Neuroanatomy Atlas in Clinical Context

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Eleventh Edition

NEUROANATOMY ATLAS IN CLINICAL CONTEXT Structures, Sections, Systems, and Syndromes

Eleventh Edition

NEUROANATOMY ATLAS IN CLINICAL CONTEXT Structures, Sections, Systems, and Syndromes

Duane E. Haines, PhD, FAAAS, FAAA Professor, Department of Neurology, and Professor, Department of Neurobiology and Anatomy, Wake Forest School of Medicine, Winston-Salem, North Carolina And Professor Emeritus, Department of Neurobiology and Anatomical Sciences and Professor, Departments of Neurology and of Neurosurgery, University of Mississippi Medical Center, Jackson, Mississippi Mary Alissa Willis, MD, FAAN, FANA Chair, Department of Neurology, University of Mississippi Medical Center, Jackson, Mississippi

Illustrator: W. K. Cunningham, BA, MSMI Photographers: G. W. Armstrong, RBP; R. W. Gray, BA

Acquisitions Editor: Crystal Taylor Development Editors: Amy Millholen, Kelly Horvath

Editorial Coordinator: Janet Jayne Marketing Manager: Danielle Klahr

Production Project Manager: Matthew West Manufacturing Coordinator: Margie Orzech Manager, Graphic Arts & Design: Stephen Druding Prepress Vendor: TNQ Technologies

Eleventh Edition

Tenth edition translations: Chinese, Simplified (Science Press) Japanese (Medical Sciences International, Ltd.)

Russian (Logosphera, Ltd.) Spanish (Wolters Kluwer)

Copyright © 2019 Wolters Kluwer Health/Lippincott Williams & Wilkins. Copyright © 2015 Wolters Kluwer Health/ Lippincott Williams & Wilkins. Copyright © 2012 Wolters Kluwer Health/Lippincott Williams & Wilkins. Copyright © 2008 Lippincott Williams & Wilkins, a Wolters Kluwer business. Copyright © 2004, 2000 by Lippincott Williams & Wilkins. Copyright © 1995 by Lippincott-Raven Publishers. Copyright © 1991, 1987 by J. B. Lippincott Company. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. govern ment employees are not covered by the above-mentioned copyright. To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at permissions@lww.com, or via our website at shop.lww.com (products and services).

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Library of Congress Cataloging-in-Publication Data

ISBN-13: 978-1-975197-29-2

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This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warran ties as to accuracy, comprehensiveness, or currency of the content of this work. This work is no substitute for individual patient assessment based upon healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data and other factors unique to the patient. The publisher does not provide medical advice or guidance and this work is merely a reference tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources. When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings and side effects and identify any changes in dosage schedule or contrain dications, particularly if the medication to be administered is new, infrequently used or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work.

Preface to the Eleventh Edition

T he first edition of this book contained several unique features, one of which was a particular emphasis on clinical information, correlations, terminology, and the integration of neuroanatom ical concepts with clinical concepts. Morphologic concepts, it could be argued, are not learned/understood for their own sake, but are learned as the basis for understanding the impaired patient. The Tenth Edition continued and expanded the approach of empha sizing clinical relevance. Clinical content was revised and increased throughout all chapters. Chapter 9 was divided into a Part I (Herniation Syndromes of the Brain and Spinal Discs) and a Part II (Representative Stroke Syndromes). This further emphasized the clinical application of basic science concepts. This new Eleventh Edition of Neuroanatomy Atlas in Clinical Context continues to (1) provide a sound anatomical base for inte grating neuroscience and clinical concepts; (2) introduce new text, artwork, and optical coherence tomography (OCT) that emphasize information and concepts that are encountered in the clinical setting; (3) utilize contemporary clinical and basic science terminology in its proper context; and (4) emphasize neuroscience information, con cepts, and images that collectively constitute a comprehensive, and clinically oriented, overview of systems neurobiology. Further, the revision, in the Tenth Edition, of existing pages, the addition of new pages, and the division of Chapter 9 into a Herniation Part and a Stroke Part resulted in an increase in the number of MRI, MRA, CT, CTA, and angiograms representing a significant increase in clinically relevant examples. Understanding systems neurobiology is an abso lutely essential element in the successful diagnosis of the neurologi cally compromised patient. Many comments, suggestions, insights, and ideas from my col leagues, medical students, residents, and graduate students have been factored into the modifications in this new edition; their candor is greatly appreciated. While minor corrections, or changes, have been made throughout the book, the new information introduced in the Eleventh Edition of Neuroanatomy Atlas in Clinical Context contin ues as follows: First , all clinical information throughout the Atlas appears in a light blue screen. This (1) makes it very easy to identify any and all clinical comments, or examples, on every page; (2) does not reduce clinical con cepts by trying to compress them into small summary boxes; (3) keeps all clinical correlations and information in their proper neuroanatomi cal context; and (4) emphasizes the overall amount—and relevance—of the clinical information presented in this Atlas. This approach allows the user to proceed from a basic point to a clinical point or from a clin ical point to a basic point, without a break in the flow of information,

