meningeal artery to the clival dura. The inferior hypophyseal artery
passes to the posterior lobe of pituitary gland and sellar oor. H, Posterior view after
removal of the dorsum sellae in another specimen. The tentorial, inferior hypophyseal,
and dorsal meningeal arteries arise directly from the cavernous carotid artery. The paired
inferior hypophyseal arteries anastomose on the posterior surface of the posterior lobe to
form an arterial circle that reaches the dura over the oor and posterior wall of sellae.
Dorello’s canal has been unroofed on the right. The dorsal meningeal artery divides into
medial and lateral branches. The lateral branch supplies the abducens nerve and the dura
around Dorello’s canal and the medial branch supplies the dura over dorsum and upper
clivus. The territory supplied by the medial branch of the dorsal meningeal artery has a
reciprocal relationship with the territory of the medial clival artery. I, Enlarged view of
the right cavernous sinus shown in H. The tentorial, dorsal meningeal, and inferior
hypophyseal arteries arise separately from the posterior bend of cavernous carotid artery.
J, Lateral view of the left cavernous sinus. The tentorial and the meningohypophyseal
arteries arise from the posterior bend of the carotid. The meningohypophyseal trunk gives
rise to the inferior hypophyseal, medial clival, and dorsal meningeal arteries. K, Lateral
view. The medial tentorial artery runs parallel to the trochlear nerve in the upper portion
of Parkinson’s triangle located between the trochlear nerve and rst trigeminal division.
The anterolateral branch of the inferolateral trunk courses between V1 and V2 and
toward the foramen rotundum. L, Superior view of the specimen shown in K. The
inferolateral trunk arises from the lateral side of the midportion of the horizontal segment
of the intracavernous carotid and passes between the abducens nerve and the rst
trigeminal division to supply the dura over the inferolateral wall of the cavernous sinus
and adjacent middle fossa. The anterior division of the inferolateral trunk gives rise to
anterolateral and anteromedial branches. The anteromedial branch passes forward and
supplies the oculomotor, trochlear, and abducens nerves and enters the orbit through the
superior orbital ssure. The medial tentorial artery has been removed. M, Superior view
of the right cavernous sinus. The roof has been opened and the oculomotor, trochlear, and
ophthalmic nerves have been retracted laterally to expose the dorsal ophthalmic artery,



'

the segment of the deep recurrent ophthalmic artery that courses inside the cavernous
sinus. The deep recurrent ophthalmic artery arises from the initial intraorbital part of the
ophthalmic artery and courses backward through the annulus of Zinn and medial portion
of the superior orbital ssure to cross the anterior venous space of the cavernous sinus.
The deep recurrent ophthalmic artery anastomoses with the anterolateral branch of the
inferolateral trunk. N, Anterior view. A right capsular artery arises from the horizontal
segment of the intracavernous carotid and runs medially to supply the dura over the oor
of the sella. O, Lateral view. The inferolateral trunk arises medial to the rst trigeminal
division, but its branches can be seen between the trigeminal divisions. The anterolateral
branch of the anterior division courses toward and gives a branch to the foramen
rotundum. The posterior division is exposed between the second and third trigeminal
divisions. P, Posterior–superior. The posterior division of the inferolateral trunk courses
above the motor root of the trigeminal ganglion and supplies the gasserian ganglion and
adjacent dura. Q, The trigeminal nerve has been removed to expose the inferolateral
trunk and its divisions. In this specimen, the superior division of the inferolateral trunk
gives rise to the medial tentorial artery, which supplies the medial third of tentorium and
posterior attachment of falx cerebri. The anterior division supplies the segment of the
oculomotor, trochlear, and abducens nerves near the superior orbital fissure. The posterior
division reaches the gasserian ganglion, mandibular nerve, and adjacent dura and
anastomoses with the recurrent artery of foramen lacerum. The dorsal meningeal artery
arises from the posterior carotid bend and supplies the abducens nerve in the region of
Dorello’s canal. A., artery; Ant., anterior; Br., branch; Caps., capsular; Car., carotid; Cav.,
cavernous; Clin., clinoid, clinoidal; Cliv., clival; CN, cranial nerve; Diaph., diaphragma;
Div., division; Dors., dorsal; For., foramen; Gr., greater; Hyp., hypophyseal; Inf., inferior,
infero; Int., internal; Lat., lateral; Lig., ligament; Med., medial; Men., meningeal;
Meningohyp., meningohypophyseal; N., nerve; Ophth., ophthalmic, P.C.A., posterior
cerebral artery; Pet., petrosal, petrous; Petroling., petrolingual; Petrosphen.,
petrosphenoid; Pit., pituitary; Post., posterior; Rec., recurrent; Seg., segment; Sup.,
superior; Tent., tentorial; Tr., trunk.
The meningohypophyseal trunk and the inferolateral trunk are the most consistent
branches of the cavernous segment of the internal carotid artery. They arise from a single
37trunk in 6% of the cavernous sinus. These vessels anastomose with their mates of the
opposite side and with the meningeal branches of the external carotid, ophthalmic, and
13vertebral arteries (see Figs. 2-1 and 2-4). The communication between the external
carotid and internal carotid through the cavernous branches is of signi cance in the
management of carotid cavernous stulae, which must be based on evaluation of all
these communicating channels. Increase in opaci cation of the cavernous carotid
branches may occur with alteration of cerebral dynamics associated with increased
intracranial pressure, a distant intracranial lesion, and in cerebrovascular disease in
13which the cavernous branches act as the rete mirabili.
Meningohypophyseal trunk
The meningohypophyseal trunk is the largest intracavernous branch of the internal
38-40carotid artery. It arises lateral to the dorsum sellae at or just proximal to the apex of

the rst curve of the intracavernous carotid (see Fig. 2-6). It is approximately the same
38size as the ophthalmic artery. In its most complete form it gives rise to the tentorial,
inferior hypophyseal, and dorsal meningeal arteries (see Fig. 2-12B–G, I, J). However,
these branches can arise separately from the internal carotid artery or in di4erent
9,36,37combinations, and the origin of some secondary arteries directly from the
meningohypophyseal trunk can give the appearance of more than the usual number of
branches (see Fig. 2-12H). The posterior bend of the internal carotid artery and the origin
of the meningohypohyseal trunk can be exposed through Parkinson’s triangle, located in
the lateral view between the trochlear and ophthalmic nerves, except when the carotid is
11,12elongated and tortuous, causing the posterior bend to rise above the trochlear nerve
(see Fig. 2-12D–F). The oculomotor and trochlear nerves enter the dural roof of the
cavernous sinus just above or slightly behind the trifurcation of the meningohypophyseal
11trunk. According to Harris and Rhoton, the meningohypophyseal trunk provides a
branch to the tentorium in 100% of 50 cavernous sinuses examined, making the tentorial
artery the most constant branch leaving this trunk.
Tentorial arteries
The tentorium has two sources of supply: the medial tentorial and the lateral tentorial
arteries. The medial tentorial artery usually arises from the meningohypophyseal trunk,
but may also arise from the inferolateral trunk, middle meningeal, accessory meningeal,
ophthalmic, and lacrimal arteries (see Fig. 2-12E, F, K, Q). It ascends to the roof of the
cavernous sinus and then posterolaterally, along the free edge of the tentorium, to
contribute to the supply of the transdural segment of the oculomotor and trochlear
12,41,42nerves, the walls of the cavernous sinus, and the medial third of the tentorium. It
departs from the cavernous sinus just beneath the entrance of the trochlear nerve and
initially courses posteriorly about 5 mm from the free margin of the tentorium (see Fig.
212D, E). As it approaches the region of the straight sinus, it curves laterally, ramifying
within tentorium and anastomosing along the base of the falx with branches from its
12,38,41mate from the opposite side (see Figs. 2-3 and 2-5). It may also anastomose with
the meningeal branches of the ophthalmic artery. Although usually described as a branch
37of the tentorial division of the meningohypophyseal trunk, the medial tentorial artery
may also arise directly from the posterior vertical or from the horizontal segment of the
cavernous carotid (as a branch of the inferolateral trunk), the accessory meningeal,
18,42intraorbital ophthalmic, lacrimal, or middle meningeal arteries.
The term Bernasconi’s artery is used as a synonym for the medial tentorial
11,12,42artery (see Table 2-1). Bernasconi and Cassinari (1956) were the rst to describe
an arterial vessel involved in the supply of the tentorium and its lesions. At that time,
39,41,43,44they thought the vessel originated from the external carotid artery but its true
38,41,44origin from the internal carotid artery later became apparent.
When visible during normal angiography, the medial tentorial artery ranges in length
from 5 to 35 mm. A pathologic lesion has been considered a possibility if the tentorial
12,39artery can be followed, in the angiogram, for a distance longer than 40 mm. Other
aspects such as increased diameter, undulating course, and multiple branching also
13suggest the presence of a lesion. Its presence on angiograms is not diagnostic of a
tentorial meningioma as rst suggested, because it can be seen in arteriovenous
malformations, gliomas with tentorial invasion, trigeminal neuromas, and even in normal
12,41,43,45patients.
The lateral tentorial artery commonly arises as a single trunk with the medial tentorial
artery (see Fig. 2-12D, E). From its origin, it passed backward, upward, and slightly
laterally to enter the tentorium along its attachment to the petrous ridge, and continued
backward to supply the tentorial area lateral to that supplied by the medial tentorial
28,42,45artery. The lateral tentorial artery anastomoses with the petrosal and
petrosquamosal branches of the middle meningeal artery and the lateral branch of the
dorsal meningeal artery (see Figs. 2-3 and 2-6).
Dorsal meningeal artery
The dorsal meningeal artery, also called lateral clival artery, is the adult remnant of the
31,36trigeminal artery. It arises from the meningohypophyseal trunk in most cases and
passes posteriorly through the cavernous sinus, to supply the dura of the dorsum sellae
and clivus and anastomose with its mate from the opposite side across midline (see Fig.
212B–E, G–J). It arose from the meningohypophyseal trunk in 90% of the 50 cavernous
11sinus studied by Rhoton and Harris. In 6% of cases, it arises directly from the lateral
surface of the posterior ascending portion of the cavernous carotid, just below the
11,12,46meningohypophyseal trunk.
The dorsal meningeal artery divides into medial and lateral branches (see Fig. 2-12H,
I). The medial branch passes below the petrosphenoid ligament, which roofs Dorello’s
31,36,38canal, to accompany and supply the abducens nerve into the canal and
anastomoses with the clival ramus of the jugular branch of the ascending pharyngeal
artery (see Figs. 2-1 and 2-6). The medial branch of the dorsal meningeal artery has a
reciprocal relationship with the medial clival artery, which arises as a direct or as a
secondary branch of the internal carotid artery from the inferior hypophyseal artery. The
medial clival arteries initial course is anterior to the posterior clinoid process, but it also
distributes to the dura over the posterior surface of dorsum sellae, where it anastomoses,
across the midline, with its counterpart from the opposite side and also with the medial
branch of the dorsal meningeal artery (see Fig. 2-12A–C). If no medial clival artery is
found, a branch arises directly from the dorsal meningeal artery or its medial branch and
courses medially and superiorly, on the posterior aspect to the posterior clinoid process
and dorsum sellae, supplying part of the territory of the medial clival artery (see Fig.
212H, I).
The lateral branch of the dorsal meningeal artery passes above the trigeminal cistern
(Meckel’s cave) and accompanies the superior petrosal sinus along the petrous ridge, thus
participating in the basal arterial arcade of the tentorium cerebelli (see Fig. 2-3). This
branch anastomoses, lateral to the trigeminal ganglion, with the lateral tentorial artery
and branches of the middle meningeal artery running over the superior surface of the
'

