The Netter Collection of Medical Illustrations VOLUME 7 PART ll

The ultimate Netter
Collection is back!

Netter’s timeless work, now arranged
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The long-awaited update of The Netter Collection of Medical
Illustrations, also known as the CIBA “green books,” is now
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and other top medical illustrators have teamed-up with
medical experts to make the classic Netter “green books” a
reliable and effective current-day reference.
• Apply a visual approach—with the classic Netter art, updated

illustrations, and modern imaging-- to normal and abnormal body
function and the clinical presentation of the patient.
• Clearly see the connection between basic and clinical sciences
with an integrated overview of each body system.
• Get a quick understanding of complex topics through a concise
text-atlas format that provides a context bridge between general and
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Frank H. Netter, MD John T. Hansen, PhD

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Ź Netter’s Histology Flash Cards, 9781416046295
Ź Netter’s Neuroscience Flash Cards, 2nd Edition, 9781437709407

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Ź Netter’s Clinical Anatomy, 2nd Edition, 9781437702729
Ź Netter’s Concise Radiologic Anatomy, 9781416056195
Ź Netter’s Concise Orthopaedic Anatomy, 2nd Edition, 9781416059875
Ź Netter’s Concise Neuroanatomy, 9781933247229
Ź Netter’s Surgical Anatomy Review P.R.N., 9781437717921

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Netter transforms your perspective. It’s how you know.

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VOLUME 7

The Netter Collection

OF MEDICAL ILLUSTRATIONS

Nervous System

Part II—Spinal Cord and Peripheral
Motor and Sensory Systems

2nd Edition

A compilation of paintings prepared by
FRANK H. NETTER, MD

Edited by

H. Royden Jones, MD Michael J. Aminoff, MD, DSc, FRCP

Jaime Ortiz-Patino Chair in Distinguished Professor and Executive
Neurology Vice Chair

Lahey Clinic Department of Neurology
Burlington, Massachusetts; School of Medicine
Clinical Professor of Neurology University of California
Harvard Medical School San Francisco, California
Boston Children’s Hospital
Boston, Massachusetts Scott L. Pomeroy, MD, PhD

Ted M. Burns, MD Bronson Crothers Professor of Neurology
Harvard Medical School
Professor and Executive Vice Chair Chair, Department of Neurology
Department of Neurology Neurologist-in-Chief
University of Virginia Boston Children’s Hospital
Charlottesville, Virginia Boston, Massachusetts

Additional Illustrations by Carlos A. G. Machado, MD

CONTRIBUTING ILLUSTRATORS
James A. Perkins, MS, MFA
Anita Impagliazzo, MA, CMI
Kristen Wienandt Marzejon, MS, MFA
Tiffany S. DaVanzo, MA, CMI
John A. Craig, MD

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

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS: ISBN: 978-1-4160-6386-5
NERVOUS SYSTEM: PART II—SPINAL CORD AND PERIPHERAL
MOTOR AND SENSORY SYSTEMS, Volume 7, Second Edition

Copyright © 2013 by Saunders, an imprint of Elsevier Inc.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic
or mechanical, including photocopying, recording, or any information storage and retrieval system,
without permission in writing from the publisher. Details on how to seek permission, further
information about the Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency can be found at our website:
www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).

Permission for Netter Art figures may be sought directly from Elsevier’s Health Science Licensing
Department in Philadelphia, PA: phone 1-800-523-1649, ext. 3276, or (215) 239-3276; or email
[email protected]

Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
treatment may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described herein. In
using such information or methods they should be mindful of their own safety and the safety of
others, including parties for whom they have a professional responsibility.

With respect to any drug or pharmaceutical products identified, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of practitioners, relying on their own
experience and knowledge of their patients, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions.

To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.
ISBN: 978-1-4160-6386-5

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Content Development Manager: Marybeth Thiel
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ABOUT THE SERIES

Dr. Frank Netter at work. Dr. Frank H. Netter exemplified the CUSHING’S SYNDROME IN A PATIENT WITH THE CARNEY COMPLEX
The single-volume “blue book” that paved the way for distinct vocations of physician,
the multivolume Netter Collection of Medical Illustrations artist,andteacher.Evenmoreimportant— Carney complex is characterized
series aff ectionately known as the “green books.” he unified them. Netter’s illustrations by spotty skin pigmentation.
always began with meticulous research Pigmented lentigines and blue
into the detailed human clinical nevi can be seen on the face–
anatomy and pathology, a philosophy including the eyelids, vermillion
that steered his broad and deep medical borders of the lips, the
understanding. He often said: “Clarifi­ conjunctivae, the sclera–and the
cation is the goal. No matter how beau­ labia and scrotum.
tifully painted, a medical illustration Additional features of the
has little value if it does not make clear Carney complex can include:
a medical point.” His greatest challenge
and greatest success was charting a Myxomas: cardiac atrium,
middle course between artistic clarity cutaneous (e.g., eyelid),
and instructional complexity. That suc­ and mammary
cess is captured in this series, beginning Testicular large-cell
in 1948, when the first comprehensive calcifying Sertoli cell tumors
collection of Netter’s work, a single Growth-hormone
volume, was published by CIBA Pharmaceuticals. It secereting pituitary adenomas
met with such success that over the following 40 years Psammomatous
the collection was expanded into an 8-volume series— melanotic schwannomas
each devoted to a single body system.
In this second edition of the legendary series, we are PPNAD adrenal glands are usually of normal size and most are
delighted to offer Netter’s timeless work, now arranged studded with black, brown, or red nodules. Most of the pigmented
and informed by modern text and radiologic imaging nodules are less than 4 mm in diameter and interspersed in the
contributed by highly respected neurologic authorities adjacent atrophic cortex.
from world-renowned medical institutions, and supple­
mented with new illustrations created by artists working A brand new illustrated plate painted by Carlos Machado,
in the Netter tradition. Inside the classic green covers, MD, for The Endocrine System, Volume 2, 2nd ed.
students and practitioners will find hundreds of original
works of art—the human body in pictures—paired with Dr. Carlos Machado at work.
the latest in expert medical knowledge and innovation
and anchored in the sublime style of Frank Netter.
Noted artist-physician, Carlos Machado, MD, the
primary successor responsible for continuing the Netter
tradition, has particular appreciation for the Green Book
series. “The Reproductive System is of special significance
for those who, like me, deeply admire Dr. Netter’s work.
In this volume, he masters the representation of textures
of different surfaces, which I like to call ‘the rhythm of
the brush,’ since it is the dimension, the direction of the
strokes, and the interval separating them that create the
illusion of given textures: organs have their external
surfaces, the surfaces of their cavities, and texture of their
parenchymas realistically represented. It set the style for
the subsequent volumes of Netter’s Collection—each an
amazing combination of painting masterpieces and
precise scientific information.”
Though the science and teaching of medicine endures
changes in terminology, practice, and discovery, some
things remain the same. A patient is a patient. A teacher
is a teacher. And the pictures of Dr. Netter—he called
them pictures, never paintings—remain the same blend
of beautiful and instructional resources that have guided
physicians’ hands and nurtured their imaginations for
more than half a century.
The original series could not exist without the dedica­
tion of all those who edited, authored, or in other ways
contributed, nor, of course, without the excellence of Dr.
Netter. For this exciting second edition, we also owe our
gratitude to the Authors, Editors, Advisors, and Artists
whose relentless efforts were instrumental in adapting
these timeless works into reliable references for today’s
clinicians in training and in practice. From all of us with
the Netter Publishing Team at Elsevier, we thank you.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS v