or the need to go to a different page. This greatly expedites the learning process. Second , since a number of new pages have been added in Chapter 8, the pagination, beginning on about p. 270, has been adjusted to accom modate these new pages. The adjustment is continuous throughout the book from that point onward. Third , Figure 8-49A introduces, in this new edition, an OCT image of a normal retina in axial plane at the level of the fovea centralis. Images in Figure 8-49B–F are examples of abnormal retinas at the same level. The OCT technology results in a clearer and more defined image than would be achievable with a regular MR. Fourth , an additional section in Chapter 8, titled “What the Patient Sees,” is new to this Eleventh Edition. It consists of examples of what the patient sees in the environment and what the image looks like when it is received in the visual cortex. This approach to illustrating the visual field is novel and gives the user of the Atlas a new look and better under standing of this important sensory system. Two further issues continue to figure prominently in this new Eleventh Edition. First , the question of whether, or not, to use eponyms in their possessive form. To paraphrase one of my clinical colleagues, “Parkinson did not die of his disease (so-called ‘Parkinson’ disease); he died of a stroke. It was never his own personal disease.” There are rare exceptions, such as Lou Gehrig disease, but the point is well taken. McKusick (1998a,b) also has made compelling arguments in support of using the nonpossessive form of eponyms. However, it is acknowl edged that views differ on this question—much like debating how many angels can dance on the head of a pin. Consultation with my neurology and neurosurgery colleagues, the style adopted by Dorland’s Illustrated Medical Dictionary (2012) and Stedman’s Medical Diction ary (2006), a review of some of the more comprehensive neurology texts (e.g., Ropper and Samuels, 2009; Rowland and Pedley, 2010), the standards established in the Council of Biology Editors Manual for Authors, Editors, and Publishers (1994), and the American Medical Association’s Manual of Style (2007) clearly indicate an overwhelming preference for the nonpossessive form. Recognizing that many users of this book will enter clinical training, it was deemed appropriate to encourage a contemporary approach. Consequently, the nonpossessive form of the eponym is used. The second issue concerns use of the most up-to-date anatomical terminology. With the publication of Terminologia Anatomica (1998), a new official international list of anatomical terms for neuroanat omy is available. This new publication, having been adopted by the International Federation of Associations of Anatomists, supersedes all previous terminology lists. Every effort has been made to incorporate

spinal cord, spinal trigeminal, cuneate, gracile, facial, inferior olivary, and parabrachial nuclei, and to the reticular formation, but does not project to the ciliary ganglion.

any applicable new or modified terms into this book. In addition, the well-reasoned modification in the Edinger–Westphal terminology that reflects its functional characteristics is also adapted for this Atlas (Kozicz et al., 2011). The Edinger–Westphal complex consists of an Edinger–Westphal preganglionic nucleus (EWpg) that projects specifi cally to the ciliary ganglion and an Edinger–Westphal centrally project ing nucleus (EWcp) that projects to a variety of targets including the

Duane E. Haines Winston-Salem, North Carolina

Mary Alissa Willis Jackson, Mississippi

REFERENCES

McKusick VA. On the naming of clinical disorders, with particular ref erence to eponyms. Medicine (Baltimore) . 1998a;77(1):1-2. McKusick VA. Mendelian Inheritance in Man: A Catalog of Human Genes and Genetic Disorders . 12th ed. The Johns Hopkins University Press; 1998b. Ropper AH, Samuels MA. Adams and Victor’s Principles of Neurology . 9th ed. McGraw-Hill Companies, Inc.; 2009. Rowland LP, Pedley TA, eds. Merritt’s Neurology . 12th ed. Lippincott Williams & Wilkins; 2010. Stedman’s Medical Dictionary . 28th ed. Lippincott Williams & Wilkins; 2006.

Council of Biology Editions Style Manual Committee. Scientific Style and Format—The CBE Manual for Authors, Editors, and Publishers . 6th ed. Cambridge University Press; 1994. Dorland’s Illustrated Medical Dictionary . 32nd ed. Saunders/Elsevier; 2012. Federative Committee on Anatomical Terminology. Terminologia Ana tomica: International Anatomical Terminology . Thieme; 1998. Iverson C, Christiansen S, Flanagin A, et al. American Medical Associ ation Manual of Style—A Guide for Authors and Editors . 10th ed. Oxford University Press; 2007. Kozicz T, Bittencourt JC, May PJ, et al. The Edinger-Westphal nucleus: a historical, structural, and functional perspective on a dichotomous terminology. J Comp Neurol . 2011;519(8):1413-1434.

Acknowledgments

O ur basic science colleagues in the Department of Neurobiology and Anatomical Sciences and our clinical colleagues in the De partment of Neurology and the Department of Neurosurgery, all at The University of Mississippi Medical Center, have been very gra cious in offering suggestions and comments, both great and small, on the revisions for this and past editions. A special thanks is due several colleagues for their important help with the Eleventh Edition. First, Dr. Mary Alissa Willis read all chapters with particular attention to clinical information, examples, comments, and terminology. Second, Dr. William Watkins (Ophthalmology, Mis sissippi) and Dr. Charlotte Taylor (Neuroradiology, Mississippi) were essential to helping us locate clinical images both normal and abnor mal. Third, Dr. Ching J. Chen (Ophthalmology, Mississippi) helped us mature some concepts on visual field. Fourth, Dr. Craig Greven (Oph thalmology, Wake Forest), Dr. William Watkins (Ophthalmology, Mis sissippi), and Dr. Manasa Gunturu (Neuro-ophthalmology, Mississippi) contributed to the inclusion of retinal OCTs. We greatly appreciate the cooperation of all of these individuals; they did a wonderful job. The modifications in this Eleventh Edition focus on the integration of basic neuroscience and its clinical applicability. The color coding of all clinical artwork has been extended to all new drawings when appropriate. A thank you is due the following individuals for their contributions to recent Editions: Drs. Bishnu Sapkota and David Sinclair, Drs. Robert McGuire and William McCluskey, Drs. Louis Harkey and Andy Parent, Dr. Alan Sinning, Mr. Ken Sullivan, and graduate student Mr. Martin O. Bohlen, medical students Ms. Kelly Brister and Mr. Jarrett R. Morgan, Dr. Tim McCowan, Dr. Jonathan Wisco (UCLA), Drs. Amy Jones and Bridgett Jones, and Drs. Kim Simpson and Jim Lynch. The external reviewers commissioned by Wolters Kluwer over the years were faculty: Dr. James D. Foster, Dr. Eustathia L. Giannaris, Dr. Joerg R. Leheste, Dr. Mary A. Matteliano, Dr. Todd A. Nolan, Dr. Omid B. Rahimi, and students: John Brandt, Rachel Krieger, Avani Patal, Ronald Sahyouni, Farooq Usmani, and Haley Zlomke. For the Eleventh Edition, we express our appreciation to the faculty external reviewers commissioned by Wolters Kluwer. Modifications, both great and small, in earlier editions to the exist ing artwork and labeling scheme, and the generation of many new ren derings, tables, and compiling plates, were predominately the work of Mr. Walter (Kyle) Cunningham (Medical Illustrator) and Mr. Michael Schenk. Mr. Chuck Runyan (Biomedical Photography), Mr. Bill Arm strong (Manager of Biomedical Photography), and Mr. Robert W. Gray (Biomedical Photography) photographed new brain and spinal cord specimens. We are enormously appreciative of the time, energy, ded ication, and professionalism of these individuals toward creating the best possible images, photographs, artwork, and finished plates for this book. Mr. Cunningham went out of his way to do an absolutely outstanding job to meet and repeatedly exceed the expectations of the