temporal bone.
Inferior hypophyseal artery
The inferior hypophyseal artery arises most frequently from the meningohypophyseal
trunk (see Fig. 2-12F, G) or directly from the medial surface of the posterior ascending
11,31,36segment of the cavernous carotid artery (see Fig. 2-12H–J, N). It passes medially
across the cavernous sinus to reach the lateral surface of the posterior lobe and capsule of
pituitary gland. The artery divides into superior and inferior branches that anastomose
with their mates of the opposite side, forming an arterial circle anterior to the dorsum
sellae (see Fig. 2-12H). The inferior branch of this arterial circle, along with the more
11,13,40,46anteriorly located capsular arteries, may supply the dura on the sellar oor.
The capsular arteries usually arise directly from the medial surface of the horizontal
cavernous carotid (see Fig. 2-12N), but may also be branches of the inferior hypophyseal
38artery. The dura of the posterior clinoid and cavernous sinus can also be supplied by
the inferior hypophyseal branch, through the medial clival artery, which can also arise
36,42directly from the cavernous carotid.
38,40Luschka, in 1860 rst identi ed the inferior hypophyseal artery in man. This
artery is the adult remnant of the primitive maxillary artery. In the lateral angiogram, the
inferior hypophyseal artery is superimposed on the carotid siphon and is therefore
36,40impossible to identify even after subtraction studies.
Inferolateral trunk
39The inferolateral trunk, also called the lateral main stem or the artery of the inferior
38cavernous sinus, arises from the lateral side of the midportion of the horizontal
segment of the intracavernous carotid, approximately 5 to 8 mm distal to the origin of the
11,46meningohypophyseal trunk (see Fig. 2-12K, L). It arises directly from the carotid
artery in 84% of the cavernous sinuses and from the meningohypophyseal trunk in
11another 6%.
47The inferolateral trunk passes above (96%) or below (4%) the abducens nerve and
descends, through or lateral to the ophthalmic nerve, and supplies the dura of the
inferolateral wall of the cavernous sinus and adjacent middle fossa up to the gasserian
ganglion (see Figs. 2-1,2-4, and 2-12K–P). The branches of the inferolateral trunk
46anastomose with the middle and accessory meningeal arteries. The branches to the
gasserian ganglion may run in the dura lateral to the ganglion or pass superior to the
motor root to reach the dura on the medial side of the ganglion (see Fig. 2-12P).
In its most complete form, the inferolateral trunk gives rise to superior, anterior, and
9,48posterior branches (see Fig. 2-12Q). The superior branch supplies the roof of the
cavernous sinus. It gives rise to a medial tentorial branch in approximately 40% of
48cases (see Fig. 2-12K, Q). The anterior and the posterior divisions divide into a medial
and a lateral branch. The medial branch of the anterior division passes forward and
supplies the oculomotor, trochlear, and abducens nerves; enters the orbit through the
'
superior orbital ssure; and terminates as the deep recurrent ophthalmic artery (see Fig.
2-12K–M). The lateral branch passes toward the foramen rotundum and supplies the dura
of the adjacent temporal fossa and maxillary nerve (see Fig. 2-12K, O, Q). The medial
branch of the posterior division is distributed to the abducens nerve, medial third of the
gasserian ganglion, and the mandibular nerve (see Fig. 2-12P). The lateral branch of the
posterior division supplies the middle and lateral thirds of the gasserian ganglion and
48adjacent dura (see Fig. 2-12Q). Because of its reciprocal relationship with the
cavernous branch of the middle meningeal artery, the posterior division may also reach
9,19the hiatus fallopi to supply the facial nerve. The posterior division of the inferolateral
trunk anastomoses with the recurrent artery of foramen lacerum (see Fig. 2-4).
McConnell’s capsular arteries
The term McConnell’s capsular arteries refers to the anterior and inferior capsular
arteries, tiny branches that arise distal to the origin of the inferolateral trunk. The inferior
capsular artery is the more proximal of the capsular arteries. It arises from the
inferomedial surface of the horizontal segment of the cavernous carotid, distal to the
origin of the inferolateral trunk, or as a secondary branch of the inferior hypophyseal
artery. It runs medially in the dural covering of the inferior surface of the anterior lobe,
giving branches to the dura of the oor of the sella turcica (see Fig. 2-12N). The anterior
capsular artery arises from the medial aspect of the internal carotid artery just before it
pierces the roof of the cavernous sinus and runs medially in the dura of the anterior
margin and roof of the sella turcica, anastomosing with its mate of the opposite side.
11,38,40,46McConnell’s capsular arteries are frequently absent, being found in 8% to
37,38,40,4650% of cavernous sinuses. This variability may be due to diN culty in
40 46injecting these arteries or its origin as a branch of the inferior hypophyseal artery.
The capsular arteries have been visualized angiographically in patients with sphenoid
13sinus carcinoma, craniopharyngioma, and parasellar meningiomas.
Recurrent artery of foramen lacerum
This tiny artery originates from the posterior ascending portion of the carotid siphon and
descends into the foramen lacerum, supplying the pericarotid autonomic nervous plexus
9,48and the arterial wall (see Figs. 2-11F and 2-12C, Q). This artery cannot be seen
angiographically after internal carotid artery injections, because of the density of the
parent carotid, but is visible after ascending pharyngeal injection because of its
anastomoses with the carotid branch of the ascending pharyngeal artery. The recurrent
artery of the foramen lacerum also anastomoses along the inferior surface of the
trigeminal ganglion with the posterior branch of the inferolateral trunk (see Figs. 2-1 and
2-4).
Supraclinoid carotid branches
The ophthalmic and anterior cerebral branches of the supraclinoid carotid may supply
the dura.Ophthalmic artery
Contributions from the ophthalmic artery to the dura derive mainly from its ethmoidal,
recurrent ophthalmic and lacrimal branches (Figs. 2-13 to 2-15).
FIGURE 2-13 Superior view. A, The anterior and posterior ethmoidal arteries arise from
the ophthalmic artery, and the anterior and posterior ethmoidal nerves arise from the
nasociliary nerves and both the arteries and nerves course medially, passing above the
optic nerve and between the superior oblique and medial rectus muscles to enter the
ethmoidal canals. B, The lacrimal artery arises from the initial segment of the ophthalmic
artery, courses laterally, and anastomoses through its recurrent meningeal or the
meningolacrimal branch with the middle meningeal artery. C, Superior view of the dura
around the cribriform plate after removal of the olfactory bulbs. The anterior ethmoidal
arteries emerge from the ethmoidal canal at the lateral edge of the cribriform plate. Theanterior ethmoidal arteries runs anterior and medially to reach and ascend in the falx,
where they continue as the anterior falcine arteries The anterior falcine artery provides
the major supply to the anterior third of falx. D, Superior view. The anterior ethmoidal
artery reaches the anterior fossa at the anterolateral edge of the cribriform plate, and the
inferior attachment of the falx to the crista galli. E, Superior view of the same specimen.
The anterior falcine artery ascends within the falx and anastomoses with the middle
meningeal branches that reach the sagittal sinus and descend on the falx and with the
falcine branches of pericallosal branch of the anterior cerebral artery. A., artery; Ant.,
anterior; CN, cranial nerve; Crib., cribriform; Eth., ethmoidal; Front., frontal; Lac.,
lacrimal; Med., medial; M., muscle; N., nerve; Nasocil., nasociliary; Obl., oblique; Olf.,
olfactory; Ophth., ophthalmic; Post., posterior; Sup., superior.
FIGURE 2-14 A, Osseous relationships. Anterior view of the right orbit. The recurrent



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meningeal (sphenoidal) branch of the lacrimal artery courses through the lateral portion
of the superior orbital ssure, to anastomose with branches of the middle meningeal
arteries. This accessory anastomotic branch between the lacrimal and middle meningeal
artery, called the meningolacrimal artery, courses through the lacrimal foramen located
just below the lesser sphenoidal wing lateral to the superior orbital ssure. B, Enlarged
view of the right orbit. The lacrimal foramen occupies a variable position relative to the
superior orbital ssure. It can be located lateral to the superior orbital ssure, con uent
with its lateral end or occupy any intermediate position between these extremes. C,
Intracranial view of the superior orbital ssure. The surface of the anterior clinoid process
exhibits the opening of a tiny bony tunnel that starts inside the optic canal and gives
passage to the super cial recurrent ophthalmic artery, which supplies the roof of
cavernous sinus and may continue posteriorly along the tentorium as the medial tentorial
artery. The lateral portion of the superior orbital ssure is enlarged (arrow) for the
passage of the recurrent meningeal (sphenoidal) artery, which anastomoses with the
anterior branch of the middle meningeal artery. D, Intracranial view of the right superior
orbital ssure and sphenoid ridge. E, Superior view of the right sphenoid ridge. The
anterior division of the middle meningeal artery may be encased in a 1- to 30-mm canal,
like that shown, in its course along the sphenoidal ridge. After reaching the upper or
distal end of the canal, the branches of the artery ascend in bony grooves on the inner
table of the skull. F, View of the medial wall of the orbit. The ethmoidal arteries and
nerves course through the ethmoidal canals, located in the suture between the orbital
plates of the frontal and ethmoid bones. A., artery; Ant., anterior; Br., branch; Clin.,
clinoid; Eth., ethmoidal; Fiss., ssure; For., foramen; Front., frontal; Gr., greater; Inf.,
inferior; Infraorb., infraorbital; Lac., lacrimal; Less., lesser; Max., maxillary; Med.,
medial; Men., meningeal; Mid., middle; Ophth., ophthalmic; Orb., orbital; Post., posterior;
Rec., recurrent; Sphen., sphenoidal; Sup., superior; Supraorb., supraorbital.