ABOUT THE EDITORS

H.Royden Jones, MD, is Chair Emeritus of the disorders. Dr. Jones has edited three other Netter pub- Ted M. Burns, MD, is Professor of Neurology at
department of neurology at Lahey Clinic in lications including the 1986 edition of this atlas and two the University of Virginia. He was born and raised
Burlington, Massachusetts, and Emeritus Director of editions of Netter’s Neurology. He has been invited to in a suburb of Kansas City, Kansas. He received his
the electromyography laboratory at Children’s Hospital speak worldwide on childhood neuromuscular disor- undergraduate and medical degrees from the University
Boston. He is Clinical Professor of Neurology at ders. Dr. Jones is a co-founder of the biennial Interna- of Kansas and then attended the University of Virginia
Harvard Medical School and a lecturer in neurology at tional Paediatric EMG Conference based at Great for neurology residency and clinical neurophysiology
Tufts Medical School. At Lahey he holds the Jaime Ormond Street Children’s Hospital, London, England. fellowship. Dr. Burns completed a second fellowship in
Ortiz-Patino Chair of Neurology. Dr. Jones graduated He has broad adult clinical interests particularly neuro- peripheral nerve disorders at Mayo Clinic in Rochester,
from Tufts College and Northwestern University immunologic and paraneoplastic neuromuscular disor- Minnesota. He was on staff at Lahey Clinic in Burling-
Medical School. After interning at Philadelphia General ders. Dr. Jones has contributed over 200 peer-reviewed ton, Massachusetts, for 2 years before joining the neu-
Hospital, he became an internal medicine resident at papers and book chapters. rology department at the University of Virginia in
Mayo, eventually specializing in neurology and clinical 2002. In 2008, he received a Harrison Distinguished
neurophysiology. Dr. Jones served over 3 years in the Dr. Jones served 8 years as a director of the American Professor Chair at the University of Virginia. Dr. Burns
United States Army as Chief of Neurology at 5th Board of Psychiatry and Neurology, becoming Chair is Vice Chair of the neurology department and Director
General Hospital, Bad Cannstatt, Germany. of its Neurology Council in 2004. During this tenure of the Neurology Residency Program and the Clinical
he was a member of the Residency Review Council Neurophysiology Fellowship Program. He is also the
He joined Lahey Clinic in 1972, initially establishing of the Accreditation Council for Graduate Medical Medical Director of the Neurology EMG Laboratory.
their neurology residency affiliations with Boston Education. In 2007 he received the American Associa-
City Hospital and later Tufts Medical Center. In 1984 tion of Neuromuscular and Electrodiagnostic Medi- Dr Burns’s clinical focus is on the care of patients
he founded Lahey’s clinical neurophysiology neuro- cine’s Distinguished Physician Award. Lahey Clinic’s with neuromuscular disease, including myasthenia
muscular disorders fellowship and subsequently trained Medical Staff Association recognized Dr. Jones in gravis. He won the Myasthenia Gravis Foundation of
a number of future leaders in this field. At Lahey he 2010 with its highest honor—the Frank Lahey Award America’s “Doctor of the Year” award for 2010. His
has also served as Chairman of the Medical Personnel for “commitment to the values of Dr. Frank Lahey: academic interests include the development and valida-
committee, Chair of Education, and Chair of the Divi- respect, teamwork, excellence, commitment to per- tion of user-friendly outcome measures for myasthenia
sion of Medicine and Medical Specialties and served on sonal best.” In 2011 he received Lahey’s Annual gravis and other neuromuscular disorders. Dr. Burns is
their Board of Governors for 19 years. He now enjoys Research Award. also interested in podcasting for the education of physi-
patient care, clinical research, and teaching responsi- cians, patients, and families. He is creator and editor of
bilities full time. He and his wife have four children. Their daughter the Neurology journal’s weekly podcast and the Ameri-
is a former New York City prosecutor, their oldest son can Association of Neuromuscular and Electrodiagnos-
In 1977 Dr. Jones joined the neurology department is a professor at the University of Rochester Simon tic Medicine’s (AANEM) podcast. He is also the creator
at Boston Children’s Hospital, founding the electromy- School of Business, and two other sons are physicians; of the MGFA’s podcast series designed to educate
ography laboratory in 1979. Noting that no clinical one is an emergency medicine specialist in rural New patients and families about practical aspects of MG.
information was then available in pediatric EMG, this Hampshire, and the other holds the Ackerman endowed
became a major clinical research interest of his, eventu- chair of the Culture of Medicine at Harvard College Dr. Burns and his wife, Bonnie, have three wonderful
ally leading to his co-editing three major textbooks on and Medical School. Photography is Dr. Jones’s major children, Charlie, Elizabeth, and Sarah. He and his
childhood clinical neurophysiology and neuromuscular avocation. family live in Charlottesville, Virginia.

vi THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

About the Editors

Michael J. Aminoff, MD, was born and educated editions, and of a number of chapters on topics related Scott L. Pomeroy, MD, PhD, graduated from
in England, graduating from University College to neurology. His published scientific contributions led Miami University and was the first graduate of the
London in 1962 and from University College Hospital to the award of a Doctorate in Science, an advanced MD/PhD program of the University of Cincinnati. He
Medical School as a physician in 1965. He subsequently doctorate in the Faculty of Science, by the University trained in pediatrics at Boston Children’s Hospital and
trained in neurology and clinical neurophysiology of London in 2000. He is the one of the two editors- in child neurology at St. Louis Children’s Hospital. In
at The National Hospital for Neurology and Neuro- in-chief of the four-volume Encyclopedia of the Neurologi- 1989, he won the Child Neurology Society Young
surgery (Queen Square) in London and also undertook cal Sciences published by Academic Press in 2003 (a new Investigator Award for work done as a postdoctoral
basic research on spinal physiology at its affiliated edition is in press). He is also one of the series editors fellow with Dale Purves at Washington University. He
Institute of Neurology, which led to the award of of the prestigious, multi-volume Handbook of Clinical has won numerous awards for his research and clinical
an MD degree (which, in England, is an advanced Neurology (Elsevier). He was Editor-in Chief of the care of children with embryonal brain tumors including
medical degree based on research) on completion of journal Muscle and Nerve from 1998 to 2007 and also the Sidney Carter Award, the Daniel Drake Medal, and
his thesis. In 1974, he moved from England to the serves on numerous other editorial boards. His other the Compassionate Caregiver Award of the Kenneth
University of California San Francisco School of interests include medical history, and he has written two Schwartz Center.
Medicine, where he has been Professor of Neurology biographies on Brown-Séquard, one published by
since 1982 and now holds the title of Distinguished Raven Press in 1993, and the other by Oxford Univer- Dr. Pomeroy currently is the Chair of the Depart-
Professor. He was Director of the Clinical NeuroÂ

FOREWORD

Combining Dr. Frank Netter’s classic medical illus- Dr. Netter’s style is absolutely distinctive. It has the
trations with a first-rate, current text is a brilliant look of mid-20th century illustration art, somewhat
idea. The choice of authors could not be better; as a like Norman Rockwell’s. Not unlike a Rockwell, one
group they are well-regarded clinicians whose experi- can recognize a Netter illustration across the room. He
ence as teachers, having national and sometimes inter- is consistent no matter what his subject; his work,
national reputations, is well illustrated by the clarity of including its vivid coloration, is always particularly
their writing. Very clearly there has been great atten- serious despite its sometimes cartoonish like appear-
tion to achieving a supple, readable style. The added ance. Netter is distinctive the way all truly great artists’
images, such as the MRIs and other visual tools, are work invariably is, no matter what the level of sophis-
very well chosen. Their clarity for teaching purposes tication. Think of Mondrian. Think of Francis Bacon.
matches the text in quality, and these are nicely inte- Totally different than Netter, they are good examples
grated with Netter’s classic imagery. The most impres- of great “high” art that are similarly distinctive and
sive thing about this effort is the marvelous embedding consistent. And such consistency, regardless of the
of Netter’s illustrations into the text with preservation subject, is surely part of what makes for genius with
of coherence. subsequent fame and greatness. Accompanied by their
new text in two detailed parts covering the brain as well
The original publication of these illustrations in the as the spinal cord and its related peripheral motor
first Netter atlas was a regular, albeit unofficial, part sensory units, Frank Netter’s art has been beautifully
of medical school neurologic learning early in my resurrected once again. These will surely provide learn-
career during the 1960s. Concomitantly, Netter’s ing with pleasure to yet another generation of medical
corollary bi-monthly white-covered slim paperback students during their neurologic studies.
Clinical Symposia was always welcome with the new
mail … more than one issue were frequently strewn on Nicholas A. Vick, MD
my desk. These were essentially mini atlases always Clinical Professor of Neurology
centered by a striking illustration immediately telling
you what the dedicated subject would be. Each new Pritzker School of Medicine
edition was always accompanied by 15 to 20 new and University of Chicago
now classic Netter illustrations. It was not clear how Chicago, Illinois;
Ciba Pharmaceutical wanted to specifically influence us
in trade for their marvelous free teaching aids. Now I Department of Neurology
wish I had saved many of them. Northshore University Healthsystem