author in earlier editions as well as this Eleventh Edition. Thank you, Kyle! A special thanks to Dr. Haines’ granddaughter, Miss Ireland G. Scott, for her excellent help with computer issues encountered in the generation of some new drawings in the Eleventh Edition. Over the years, many colleagues, friends, and students (now faculty or medical/dental practitioners) have made many helpful comments. They are again acknowledged here, because these earlier suggestions continue to influence this book: Drs. A. Agmon, A. Alqueza, B. Ander son, C. Anderson, R. Baisden, S. Baldwin, R. Borke, J. Brandt, P. A. Brewer, A. S. Bristol, Patricia Brown, Paul Brown, A. Butler, T. Castro, B. Chronister, C. Constantinidis, A. Craig, J. L. Culberson, P. DeVasto, V. Devisetty, E. Dietrichs, L. Ehrlichman, J. Evans, E. M. Fallon, B. Falls, C. Forehand, J. D. Foster, R. Frederickson, G. C. Gaik, E. Garcis-Rill, E. L. Giannaris, G. Grunwald, B. Hallas, T. Imig, J. King, J. A. Kmiec, R. Krieger, P. S. Lacy, A. Lamperti, J. R. Leheste, G. R. Leichnetz, E. Levine, R. C. S. Lin, J. C. Lynch, T. McGraw-Ferguson, G. F. Martin, M. A. Matteliano, A. Miam, G. A. Mihailoff, M. V. Mishra, B. G. Mollon, T. A. Nolan, R. L. Norman, R. E. Papka, A. Patel, A. N. Perry, K. Peusner, C. Phelps, B. Puder, O. B. Rahimi, H. J. Ralston, J. Rho, L. T. Robertson, D. Rosene, A. Rosenquist, I. Ross, R. Sahyouni, J. D. Schlag, M. Schwartz, J. Scott, V. Seybold, L. Simmons, K. L. Simpson, A. Singh, D. Smith, S. Stensaas, C. Stefan, D. G. Thielemann, M. Thomadaki, S. Thomas, M. Tomblyn, J. A. Tucker, D. Tolbert, F. Usmani, F. Walberg, S. Walkley, M. Woodruff, M. Wyss, R. Yezierski, H. Zlomke, and A. Y. Zubkov. We have greatly appreciated their comments and suggestions. The stained sections used in this Atlas are from the teaching collection in the Depart ment of Neurobiology and Anatomy at West Virginia University School of Medicine. Dr. Haines, who was on the faculty at WVU from 1973 to 1985, expresses his appreciation to Mr. Bruce Palmer. This Eleventh Edition would not have been possible without the interest and support of the publisher, Wolters Kluwer. We want to express thanks to our edi tors, Crystal Taylor (Senior Acquisitions Editor), Amy Millholen (Senior Development Editor), Janet Jayne (Editorial Coordinator), Matthew West (Production Project Manager), Parisa Saranj (Editorial Assistant), and especially Kelly Horvath (Freelance Development Editor) for their encouragement, continuing interest, and confidence in this project. Kelly was absolutely an essential key in the process and we greatly appreciate her hard work and wonderful cooperation. Their cooperation has given us the opportunity to make the improvements seen herein. Lastly, but clearly not least, we want to express a special thanks to Dr. Haines’ wife, Gretchen. The significant changes made in this edition required attention to many, and multiple, details. She carefully and critically reviewed the text, patiently listened to more neurobiol ogy than she could have ever imagined, and gleefully informed him about rules of grammar and punctuation that he is not sure he even knew existed. She also got a kick out of arguing about the singular versus plural form of Latin terms. We gladly dedicate this Eleventh Edition to Gretchen.