FIGURE 2-15 Superolateral view. A, Part of the roof and lateral wall of the left orbit
have been removed and the intraorbital structures exposed to demonstrate the
anastomotic pathways between lacrimal and middle meningeal arteries. The anterior
division of the middle meningeal artery gives o4 a medial branch, which runs medially
along the sphenoid ridge and anastomoses with the lacrimal branch of the ophthalmic
system. In this specimen, there is a dual connection between the middle meningeal and
lacrimal arteries. The most lateral artery is the meningolacrimal branch, a recurrent
meningeal branch that pierces the sphenoid wing by passing through the lacrimal
foramen. Another vessel, called the recurrent meningeal artery or sphenoid artery (shown
in B), courses through the superior orbital ssure to create a second anastomosis between
the anterior division of the middle meningeal and the ophthalmic system. B, Enlarged
view of A. The meningolacrimal artery has been depressed to expose the tortuous course
of the recurrent meningeal artery, also called the sphenoidal artery, which courses
through the lateral edge of the superior orbital ssure to reach the dura of the middle
fossa and parasellar area. C, Lateral view of the left frontal dura. A frontal branch that
arises from the ophthalmic artery passes through the orbital roof to supply the frontal
dura, reaching forward to the dura that covers the frontal pole. A., artery; Ant., anterior;
Br., branch; CN, cranial nerve; Div., division; Front., frontal; Lac., lacrimal; Lat., lateral;
M., muscle; Men., meningeal, meningo; Mid., middle; Ophth., ophthalmic; Orb., orbital;
Post., posterior; Sphen., sphenoidal.
Ethmoidal arteries
The anterior and posterior ethmoidal arteries arise from the ophthalmic artery in the
medial third of the orbit (see Fig. 2-13A, B) and range in diameter between 0.5 and 1
49mm in diameter. These arteries enter the anterior and posterior ethmoidal canals with
their corresponding ethmoidal nerves and leave the canals to enter the anterior cranial
fossa at the anterior and posterior ends of the lateral edge of the cribriform plate (see Fig.
2-13A–D). The orbital opening of the ethmoidal canals are located at the junction of the
roof and medial wall of the orbit, along the frontoethmoid suture formed by the medial
edge of the orbital plate of the frontal bone above and the perpendicular plate of the
ethmoid below (see Fig. 2-14F). Intracranially, the ethmoidal canals open on the suture
between the orbital part of the frontal bone and the cribriform plate. Before reaching the
intracranial cavity, the ethmoidal arteries send branches to the ethmoid sinuses and nasal
cavity and septum. The ethmoidal arteries are prominently enlarged in vascular tumors
or dural arteriovenous malformations of the anterior fossa.
Intracranially, the anterior ethmoidal artery has been also called the anterior
meningeal artery, especially when its territory extends to the dura of the frontal
50convexity (see Fig. 2-2). It gives origin to the artery of the falx cerebri, also called the
50-52anterior falcine artery, which enters the falx at the cribriform plate and supplies the
anterior portion of the falx cerebri and adjacent dura covering the frontal pole that
borders with the dural territory of the middle meningeal artery (see Fig. 2-13C–E). The
anterior falcine artery may be present on both sides but either the right or left may
52predominate. It artery is frequently seen, on normal carotid angiograms, ascending in
52the falx near its attachment to the convexity dura. It may enlarge in falx meningiomas



'
51and occlusive cerebrovascular diseases. The anterior meningeal branches of the
ethmoidal arteries often supplies meningiomas from the olfactory groove and may be
28seen on angiography to be displaced in arch along the surface of the tumor. The
anterior falcine artery is not shifted laterally by intracranial masses because it courses
52within the rigid falx.
The posterior ethmoidal artery passes through the posterior ethmoidal canal and enters
the dura at the posterior margin of the cribriform plate and supplies the dura of the
medial third of the oor of the anterior cranial fossa, including the planum sphenoidale,
anterior clinoid process, and chiasmatic groove (see Fig. 2-1). It anastomoses posteriorly
with the branches of the internal carotid artery, laterally with branches of the middle
meningeal artery, and anteriorly with the meningeal branches of the anterior ethmoidal
artery (see Figs. 2-1 and 2,4).
Recurrent ophthalmic arteries
The ophthalmic arteries may give rise to two recurrent ophthalmic arteries, one
super cial and one deep that supply the dura. The super cial recurrent ophthalmic
artery generally arises at a sharp angle, from the proximal portion of the ophthalmic
artery in the optic canal, and passes backwards, to supply the dura over the anterior
clinoid, adjacent lesser sphenoid wing, and the anterior and medial parts of the middle
50fossa (see Fig. 2-14C) and anastomoses with branches of the middle meningeal artery
and posterior ethmoidal artery (see Figs. 2-1 and 2-4). It supplies the dural roof of the
cavernous region and may continue as the medial tentorial artery (see Table 2-1). In the
lateral angiographic view it projects above the C4 portion of the carotid siphon crossing
the C3 portion under or on the anterior clinoid process somewhat more cephalad than the
53deep recurrent ophthalmic artery.
The deep recurrent ophthalmic artery arises from the initial intraorbital part of the
ophthalmic artery, courses laterally, through the annulus of Zinn and the medial portion
of the superior orbital ssure, crossing the anterior venous space in the cavernous sinus to
supply the dura adjacent to the wall of cavernous sinus, bordering the territory of the
inferolateral trunk (see Fig. 2-12M). The presence of the deep recurrent ophthalmic artery
is closely related to the embryological process that results in the adult form of the
ophthalmic artery. Initially the primitive ophthalmic artery arises from two sources, the
anterior cerebral artery and the intracavernous carotid artery. The ophthalmic artery,
arising from the anterior cerebral artery, undergoes a process of migration to arise from
the paraclinoid internal carotid artery. The ophthalmic artery, arising from the cavernous
48carotid, also undergoes regression to become the deep recurrent ophthalmic artery. A
cavernous origin of the ophthalmic artery, either with or without an ophthalmic artery
11arising in the usual intradural location, has been reported in 6% to 8% of the cases, a
nding explained by the persistence of the dorsal primitive ophthalmic artery. When
there are two ophthalmic arteries, one passing through the optic canal and one through
the superior orbital fissure either may be dominant.
Lacrimal branch'


'
54The most important collateral blood supply to the orbit is the middle meningeal artery
and, in reverse fashion, the ophthalmic arterial system can provide ow to the territory of
the middle meningeal artery and its branches through the anastomoses between the
anterior branch of the middle meningeal artery and the lacrimal branch of the
ophthalmic artery (see Fig. 2-15). The presence of arterial connections between the
ophthalmic arterial system and the middle meningeal artery has its origin in the
55embryonic development of the stapedial artery and involves persistence of anastomoses
24,56that are normal at one stage of the development but later regress. In a 20-mm
embryo the stapedial artery (a branch of the hyoid artery) divides into
maxillomandibular and supraorbital divisions. The maxillo-mandibular division
penetrates the foramen spinosum and is eventually annexed by the external carotid
artery, to form the maxillary artery and extracranial segment of the middle meningeal
artery. The supraorbital division, arises in the middle fossa and reaches the superior
orbital ssure, providing retro- and intraorbital branches that will, in the adult, become
the site for the anastomose of the lacrimal with the middle meningeal artery. The
supraorbital division of the primitive stapedial artery is thus responsible for formation of
the intracranial segment of the middle meningeal artery and the extraocular ophthalmic
56,57artery. The supraorbital division also gives o4 a branch near the superior orbital
ssure that courses medially along the posterior edge of the lesser wing of the sphenoid to
be distributed to the anterior clinoid process and roof of the cavernous sinus,
participating in the supply of the oculomotor and trochlear nerves and sometimes
coursing posteriorly as the marginal artery of the tentorium. This arterial branch provides
the link between the intraorbital vessels (lacrimal or ophthalmic) and the posterior
42,48branches of the carotid siphon. In the adult, this artery possibly corresponds to the
superficial recurrent ophthalmic artery.
Partial or complete persistence of intraorbital and retro-orbital branches of the
supraorbital artery explains both the dependence of the orbital vascularizarion on the
middle meningeal artery and the variable participation of the ophthalmic artery in
56,58vascularization of the convexity dura (see Fig. 2-15C). If the proximal portion of the
ophthalmic artery regresses, the adult ophthalmic artery originates, not from the internal
24,54carotid artery, but from the middle meningeal artery. Unilateral middle meningeal
artery origin of the ophthalmic artery was seen in 2 of 170 anatomic specimens and 3 of
3500 cerebral angiograms. Demonstration of this anomaly bilaterally is extremely rare;
59only 4 cases have been reported. Ophthalmic origin of the middle meningeal artery can
be detected in skulls by the absence or reduced size of the foramen spinosum and/or
absence, attenuation or interruption of the osseous sulcus for the middle meningeal artery
44,54,60along the oor of the middle fossa, and has been found in 10% of specimens.
Elevating the dura from the greater and lesser wings of the sphenoid, removing the
sphenoid ridge, or embolization procedures involving the external carotid artery risk
24,56,59blindness in patients with a middle meningeal origin of the ophthalmic artery. If
the supraorbital stapedial branch persists, but its embryonic anastomoses with the
primitive ophthalmic artery regresses, the resultant anomaly includes an ophthalmic
artery that supplies only the globe and remains separated from intraorbital extraocular


'