Evanston, Illinois

viii THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

PREFACE, ACKNOWLEDGMENTS, AND DEDICATION

PREFACE many Netter-illustrated medical texts and atlases that the art and science of neurology. We also express our
This new edition of The Netter Collection of Medical include some fine new artwork created by a superb admiration and thanks to our artist colleagues Carlos
Illustrations: Nervous System recognizes the enduring group of medical artists carrying forward Frank A. G. Machado, MD, John A. Craig, MD, James A.
nature of Dr. Frank Netter’s incomparable artistic Netter’s tradition. Perkins, MS, MFA, Anita Impagliazzo, MA, CMI,
genius and his immense educational vision. Dr. Netter’s Tiffany S. DaVanzo, MA, CMI, and Kristen Wienandt
initial atlas dedicated to neurology, first published in As editors of the current two-part volume, we have Marzejon, MS, MFA, who have so carefully upheld
1957, provided a very concise introduction to the combined basic science information with clinical mate- Frank Netter’s approach to medical illustration. These
nervous system for generations of students of medicine rial, discussing the anatomy, physiology, pathology, and dedicated artists have expertly created a number of out-
and the health sciences. His ability to simplify the clinical presentation of many neurologic disorders, thus standing new plates for these volumes. Additionally,
essentials of very important components, namely the supplementing the system-based approach now used Barry Arnason, MD, the primary author of the multiple
cerebral cortex and diencephalon, the complexities of in many medical school curricula. We have been sclerosis section in Part 1, significantly contributed to
the hypothalamus, fiber tracts within the brainstem and most privileged during our careers to participate in the the final artwork seen in Plates 10-6 through 10-12 and
spinal cord, the cranial nerves, and the peripheral exponential technologic advances leading to our very 10-14, providing his own detailed sketches, direction,
motor-sensory unit, was very remarkable. Furthermore, detailed understanding of the various neurologic disor- and feedback to an artist. These unique drawings rep-
Dr. Netter’s illustrations are absolutely outstanding in ders, particularly the rapid growth in diagnostic and resent a very special artistic contribution by an author
comparison to those available in other texts. His paint- management options now available. However, although of this text. Most MRI and CT images for many previ-
ings are as vital today as at their artistic inception. these represent wonderful accomplishments not envi- ous plates used in this atlas were supplied by Richard
sioned at the time of the last printing of this publica- A. Baker, MD, of the Lahey Clinic, who has expertly
The initial single-part publication, providing an tion, such advances have created pleasant challenges for and tirelessly worked with Royden Jones on four Netter
interaction between the basic neurologic sciences and us both in organization and in definition of the scope projects during the past 30 years. Finally, the entire
clinical neurology, offered a stimulating introduction to of the topics discussed. Elsevier editorial team, particularly Marybeth Thiel
many intriguing and important clinical aspects of neu- and Elyse O’Grady, have been gracious and cooperative
rologic medicine. Although the scope was somewhat Each of us is ever mindful of the many unanswered in supporting our goals. It has been a distinct pleasure
limited in its clinical depth, its vivid and intriguing questions, particularly regarding Alzheimer disease and having such professional and dedicated colleagues.
plates provided a unique catalyst for students, making other neurodegenerative disorders, various epilepsies,
the challenge of learning the neurosciences both excit- autism, schizophrenia, cerebral aneurysms, glioblas- DEDICATION
ing and rewarding. Indeed, Netter’s initial volume was toma, multiple sclerosis, and amyotrophic lateral scle- These two volumes are dedicated to our wives, chil-
a major influence in leading some of us to consider a rosis, to name a few disorders that we hope will enjoy dren, and grandchildren, whose love and support gave
neurologic career. major advances during our lifetimes. We have confi- us the time to work on this project; to our students,
dence that our younger colleagues will shed further residents, and fellows, who challenged us to be fine
Much of the anatomy of the peripheral nervous light on these very enigmatic clinical riddles and bring teachers; and to our many and dear patients for whom
system and many central and peripheral clinical neuro- comfort and help to future generations of neurologic we have been honored and blessed to care.
logic disorders were lacking in Netter’s original patients.
Nervous System. To expand the scope of neuroanatomy H. Royden Jones
and clinical disorders, a second volume was published Each of us also hopes that today’s medical students Ted Burns
in 1986. Although their publications were separated will find this new edition of the Nervous System an excit-
in time, these two parts are referred to as the “first ing introduction to the many challenges and rewards Michael J. Aminoff
edition.” We now present a second edition, which is incumbent in a clinical neuroscience career. Scott Pomeroy
more comprehensive, carrying forward the vision that December 2012
Frank Netter, MD, so brilliantly developed. Since the ACKNOWLEDGMENTS
first editions, Elsevier purchased the publishing rights The editors thank their many neuroscience colleagues
to the entire Netter art library, and it now has a who contributed to this text, as listed on pp. xiv-xvi, as
dedicated division responsible for the publication of well as our many patients through whom we learned

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS ix

FRANK NETTER, MD: A PERSONAL RECOLLECTION

While attending a major medical meeting more every four days. He worked with vigor every day of the
than two decades after using the first Netter week until his death at age 85.
Nervous System, published in 1957, I met a representa-
tive of the Ciba Pharmaceutical Medical Education Unknown to me when we initially met, Frank previ-
division—the corporation that sponsored Dr. Frank ously had commenced his work on a new edition of his
Netter’s medical artistic career for more than 40 years— Neuroscience Atlas, having recognized the relatively
and inquired about the possibility of having him create limited scope of his initial volume. After we worked
paintings relevant to the peripheral motor and sensory together for a while, he showed this project to me,
unit and, particularly, the major peripheral nerves. noting that it had remained dormant for a few years;
Within a few months, I was surprised to receive a hand- subsequently he asked me to become its clinical editor.
written letter from Dr. Netter, asking for more detailed There were to be two parts. Part I, dedicated to tradi-
suggestions. This led to an invitation to meet with him tional basic neuroanatomy and neurophysiology, was
at his Florida beachfront home and to advise him in essentially completed. The clinical portion of his
reference to his current orthopedic disorders project. revised atlas, Part II Neurologic and Neuromuscular Dis-
orders, required extensive new artwork and text and was
Frank was a humble and engaging person entirely first published in 1986. However production costs and
dedicated to his goal of illustrating all human anatomy time restraints limited its clinical breadth and depth.
and related clinical disorders. A day in his studio might Therefore , Frank and I envisioned production of a
be dedicated to interviewing physicians to discuss their more complete set of texts within 5 to 10 years to add
area of expertise, who would provide him with a full further to these volumes. Although long overdue,
appreciation of the subject before he started on his thanks to the foresight of Elsevier, these volumes are
drawings. Sometimes after lunch he took a break from now completed. There is no doubt that Dr. Netter
his ever-present cigars and his studio to play two or would be extremely pleased with these results subse-
three holes of golf before returning to his various chal- quent to the dedication of so many expert neurologic
lenges. Most other days were dedicated to conceptual- physicians. The new two-part volume supports his
ization, drawing, or painting sessions. Dr. Netter had dream of very comprehensive, relevant, and totally up-
an unbridled passion for his work. His artistic abilities to-date neuroscience atlases.
were truly amazing—he was under contract to provide
93 new illustrations annually, which amounts to one H. Royden Jones, MD

x THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

INTRODUCTION TO THE FIRST EDITION

INTRODUCTION TO PART I developmental disorders not only prompted presenta- with preparing this volume. They are all credited sepa-
The Ciba Collection of Medical Illustrations was originally tion of those disorders but emphasized the importance rately herein. I admire their erudition and I thank them
conceived as a series of atlases picturing the anatomy, of including a section on neuroembryology. for the time they gave me and the knowledge they
embryology, physiology, pathology, and diseases of imparted to me. It was a great pleasure for me to learn
mankind, system by system. The creation of these Accordingly, it has for many years been my desire to from them, and I cherish the friendships we established
atlases has been for me a labor of love to which I have revise and expand this atlas in a new edition. I was, during our collaboration. The creation of this volume
devoted most of my working career. The first volume however, so busy with preparing other volumes of the would have been impossible without their help. I also
of this series was Nervous System. That volume was Ciba Collection that it took me a long time to accomplish thank the CIBA-GEIGY Corporation and its executives
very well received and acclaimed by students, physi- it. This was, to a certain extent, fortuitous, for it allowed for the free hand they have given me in this project, and
cians, and members of allied professions throughout the me to include newer material that would not have been the members of the editorial staff for their very helpful
world. It has been reprinted many times and published available for an earlier revision. But the volume of illus- and dedicated cooperation.
in a number of languages. The multitude of letters of trations and accompanying texts grew to such an extent
appreciation I have received in the more than 30 years that they could not all be included in a single book. It Since the foundation for this volume was laid in
since its first publication have been a great source of was therefore decided to issue the atlas in two parts; its earlier edition, I reiterate here, with much nostalgia,
satisfaction to me, even as I progressed with other Part I to include anatomy, embryology, physiology, and my appreciation for the great men who guided
volumes in the series. functional neuroanatomy; and Part II, shortly forth- me through that original endeavor. They were:
coming, to include all neurologic and neuromuscular Dr. Abraham Kaplan, neurosurgeon and gifted student
From the beginning, however, certain deficiencies in diseases. of Dr. Harvey Cushing; Dr. Albert Kuntz, pioneer
the Nervous System volume became evident. It con- in unraveling the mysteries of the autonomic nervous
tained, for example, practically no coverage of the At the same time that I was working on this revision system; Dr. Gerhardt von Bonin, brilliant neuroÂ