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Faculty Reviewers

Keith Bishop, PhD, PT Texas Tech University Health Sciences Center Lubbock, Texas Abimbola Farinde, PhD Columbia Southern University

Priti Lacy, PhD Des Moines University Des Moines, Iowa

Forshing Lui, MD, FAAN (UK), FRCP (Edinburg) California Northstate University, College of Medicine

Orange Beach, Alabama James D. Foster, PhD Alabama College of Osteopathic Medicine Dothan, Alabama Jonathan R. Hill, MBA, MD/PhD Candidate The University of Queensland, Ochsner Clinical School New Orleans, Louisiana

Elk Grove, California Barbara Sawyer, PhD Texas Tech Health Sciences Center Lubbock, Texas Gregg Stanwood, PhD Florida State University, College of Medicine Tallahassee, Florida

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Table of Contents

Preface to the Eleventh Edition V

Acknowledgments VII

Introduction and User’s Guide 1

External Morphology of the Central Nervous System 9 The Spinal Cord: Gross Views and Vasculature 10 The Brain: Lobes, Principle Brodmann Areas, Sensory–Motor Somatotopy 13 The Brain: Gross Views, Vasculature, and MRI 16 The Cerebellum: Gross Views and MRI 36 The Insula: Gross View, Vasculature, and MRI 38 Vascular Variations of Clinical Relevance 40

Cranial Nerves 45

Synopsis of Cranial Nerves 46 Cranial Nerves in MRI 48 Deficits of Eye Movements in the Horizontal Plane 55 Cranial Nerve Deficits in Representative Brainstem Lesions 56 Cranial Nerve Cross Reference 57

Meninges, Cisterns, Ventricles, and Related Hemorrhages 59 The Meninges and Meningeal and Brain Hemorrhages 60 Meningitis 62 Epidural and Subdural Hemorrhage 64 Cisterns and Subarachnoid Hemorrhage 66 Meningioma 68 Ventricles and Hemorrhage into the Ventricles 70 4 Copyright © Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. 2024

The Choroid Plexus: Locations, Blood Supply, Tumors 74 Hemorrhage into the Brain: Intracerebral Hemorrhage 76

Internal Morphology of the Brain in Unstained Slices and in MRI 77

Part I: Brain Slices in the Coronal Plane Correlated with MRI 77 Part II: Brain Slices in the Axial Plane Correlated with MRI 87

Internal Morphology of the Spinal Cord and Brain: Functional Components, MRI, Stained Sections 97 Functional Components of the Spinal Cord and Brainstem 98 The Spinal Cord with CT and MRI 100 Arterial Patterns within the Spinal Cord with Vascular Syndromes 110 The Degenerated Corticospinal Tract 112 The Medulla Oblongata with MRI and CT 114 Arterial Patterns within the Medulla Oblongata with Vascular Syndromes 126 The Cerebellar Nuclei 128 The Pons with MRI and CT 132 Arterial Patterns within the Pons with Vascular Syndromes 140 The Midbrain with MRI and CT 142 Arterial Patterns within the Midbrain with Vascular Syndromes 154 The Diencephalon and Basal Nuclei with MRI 156 Arterial Patterns within the Forebrain with Vascular Syndromes 176

Internal Morphology of the Brain in Stained Sections: Axial–Sagittal Correlations with MRI 179 Axial–Sagittal Correlations with MRI 180

Tracts, Pathways, and Systems in Anatomical and Clinical Orientation 191 Orientation 192

Sensory Pathways 194 Motor Pathways 212 Cranial Nerves 228 Spinal and Cranial Nerve Reflexes 236 Cerebellum and Basal Nuclei 244 Visual, Auditory, and Vestibular Systems 264 Internal Capsule and Thalamocortical Connections 288 Limbic System: Hippocampus and Amygdala 292 Hypothalamus and Pituitary 300

Clinical Syndromes of the CNS 309 Part I: Herniation Syndromes of the Brain and Spinal Discs 309 Part II: Representative Stroke Syndromes 321

Anatomical–Clinical Correlations: Cerebral Angiogram, MRA, and MRV 329 Cerebral Angiogram, MRA, and MRV 330 Overview of Vertebral and Carotid Arteries 341

Q&As: A Sampling of Study and Review Questions, Many in the USMLE Style, All with Explained Answers 343

Sources and Suggested Readings

See online Interactive Atlas

Index 355

Duane E. Haines, PhD, FAAAS, FAAA

Mary Alissa Willis, MD, FAAN, FANA

Recipient of the 2008 Henry Gray/Elsevier Distinguished Educator Award from the American Association for Anatomy Elected a Fellow of the American Association for Anatomy and a Fellow of the American Association for the Advancement of Science Recipient of the 2010 Alpha Omega Alpha Robert J. Glaser Distinguished Teacher Award from AOA and the Association of American Medical Colleges Neuroanatomy Consultant for Stedman’s Medical Dictionary and for Dorland’s Illustrated Medical Dictionary Co-recipient, International Society for the History of Neuroscience, 2017 Outstanding Articles Award, Journal of the History of the Neurosciences

Fellow, American Academy of Neurology Fellow, American Neurological Association Executive Council, Association of University Professors of Neurology Associate Editor, International Journal of MS Care