branches (muscular and lacrimal branches), which are then supplied by the middle
meningeal artery.
The ophthalmic artery complex can supply the dura of the convexity and related
lesions by three different anomalous meningeal vessels. The commonest found, in 0.5% of
angiograms, is the middle meningeal artery that originates from the ophthalmic artery.
This results from failure of the proximal intraorbital stapedial branches to involute in
association with the involution of the maxillomandibular division of the stapedial artery.
The ophthalmic artery may also supply dural lesions through the anterior branch of the
middle meningeal, as occurs if there is a partial involution of retro-orbital stapedial
branches. The accessory meningeal artery can also arise from the ophthalmic artery. The
anatomico–radiologic features of anomalous meningeal branches arising from the
ophthalmic artery are typical. These vessels usually arise at the point that the ophthalmic
artery passes above the intraorbital optic nerve near the origin of the posterior ethmoidal
artery, and pass upward through the superior orbital ssure to reach the cranial dura.
Meningeal vessels of ophthalmic origin and related lesions are opaci ed exclusively by
internal carotid artery injection whereas external carotid artery injection fails to visualize
them. The anterior branch of the middle meningeal artery and the accessory meningeal
artery of ophthalmic origin may be distinguished on angiograms from the anterior
meningeal artery or artery of the falx, because this later branch courses near the midline
in anteroposterior view and a few millimeters inside the frontal convexity in the lateral
view, while the anterior branch of the middle meningeal artery and the accessory
meningeal artery of ophthalmic origin have a more lateral course, away from the midline
56in the AP view and posterior to the frontal convexity in the lateral view.
48,53In 30% of the cases in which the orbital branch of the supraorbital artery divides
proximally, within the middle cranial fossa, the sphenoid bone, which ossi es later, will
allow more than one transosseous route for these vessels. The anastomotic ramus between
the lacrimal and the middle meningeal artery usually enter the orbit through the superior
orbital ssure; however, in as much as 50% of dissected specimens an additional foramen
60can be seen in the greater wing of the sphenoid (see Fig. 2-14A–C). This foramen has
been given several names including the lacrimal, Hyrtl, meningorbital, cranio-orbital,
54,60sinus canal, or sphenofrontal foramen.
The lacrimal foramen is composed of multiple openings in 5% to 15% of the cases and
54,60occupies a variable position relative to the superior orbital ssure. The lacrimal
foramen can be located lateral to the superior orbital ssure or con uent with its lateral
54end (see Fig. 2-14A–C). Two middle meningeal branches can coexist: one penetrating
the orbit through the superior orbital ssure and the other, the lacrimal foramen. The
branch that passes through the lacrimal foramen is referred to as the meningolacrimal
artery, and the one entering the orbit through the superior orbital ssure is called
sphenoidal artery or recurrent meningeal artery or orbital branch of the middle
meningeal artery (see Fig. 2-15A, B).
Sometimes the meningolacrimal artery is intact distally but fails to anastomose
proximally with the middle meningeal artery and instead breaks up into a ne
54anastomotic plexus within the dura. The recurrent meningeal artery runs in the
sphenoparietal sulcus, on the lower edge of the sphenoid ridge, with the sphenoparietal
sinus. This artery is long and tortuous while the meningolacrimal has a short, straight
path to the orbit and to its anastomosis with the lacrimal artery (see Fig. 2-15A, B). The
recurrent meningeal artery may be associated with a laterally expanded superior orbital
fissure (see Fig. 2-14C). The meningeal branches of the ophthalmic artery, because of this
variable distribution, should be carefully studied in sphenoid ridge, frontobasal, and
anterior falcine tumors. A common angiographic nding in these lesions is enlargement
50of the ophthalmic artery.
Anterior cerebral artery
9Dural branches can arise at two levels along the anterior cerebral artery. The olfactory
branches from the anterior cerebral artery, which course on the olfactory bulb may
anastomose with the olfactory branches from the ethmoidal arteries in the region of the
cribriform plate; and the pericallosal artery can send branches to the free margin of falx,
anastomosing anteriorly with the anterior falcine branch of the ophthalmic artery and
9posteriorly with the dural branches from the posterior cerebral artery (see Figs. 2-1 and
2-4).
Vertebrobasilar system
The vertebral, anterior inferior cerebellar, or posterior cerebral arteries may o4er
branches to the dura.
Vertebral artery branches
The anterior and posterior meningeal arteries arise from the extracranial segment of the
vertebral artery to supply a portion of the posterior fossa dura (Fig. 2-16).
FIGURE 2-16 A, Posterior view. The anterior meningeal artery arises from the
anteromedial surface of the extracranial vertebral artery, between the C2 and C3
transverse processes. The anterior meningeal artery anastomoses with the hypoglossal
and jugular branches of the ascending pharyngeal artery to supply the dura of the lateral
portion of foramen magnum. The second, third, and fourth segments of the vertebral
artery are labeled. B, Posterior view. The posterior meningeal artery arising from the
third segment of the vertebral artery, which courses in a bony sulcus on the upper edge of
C1. C, Enlarged view of B after a suboccipital craniotomy. The third segment of the
vertebral artery is located between the transverse process of atlas and the dural entrance
and gives rise to the posterior meningeal artery near the dura entrance than the
transverse process of C1. A lateral branch of the posterior meningeal artery runs toward
the occipital condyle. The posterior condylar vein passes through the condylar canal. D,
The posterior meningeal artery ascends, nearly parallel to the internal occipital crest, to
reach the dura over the medial cerebellar fossae and falx cerebelli and above the torcula
to reach the dura of the falx cerebri. E, Posterior view of the torcula area. The posterior
meningeal artery anastomoses with the meningeal branches of the ascending pharyngeal
artery and mastoid branch of the occipital artery at the level of the foramen magnum and
over the cerebellar fossae. Above the torcula, the posterior meningeal artery anastomoses
with the petrosquamosal and parieto-occipital branches of the middle meningeal arteries.
F, Posterior view. The left posterior meningeal artery has an anomalous origin from
posterior inferior cerebellar artery. At the level of the cisterna magna, the caudal loop of
the posterior inferior cerebellar artery gives rise to a meningeal branch, which pierces the
arachnoid to supply the territory of the posterior meningeal artery. G, Posterior view of
the right cerebellopontine angle. The anterior inferior cerebellar artery gives o4 the
subarcuate and labyrinthine arteries. H, Posterior view of the right petrous bone adjacent
to the subarcuate fossa. A., artery; A.I.C.A., anterior inferior cerebellar artery; Ant.,
anterior; Asc., ascending; Atl., atlas, atlantal; Br., branch, C1, rst cervical nerve; C2,



'
second cervical nerve; C3, third cervical nerve; CN, cranial nerve; Cap., capitis; Cond.,
condylar; Dors., dorsal; Endolimph., endolymphatic; Flocc., occulus; For., foramen;
Gang., ganglion; Int., internal; Intermed., intermedius; Jug., jugular; Labyr., labyrinthine;
Lat., lateralis; M., muscle; Maj., major; Men., meningeal; Mid., middle; Min., minor; N.,
nerve, nervous; Occip., occipital; Pet., petrosal; Pharyng., pharyngeal; P.I.C.A., posterior
inferior cerebellar artery; Post., posterior; Subarc., subarcuate; Suboccip., suboccipital;
Sup., superior; Transv., transverse; V., vein; V.A.2, vertebral artery second segment;
V.A.3, vertebral artery third segment; V.A.4, vertebral artery fourth segment.
Anterior meningeal artery
The anterior meningeal artery arises from the vertebral artery at the level of the C2,
passes medially through the C2–C3 foramen in front of the C3 root, and courses upward
near the midline, sending several twigs to the anterior dura along its course (see Fig.
216A). These paired arteries join to form an arch in the dura at the level of the apex of the
dens, which gives o4 multiple ne rami to the dura in the atlanto-occipital
16,60-62space. Intracranially, the anterior meningeal artery anastomoses with the
16,61,63,64hypoglossal branch of the ascending pharyngeal artery (see Figs. 2-1 and 2-6).
The anterior meningeal artery can be identi ed in approximately 50% of subtraction
60angiograms. Its small size, results in only the rst 1 to 1.5 cm of its course being seen
17,61angiographically. In the frontal angiogram, it is seen to arise from the medial aspect
of vertebral artery and courses upward toward the foramen magnum. In the lateral
angiogram, its initial segment is projected behind the vertebral artery, but it is
subsequently seen into the anterior portion of the spinal canal, immediately posterior to
16,61,65the vertebral bodies, and anterior to the anterior spinal artery.
Posterior meningeal artery
The posterior meningeal artery usually arises from the segment of the vertebral artery
that runs in the groove for the vertebral artery on the upper edge of the posterior arch of
atlas (V3 segment) (see Fig. 2-16B–D). Its origin is usually closer to the dural entrance
than to the transverse foramen of the atlas. Its initial course is along the upper posterior
aspect of the extradural vertebral artery toward the posterolateral edge of foramen
magnum, where it enters the intracranial dura (see Fig. 2-16B). It ascends
posterosuperiorly, nearly parallel to the internal occipital crest, to reach the attachment
of the cerebellar falx. Around the level of the external occipital protuberance, the artery
bifurcates and anastomoses with the meningeal branches of the occipital and middle
6meningeal arteries (see Figs. 2-7 and 2-14D).
The posterior meningeal artery can be divided into an extracranial and an intracranial
portion. The extracranial portion is tortuous, probably as a response to the motility of the
16neck and extends from origin to the atlanto-occipital space. The intracranial portion
17shows a relatively straight con guration (see Fig. 2-14B–D). This pattern, on
angiography, facilitates di4erentiation of the posterior meningeal artery from the
branches of the posterior inferior cerebellar artery. The posterior meningeal artery, seen



16,17on 30% to 40% of angiograms, is easier to identify on lateral films.
The posterior meningeal artery may also originate from the occipital artery, the
hypoglossal branch of the ascending pharyngeal artery, the cervical internal carotid
66 6artery, and the posterior inferior cerebellar artery. Its origin from an artery supplying
the brain parenchyma can result from the persistence of the preexisting anastomotic
channels between the primitive cerebral and meningeal vessels, and regression of the
proximal stem of the posterior meningeal artery (see Fig. 2-14F).
Anterior inferior cerebellar artery
The subarcuate artery usually originates from the lateral pontine segment of the anterior
inferior cerebellar artery (AICA), medial to the porus, penetrates the dura covering the
subarcuate fossa, and enters the subarcuate canal (see Fig. 2-14G). It may arise as a
branch of the labyrinthine artery, which also arises from AICA or as a single trunk from a
cerebellar branch of AICA (cerebellosubarcuate artery). In the few cases in which the
artery arises inside the internal acoustic canal, it reaches the subarcuate canal after a
12short recurrent segment or by piercing the meatal roof. The subarcuate artery
anastomoses with the branches of the stylomastoid artery within the petrous bone, the
branches of the middle meningeal artery running over the superior surface of the petrous
bone and the mastoid branches of the occipital artery. It supplies the dura of the internal
acoustic meatus and adjacent posterior surface of the petrous bone as well as the bone in
the region of the semicircular canals. Although not seen angiographically, the subarcute
artery is involved in the formation of the dural collateral circulation that joins the
48,58leptomeningeal collaterals in cases of anterior inferior cerebellar artery occlusion.
Posterior cerebral artery
The posterior part of the falx cerebri and the adjacent medial part of tentorium may be
supplied in part by a meningeal branch of the posterior cerebral artery. Wollschlaeger
67and Wollschlaeger rst described this meningeal branch during anatomical dissections
and named it the artery of Davido4 and Schechter, in honor of their mentors (see Figs.
23 and 2-5). This artery originates from the peduncular or ambient segment of the
posterior cerebral artery, courses around the brainstem to the midline and makes a sharp
angulated upward turn to pierce the tentorium and supplies the tentorium and adjacent
falx cerebri along the falcotentorial angle. An enlarged meningeal branch of the posterior
cerebral artery has been identi ed angiographically in vascular tumors and arteriovenous
68malformations involving the falcotentorial junction. A meningeal branch of the
posterior cerebral artery could not be identi ed in this study or in a prior study from this
69laboratory. However the senior author (ALR) has noted the presence of this variation in
studies related to other areas.
Dural Sinuses and Veins
The sinuses are compartments of dura, lined with endothelium, which collect venous
blood from the super cial and deep cerebral venous systems. They include the superior
and inferior sagittal, straight, transverse, tentorial, cavernous, superior, and inferior
petrosal sinuses.
Superior sagittal sinuses
Superior sagittal sinus is attached to the falx cerebri superiorly, to crista galli anteriorly
and tentorium, posteriorly. It is triangular in cross section and has right and left lateral
angles at its junction with the dura mater covering the convexities and an inferior angle
at its junction with the falx. The superior sagittal sinuses courses in the midline in the
shallow groove on the inner table of the cranium, and grows larger as it continues
posteriorly. In approximately 60% of cases, superior sagittal sinus ends by becoming the
70-74right transverse sinus. At the termination of the superior sagittal sinus is a
dilatation, known as confluence of the sinuses or torcular herophili.
The superior sagittal sinus also communicates with veins in the scalp through emissary
veins passing through foramina, as the example of the parietal foramen, which transmits
venous connections to the superior temporal vein and may serve as a collateral route of
venous drainage.
The cortical veins may pass directly to the superior sagittal sinus, or they may rst join
the meningeal veins. Enlarged venous spaces, called lacunae, are contained in the dura
mater adjoining the superior sagittal sinus. The lacunae are largest and most constant in
the parietal and posterior frontal regions. Smaller lacunae are found in the occipital and
anterior frontal regions. The lacunae receive predominantly the drainage of the
meningeal veins, which accompany the meningeal arteries in the dura mater but cortical
72-77veins can also pierce its deeper surface (Figs. 2-17, 2-18, and 2-19).'
FIGURE 2-17 Dural sinuses and bridging veins. A, Oblique superior view. B, Direct
superior view with the falx and superior sagittal sinus removed. A and B, The veins are
divided into four groups based on their site of termination: a superior sagittal group (dark
blue), which drains into the superior sagittal sinus; a tentorial group (green), which
drains into the transverse or lateral tentorial sinus; a sphenoidal group (red), which
drains into the sphenoparietal or cavernous sinus; and a falcine group (purple), which
drains into the straight or inferior sagittal sinus either directly or through the basal, great,
or internal cerebral veins. The carotid arteries pass through the cavernous sinuses. The
meningeal sinuses in the oor of the middle cranial fossae course with the middle
meningeal arteries. The medial tentorial sinuses receive tributaries from the cerebellum
and join the straight sinus. The basilar sinus sits on the clivus. Pacchionian granulations
protrude into the venous lacunae.FIGURE 2-18 A, Superior view. The dura covering the cerebrum has been removed to
expose the cortical veins entering the superior sagittal sinus. B, Venous lacunae and
bridging veins to the superior sagittal sinus. A large venous lacunae adjoining the sagittal
sinus extends above the bridging veins emptying into the superior sagittal sinus. The veins
from the right hemisphere emptying into the superior sagittal sinus are the anterior,
middle, and posterior frontal, central, postcentral, and anterior parietal veins. C,
Posterior view of the cerebral and cerebellar hemispheres. The superior sagittal sinus is
connected through the torcula with the transverse sinuses. The right transverse sinus is
slightly larger than the left. The veins arising along the posterior part of the hemisphere
are directed forward and join the superior sagittal sinus well above the torcula, leaving a
void along the medial occipital lobe where there are no bridging veins emptying into the
sinus. D, Superior view of the tentorial sinuses. The long vein on the left basal surface
empties into the tributary of the left tentorial sinus shown by the red arrow. The
temporobasal veins on the right side empty into the right tentorial sinus with multiple
tributaries. The vein empties into the tributary of right tentorial sinus shown with a
yellow arrow.FIGURE 2-19 A, Superior view. There is commonly an area devoid of bridging veins
entering the superior sagittal sinus just in front of the coronal suture, as shown, that
would be a suitable site for a transcallosal approach. B, Posterolateral view. Both
hemispheres removed to show falx and tentorial incisura. C, Anterolateral view. D, Falx
was removed. Inferior sagittal sinus, superior sagittal sinus, and straight sinus are
preserved. E, Medial surface of the right cerebral hemisphere. The falx except for the
inferior sagittal sinus and straight sinus is removed.
The inferior sagittal sinus
Inferior sagittal sinus occupies the posterior two thirds of the free inferior edge of the falx
cerebri. It ends by joining the great cerebral vein to form straight sinus. It arises from the
union of veins from the adjacent part of the falx, corpus callosum, and cingulated gyrus.
The largest tributaries of the inferior sagittal sinus are the anterior pericallosal veins. The
superior sagittal sinus may communicate through venous channels in the falx with the
70,75inferior sagittal sinus (see Figs. 2-17 and 2-19).