Introduction to the First Edition

INTRODUCTION TO PART II system of the body as portrayed in other volumes of I express here also my appreciation for the help and
In the introduction to Part I of this volume on the the Ciba Collection. The association is, however, most encouragement which I received from Dr. William
nervous system, I wrote of why, after almost 35 years of marked with the musculoskeletal system. Indeed, there (Bill) Fields, professor and chairman of the department
widespread acceptance, it was necessary to revise and is great overlap between the fields of neurology and of neuro-oncology at the MDAnderson Hospital and
update the original atlas, Volume 1 of The Ciba Collection neurosurgery with the field of orthopedics, both diag- Tumor Institute, Houston. He was not only a definitive
of Medical Illustrations. I also told there of how, as I nostically and therapeutically. Cerebral palsy and polio- collaborator for some specific subjects, but readily gave
progressed with the revision, the amount of material to myelitis are, of course, basically neurologic diseases, me much practical advice and counsel throughout the
be included grew to such a magnitude that it was and they are so presented in this volume. But the undertaking. I thank Mr. Philip Flagler, director of
decided to publish it in two parts. Part I, published in aftercare, corrective surgery, and rehabilitation of Medical Education for the CIBA Company, and Dr.
1983, contained a depiction of what may be called the such patients are usually in the hands of the orthope- Milton Donin, a relative newcomer to our team, for
“basic science” of the nervous system, that is, the bony dists. Accordingly, those aspects of these diseases will their continuous efforts in coordinating the varied
encasements, the gross anatomy, and the vasculature of be covered in the forthcoming atlases on the musculo- aspects of the undertaking, to keep it moving along, and
the brain and spinal cord, the autonomic nervous skeletal system, on which I am now at work. Interver- to ensure that each person involved understood and felt
system, the cranial nerves, the nerve plexuses and tebral disc herniation and spinal stenosis likewise fall happy in their contribution to it. My accolades go also
peripheral nerves, the embryology, and the physiology into both fields of practice, and thus, while presented to Ms. Gina Dingle for her diverse editorial activities,
and functional neuroanatomy of the nervous system. herein, their management will be amplified in the mus- for her untiring and patient attention to frustrating
Part II, presented herewith, is devoted to portraying the culoskeletal volume. The neuromuscular diseases are details, for her great organizing accomplishments, and
disorders and diseases of the nervous system. But once among many other examples of overlap between the especially for her ever-present personality. Finally, I
again, to my dismay, as I progressed with picturing the two disciplines. express once more my appreciation of the CIBA Phar-
pathology and clinical aspects of those multitudinous maceutical Company and its executives for their under-
ailments, the volume of material grew to such an extent The trials and tribulations of the production of this standing of the significance of this project and for the
that I was hard put to confine it to the limits of one atlas were far outweighed by the pleasure and stimula- free hand they have given me in its creation.
book. Furthermore, the fantastic progress that was tion I received from working on it. This was largely due
being made in the field even as I worked added to the to those wonderful people, my consultants and collabo- Frank H. Netter, 1986
difficulty of space limitation. Accordingly, I tried to rators, who helped me, taught me, advised me, and
place emphasis on those disorders most threatening to supplied me with the pertinent reference material as a
mankind because of incidence or severity, with due basis for many of my illustrations. They are all listed
consideration for timeliness, diagnostic difficulty, and separately herein and I thank them, each and every one,
potential for beneficial management. for the knowledge they imparted to me and for the time
they so graciously gave me.
I believe that, in studying many of the conditions
portrayed in this book, the reader will find it most I was especially fortunate to have had the guidance
helpful to refer repeatedly to Part I of this volume for and counsel of that delightful personality, Dr. H.
an understanding of the basic science aspects underly- Royden Jones, Jr. (“Roy” to me), of the Lahey Clinic.
ing the disorder. For example, study of stroke in this The many long hours we spent together planning and
book may be enhanced by reference to the arterial organizing the material to be included were not only
supply and functional subdivisions of the brain, as informative and productive but exceedingly pleasurable
covered in Part I. Likewise, study of the peripheral as well. I was constantly impressed by his broad knowl-
neuropathies may call for a review of nerve conduction edge, his unique ability to define the essence of each
as well as of the course and distribution of the periph- subject we dealt with, and his ability to call upon knowl-
eral nerves. edgeable consultants for special topics, yet maintaining
an overall perspective of the project in relation to the
But the nervous system is not an isolated entity. It is total field of medical practice and neurology in particu-
intimately involved with the function of every other lar. Our collaboration thus developed into a lasting
friendship that I cherish highly.

xii THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

ADVISORY BOARD

Prof. Eugenio Gaudio, MD Professor Christopher Kennard, PhD, Dra. Patricia M. Herrera Saint-Leu
Full Professor and Director FRCP, FMedSci Jefa del Departamento de Anatomía
Department of Human Anatomy Professor of Clinical Neurology Facultad de Medina
Sapienza University of Rome Head, Nuffield Department of Clinical Neurosciences The National Autonomous University of
Rome, Italy University of Oxford, John Radcliffe Hospital
Sung-Tsang Hsieh, MD, PhD Oxford, United Kingdom Mexico (UNAM)
Institute of Anatomy and Cell Biology Mexico City, Mexico
National Taiwan University College of Medicine
Department of Neurology Prof. Subramaniam Krishnan
National Taiwan University Hospital Professor of Anatomy
Taipei, Taiwan Head of Department (retired)
Faculty of Medicine
University of Malaya
Kuala Lumpur, Malaysia

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS xiii

CONTRIBUTORS

EDITORS-IN-CHIEF Katarzyna H. Czerniecka, MD Maria E. Frazer, BS
H. Royden Jones, MD Department of Neurosurgery Translational Pain Research
Jaime Ortiz-Patino Chair in Neurology University of Rochester School of Medicine Department of Neurosurgery
Lahey Clinic University of Rochester School of Medicine
Burlington, Massachusetts; and Dentistry
Clinical Professor of Neurology Rochester, New York and Dentistry
Harvard Medical School Plates 8-1â•–› â•8› -6, 8-12, 8-13, 8-18, 8-19, 8-22, 8-23 Rochester, New York
Boston Children’s Hospital Dr. Basil T. Darras, MD Plates 8-7â•–› â•8› -9, 8-15
Boston, Massachusetts Professor of Neurology (Pediatrics) Namita Goyal, MD
Editor: Part I: Sections 4, 5, 8, 9, 10, 13; Joseph J. Volpe Chair in Neurology Instructor of Neurology
Harvard Medical School Harvard Medical School
Part II: Sections 5, 8, 9, 11, 12 Associate Neurologist-in-Chief Massachusetts General Hospital
Author: Part I: Plates 10-17, 10-18; Director, Division of Clinical Neurology Boston, Massachusetts
Director, Neuromuscular Program Plates 11-6, 11-7, 11-11, 12-7, 12-11â•–› â•1› 2-21
Part II: Plates 5-3–5-22, 9-3 Department of Neurology Kelly G. Gwathmey, MD
Ted M. Burns, MD Boston Children’s Hospital Fellow Physician
Professor and Executive Vice Chair Boston, Massachusetts University of Virginia
Department of Neurology Plates 9-1, 9-4, 12-8â•–› â•1› 2-10 Department of Neurology
University of Virginia William S. David, MD, PhD Charlottesville, Virginia
Charlottesville, Virginia Associate Professor of Neurology Plates 1-1â•–› â•1› -6, 1-18â•–› â•1› -46
Editor: Part I: Section 2; Part II: Sections 1, 4, 6, 10 Harvard Medical School Hans-Peter Hartung, MD
Author: Part II: Plates 5-1, 5-2, 6-26, 11-9 Director of EMG Laboratory and Neuromuscular Professor and Chairman of Neurology
Michael J. Aminoff, MD, DSc, FRCP Heinrich-Heine-University
Distinguished Professor and Executive Vice Chair Diagnostic Center Department of Neurology
Department of Neurology Massachusetts General Hospital Duesseldorf, Germany
University of California Boston, Massachusetts Plate 6-26
San Francisco, California Plates 10-5â•–› â•1› 0-11 India K. Johnson, BS
Editor: Part I: Sections 6, 7, 11, 14; Feza Deymeer, MD, MS (Epid) Medical Student
Professor of Neurology University of Rochester School of Medicine
Part II: Sections 2, 3, 7 Department of Neurology
Author: Part I: Plates 4-10, 7-18, 11-12, 11-13, 11-14, Istanbul Medical Faculty and Dentistry
Istanbul University Rochester, New York
11-18–11-20, 11-22; Part II: Plates 2-1–2-29, 4-3 Istanbul, Turkey Plates 8-10, 8-20, 8-21
Scott L. Pomeroy, MD, PhD Plate 11-10
Bronson Crothers Professor of Neurology
Harvard Medical School William P. Dillon, MD Justin Johnston, MS-3
Chair, Department of Neurology Elizabeth A. Guillaumin Professor of Radiology Drexel University College of Medicine
Neurologist-in-Chief University of California San Francisco Philadelphia, Pennsylvania
Boston Children’s Hospital Executive Vice Chair of Radiology Plates 3-1â•–› â•3› -18
Boston, Massachusetts Chief of the Section of Neuroradiology Peter B. Kang, MD
Editor: Part I: Sections 1, 3, 5, 12 San Francisco, California Assistant Professor of Neurology
Imaging for Plates 2-20â•–› â•2› -25 Harvard Medical School
CONTRIBUTORS Elliot L. Dimberg, MD Director, Electromyography Laboratory
Gregory J. Allam, MD Assistant Professor of Neurology Children’s Hospital Boston
Assistant Professor of Neurology Mayo Medical School Boston, Massachusetts
Harvard Medical School Department of Neurology Plate 9-5
Department of Neurology/Division of Stroke Mayo Clinic Kerry H. Levin, MD
Brigham and Women’s Hospital Jacksonville, Florida Professor of Medicine (Neurology)
Stroke Director South Shore Hospital Plates 12-1â•–› â•1› 2-6 Cleveland Clinic Lerner College of Medicine
Boston, Massachusetts P. James B. Dyck, MD Chairman, Department of Neurology
Plates 1-1â•–› â•1› -6, 1-18â•–› â•1› -46 Professor of Neurology Director, Neuromuscular Center
Valerie Biousse, MD Mayo Medical School Cleveland Clinic
Cyrus H. Stoner Professor of Ophthalmology Head of the Peripheral Nerve Section and Laboratory Cleveland, Ohio
Professor of Ophthalmology and Neurology Department of Neurology Plates 4-1â•–› â•4› -17
Emory University School of Medicine Mayo Clinic Jeff W. Lichtman, MD, PhD
Atlanta, Georgia Rochester, Minnesota Jeremy R. Knowles Professor of Molecular and
Plates 1-7â•–› â•1› -17, Imaging Plate 9-7 Plates 6-3, 6-7â•–› â•6› -25, 6-27â•–› â•6› -29
David A. Chad, MD JaNean K. Engelstad, HT Cellular Biology
Associate Professor of Neurology Peripheral Nerve Laboratory Harvard University
Harvard Medical School Mayo Clinic Cambridge, Massachusetts
Department of Neurology Rochester, Minnesota Plates 10-2, 11-1, 11-2
Massachusetts General Hospital Plates 6-3, 6-7â•–› â•6› -25, 6-27â•–› â•6› -29
Boston, Massachusetts
Plates 11-6, 11-7, 11-11, 12-7, 12-11â•–› â•1› 2-21 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