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chapter

and Related Hemorrhages 4

Meninges, Cisterns, Ventricles,

T he meninges consist of dura mater ( pachymeninx ), arachnoid mater , and pia mater; the latter two form the leptomeninx . The meninges are composed of fibroblasts modified in different layers to serve specific functions. The outer layers, the periosteal dura and men ingeal dura , are composed of elongated fibroblasts and large amounts of collagen and have great strength. Vessels in the pachymeninx are located at the dura-skull interface generally forming indentations/grooves in the inner table of the skull. The periosteal dura forms the periosteum on the inner table of the skull, is tightly adherent to the inner table particularly at suture lines, and is located external to the dural sinuses. The meningeal dura forms the dural reflections ( falx cerebri , tentorium cerebelli , dia phragma sellae , falx cerebelli ) that are located internal to specific venous sinuses. Extradural ( epidural ) hemorrhages or hematomas are sequestered between the inner table of the skull and the periosteal dura. The innermost part of the dura, the dural border cell layer , is attached to the externally located meningeal dura and to the internally located arachnoid mater. It is made up of sinuous elongated fibroblasts separated by extracellular spaces containing an amorphous material but no collagen; this layer has markedly few cell junctions. The dural border cell layer is a structurally weak plane at the dura-arachnoid interface; so-called subdural hemor rhages or hematomas are sequestered within this layer. There are no naturally occurring spaces between the inner table and the periosteal dura or external to, within, or internal to, the dural bor der cell layer. Consequently, epidural hematoma and the so-called sub dural hematoma , with their characteristic shapes, extents, and clinical sequelae are usually the result of a traumatic or pathologic event. There is a naturally occurring spinal epidural space between the spinal dural sac and vertebral column; the vertebrae have their own periosteum.

The arachnoid mater is composed of cells that are less elongate, tightly packed with little/no extracellular space, and attached to each other by desmosomes and tight junctions. The arachnoid membrane is located internal to the dural border cell layer and, along with the menin geal dura, forms the various dural reflections . This layer is generally two to four cells thick and forms a barrier against the movement of cerebrospinal fluid (CSF), hence its designation as the arachnoid bar rier cell layer . The naturally occurring subarachnoid ( leptomeningeal ) space ( SAS ) is located between the arachnoid and pia and provides for the egress of CSF from the ventricles, circulation around the brain and spinal cord, and reabsorption into the venous system particularly at the arachnoid villi . Arachnoid cap cells generally found in the vicinity of these villi are a primary source of cells that develop into meningioma . Blood within the SAS ( subarachnoid hemorrhage ) is most commonly seen following trauma and secondarily after rupture of an intracranial aneurysm. The causative agents for bacterial or viral meningitis may be found in the leptomeningeal space. The arachnoid trabeculae are com posed of numerous elongated sinuous fibroblasts that traverse the SAS. These have cell junctions with the arachnoid layer and with the pia and may contain collagen in folds of their cell membranes. The fibroblasts forming the pia mater are adherent to the CNS sur face and follow all of its various undulations, in some places forming a single layer. Taken together the pia mater and the glial limiting mem brane (protoplasmic astrocyte cell processes at the CNS surface) form the pial-glial membrane . Occasional small subpial spaces containing collagen fibers are found at the pia-brain interface. Large vessels located in the SAS may be partially, or totally, enveloped by pial cell and/or trabecular cell processes.

Skull

Location of epidural hematoma

Periosteal dura

Dura mater

Meningeal dura

Dural border cell layer

Location of subdural hematoma

Arachnoid trabeculae in SAS

Position of subarachnoid hemorrhage

Subarachnoid space (SAS)

Collagen

Pia mater

Pia–glia membrane (intima pia) Occasional subpial space

Pia–glia membrane (intima pia)

Basement membrane

Brain surface

60 CHAPTER 4 / MENINGES, CISTERNS, VENTRICLES, AND RELATED HEMORRHAGES

TABLE 4-1 Comparison of Cerebral Versus Spinal Meninges

C erebral

S pinal

Dura

• Adherent to inner table of skull (no epidural space) • Composed of two fused layers (periosteal, meningeal), which split to form sinuses, and of the dural border cell layer (DBC)

• Separated from vertebrae by epidural space • Composed of meningeal dura only (vertebrae have their own perios teum), and of the DBC layer

Arachnoid (outer part of leptomeninges)

• Attached to dura in living condition (no preexisting subdural space) • Arachnoid villi (in superior sagittal sinus) • Arachnoid trabeculae in SAS • Subarachnoid space with many cisterns

• Attached to dura in living condition (no preexisting subdural space) • No arachnoid villi • Few or no arachnoid trabeculae but larger arachnoid septae • Subarachnoid space with one main cistern • Intimately adherent to surface of cord • Specializations in the form of denticulate ligaments, filum terminale, and linea splendens • Follows vessels as they pierce the cord Pia (inner part of leptomeninges)

Pia (inner part of leptomeninges) • Intimately adherent to surface of brain • No pial specializations • Follows vessels as they pierce the brain

MENINGITIS, MENINGEAL HEMORRHAGES, AND MENINGIOMA A wide variety of disease processes and lesions may involve the menin ges; only a few examples are mentioned here. Infections of the meninges ( bacterial meningitis ) may be called lep tomeningitis because the causative organisms localize to the SAS and involve the pia and arachnoid . Extension into the dura is called pachy meningitis . A variety of organisms cause bacterial meningitis ; bacteria most commonly associated with certain age groups or with trauma are as follows: neonate = Streptococcus ( S. ) agalactiae , Escherichia ( E. ) coli , Listeria (L.) monocytogenes ; neonate to about 24 months = S. agalactiae , E. coli , Haemophilus (H.) influenzae ; about 2–50 years = S. pneumoniae , Neisseria ( N. ) meningitidis ; about 50 years + = S. pneu moniae , N. meningitidis , L. monocytogenes ; basal skull fracture = S. pneumoniae , H. influenzae ; head trauma = Staphylococcus . The patient becomes acutely ill (i.e., headache , photophobia, confusion , fever , stiff neck [ nuchal rigidity ], stupor ), may have generalized or focal signs/ symptoms, and, if not rapidly treated (with appropriate antibiotics), will likely die. Patients with viral meningitis may become ill over a period of several days, experience headache , confusion , and fever , but most will recover in 1–2 weeks with supportive care. The most common cause of an epidural ( extradural ) hematoma (~85% of cases) is a skull fracture that results in a laceration of a major dural vessel, such as the middle meningeal artery . In approximately 15% of cases, bleeding may come from a venous sinus. The extrava sated blood dissects the dura mater off the inner table of the skull; there is no preexisting cerebral extradural space for the blood to enter. These lesions are frequently large, lens ( lenticular ) shaped, may appear locu lated, and are “ short and thick” compared with subdural hematomas (see Figure 4-4). The fact that epidural hematomas do not cross suture lines correlates with their characteristic shape. The patient may have headache , seizure , vomiting , hyperactive reflexes , or lapse into a coma , and, if the lesion is left untreated, death may result. In some cases, the patient may be unconscious initially , followed by a lucid interval (the patient is wide awake), then subsequently deteriorate rapidly and die; this sequela is called “ talk and die .” Treatment of choice for large lesions is surgical removal of the clot and coagulation of the damaged vessel. Tearing of bridging veins (veins passing from the brain outward through the arachnoid and dura), usually the result of trauma, is a common cause of subdural hematoma . This designation is somewhat