Straight sinuses
This venous sinus is formed by the union of the inferior sagittal sinus with the great
cerebral vein. It is attached to the tentorium cerebelli and drains either into the right or,
72-74,77most commonly, the left transverse sinus. (see Figs. 2-17 and 2-19).
Transverse sinuses
The right and left transverse sinuses originate at the torcular herophili and course
laterally from the internal occipital protuberance in a shallow groove between the
attachments of the tentorium to the inner surface of the occipital bone. The right
transverse and sigmoid sinus and the right jugular vein are the main eQ uent route to the
super cial venous system, whereas the left transverse and sigmoid sinus and the left
internal jugular vein drain the venous blood mainly from the deep venous system of the
77brain, which comprise the internal cerebral, basal and great veins (see Figs. 2-17 and
2-18).
Tentorial sinuses
76These sinuses divide into the medial and lateral groups. The medial tentorial sinuses
are formed by the convergence of veins from the superior surface of the cerebellum, and
the lateral tentorial sinuses are formed by the convergence of veins from the basal and
lateral surfaces of the temporal and occipital lobes. The medial group drains into
transverse sinuses and the lateral group drains into both straight and transverse
77sinuses.
Cavernous sinuses
These large sinuses are approximately 2 cm long and 1 cm wide. They are located on
each side of sella turcica and the body of the sphenoid bone. There are many trabeculae
that contain blood channels. Each cavernous sinus receives blood from the superior and
inferior ophthalmic veins, the super cial middle cerebral vein in the lateral ssure of the
cerebral hemispheres. The cavernous sinus communicates through the superior petrosal
sinus with the junction of the transverse and sigmoid sinuses and through the inferior
77petrosal sinus with the sigmoid sinus (see Fig. 2-17).
Superior petrosal sinuses
These venous sinuses are small channels that drain the cavernous sinuses. They run from
the posterior ends of the cavernous sinuses to the transverse sinuses. Both of petrosal
sinuses lie in the attached margins of the tentorium cerebella to the petrous ridge. The
super cial sylvian veins may empty into an infrequent tributary of the superior petrosal
77sinus called the sphenopetrosal sinus (see Fig. 2-17).
Inferior petrosal sinuses
The inferior petrosal sinuses start at the posteroinferior margin of cavernous sinus and
drain the cavernous sinuses into the internal jugulae veins. They run in a groove between
78petrous bone and occipital bone.
Meningeal veins
The small venous channels that drain the dura mater covering the cerebrum are called
the meningeal veins. They are small sinuses that usually accompany the meningeal
arteries. The meningeal veins that accompany the meningeal arteries course between the
arteries and the overlying bone. The fact that the artery presses into the veins gives them
the appearance ofparallel channels on each side of their respective arteries. The largest
meningeal veins accompany the middle meningeal artery. The meningeal veins drain into
the large dural sinuses along the cranial base at their lower margin and into the venous
lacunae and superior sagittal sinus at their upper margin. The veins accompanying the
anterior branch of the middle meningeal artery join the sphenoparietal or cavernous sinus
or may pass through the sphenoidal emissary veins. The meningeal veins accompanying
the posterior branch of the middle meningeal artery join the transverse sinus. The
meningeal veins may course through a super cial tunnel on the inner surface of the bone
so that they have both an intradiploic and an intradural course. The meningeal veins
77receive diploic veins from the calvarium (Fig. 2-20).
FIGURE 2-20 A, The outer table of the skull has been removed, while preserving the
sutures, to expose the diploic veins (red arrows) coursing between the inner and outer
tables. B, The inner table has been removed to expose the meningeal sinuses coursing
along the middle meningeal artery while preserving the large posterior diploic vein in the
bone. The upper end of the diploic vein joins the venous sinuses around the middle
meningeal artery at the yellow arrow. C, Superior view. The dura covering the cerebral


'