xiv

Monique M. Ryan, M Med, BS, FRACP Contributors
Clinical Associate Professor
John D. Markman, MD University of Melbourne Jinny Tavee, MD
Associate Professor Paediatric Neurologist Assistant Professor of Medicine (Neurology)
Department of Neurosurgery Research Fellow, Murdoch Childrens Research Cleveland Clinic Lerner College of Medicine
University of Rochester School of Medicine and Neuromuscular Center
Institute Neurological Institute
Dentistry The Royal Children’s Hospital Melbourne Cleveland Clinic
Director, Translational Pain Research Melbourne, Australia Cleveland, Ohio
Director, Neuromedicine Pain Management Center Plates 6-3, 6-7â•–› â•6› -25, 6-27â•–› â•6› -29 Plates 4-1â•–› â•4› -17
Rochester, New York Steven Shook, MD Jennifer A. Tracy, MD
Plates 8-1â•–› â•8› -23 Staff Physician, Neuromuscular Center Assistant Professor
Matthew N. Meriggioli, MD Department of Neurology Mayo Medical School
Associate Professor Cleveland Clinic Department of Neurology
University of Illinois Hospital and Health Sciences Cleveland, Ohio Mayo Clinic
Plates 4-1â•–› â•4› -17 Rochester, Minnesota
System Jayashri Srinivasan, MD, PhD, FRCP Plates 6-3, 6-7â•–› â•6› -25, 6-27â•–› â•6› -29
Director of Section of Neuromuscular Medicine Staff Neurologist and Vice Chairman Ezgi Tiryaki, MD
Department of Neurology and Rehabilitation Division of Medicine Assistant Professor of Neurology
Lahey Clinic University of Minnesota
Medicine Burlington, Massachusetts; Director of EMG Laboratory and ALS Clinic
Chicago, Illinois Associate Professor Hennepin County Medical Center
Plate 11-8 Tufts University School of Medicine Minneapolis, Minnesota
Nancy J. Newman, MD Boston, Massachusetts Plates 10-5â•–› â•1› 0-11
LeoDelle Jolley Professor of Ophthalmology Plates 5-1â•–› â•5› -22, 7-1â•–› â•7› -27 Jack Wilberger, MD, FACS
Professor of Ophthalmology and Neurology Kathryn J. Swoboda, MD, FACMG Professor and Chairman, Department of
Instructor in Neurological Surgery Associate Professor of Neurology and Pediatrics
Emory University School of Medicine University of Utah School of Medicine Neurosurgery
Atlanta, Georgia Director, Pediatric Motor Disorders Research Drexel University College of Medicine
Plates 1-7â•–› â•1› -17, Imaging Plate 9-7 Allegheny General Hospital
Dennis Roberts, MD Program Vice President, Graduate Medical Education
Department of Neurosurgery Department of Neurology West Penn Allegheny Health System
Allegheny General Hospital Salt Lake City, Utah Designated Institutional Official
Drexel University College of Medicine Plates 9-2, 10-5â•–› â•1› 0-11 Chairman, Graduate Medical Education Committee
Pittsburgh, Pennsylvania AGH-WPH Medical Education Consortium
Plates 3-1â•–› â•3› -18 Pittsburgh, Pennsylvania
Devon I. Rubin, MD Plates 3-1â•–› â•3› -18
Associate Professor of Neurology
Mayo Medical School
Department of Neurology
Mayo Clinic
Jacksonville, Florida
Plates 6-1, 6-2, 6-4â•–› â•6› -6, 10-1â•–› â•1› 0-4, 11-3â•–› â•1› 1-5

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS xv

CONTENTS OF COMPLETE VOLUME 7—
NERVOUS SYSTEM: TWO-PART SET

PART I Brain

SECTION 1 Normal and Abnormal Development
SECTION 2 Cerebral Cortex and Neurocognitive Disorders
SECTION 3 Epilepsy
SECTION 4 Psychiatry
SECTION 5 Hypothalamus, Pituitary, Sleep, and Thalamus
SECTION 6 Disorders of Consciousness
SECTION 7 Basal Ganglia and Movement Disorders
SECTION 8 Cerebellum and Ataxia
SECTION 9 Cerebrovascular Circulation and Stroke
SECTION 10 Multiple Sclerosis and Other Central Nervous

System Autoimmune Disorders
SECTION 11 Infections of the Nervous System
SECTION 12 Neuro-Oncology
SECTION 13 Headache
SECTION 14 Head Trauma
ISBN: 978-1-4160-6387-2

PART II Spinal Cord and Peripheral
Motor and Sensory Systems

SECTION 1 Cranial Nerve and Neuro-Ophthalmologic
Disorders

SECTION 2 Spinal Cord: Anatomy and Myelopathies
SECTION 3 Spinal Trauma
SECTION 4 Nerve Roots and Plexus Disorders
SECTION 5 Mononeuropathies
SECTION 6 Peripheral Neuropathies
SECTION 7 Autonomic Nervous System and Its Disorders
SECTION 8 Pain
SECTION 9 Floppy Infant
SECTION 10 Motor Neuron and Its Disorders
SECTION 11 Neuromuscular Junction and Its Disorders
SECTION 12 Muscle and Its Disorders
ISBN: 978-1-4160-6386-5