a misnomer because the extravasated blood actually dissects through a specialized, yet structurally weak, cell layer at the dura-arachnoid inter face: the dural border cell layer . There is no preexisting “subdural space” in the normal brain. Acute subdural hematomas , more commonly seen in younger patients, usually are detected immediately or within a few hours after the precipitating incident. Chronic subdural hematomas , usually seen in the elderly or in patients on anticoagulation therapy, are frequently of unknown origin. They may take days or weeks to become symptomatic and, in the process, cause a progressive change in the men tal status of the patient. This lesion appears “long and thin” compared with an epidural hematoma, follows the surface of the brain, and may extend for considerable distances (see Figures 4-4 and 4-5). Treatment is surgical evacuation (for larger or acute lesions) or close monitoring for small, asymptomatic, or chronic lesions. The most common cause of subarachnoid hemorrhage is trauma. In approximately 75% to 80% of patients with spontaneous (nontrau matic) subarachnoid hemorrhage , the precipitating event is rupture of an intracranial aneurysm. Symptomatic bleeding from an arteriovenous malformation occurs in ~5% of cases. Blood collects in and percolates through the SAS and cisterns (see Figure 4-7). Sometimes, the deficits seen (assuming the patient is not in a coma) may be a clue as to loca tion, especially if cranial nerves are nearby. Onset is sudden; the patient complains of a sudden and excruciatingly painful headache (“the worst of my life,” or “thunderclap”) and may remain conscious , may become lethargic and disoriented , or may be comatose . Treatment of an aneu rysm is to surgically separate the sac of the aneurysm from the parent vessel (by surgical clip or endovascular coil), if possible, and to protect against the development of vasospasm. Tumors of the meninges ( meningiomas ) are classified in different ways, but usually they arise from arachnoid cap/stem cells (a small number are dural in origin) around the villi or at places where ves sels or cranial nerves penetrate the dura-arachnoid. These tumors may present with signs/symptoms based on their location and size. They grow slowly (symptoms may develop almost imperceptibly over years), are histologically benign , may result in hyperostosis of the overlying skull, and frequently contain calcifications . In decreasing order, meningiomas are found in the following locations: parasagittal area + falx cerebri (together 29%), convexity 15%, sellar 13%, sphe noid ridge 12%, and olfactory groove 10%. Treatment is primarily by surgical removal, although in some cases meningiomas are treated by radiotherapy.

THE MENINGES AND MENINGEAL AND BRAIN HEMORRHAGES 61

Superior sagittal sinus

Arachnoid villus

Lateral lacunae Dura mater: Periosteal dura Meningeal dura

Skull

Cerebrum

Arachnoid mater

Arachnoid trabeculae

Pia mater

Transverse sinus

Falx cerebri

Tentorium cerebelli

Cerebellum

Cistern

Skull

Dura mater: Periosteal dura Meningeal dura

Subarachnoid space

Cerebral vessel and branch Arachnoid mater

Pia mater

Arachnoid trabeculae

Vertebrae

Spinal nerves

Spinal vessel

Meningeal dura

Dura mater

Intervertebral ligament

Epidural space

Conus medullaris

Vertebra Arachnoid mater

Cauda equina

Lumbar cistern

Filum terminale (internum)

Denticulate ligament

Pia mater

ventricular system ( small arrows ) and enters the subarachnoid space via the medial foramen of Magendie and the two lateral foramina of Luschka. In the normal healthy person, the arachnoid is attached to the inner surface of the dura. There is no actual or potential subdural space. Creation of this subdural space results from a traumatic, infec tious, or pathologic process.

4-1 Semi-diagrammatic representation of the central nervous sys tem and its associated meninges. The details show the rela tionships of the meninges in the area of the superior sagittal sinus, on the lateral aspect of the cerebral hemisphere, and around the spinal cord. Cerebrospinal fluid is produced by the choroid plexuses of the lateral, third, and fourth ventricles. It circulates through the

62 CHAPTER 4 / MENINGES, CISTERNS, VENTRICLES, AND RELATED HEMORRHAGES

Mastoiditis

Sigmoid sinus

Middle cerebral artery

Position of tentorium cerebelli

Falx cerebri

is almost always accompanied by other disease processes, most notably acute or chronic otitis media . The close association of mastoid air cells to the sigmoid sinus represents one comparatively direct route into the central nervous system. Once an infection of the mastoid accesses the central nervous sys tem, it may involve the venous sinuses ( A ), which appear bright when enhanced. The infection will layer out over the surface of brain within the SAS, enter the sulci, and occupy the SAS immediately above and below the tentorium cerebelli (see arrows in A , B , C ). The SAS and the sulci enhance when the patient is given IV gadolinium ( C , D ) and appear bright in the image. In addition to these features, small enhancements may appear within the SAS ( D , arrows) that indicate the formation of small abscesses. This inflammation may also extend to involve the dura mater in which case it is called pachymeningitis . Copyright © Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. 2024