hemispheres contains a plexus of small meningeal sinus veins that follow the branches of
the meningeal arteries. The largest meningeal sinuses course along the anterior and
posterior branches of the middle meningeal artery and extend up to the superior sagittal
sinus and the region of the venous lacunae.
NEURAL SUPPLY TO THE CRANIAL DURA MATER
The neural supply of the cranial dura matter is mainly from the three divisions of the
trigeminal nerve, the first three cervical spinal nerves, and cervical sympathetic trunk.
In the anterior cranial fossa, the dura is innervated by meningeal branches of the
anterior and posterior ethmoidal nerves and the meningeal branch of the maxillary
(nervus meningeus medius) and mandibular (nervus spinosus) divisions of the trigeminal
nerve. The trigeminal ganglion also gives o4 a small branch. Nervus meningeus medius
and spinosus are largely distributed to the middle cranial fossa. The nervus spinosus is a
branch from the mandibular division, and enters the cranium through the foramen
spinosum accompanying the middle meningeal artery. It divides into anterior and
posterior branches that accompany the main divisions of the artery and supply the dura
mater in the middle cranial fossa.
The tentorium is supplied by recurrent tentorial nerve from the ophthalmic division.
The posterior fossa dura is innervated by upper cervical nerves that give o4 ascending
meningeal branches. Meningeal branches from the rst and second cranial nerves enter
the cranium through the hypoglossal canal and jugular foramen. Meningeal branches
from the second and third cervical nerves enter the cranium through anterior part of the
foramen magnum. These meningeal rami contain both sensory bers from the upper
cervical nerves and sympathetic bers from the superior cervical sympathetic ganglion.
Involvement of meningeal branches from hypoglossal and and vagus nerve and possibly
from facial and glossopharyngeal nerve has been described. The branch from vagus starts
from superior ganglion and supply posterior fossa dura. The bers from the hypoglossal
nerve arise inside the hypoglossal canal and supply the occipital dura, the dura covering
the anterior walls and oor of the posterior fossa, and the inferior petrosal sinuses dural
layers.
The arachnoid and pia matter do not contain nerve bers. Only dura matter and blood
78vessels have a neural supply.
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[78] Gray’s Anatomy, 39th ed. Elsevier, Philadelphia, 2005.CHAPTER 3
The Origin of Meningiomas
Serdar Baki Albayrak, Peter M. Black
INTRODUCTION
Meningiomas account for approximately 30% of all primary brain tumors constituting
1-3the largest subset of all intracranial tumors. They can occur at any age, but most
commonly in middle age. Women are more likely to develop intracranial meningiomas,
with a female:male ratio of nearly 2:1. Even though it is generally agreed that
meningiomas are of neuroectodermal in origin and arise from the arachnoidal
(meningothelial, arachnoid cap) cells based on the ultrastructural and histologic
similarities between meningiomas and arachnoid cells, the cellular origins of
4-21meningiomas still have not been identi( ed clearly. The histologic expression of
diverse meningioma subtypes ranging from meningothelial to ( broblastic patterns
matches well with the various non-neoplastic cells in the arachnoid villi in a similar range
of meningeal to ( broblastic cells. Thus, the critical question merges at this point: Is there
a universal pluripotent cell that gives rise to all different subtypes of meningiomas or does
each meningioma subtype takes origin from di, erent tumor initiating cells in various
subsets of cells in the arachnoid villi? The answer to this questions still remains obscure
because there is no as yet identi( ed subset of meningioma cells with unique molecular
signatures that may give rise to all meningioma subtypes.
Even though it was possible to characterize meningiomas well cytogenetically in the
past several decades, they are still poorly understood and de( ned molecularly. Hence
histopathologic grading of the tumor does not necessarily predict its clinical course,
22,23particularly in atypical meningiomas. Current ( ndings in molecular genetics
provide convincing evidence that meningiogenesis is a dynamic process whereas
histopathologic grading, which re1ects only a snapshot of tumor behavior, falls short in
capturing the complexity of the underlying molecular dynamics of the neoplastic process.
Recently, in addition to the well known tumor suppressor NF-2 gene deletion on
chromosome 22, several other genetic aberrations including the deletion of the
INK4aARF locus have been discovered, and altered biological pathways that potentially
22,24-28promote tumor growth have been suggested.
Even though these ( ndings may provide more insight into the ongoing molecular
alterations and thus various clinical courses of meningiomagenesis, the ultimate challenge
still remains: the origin and evolution of meningiomas.
In this chapter, we report the latest ( ndings regarding the cellular origins of
meningiomas. As well known, the classically described “arachnoid-cell derived
meningioma” concept is based on histopathologic and electron microscopic studies. Inaddition, recent molecular and genetic studies in animal models have shown that biallelic
inactivation of the NF2 gene has resulted in meningioma formation, which further
supports the concept of “arachoid cell-derived meningioma” at the molecular and genetic
29,30levels.
The further objective of meningioma research in this sense is to identify whether there
are any universal meningioma stem cells, and if so, what their molecular signatures
would be. Isolating candidate meningioma “stem cells” from human meningioma tissue
samples and establishing a novel in vivo meningioma animal model are the ( rst steps in
accomplishing this goal. The next step would be to demonstrate that the molecular and
genetic pro( les of the initial and in vivo formed tumor cells are identical, which would
verify the presence of the meningioma stem cells.
HISTOLOGIC AND ULTRASTRUCTURAL SIMILARITIES BETWEEN
ARACHNOID CELLS AND MENINGIOMAS
Arachnoid granulations, or arachnoid villi, are small projections of the arachnoid
membrane into the superior sagittal sinus and its major tributaries, involved in the
absorption process of cerebrospinal 1uid (CSF). There is a general agreement that
meningiomas take origin from these granulations. In 1831, Bright noticed the histologic
similarities between meningioma cells and arachnoid villi cells. Cleland and Robin
proposed for the ( rst time that meningiomas derive from arachnoid cells. Soon after,
Schmidt observed obvious histologic similarities between meningioma and arachnoid
cells at the ultrastructural level, and with respect to cell adhesion mechanisms and the
11,13components of extracellular matrix (Table 3-1).
TABLE 3-1 Ultrastructural and histological features of non-neoplastic arachnoid cells and
meningioma cells.
Arachnoid cells Meningioma cells
Arachnoid Psammoma bodies Psammoma bodies
cap cell
aggregates
Polygonal Numerous junctional complexes and Fewer junctional
arachnoid interdigitations complexes and
cells interdigitations
Phospholipid Phosphatidyl choline-multilamellar Phosphatidyl serine
composition bodies to lubricate the surfaces of ribbonlike rings in
arachnoid cells thus facilitating the flow meningioma whorls are
or absorption of CSF thought to be the
precursors of psammoma
bodies
E-cadherin Localized at the intermediate junctions Distributed along the cellexpression and anchored to cytoskeleton via borders and variations
intracytoplasmic microfilaments in exist between the
normal arachnoid cells expressions of E-cadherin
in different meningioma
subtypes
Prostaglandin Mainly localized in the rough The exact role of PGDS
D synthase endoplasmic reticulum of arachnoid cells in meningioma cells is2
and detected in higher concentrations in yet to be identified,(PGDS)
the core arachnoid cells suggesting that it besides being a
may play role in the absorption process candidate as a cell
of CSF marker for meningiomas
Ultrastructural Similarities
Human arachnoid villi are composed of ( ve layers: endothelial layer, ( brous capsule,
arachnoid cell layer, cap cells, and central core. The outermost layer, an endothelial
lining has a pivotal role in the absorption process of CSF, and displays a number of
micropinocytotic vesicles, intracytoplasmic vacuoles, and villous projections. Endothelial
cells are interconnected to each other by tight junctions. The arachnoid cell layer of the
villus is the direct continuation of arachnoid membrane itself. This arachnoid cell layer
forms cap cell aggregates that contains calci( ed organelles (psammoma bodies), which
are also one of the histopathologic features of meningiomas. The arachnoid cell layer
contains numerous extracellular cisterns that may contain granular material and
multilamellar phospholipids. These cisterns form channels from the central core into the
venous lumen and are involved in the transport of CSF. In addition, polygonal arachnoid
cells are tightly attached via junctional complexes that are less frequently seen in
13meningioma cells. Several studies in the literature revealed that syncytial areas of
meningiomas and normal arachnoid villi are similar ultrastructurally; however, the
ultrastructure of the meningioma cells are less organized and display fewer
11,13,31interdigitations.
Yamashima and colleagues investigated two forms of phospholipids in arachnoid villi
and meningiomas: phosphatidyl choline and phosphatidyl serine. Human arachnoid villi
display multilamellar bodies that are similar to pulmonary surfactant and are assumed to
lubricate the surfaces of arachoid cells thus facilitating the 1ow or absorption of CSF.
Conversely, phosphatidyl serine appeared as ribbonlike rings in meningioma whorls that
32are thought to be the precursors of psammoma bodies.
Cell Adhesion Mechanisms
During formation of a tumor, the tumor cells attach to each other via adhesion molecules.
Adhesion molecules are divided into subgroups including cadherins, immunoglobulins,
selectins, integrins, and mucins. These molecules have a pivotal role in tumor cell–tumor
cell adhesion, tumor cell–endothelial cell adhesion, or tumor cell–extracellular matrixadhesion, all of which are of paramount importance at di, erent stages in primary tumor
formation or metastasis. Here, we discuss some of the common adhesion molecules that
are expressed in both non-neoplastic arachnoid tissue and meningioma cells.
Cadherins
Cadherins are a group of glycoproteins playing a crucial role in cell adhesion and known
to be one of the fundamental elements in embryologic morphogenesis similar to
immunoglobulins and integrins. Cadherins are divided into four subtypes based on the
tissue distribution: epithelial (E), neuronal (N), placental (P), and vascular (V).
Epithelial (E)-cadherin is a transmembrane glycoprotein and functions in cell–cell
adhesion via β-catenin that indirectly binds E-cadherin to actin ( laments. This results in
strong adhesive forces between the adjacent arachnoid cells in arachnoid villi, thus
enabling individual arachnoid cells to undergo conformational changes during CSF
33,34absorption.
E-cadherin–dependent cell adhesion is a calcium-dependent process and is regulated
by a number of cytoplasmic proteins such as alpha-catenin, moesin, exrin, and radixin.
Recent evidence has shown that cadherin-mediated cell–cell adhesion is also controlled
b y NF2 gene–coded merlin protein, which is lost or inactivated in the majority of
meningioma cells.
Apart from their involvement in CSF absorption process in arachnoid villi, cadherins
have profound roles in embryogenesis, normal tissue growth, and maintenance of the
tumor cell nest. Shimoyama and colleagues reported that E-cadherin is expressed in all
epithelial tissues and cancer cells, loss of which may contribute to the invasiveness of
cancer cells. Interestingly, most meningiomas display en block growth, compressing the
surrounding brain without in( ltration. This growth pattern can be partly explained by
the expression of E-cadherins, particularly in syncytial and transitional types of
meningiomas. Several experimental studies reported an inverse correlation between the
invasiveness of meningiomas and the expression of E-cadherins. Further, variations exist
between the expressions of E-cadherin in di, erent meningioma subtypes: It is expressed
di, usely in syncytial type, less in transitional type, and not expressed in the ( broblastic
type. This variation in the expression of E-cadherins in meningioma types correlates with
33the proposed corresponding cell types in arachnoid villi. Tohma and colleagues
claimed that meningiomas may derive from arachnoid cells or ( broblasts (( brous
capsule) in the arachnoid villi rather than a single uniform cell based on the expression
pattern of E-cadherin in di, erent meningioma types. It is noteworthy that whereas
( brous capsule and the ( broblastic type of meningiomas do not express E-cadherin, the
rest of the layers of arachnoid villi (cap cell cluster, arachnoid layer, and core arachnoid
cells), and the proposed corresponding meningioma types do express E-cadherins. Tohma
and colleagues also demonstrated ultrastructurally that E-cadherins are distributed along
the cell borders in meningioma cells whereas they are localized at the intermediate
junctions and anchored to cytoskeleton via intracytoplasmic micro( laments in normal
33arachnoid cells. This change in the distribution of E-cadherin was thought to be at the