xvi THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

CONTENTS

SECTION 1—CRANIAL NERVE AND VAGUS (X) NERVE 3-5 Internal Craniocervical Ligaments,╇ 84
NEURO-OPHTHALMOLOGIC DISORDERS 1-40 Vagus (X) Nerve,╇ 42 3-6 Thoracic Vertebrae,╇ 85
1-41 Vagus Nerve Branches and 3-7 Lumbar Vertebrae and Intervertebral
OVERVIEW OF CRANIAL NERVES
1-1 Distribution of Motor and Sensory Disorders,╇ 43 Disk,╇ 86
ACCESSORY (XI) NERVE 3-8 Ligaments of Spinal Column,╇ 87
Fibers,╇ 2 1-42 Accessory (XI) Nerve,╇ 44 3-9 Sacrum and Coccyx,╇ 88
1-2 Nerves and Nuclei Viewed in Phantom 1-43 Clinical Findings in Cranial Nerve XI 3-10 Ligaments of Sacrum and Coccyx,╇ 89
3-11 Distractive Flexion,╇ 90
from Behind,╇ 4 Damage,╇ 45 3-12 Compressive Flexion,╇ 91
1-3 Nerves and Nuclei in Lateral Dissection,╇ 5 HYPOGLOSSAL (XII) NERVE 3-13 Distractive Extension,╇ 92
OLFACTORY (I) NERVE 1-44 Hypoglossal (XII) Nerve,╇ 46 3-14 Cervical Spine Injury: Prehospital,
1-4 Olfactory Pathways,╇ 6 1-45 Intramedullary Course,╇ 47
1-5 Olfactory Receptors,╇ 7 1-46 Disorders of Hypoglossal Nucleus and Emergency Room, and Acute
1-6 Olfactory Bulb and Nerve,╇ 8 Management,╇ 93
OPTIC (II) NERVE Nerve,╇ 48 3-15 Traction and Bracing,╇ 94
1-7 Eye,╇ 9 3-16 Anterior Cervical Spine Decompression
1-8 Visual Pathways,╇ 10 SECTION 2—SPINAL CORD: ANATOMY and Stabilization,╇ 95
1-9 Optic Nerve Appearance,╇ 11 AND MYELOPATHIES 3-17 Posterior Cervical Stabilization and
1-10 Retinal Projections to Thalamus, 2-1 Spinal Cord,╇ 50 Fusion,╇ 96
2-2 Spinal Membranes and Nerve 3-18 Spinal Cord Injury Medical Issues,╇ 97
Midbrain, and Brainstem,╇ 12
1-11 Pupillary Light Reflex and the Roots,╇ 51 SECTION 4—NERVE ROOTS AND
2-3 Arteries of Spinal Cord,╇ 52 PLEXUS DISORDERS
Accommodation Reflex,╇ 13 2-4 Arteries of Spinal Cord: Intrinsic 4-1 Cervical Disk Herniation,╇ 100
OCULOMOTOR (III), TROCHLEAR (IV), 4-2 Radiographic Diagnosis of
AND ABDUCENS (VI) NERVES Distribution,╇ 53
1-12 Oculomotor (III), Trochlear (IV), and 2-5 Veins of Spinal Cord, Nerve Roots, and Radiculopathy,╇ 101
4-3 Examination of Patient with Low Back
Abducens (VI) Nerves,╇ 14 Vertebrae,╇ 54
1-13 Nerves of Orbit and Cavernous Sinus,╇ 15 2-6 Principal Fiber Tracts of Spinal Pain,╇ 102
1-14 Control of Eye Movements,╇ 16 4-4 Lumbar Disk Herniation: Clinical
1-15 Control of Eye Cord,╇ 55
2-7 Somesthetic System of Body,╇ 56 Manifestations,╇ 103
Movements—Pathology,╇ 17 2-8 Corticospinal (Pyramidal) System: Motor 4-5 L4-5 Disk Extrusion,╇ 104
1-16 Control of Eye Movements—Pathology 4-6 Lumbosacral Spinal Stenosis,╇ 105
Component,╇ 57 4-7 Spinal Nerves,╇ 106
(Continued),╇ 18 2-9 Rubrospinal Tract,╇ 58 4-8 Dermal Segmentation,╇ 107
1-17 Autonomic Innervation of the Eye,╇ 19 2-10 Vestibulospinal Tracts,╇ 59 4-9 Thoracic Nerves,╇ 108
TRIGEMINAL (V) NERVE 2-11 Reticulospinal and Corticoreticular 4-10 Thoracic Spinal Nerve Root
1-18 Trigeminal (V) Nerve,╇ 20
1-19 Trigeminal Nuclei: Afferent and Central Pathways,╇ 60 Disorders,╇ 109
2-12 Spinal Origin or Termination of Major 4-11 Diabetic Lumbosacral Radiculoplexus
Connections,╇ 21
1-20 Trigeminal Nuclei: Central and Peripheral Descending Tracts and Ascending Neuropathy,╇ 110
Pathways,╇ 61 4-12 Lumbar, Sacral, and Coccygeal
Connections,╇ 22 2-13 Cytoarchitecture of Spinal Cord Gray
1-21 Ophthalmic (V1) and Maxillary (V2) Matter,╇ 62 Plexuses,╇ 111
2-14 Spinal Effector Mechanisms,╇ 63 4-13 Brachial Plexus,╇ 112
Nerves,╇ 23 2-15 Spinal Reflex Pathways,╇ 64 4-14 Brachial Plexus and/or Cervical Nerve
1-22 Mandibular Nerve (V3),╇ 24 2-16 Motor Impairment Related to Level of
1-23 Trigeminal Nerve Disorders,╇ 25 Spinal Cord Injury,╇ 65 Root Injuries at Birth,╇ 113
FACIAL (VII) NERVE 2-17 Sensory Impairment Related to Level of 4-15 Brachial Plexopathy,╇ 114
1-24 Facial (VII) Nerve,╇ 26 Spinal Cord Injury,╇ 66 4-16 Lumbosacral Plexopathy,╇ 115
1-25 Muscles of Facial Expression: Lateral 2-18 Incomplete Spinal Cord Syndromes,╇ 67 4-17 Cervical Plexus,╇ 116
2-19 Acute Spinal Cord Syndromes: Evolution
View,╇ 27 of Symptoms,╇ 68 SECTION 5—MONONEUROPATHIES
1-26 Central Versus Peripheral Facial 2-20 Acute Spinal Cord Syndromes: Pathology, 5-1 Compression Neuropathies,╇ 118
Etiology, and Diagnosis,╇ 69 5-2 Chronic Nerve Compression,╇ 119
Paralysis,╇ 28 2-21 Spinal Tumors,╇ 70 5-3 Electrodiagnostic Studies in Compression
1-27 Facial Palsy,╇ 29 2-22 Spinal Tumors (Continued),╇ 71
TASTE RECEPTORS AND PATHWAYS 2-23 Neuroimaging (MRI) Characteristics of Neuropathy,╇ 120
1-28 Anatomy of Taste Buds and Their Spinal Tumors,╇ 72 5-4 Radiologic Studies in Compression
2-24 Syringomyelia,╇ 73
Receptors,╇ 30 2-25 Subacute Combined Degeneration,╇ 74 Neuropathy,╇ 121
1-29 Tongue,╇ 31 2-26 Spinal Dural Fistulas and Arteriovenous 5-5 Proximal Nerves of the Upper Extremity:
VESTIBULOCOCHLEAR (VIII) NERVE Malformations,╇ 75
1-30 Vestibulocochlear (VIII) Nerve,╇ 32 2-27 Cervical Spondylosis,╇ 76 Spinal Accessory Nerve,╇ 122
1-31 Pathway of Sound Reception,╇ 33 2-28 Cervical Disk Herniation Causing Cord 5-6 Proximal Nerves of the Upper Extremity:
1-32 Pathologic Causes of Vertigo,╇ 34 Compression,╇ 77
1-33 Canalith Repositioning (Epley 2-29 Infectious and Hereditary Suprascapular and Musculocutaneous
Myelopathies,╇ 78 Nerves,╇ 123
Maneuver),╇ 35 5-7 Median Nerve,╇ 124
1-34 Afferent Auditory Pathways,╇ 36 SECTION 3—SPINAL TRAUMA 5-8 Proximal Median Neuropathies,╇ 125
1-35 Centrifugal Auditory Pathways,╇ 37 3-1 Spinal Column,╇ 80 5-9 Distal Median Nerve,╇ 126
1-36 Vestibular Receptors,╇ 38 3-2 Atlas and Axis,╇ 81 5-10 Distal Median Neuropathies: Carpal
1-37 Cochlear Receptors,╇ 39 3-3 Cervical Vertebrae,╇ 82 Tunnel Syndrome,╇ 127
GLOSSOPHARYNGEAL (IX) NERVE 3-4 External Craniocervical Ligaments,╇ 83 5-11 Proximal Ulnar Nerve,╇ 128
1-38 Glossopharyngeal (IX) Nerve,╇ 40 5-12 Ulnar Mononeuropathies: Potential
1-39 Otic Ganglion,╇ 41 Entrapment Sites,╇ 129
5-13 Radial Nerve,╇ 130

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS xvii

Contents

5-14 Radial Nerve Compression/Entrapment 7-3 Autonomic Reflex Pathways,╇ 176 8-22 Neurologic Evaluation of the Somatoform
Neuropathies,╇ 131 7-4 Cholinergic and Adrenergic Nerves,╇ 177 Patient: Cutaneous Distribution of
7-5 Autonomic Nerves in Head,╇ 178 Peripheral Nerves,╇ 223
5-15 Femoral and Lateral Femoral Cutaneous 7-6 Autonomic Nerves in Neck,╇ 179
Nerves,╇ 132 7-7 Autonomic Distribution to the Head and 8-23 Neurologic Evaluation of the Somatoform
Patient: Somatoform Conversion
5-16 Iliohypogastric, Ilioinguinal, the Neck,╇ 180 Reactions,╇ 224
Genitofemoral, and Obturator 7-8 Ciliary Ganglion,╇ 181
Nerves,╇ 133 7-9 Thoracic Sympathetic Chain and SECTION 9—FLOPPY INFANT
9-1 Neonatal Hypotonia,╇ 226
5-17 Gluteal Nerves,╇ 134 Splanchnic Nerves,╇ 182 9-2 Spinal Muscular Atrophy Type I (Werdnig-
5-18 Sciatic and Posterior Femoral Cutaneous 7-10 Innervation of Heart,╇ 183
7-11 Innervation of Blood Vessels,╇ 184 Hoffmann Disease),╇ 227
Nerves,╇ 135 7-12 Carotid Body and Carotid Sinus,╇ 185 9-3 Infantile Neuromuscular Junction (NMJ)
5-19 Fibular (Peroneal) Nerve,╇ 136 7-13 Autonomic Nerves and Ganglia in
5-20 Tibial Nerve,╇ 137 Disorders,╇ 228
5-21 Cutaneous Innervation,╇ 138 Abdomen,╇ 186 9-4 Congenital Myopathies,╇ 229
5-22 Dermatomes,╇ 139 7-14 Innervation of Stomach and Proximal 9-5 Arthrogryposis Multiplex Congenita,╇ 230