4-2 Examples of meningitis ( A – D , all axial) in the adult. Meningitis is a disease that generally involves the subarach noid space (SAS) and the membranes bordering on this space, namely, the arachnoid mater and pia mater. Consequently, it is commonly called leptomeningitis ( arachnoiditis, or pia-arachnitis ). Meningitis may preferentially affect one side more than the other and, in some cases, present with unilateral deficits. Bacterial meningitis is a medical emergency ; it may present suddenly, progress rapidly, and must be treated quickly or death may result. Patients with viral meningitis may become ill over several days versus potentially hours, and after a short acute period, and with supportive care, most will recover with no per manent deficits. Sources of infections that may lead to meningitis are those involving the paranasal sinuses or the mastoid air cells ( mastoiditis, A ). Mastoiditis

MENINGITIS 63

Position of tentorium cerebelli

SSS

Falx cerebri

Superior sagittal sinus

Falx cerebri

Superior sagittal sinus

is also apparent that the meningeal inflammation and the inflamma tion within the SAS are more subtle than lesions such as meningioma, hemorrhage, or brain tumor. While these may enhance in similar ways, such as a mild subarachnoid hemorrhage versus leptomeningitis, each has its unique clinical features and presentation that lead to a cor rect diagnosis. Vessels located within the subarachnoid space may also enhance as they most likely contain infectious material and the organ isms may infiltrate the vessel walls. As noted in Figure 4-2, the inflam mation may also extend to involve the dura mater ( pachymeningitis ). The more common causative agents for meningitis, and the age groups with which they are more frequently associated, are discussed earlier in this chapter. Copyright © Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. 2024

4-3 Examples of meningitis ( pachymeningitis ) that extensively involves both sides of the central nervous system ( A – D , all axial) in the adult. In A and B , note the enhancement of the meninges over the temporal lobe (arrows), at the location of the tentorium cerebelli, and of the venous sinuses (SSS, superior sagittal; S, sigmoid; TS, transverse). At different axial levels, enhancement is clearly visible on the brain surface ( B , C , arrows), along the dural reflections (tentorium cerebelli and falx cerebri, B – D ), and within the sulci ( C ). In addition, enhancements over the curvature of the hemisphere ( D ) are suggestive of focal collections of inflammation largely sequestered in the leptomeninges . As seen in these samples, meningitis can be imaged using gadolinium and to a reasonable level its degree and extent visualized. However, it

64 CHAPTER 4 / MENINGES, CISTERNS, VENTRICLES, AND RELATED HEMORRHAGES

Hemorrhage in brain

epidural lesions. The patient in E also has small hemorrhages into the substance of the brain in the region of the genu of the internal capsule. Images A – E are CT without contrast. For additional comments on epi dural and subdural hemorrhages, see p. 58. The treatment of choice for epidural hematoma , especially if the patient is symptomatic, or if the patient is asymptomatic but the acute lesion is greater than 1 cm thick at its widest point and has a volume of greater than 30 cm 3 , is surgical removal and hemostasis of bleeders. In subdural hematoma, surgical evacuation is the preferred treatment in symptomatic patients with acute lesions that are 1 cm thick (0.5 cm in pediatric patients) and where there is a midline shift of greater than 5 mm. On the other hand, asymptomatic patients with thin subdural lesions may be followed medically and may not require surgery. Copyright © Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited. 2024

4-4 Examples of epidural ( extradural ) hemorrhage / hematoma ( A , B ) and of acute ( C , D ) and subacute ( E ) subdural hematoma/ hemorrhage . Note the lenticular shape of the epidural lesions (they do not cross suture lines— A , B ), their loculated appearance , and their loca tion external to the substance of the brain (see also Figure 4-5). In con trast, the acute subdural lesions ( C , D , arrows ) are quite thin and extend over a longer distance on the cortex; they are not constrained by suture lines. Note the midline shift in patients ( A , D ). In E , the subdural hematoma has both chronic and subacute phases. The chronic phase is indicated by the upper two and lower two arrows where the blood is replaced by fluid, and the subacute phase by the mid dle arrow, where fresher blood has entered the lesion. Note the extent of this lesion on the surface of the cortex and its thinness compared with

EPIDURAL AND SUBDURAL HEMORRHAGE 65

and do occur in cases where trauma is not involved. In these examples, trauma on the right side of the head ( C , soft tissue damage at arrows) resulted in a large acute subdural hematoma on the patient’s right side, and trauma on the left side of the head ( D , soft tissue damage at arrows ) resulted in a subdural lesion on the patient’s right. This latter lesion is a type of contrecoup injury in which the lesion is on the side opposite the initial impact. Note that the larger subdural lesion ( C ) has caused considerable midline shift . Subdural hematomas are not restrained by suture lines. Therefore, damage to the dural border cell layer may dissect this friable cell layer over considerable distances and the resultant lesion is thin and long . As seen in B and C in this figure, and in Figure 4-4A and D on the facing page, epidural and subdural lesions may be sufficiently large to result in effacement of the midline as indicated by a shift in the position of the falx cerebri. This appearance, plus the frequent loss of sulci and sometimes cisterns on the side of the lesion, foretells the very real pos sibility of brain herniation. This may present as a subfalcine herniation , which may impinge on both hemispheres, or morph into a transtentorial herniation ; all result in characteristic deficits (see Chapter 9 for further information of herniation syndromes).