receptor level, rendering the E-cadherin inactive and thus resulting in more arbitraryarchitecture and the increased motility of embryonic and meningioma cells.
Prostaglandin D synthase2
Prostaglandin D synthase (PGDS or β-trace) is an enzyme playing a role in the synthesis2
9,35of prostaglandin D in the central nervous system (CNS). The function of PGDS in2
arachnoid and meningioma cells was reported in detail by Yamashima and colleagues in
1997. This study demonstrated that PGDS is localized mainly in the rough endoplasmic
reticulum of arachnoid cells and detected in higher concentrations in the core arachnoid
9cells, suggesting that it may play role in the CSF absorption process.
The authors also showed di, use expression of PGDS in meningioma cells. However, the
exact role of PGDS in meningioma cells is yet to be identi( ed, besides its being a
candidate universal cell marker for meningiomas as proposed by Yamashima and
colleagues.
Extracellular Matrix
In the literature, there is convincing evidence that meningiomas are derived from
arachnoid cells based on the similarities in the composition and the distribution of the
components of extracellular matrix in arachnoid cells and meningiomas.
It is also reported that the two basic subtypes—meningothelial and ( broblastic
meningiomas—display common ultrastructural features of intermediate ( laments such as
11,36 37vimentin, interdigitations, and desmosomes. Bellon and colleagues have shown
extracellular deposition of type 4 collagen in the transitional type. Likewise, McComb and
38Bigner demonstrated the ( brillar distribution of the laminin in the transitional and the
39( broblastic types but not in the meningothelial type. Further, Kubota and colleagues
found that whereas type I, III, and IV collagens and laminin occurred di, usely in
between the tumors cells of ( broblastic types, these extracellular matrix proteins were
detected in the ( brous septum of the meningothelial type that separates the clusters of
tumor cells. In addition, Rutka and colleagues demonstrated that cultured meningioma
cells express type I and III procollagens, type IV collagen, and laminin independent of the
40histologic subtypes.
In short, the components of extracellular matrix in meningioma cells and
nonneoplastic arachnoid cells display signi( cant similarities in terms of amount and type of
proteins. It is also noteworthy that expressions of extracellular matrix proteins in
meningothelial and ( broblastic subtypes of meningiomas show a di, erent distribution
pattern, which might suggest that these two basic meningioma subtypes may originate
from different cell types.
ORIGINS OF MENINGIOMAS AT THE GENETIC AND MOLECULAR LEVELS
The majority of meningiomas occur spontaneously or in association with the inherited
autosomal dominant disorder, neuro( bromatosis 2 (NF2). Mutation of the
neuro( bromatosis 2 (NF2) gene on chromosome 22q12 is an early aberration inmeningioma tumorigenesis and individuals with NF2 are at signi( cantly elevated risk for
10,26,41-43developing meningiomas. Mutations in the both alleles of NF2 tumor
suppressor gene result in the loss of merlin protein, which is thought to play a central role
in regulating leptomeningeal cell proliferation. Biallelic inactivation of the NF2 gene is
the initial and most common genetic defect present in at least 50% (30% to 70%) of
26,29,30,42spontaneous meningiomas. In addition, recent studies have identi( ed merlin
inactivation through calpain-mediated proteolysis or aberrant methylation in the 5′
7,8,44region of the NF2 gene in the remaining approximately 50% of meningiomas.
Merlin is a radixin-like protein that is localized underneath the cell membrane and is
implicated in the control of cell membrane–cytoskeletal interaction. Merlin acts on
linking cell membrane proteins and actin ( laments, thus leading to contact inhibition of
normal cell growth. Notably, meningioma cells exhibit weak immunostaining for merlin
compared to non-neoplastic arachnoid cells. Recent studies have reported that
merlinde( cient meningioma cells are prone to develop cytoskeletal and cell contact defects,
41,44,45altered cell morphology, and delayed cellular apoptosis.
Another protein called 4.1 B belonging to the same protein superfamily as merlin was
localized in DAL1 gene locus on chromosome 18p11.32. Although several studies have
demonstrated the loss of 4.1 B protein expressions in up to 76% of cases, no genetic or
46epigenetic change on the DAL1 gene locus itself could be identi( ed. Similarly, no
mutations have been identi( ed in the genes coding for ezrin, radixin, and moesin which
26,27,47are structural relatives of merlin.
Atypical and malignant meningiomas have more intricate genetic aberrations with
losses of the G1–S phase cell cycle checkpoint regulators, CDKN2A and CDKN2B, and
p14ARF on chromosome 9p contributing to more aggressive meningioma
25,28phenotypes. Recently, Kalamarides and colleagues showed that there is a synergy of
Ink4aNF2 and p16 mutations in the natural history of meningioma development in mice
30with biallelic inactivation of NF2. In this study, authors investigated that additional
Ink4aloss of the p16 locus increased the frequency of meningioma and meningothelial
proliferation in NF2 knockout mice regardless of the tumor grade. Likewise, Kalamarides
and colleagues developed an animal model earlier. In this animal model, they targeted
29Cre recombinase to the leptomeninges of NF2 knockout mice by adenoviral delivery.
Consequently, these mice developed a range of meningioma subtypes mimicking human
meningiomas; hence the authors concluded that NF2 biallelic gene activation in
arachnoid cells is rate-limiting for meningioma development in the mouse.
However, in contrast to spontaneous meningiomas, radiation-induced meningiomas
express fewer NF2 mutations or losses on chromosome 22. Radiation-induced
meningiomas arise in fewer than 1% of irradiated patients and tend to be multifocal and
26,41more aggressive, possibly due to additional chromosomal losses on 1p, 6q, and 7p.
The correlation between the aforementioned genetic aberrations and the corresponding
alterations in molecular pathways during meningiomagenesis presents a challenge.
Several studies have been investigating the global gene expression pro( les ofmeningiomas with the goal of providing more insight into the molecular biology of these
neoplasms. A recent study by Lal and colleagues has demonstrated that meningiomas of
all three histopathologic grades can be divided into two main
subgroups—lowproliferative and high-proliferative meningiomas—based on the global gene pro( les and
11underlying molecular mechanisms. The results of this study rede( ned the grade II
meningiomas as either grade I or grade III based on their gene-expression patterns. In this
study, gains and losses of chromosomes were described, but no gene ampli( cations were
found in 23 meningioma specimens studied. The frequency of chromosome losses in
descending order was chromosome 22, 14q, and 1p. Aberrations have also been detected
on chromosomes 3p, 6q, 10, 14q, and 18, and gains on chromosome 1q. The study also
claimed that alterations in the transforming growth factor-β (TGF-β) pathway may
contribute to the anaplasia of grade III meningiomas, as a striking di, erence in the
number of aberrations in genes that regulate TGF-β pathway was observed between the
grade I and grade III meningiomas.
The proposed classi( cation of meningiomas in this study also provided signi( cant
clinical relevance in that it retrospectively showed longer survival in the atypical
lowproliferative group than in the atypical high-proliferative group. However, more studies
are needed to bridge the gap between genetic mutations and intracellular signaling
pathways in meningiogenesis.
THE MENINGIOMA STEM CELL CONCEPT AND ITS IMPLICATIONS IN THE
ORIGIN OF MENINGIOMAS
Stem cells can be described as self-renewing, omnipotent cells that may eventually form
various cell types with multilineage di, erentiation. Likewise, the concept of “cancer stem
cells” denotes cancer cells with stem cell–like features that are responsible for tumor
initiation, tumor renewal, and resistance to antineoplastic medications. Initially, this
concept took its origin from the obvious similarities between the self-renewal mechanisms
of stem cells and cancer cells derived from leukemia, multiple myeloma, and breast
cancer. More than a decade ago, Singh and colleagues presented striking evidence
48regarding the existence of cancer stem cells in medulloblastomas and gliomas. This
+study demonstrated that CD133 cancer cells had the potential to form clusters of cells
resembling neurospheres with self-renewal and di, erentiation abilities. The authors
posted that the origin of cancer initiating cells might be a normal CD133 expressing
neural stem cell, because CD133, a neural stem cell surface marker, was also detected in
the normal human fetal brain. Several more recent studies have also revealed similar
findings suggestive of a linkage between the normal neurogenesis and carcinogenesis.
Currently, there are no known exclusive markers that are unique to cancer stem cells.
Even though CD133 appears to be di, usely expressed by glioma and
medulloblastomainitiating stem cells, it is also present on normal brain stem cells and numerous non-stem
cells in di, erent tumors and normal tissues. The same applies to the other frequently
proposed cancer stem cell markers including CD44, Scal, and Thyl.
Recently, microarray and genomic hybridization techniques enabled the identi( cationof several genes and signaling pathways, including Bmi-1, Tie-2, Shh, Notch, and
Wnt/βcatenin, that may exert control over stem cells. Nevertheless, these genes also function in
other non-neoplastic cell types. In conclusion, there is still no exclusively identi( ed gene,
epigenetic signature, or corresponding signaling pathway for cancer stem cells.
The idea of a “meningioma stem cell” is the extension of the cancer stem cell concept
47in other various solid tumors.
The hypothetical approach for the identi( cation of potential meningioma stem cells
should include the consecutive steps as follows:
1. Cultivation of meningioma cells from the patient specimens in serum-free neural stem
cell (NSC) medium
2. Isolation of the potential meningioma stem cells using histopathologic (e.g.,
immunostaining), molecular (e.g., Western blot), and genetic tools (e.g., global gene
profiling)
3. Establishment of an in vivo meningioma animal model by implanting isolated
meningioma “stem cells”
4. Histopathologic, molecular, and genetic comparison of the in vivo formed
meningioma cells with the initial meningioma tumor sample for verification.
Preliminary Results Supporting the Concept of Meningioma Stem
Cells
Considering the cell surface markers of tumor-initiating cells, or, in other words, “cancer
stem cells,” several transmembrane glycoproteins including CD24, CD34, CD44, CD133,
and CD166 were studied in cultured meningioma cells in neural stem cell medium and on
paraN n-embedded tissue sections obtained from grade I to III meningiomas. In addition,
double staining with the proliferation marker Ki-67 was performed with each of the
aforementioned cell surface markers to show the co-localization of Ki-67 staining with
any of the stem cell markers. We observed consistent co-localization of CD133 and CD44
with the nuclear proliferation marker Ki-67 in vivo and in vitro. These ( ndings suggested
+ + – –that meningioma stem cells may arise from CD133 CD44 CD24 CD166
+ + – –meningioma cells. Further, CD133 CD44 CD24 CD166 meningioma cell populations
had signi( cantly longer survival times and increased proliferation rates in vitro. In the
literature we reviewed, breast cancer stem cells displayed similar expression of surface
+ + –markers as CD133 CD44 CD24 (Table 3-2).
TABLE 3-2 Cell surface markers of cancer stem cells in various solid tumors.It is also noteworthy that breast carcinoma is also predominantly seen in females; thus
it may be feasible to investigate further to clarify any common intracellular signaling
pathways and genetic aberrations in both meningiomas and breast carcinomas.
Phase-contrast and immuno1uorescence (IF) microscopy con( rmed the growth of
cultured meningioma cells in serum-free (NSC) media.
Expression of epithelial membrane antigen and vimentin
In numerous studies, IF staining has demonstrated strong positivity for epithelial
membrane antigen (EMA) and vimentin in cultured meningoma cells in NSC medium.
Expression of prostaglandin D synthase
Prostaglandin D synthase (PGDS) is one of the proposed meningioma cell markers in vivo,
and its physiologic role in arachnoid cells was explained earlier. IF staining for PGDS in
our cultured meningioma cells was positive, which may be evidence supporting the
differentiation of potential meningioma stem cells into meningioma cells.
Expression of CD44
CD44 is a widely distributed cell surface marker and cell adhesion molecule. The
insertion of alternatively spliced exons into the CD44 mRNA creates various isoforms of
CD44, each involved in diverse biologic functions. Suzuki and colleagues demonstrated
49the di, erential expression of CD44 in various meningioma subtypes. In this study, only
the secretory meningiomas appeared to express variant forms of CD44, favoring tumor
cell di, erentiation to epithelial type, whereas meningothelial, ( brous, and malignant
meningiomas express the standard form of CD44. Further, several other studies in the
literature revealed convincing evidence that the overexpression of CD44 was often