SECTION 6—PERIPHERAL NEUROPATHIES Duodenum,╇ 187 SECTION 10—MOTOR NEURON AND
6-1 Anatomy of Peripheral Nerve,╇ 143 7-15 Innervation of Intestines,╇ 188 ITS DISORDERS
6-2 Histology of Peripheral Nerve,╇ 144 7-16 Autonomic Innervation of Small 10-1 Peripheral Nervous System:
6-3 Cell Types of Nervous System,╇ 145
6-4 Resting Membrane Potential,╇ 146 Intestine,╇ 189 Overview,╇ 232
6-5 Ion Channel Mechanics and Action 7-17 Enteric Plexuses,╇ 190 10-2 Spinal Cord and Neuronal Cell Body with
7-18 Innervation of Liver and Biliary
Potential Generation,╇ 147 Motor, Sensory, and Autonomic
6-6 Neurophysiology and Peripheral Nerve Tract,╇ 191 Components of the Peripheral
7-19 Innervation of Adrenal Glands,╇ 192 Nerve,╇ 233
Demyelination,╇ 148 7-20 Autonomic Nerves and Ganglia in 10-3 Motor Unit,╇ 234
6-7 Impulse Propagation,╇ 149 10-4 Motor Unit Potentials,╇ 235
6-8 Conduction Velocity,╇ 150 Pelvis,╇ 193 10-5 Primary Motor Neuron Disease,╇ 236
6-9 Visceral Efferent Endings,╇ 151 7-21 Autonomic Innervation of Kidneys and 10-6 Clinical Manifestations of Amyotrophic
6-10 Cutaneous Receptors,╇ 152 Lateral Sclerosis,╇ 237
6-11 Pacinian Corpuscle,╇ 153 Upper Ureters,╇ 194 10-7 Clinical Manifestations of Amyotrophic
6-12 Muscle and Joint Receptors,╇ 154 7-22 Innervation of Urinary Bladder and Lower Lateral Sclerosis (Continued),╇ 238
6-13 Proprioceptive Reflex Control of Muscle 10-8 Mimics of Amyotrophic Lateral
Ureter,╇ 195 Sclerosis,╇ 239
Tension,╇ 155 7-23 Innervation of Male Reproductive 10-9 Diagnosis of Amyotrophic Lateral
6-14 Hereditary Motor and Sensory Sclerosis,╇ 240
Organs,╇ 196 10-10 Treatment of Amyotrophic Lateral
Neuropathies (HMSN, i.e., Charcot-Marie- 7-24 Innervation of Female Reproductive Sclerosis,╇ 241
Tooth Disease),╇ 156 10-11 Spinal Muscular Atrophy and Spinal
6-15 Hereditary Motor and Sensory Organs,╇ 197 Bulbar Muscular Atrophy,╇ 242
Neuropathy Types I and II,╇ 157 7-25 Autonomic Testing,╇ 198
6-16 Other Hereditary Motor and Sensory 7-26 Abnormal Pupillary Conditions,╇ 199 SECTION 11—NEUROMUSCULAR
Neuropathies (Types III, IV, and X),╇ 158 7-27 Clinical Presentation of Autonomic JUNCTION AND ITS DISORDERS
6-17 Hereditary Sensory and Autonomic 11-1 Structure of Neuromuscular
Neuropathy,╇ 159 Disorders,╇ 200
6-18 Guillain-Barré Syndrome,╇ 160 Junction,╇ 244
6-19 Guillain-Barré Syndrome SECTION 8—PAIN 11-2 Physiology of Neuromuscular
(Continued),╇ 161 8-1 Somatosensory System,╇ 202
6-20 Chronic Inflammatory Demyelinating 8-2 Somatosensory Afferents and Principal Junction,╇ 245
Polyradiculoneuropathy,╇ 162 11-3 Somatic Neuromuscular
6-21 Diabetic Neuropathies,╇ 163 Fiber Tracts,╇ 203
6-22 Monoclonal Protein–Associated 8-3 Pain Pathways,╇ 204 Transmission,╇ 246
Neuropathies: Amyloid Neuropathy,╇ 164 8-4 Endorphin System,╇ 205 11-4 Pharmacology of Neuromuscular
6-23 Monoclonal Protein–Associated 8-5 Spinothalamic and Spinoreticular
Neuropathies: Distal Acquired Transmission,╇ 247
Demyelinating Symmetric (DADS) Nociceptive Processing in the Spinal 11-5 Repetitive Motor Nerve Stimulation,╇ 248
Neuropathy,╇ 165 Cord,╇ 206 11-6 Myasthenia Gravis: Clinical
6-24 Vasculitic Neuropathy and Other 8-6 Central Nervous System
Connective Tissue Disorders Neurotransmitters, Receptors, and Drug Manifestations,╇ 249
Associated with Neuropathy: Targets,╇ 207 11-7 Myasthenia Gravis: Etiologic and
Fibrinoid Necrosis,╇ 166 8-7 Thalamic Pain Syndrome,╇ 208
6-25 Vasculitic Neuropathy and Other 8-8 Clinical Manifestations Related to Pathophysiologic Concepts,╇ 250
Connective Tissue Disorders Thalamus Site in Intracerebral 11-8 Immunopathology of Myasthenia
Associated with Neuropathy: Hemorrhage,╇ 209
Sjögren Syndrome,╇ 167 8-9 Complex Regional Pain,╇ 210 Gravis,╇ 251
6-26 Immunopathogenesis of Guillain-Barré 8-10 Herpes Zoster,╇ 211 11-9 Presynaptic Neuromuscular Junction
Syndrome,╇ 168 8-11 Occipital Neuralgia,╇ 212
6-27 Peripheral Neuropathy Cause by Heavy 8-12 Myofascial Factors in Low Back Transmission Disorders: Lambert-Eaton
Metal Poisoning,╇ 169 Pain,╇ 213 Myasthenic Syndrome and Infantile
6-28 Metabolic, Toxic, and Nutritional 8-13 Myofascial Factors in Low Back Pain Botulism,╇ 252
Peripheral Neuropathies,╇ 170 (Continued): Posterior Abdominal Wall: 11-10 Congenital Myasthenic Syndromes,╇ 253
6-29 Leprosy and Other Infections Sometimes Internal View,╇ 214 11-11 Foodborne Neurotoxins,╇ 254
Causing Peripheral Neuropathies,╇ 171 8-14 Lumbar Zygapophyseal Joint Back
Pain,╇ 215 SECTION 12—MUSCLE AND
SECTION 7—AUTONOMIC NERVOUS 8-15 Low Back Pain and Effects of Lumbar ITS DISORDERS
SYSTEM AND ITS DISORDERS Hyperlordosis and Flexion on Spinal 12-1 Muscle Fiber Anatomy: Basic Sarcomere
7-1 General Topography of Autonomic Nerves,╇ 216
8-16 Examination of the Low Back Pain Subdivisions,╇ 256
Nervous System,╇ 174 Patient,╇ 217 12-2 Muscle Fiber Anatomy: Biochemical
7-2 General Topography of Autonomic 8-17 Osteoporosis,╇ 218
8-18 Diagnosis of Hip, Buttock, and Back Mechanics of Contraction,╇ 257
Nervous System (Continued),╇ 175 Pain,╇ 219 12-3 Muscle Membrane, T Tubules, and
8-19 Hip Joint Involvement in
Osteoarthritis,╇ 220 Sarcoplasmic Reticulum,╇ 258
8-20 Peripheral Nerves of Feet, Painful 12-4 Muscle Response to Nerve
Peripheral Neuropathies,╇ 221
8-21 Peripheral Neuropathies: Clinical Stimulation,╇ 259
Manifestations,╇ 222

xviii THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

12-11 Myotonic Dystrophy and Other Myotonic Contents
Disorders,╇ 267
12-5 Metabolism of Muscle Cell,╇ 260 12-18 Endocrine, Toxic, and Critical Illness
12-6 Muscle Fiber Types,╇ 261 12-12 Myotonic Dystrophy and Other Myotonic Myopathies,╇ 274
12-7 Overview of Myopathies: Clinical Disorders (Continued),╇ 268
12-19 Myopathies: Hypokalemia/Hyperkalemia
Approach,╇ 262 12-13 Other Types of Muscular Dystrophy,╇ 269 and the Periodic Paralyses
12-8 Dystrophinopathies: Duchenne 12-14 Polymyositis and Dermatomyositis,╇ 270 Channelopathies Myopathies Associated
12-15 Polymyositis and Dermatomyositis with Disorders of Potassium
Muscular Dystrophy—Gower’s Metabolism,╇ 275
Maneuver,╇ 264 (Continued),╇ 271
12-9 Dystrophinopathies: Duchenne Muscular 12-16 Inclusion Body Myositis,╇ 272 12-20 Metabolic and Mitochondrial
Dystrophy,╇ 265 12-17 Immunopathology for Inflammatory Myopathies,╇ 276
12-10 Dystrophinopathies: Molecular Genetic
Testing,╇ 266 Myopathies,╇ 273 12-21 Myoglobinuric Syndromes Including
Malignant Hyperthermia,╇ 277

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS xix

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SECTION 1â•…

CRANIAL NERVE
AND NEURO-

OPHTHALMOLOGIC
DISORDERS

Plate 1-1â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
DISTRIBUTION OF MOTOR AND SENSORY FIBERS

II III
Optic Oculomotor
I Eye Medial rectus, superior Ophthalmic
Olfactory rectus, inferior rectus, inferior MMaaxnidlliabruy lar
Nasal cavity oblique, levator palpebra,
ciliary muscle, and iris sphincter
V
IV Trigeminal Motor—muscles of
Trochlear Sensory—face, mastication: tensor tympani,
VI Abducens Superior oblique muscle tensor veli palatini,
Lateral rectus sinuses, teeth, orbit mylohyoid, anterior
and oral cavities, belly of digastric
muscle dura mater

VII Intermediate nerve
Facial Motor—submandibular,
Muscles of face stapedius, sublingual, lacrimal glands
posterior belly of digastric,
stylohyoid, occipitalis, Taste—anterior 2⁄3 of
auricularis muscles tongue, sensory soft palate

VIII
Cochlear Vestibulocochlear

Vestibular

XII XI X IX
Hypoglossal Accessory Vagus Glossopharyngeal
Sternocleidomastoid, Motor—heart, lungs, palate, pharynx, Taste—posterior 1⁄3 of tongue
Tongue trapezius muscles larynx, trachea, bronchi, GI tract Sensory—tonsil, pharynx, middle ear
muscles Sensory—heart, lungs, trachea, Motor—stylopharyngeus,
bronchi, larynx, pharynx,
GI tract, external ear parotid gland