4-5 Examples of epidural ( extradural ) hemorrhage/hematoma ( A , B ) and subdural hematoma/hemorrhage ( C , D ) resultant to trauma to the head; all are CTs without contrast, and all are in the axial plane. Epidural hematoma may occur in cases of skull fracture ( A , on the right side) in which the middle meningeal artery (or its larger branches) is lacerated. The resulting hematoma is formed between the inner table of the skull and the outer aspect of the dura ( epidural, B , on the right). In this significant trauma, there is a large epidural hematoma, a small lesion, probably also an epidural (small arrows), and small amounts of air within the cranial cavity ( B, black dots ). The mechanism of epidural hematoma formation is most likely two fold. First, the dura is stripped from the inner table of the skull dur ing the traumatic event creating an artifactual space. Second, the sharp edges of bone lacerate arteries, which bleed into this space, and, it is believed, may further dissect the dura from the skull. Epidural hemat omas, however, do not cross suture lines. Once the dissection reaches a suture line it stops and the lesion becomes lenticular shaped. Trauma to the head, without skull fracture, may also result in sub dural hemorrhage/hematoma; in such cases, it is called acute subdural hematoma ( C , D ). Subdural hematomas may also be subacute or chronic

66 CHAPTER 4 / MENINGES, CISTERNS, VENTRICLES, AND RELATED HEMORRHAGES

Paracallosal cistern

Quadrigeminal cistern

Lamina terminalis cistern

Fourth ventricle B

Chiasmatic cistern Interpeduncular cistern

Prepontine cistern

Premedullary cistern

Cisterna magna

Lamina terminalis cistern Optic tract

Sylvian cistern Crural cistern Midbrain

Interpeduncular cistern

Ambient cistern

Quadrigeminal cistern

Inferior colliculus

Prepontine cistern

Trigeminal nerve

Basilar artery

Superior cerebellopontine cistern

Basilar pons

Fourth ventricle

Premedullary cistern

Medulla

Inferior cerebellopontine cistern

Cisterna magna

Tonsil of cerebellum

4-6 A median sagittal MRI ( A , T2-weighted) of the brain showing the positions of the major cisterns associated with midline structures. Axial views of the midbrain ( B , T1-weighted), pons ( C , T2-weighted), and medulla ( D , T2-weighted) represent the correspond ing planes indicated in the sagittal view ( A ). Cisterns are the enlarged portions of the subarachnoid space that contain arteries and veins , roots of cranial nerves , and, of

course, cerebrospinal fluid . Consequently, the subarachnoid space and cisterns are continuous one with the other. In addition, the sub arachnoid space around the brain is continuous with that around the spinal cord (Figure 4-1). Compare the locations and shapes of these cisterns with the blood-filled parts of the subarachnoid space and contiguous cisterns shown in Figure 4-7 on the facing page.

CISTERNS AND SUBARACHNOID HEMORRHAGE 67

Subdural hemorrhage

Lamina terminalis cistern

Supraoptic recess

Sylvian cistern

Interpeduncular cistern

Crural cistern

Temporal horn

Blood on insular cortex

Ambient cistern

Midbrain Blood on tentorium cerebelli

Cerebellum

Quadrigeminal cistern

Third ventricle

Lamina terminalis cistern

Sylvian cistern

Blood on insula

Interpeduncular cistern

Crural cistern

Cerebello pontine cistern

Ambient cistern

Cerebellum

Rostral part of fourth ventricle

Blood on tentorium cerebelli

4-7 Blood in the subarachnoid space and cisterns ( subarachnoid hemorrhage ). In these CT examples, blood occupies the sub arachnoid space and cisterns, outlining these areas in various shades of white. Consequently, the shape of the cisterns is indicated by the config uration of the white area, the white area representing blood. Around the base of the brain ( A ), it is easy to identify the cisterns related to the midbrain, the supraoptic recess , which is devoid of blood, and blood extending laterally into the Sylvian cistern . In some cases ( B ), subdural hemorrhage may penetrate the arachnoid membrane and result in blood infiltrating between gyri, such as this example with blood on the cortex of the insula. In C , the blood is located around the mid brain ( crural and ambient cisterns ), extends into the Sylvian cistern , and into the cistern of the lamina terminalis . The sharp interface between the lamina terminalis cistern (containing blood) and the third ventricle (devoid of blood) represents the position of the lamina terminalis . In D , blood is located in cisterns around the pons but avoids the rostral part of the fourth ventricle. Also note the clearly enlarged temporal horn of

the lateral ventricle in D ; enlargement of this particular part of the ven tricle is indicative of increased pressure within the ventricular system. In fact, the presence of subarachnoid blood in the cisterns is in frank contrast to the stark and total lack of blood in the ventricles ( A – D ). Subarachnoid hemorrhage (SAH ) is always a serious medical event. In the case of SAH resulting from aneurysm rupture (about 75%–80% of all spontaneous cases), 10%–15% die prior to receiving medical attention and about 20% after hospital admission; about 30% have permanent disability; approximately 30% who survive may have mod erate to severe deficits, particularly depression and cognitive compro mise. Other comparable statistics indicate that about 45% to 50% die within the first 2–4 weeks and about 30% have moderate to severe deficits. More than one-third of patients who have aneurysms surgically clipped or endovascularly coiled have a poor functional outcome at 10 years. Compare these images with the locations of some of the com parable cisterns as seen in Figure 4-6. Images A–D are CT.

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