49,50associated with increased migration ability and anaplasia in meningioma cells.
Sainio and colleagues demonstrated the co-localization of NF2 gene–encoded merlin
protein with CD44 and noted the interaction of CD44 and cytoskeleton via ezrin, radixin,
and moesin proteins which are structurally related to merlin protein. Similarly, Morrisonand colleagues presented additional evidence regarding the role of merlin-mediated
contact inhibition of cell growth through interactions with CD44 in schwannoma cell
lines.
We observed co-localization of CD44 with the proliferation marker Ki-67 in paraN
nembedded slides and in vitro under an IF microscope.
Expression of CD133
CD133 (Prominin I), a cell-surface antigen, is the ( rst in a class of pentaspan membrane
proteins. CD133 is a 97-kDa glycoprotein with ( ve transmembrane domains, binds to the
cell membrane cholesterol, and is associated with a particular membrane microdomain in
a cholesterol-dependent manner. Even though the exact biologic function of CD133 is not
known, it has been shown as a marker for stem and progenitor cells including neural and
embryonic stem cells as well as hematopoietic stem and progenitor cells in both humans
and mice. It was also shown to be expressed in cancers, including some leukemias and
brain tumours, mostly in gliomas and medulloblastomas.
Immunostaining of paraN n-embedded slides has revealed the co-localization of CD133
with the nuclear proliferation marker Ki-67.
We also detected the di, use expression of CD133 in meningioma cell culture plates
The double-staining of CD133 with EMA also revealed positive results in some cells. It
was particularly noteworthy to observe the co-staining of CD133 and EMA. Because EMA
is an important marker in histologic diagnosis of meningiomas, it is conceivable that
meningioma cells displaying positive staining for CD133 and EMA simultaneously may be
“candidate meningioma stem cells.” The CD133 might serve as a potential “surface
marker” for these meningioma “stem cells.”
Expression of CD166
CD166 (ALCAM) is an activated leukocyte cell adhesion molecule that binds to cell
surfaces via CD6. It is a glycoprotein belonging to the immunoglobulin superfamily and is
localized mostly on epithelial cells at intercellular junctions as part of the adhesive
complex that maintains tissue architecture. CD166 has been detected in numerous
malignancies, including melanoma, prostate carcinoma, breast cancer, colorectal
carcinoma, bladder cancer, and esophageal squamous cell carcinoma. A recent
experimental study has revealed CD166 at intercellular junctions in cultured endothelial
cells and at the sites of cell–cell contact in the epithelium of several organs. The CD166
expression on meningiomas has not been reported in the literature so far. We detected
di, use positive IF staining for CD166 on our cultured meningioma cells suggesting a
potential role for it on the di, erentiation and proliferation on meningioma “stem cells.”
However, we did not detect persistent staining of CD166 on paraffin-embedded slides and
did not observe any co-localization with Ki-67.
CONCLUSION
Classical data regarding the origin of meningiomas are mostly based on electron
microscopic and immunohistochemical ( ndings showing that meningiomas arise fromarachnoid cells. However, arachnoid cells are not uniform and exhibit a wide range of
cellular diversity including meningothelial, ( broblastic, endothelial cells, and the cells at
the dura–arachnoid border. Recent studies have further supported the idea of
“arachnoid-derived meningioma” concept: biallelic NF2 gene inactivation in arachnoid
cells in nude mice led to meningioma formation. Taken together, these classical ( ndings
and recent evidence strongly suggested that arachnoid cells are the origins of
meningiomas. Nevertheless, it is still not clear what particular type of arachnoid cell or
cells are the meningioma-initiating cells. At this point, menigioma stem cell research
would serve to investigate the meningioma-initiating cell/cells. Further, the concept of a
“meningioma stem cell” does not seem too farfetched in light of current exciting ( ndings.
The next challenge is to develop a in vivo animal model that would mimic the natural
course of meningioma formation.
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#
CHAPTER 4
Epidemiology and Natural History of Meningiomas
Lisa Calvocoressi, Elizabeth B. Claus
INTRODUCTION
In this chapter, we (1) provide descriptive data on the impact of meningiomas; (2)
describe the natural history of these tumors; and (3) review risk and protective factors.
Throughout, we critically evaluate the literature and identify gaps in knowledge. We
identi ed studies on natural history and risk factors through MEDLINE using the PubMed
system to retrieve articles published through February, 2008. We conducted searches,
restricted to articles written in English, using the key words “meningioma” or
“meningiomas” in conjunction with “biology,” “natural history,” “long-term,” “outcome,”
surgery/microsurgery, “radiotherapy,” “radiation (ionizing),” “radiation e3ects,”
cellular/mobile telephone/s, “occupation,” “head trauma,” “head injury,” “allergy,”
breast cancer/carcinoma, “oral contraceptives,” hormone/estrogen replacement therapy,
“hormone receptors,” genetic/s, and “epidemiology.” We obtained additional references
1-4from those articles and from several recent epidemiologic reviews of brain tumors. We
obtained descriptive statistics from articles identi ed through PubMed key word searches
combining meningioma/s with “incidence,” “prevalence,” “survival,” “recurrence,” and
“descriptive epidemiology,” and from the most recent report of the Central Brain Tumor
Registry of the United States (CBTRUS) that is based on voluntary reporting by 18
5registries from 1998 to 2002.
DESCRIPTIVE STATISTICS
By histology, meningiomas were the most frequent primary brain and central nervous
system (CNS) tumors reported to CBTRUS between 1998 and 2002, accounting for
19,190 (30.1%) of all 63,698 tumors reported (Fig. 4-1). Ninety-three percent of the
5meningiomas were nonmalignant.FIGURE 4-1 Histologic distribution of primary brain tumors and CNS tumors, CBTRUS
1998–2002, n = 63,698.
Incidence
CBTRUS rates per 100,000 person years, age-adjusted to the 2000 U.S. standard
population, demonstrated an overall meningioma incidence rate of 4.52. Rates di3ered
little by race/ethnicity (4.46 in non-Hispanic whites; 4.58 in non-Hispanic blacks, and
4.61 in Hispanics of any race), but more than twice as many new cases were diagnosed
5among women than men (6.01 vs. 2.75). Meningiomas are uncommon in children,
accounting for approximately 3% of all childhood tumors; their incidence increases
5linearly with age (Fig. 4-2). Mean age at diagnosis was 64 years.
FIGURE 4-2 Age-adjusted incidence rates of meningioma, 1998–2002. Central Brain
Tumor Registry of the United States.
In the United States, data collected by CBTRUS between 1985 and 1994 from six
6population-based registries did not show an increase in incidence of meningioma, nor
7did a study of the population of Rochester, Minnesota, 1950–1990. However, data from
the Danish Cancer Registry (1943–1997) demonstrated an increase in new cases of
meningioma from 0.61 to 2.42 per 100,000 population, with an accelerating increase
8over time. A similar trend was observed across Denmark, Sweden, Norway, and Finland
9between 1968 and 1997, whereas in Japan, based on 1973–1993 data, an increase in#
#
10incidence was seen before 1980, followed by stable subsequent rates. Where an
increasing trend has been observed, it has been attributed to increased use of advanced
9,10imaging techniques, increased exposure to potential risk factors, and di3erential
8histologic classification of meningioma over time.
Survival, Prevalence, and Recurrence
Data from the Hospital-based National Cancer Data Base collected from 1985 to 1988
and 1990 to 1992 estimated 5-year survival rates for benign, atypical, and malignant
11,12meningiomas in the United States at 70.1%, 74.5%, and 54.6%. Population-based
data from Finland, Australia, and Sweden have found that 5-year survival rates for all
13-15meningioma histologic subtypes combined ranged from 73% to 94%. This relatively
high 5-year survival is reFected in the number of prevalent cases. Registry data from
Connecticut and Utah estimated that 138,000 individuals were living with this tumor in
16the United States in the year 2000, a prevalence rate of 50.4 per 100,000 population.
In addition, meningiomas may recur. At 5 years, 19.2% of persons with benign tumors
and 32.4% of persons with malignant meningioma had su3ered a recurrence of
11symptoms.
These data likely represent a lower limit of the number of persons with meningioma, as
many patients presumed to have such a lesion are managed conservatively (i.e., without
surgical intervention and pathologic con rmation), and hence may not be included in
national databases that produce estimates of tumor incidence and prevalence. The
di3erent incident trends across nations reported here may reFect real di3erences, but are
diG cult to compare owing to di3erences in the time periods assessed and in the quality
and methods of reporting. The Danish Cancer Registry is considered valid and 95% to
899% complete. In contrast, case reporting in the United States may be hampered by
information and selection biases. Although CBTRUS has worked collaboratively with state
cancer registries since the 1980s to collect information on all primary brain tumors,
including tumors of benign and uncertain behavior, such reporting was voluntary and
necessarily incomplete until recently, primarily reFecting patterns for the white
6population of the northeastern United States. In 2004, the United States Congress passed
the Benign Brain Tumor Registry Amendment Act (Public Law 107-206) that mandated
all United States cancer registries within the National Program of Cancer Registries
(NPCR) to collect data on nonmalignant brain tumors. The accuracy of future population
estimates in the United States will improve once these data become available.
NATURAL HISTORY AND LONG-TERM FOLLOW-UP
Some meningiomas may be asymptomatic and found incidentally. Other meningiomas
may cause devastating symptoms with relatively abrupt onset. Or, because of the slow
growth, some tumors may cause more subtle neurologic symptoms including diG culty
concentrating or nding words and weakness or numbness in arms or legs with resultant
1problems with gait and walking. In addition, whereas more than 90% of meningiomas
are benign (WHO Grade I), approximately 5% are atypical/borderline, and 3% to 5% are#
#
1malignant. In addition, these tumors di3er in size, site, and relationship to important
17vascular and neural structures. These varied presentations require di3erent treatment
strategies, each with associated risks and bene ts. Case series that examine long-term
outcomes of patients who were conservatively managed, and those who received surgery
or radiation therapy, or both, may aid decision making regarding treatment options. We
reviewed long-term follow-up studies of tumor progression and recurrence, survival,
symptoms, and quality of life among patients with meningioma by treatment modality
and histologic grade.
Incidental Findings and Conservative Management
With increasing use of magnetic resonance imaging (MRI) and computed tomography
(CT) in clinical settings, asymptomatic meningiomas are more often coming to medical
18attention, with attendant questions about their clinical management. Several studies
with fairly small samples (n = 17–67) have reported on patients with conservatively
treated, incidental and asymptomatic tumors across meningioma sites. During mean
follow-up times that ranged from 2.7 to 6.2 years, the proportion of patients who became
19-22symptomatic was small, ranging from 0% to 16%. In addition, during mean
followup of 1.3 to more than 5 years, a majority of patients (between 63% and 100%)
3 18,20-24demonstrated no or limited (<1> per year) tumor growth. However, there was
substantial variability. For example, in a study of 41 patients over a 3.6-year follow-up,
the range in growth rate was 0.48% to 72% and calculated tumor doubling time varied
18from 1.27 to 143.5 years.
Whereas the aforementioned studies examined the natural history of meningiomas
across tumor locations in asymptomatic individuals, the natural history of skull base
tumors, speci cally, was examined in cohorts of conservatively managed patients, many
of whom were symptomatic but did not undergo more aggressive treatments owing to
advanced age, patient preference, medical contraindications, or tumors considered
inoperable. These patients presented with symptoms that included headaches, dizziness
and vertigo, seizures, hearing and vision loss, facial palsy, trigeminal neuropathy,
25,26swallowing problems, and gait disturbance. Of 21 consecutive patients with
petroclival tumors followed on average 6.8 years, tumor growth was observed in 76% of
cases, 58% experienced functional deterioration, and two succumbed to tumor-related
26deaths. Among 40 patients with petroclival, cavernous sinus, and anterior clinoid
tumors at 10-year radiographic follow-up, 58% of tumors evidenced some growth. After a
mean 6.9 years of clinical follow-up, 11 patients (28%) experienced new or worsening
neuropathy; 23 (58%) developed paralysis or long tract signs; 2 (5%) had lost sight in
25one eye; and two became disabled.
Surgery and Radiation Treatments
Benign tumors
Among selected case series that included exclusively or predominantly benign