Strap Spinal nerve
muscles fibers
(C1, 2, 3 Efferent (motor)
fibers) fibers
Afferent (sensory)
fibers

Overview of Cranial Nerves

The brainstem is the source of all the cranial nerves and nerve serves a regional skull area and may provide more series. The manifestations of multiple cranial neuropa-
provides sensory, motor, and, through the vagus nerve, than one function to that area and therefore is not thies reflect the sites of injury and function of the
parasympathetic preganglionic innervation to the face, restricted to a single nucleus or nerve type. For example, cranial nerves affected. The many different causes of
head, thorax, and most of the abdominal viscera. Dis- the facial nerve provides voluntary motor innervations multiple cranial neuropathies include infectious, neo-
tinct motor and sensory nuclei within the brainstem to the face as well as taste special sensation to the ante- plastic, autoimmune disease, trauma, and vascular
project to the various structures of the head to provide rior tongue. The pure motor nerves (except for perhaps disease. Infections associated with multiple cranial
(1) general sensory information from the face, ears, some proprioceptive function) are the oculomotor III, neuropathies include Lyme disease, tuberculous men-
and oropharynx and (2) motor innervations for facial trochlear IV, abducens VI, spinal accessory nerve XI, ingitis, cryptococcus, histoplasmosis, botulism, mucor-
movement and expression, mastication, extraocular eye and hypoglossal XI. The special sensory nerves are the mycosis, certain viruses (e.g., herpes simplex virus,
movements, and complex functions such as speech and olfactory, optic, and vestibulocochlear. Mixed cranial varicella-zoster virus) and bacterial meningitis.
swallowing. The specialized olfactory, visual, auditory, nerves are the trigeminal V, facial VII, glossopharyngeal Guillain-Barré syndrome (GBS) and the Miller Fisher
and gustatory senses are provided by highly specialized IX, and vagus X. A summary of the origin, course, and variant of GBS are monophasic, autoimmune polyra-
receptor cells and end organs, with ultimately wide cor- distribution of each cranial nerve is outlined on the next diculoneuropathies that can frequently involve multiple
tical projections. plates. cranial nerves. Neoplasms cause multiple cranial neu-
ropathies either by direct compression and local exten-
Cranial nerve motor nuclei are located medially, Cranial neuropathies may manifest as a single cranial sion, such as with meningiomas, schwannomas, and
whereas the sensory nuclei are found generally more neuropathy or, less commonly, as multiple cranial neu- nasopharyngeal tumors, or by diffuse dissemination
lateral. Three types of motor nuclei are present inner- ropathies. Single cranial neuropathies are discussed in and meningeal infiltration, such as with lymphoma and
vating voluntary striated muscles (somatic), muscles their respective sections. For example, Bell palsy is various carcinomas. Myasthenia gravis (MG) mimics
of facial expressions and mastication (special motor reviewed in the cranial nerve VII (facial nerve) section. multiple cranial neuropathies but the site of autoim-
derived from embryonic branchial arch structures), and Multiple cranial neuropathies involve any combination mune attack in MG is directed against the postsynaptic
autonomic smooth muscles (visceral). Each cranial of cranial nerves, although cranial nerves III, V, VI, and muscle end rather than the nerve.
VII are the most commonly affected in most clinical

2 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Cranial Nerve and Neuro-Ophthalmologic Disorders

Name and number: Origin, course, and distribution Chief functions
Type of fibers
Olfactory cells in nasal mucosa aggregate into olfactory nerves that penetrate the cribriform plate and Smell
Olfactory (I): join to form the olfactory bulb. The bulb’s posteriorly extending tract divides into a medial branch,
Special sensory which fans into the parolfactory and subcallosal areas, and a lateral branch, which ends in the uncus
and the parahippocampal gyrus.
Optic (II):
Special sensory Axons of the inner retinal ganglion cell layer form the retina’s nerve fiber layer and gather at the optic Vision
disk (optic nervehead) before turning 90° and penetrating the scleral canal to exit the globe, now
myelinated, as the optic nerve. The optic chiasm is the intersection of the optic nerve from each eye
coming through the optic canal and is located above the pituitary body within the sella turcica. Axons
from the temporal retina (nasal field) remain ipsilateral as they pass through the chiasm to the optic
tract. In contrast, the nasal retinal fibers decussate, carrying temporal visual field information to the
contralateral side. Inferior nasal fibers decussate within the chiasm more anteriorly than superior ones.
As the inferior nasal retinal fibers approach the posterior aspect of the chiasm, the fibers shift to occupy
the lateral aspect of the contralateral optic tract. The optic tract leads to the lateral geniculate bodies.
The lateral geniculate nucleus (LGN) is a thalamic nucleus that serves as the synapse point as the retinal
ganglion cells and relays visual information through the optic radiations to the striate and occipital cortex.

Oculomotor (III): This nerve emerges as a collection of nine rostral midbrain subnuclei located ventral to the aqueduct Somatic motor: Upper lid
Motor at the level of the superior colliculus and includes the accessory autonomic (Edinger-Westphal) nucleus. elevation (levator palpebrae
Visceral motor Axons from the CNIII subnuclei gather into a fascicle that arcs through the red nucleus and emerges superioris) and extraocular
at the medial surface of the cerebral peduncle. In the interpeduncular cistern, the nerve passes beneath movements upward,
the posterior cerebral artery, then pierces the dura crossing next to the internal carotid artery en route medially, and downward
to the cavernous sinus. From the lateral wall of the cavernous sinus, it enters the orbit through the Visceral motor: Para-
superior orbital fissure to supply the superior rectus, medial rectus, inferior rectus, and inferior oblique. sympathetically mediated
The fibers subserving pupillary constriction are located superficially and are susceptible to compression pupillary constriction and
but are less prone to microvascular or ischemic changes than the deeper fibers are. These parasympathetic accommodation reflex
fibers split off the oculomotor nerve in the orbit and synapse in the ciliary ganglion from which postgang-
lionic short ciliary nerves supply the pupillary sphincter and ciliary muscles.

Trochlear (IV): The CNIV nuclei are located in the midbrain at the level of the inferior colliculi off midline at the anterior Somatic Motor: Superior
Motor edge of the periaqueductal gray. Axons from the trochlear nucleus arc posteriorally around the oblique muscle, extraocular
periaqueductal gray and cross the midline to emerge laterally beneath the inferior colliculus and wrap eye movement downward
Trigeminal (V): forward around the medial border of the brachium conjuctivum. CNIV completely decussates, a unique and intorsion
Somatic sensory feature among the cranial nerves, and exits the brainstem from its posterior aspect. It passes the ambient
and special motor cistern and through the lateral wall of the cavernous sinus to then enter the orbit via the superior orbital
fissure. The trochlear nerve innervates a single extraocular muscle, the superior oblique.
Abducens (VI):
Motor The trigeminal somatic sensory column is a posterolateral series of nuclei extending from the mid pons to Somatic sensory (touch, pain
the upper cervical cord and receive general sensory input from the eye, orbit, face, forehead, upper and and temperature): Eyes, face,
lower jaws, sinuses, teeth, and nasopharynx. Proprioceptive receptors in the extraocular and masticatory anterior scalp, sinuses, teeth,
muscles end in the mesencephalic nucleus. Pain, touch, and temperature fibers end in the principal oral and nasal cavities as
(pontine) sensory nucleus and spinal nucleus of trigeminal nerve. Trigeminal motor nucleus in the upper well as the dura mater
part of the pons is the origin of special branchiomotor fibers to the muscles of mastication.

Large sensory and smaller motor roots enter and emerge laterally at the midpons level. As the trigeminal Proprioceptive sensory (deep
nerve exits the posterior fossa, it expands over the apex of the petrous temporal bone into the trigeminal pressure, position, and move-
(semilunar) ganglion made of sensory nuclei from the ophthalmic, maxillary, and mandibular nerves that ment): Teeth, temporomand-
pass through the superior orbital fissure, foramen rotundum, and foramen ovale, respectively. The ibular joint, hard palate, and
ophthalmic nerve divides into lacrimal, frontal, and nasociliary branches, which participate in innervating muscles of mastication
eye, nose, and scalp. The maxillary nerve traverses the pterygopalatine fossa, enters the infraorbital groove Special motor: Branchio-
(canal), and emerges as the infraorbital nerve through infraorbital foramen; supplies meningeal, zygomatic, motor fibers to the muscles
superior alveolar, inferio-palpebral, nasal, and superior labial branches, and is connected with of mastication, anterior belly
pterygopalatine ganglion through which it supplies orbital, nasal, palatine, and pharyngeal branches. of the digastrics, tensor
The mandibular nerve is joined by entire motor root of trigeminal nerve in the foramen ovale and gives tympani, and tensor veli
off meningeal, buccal, auriculotemporal, lingual, and inferior alveolar branches, as well as motor nerves palatini mylohyoid
supplying mastricatory muscles, the tensors of the soft palate, and the tympanic membrane.

The abducens CNVI nucleus is in the floor of the fourth ventricle just lateral to the median eminence of Somatic motor: Lateral
the pons. It is enveloped by looping CNVII fibers (genu) that form the facial colliculus. rectus muscle extraocular
The CNVI nucleus contains two physiologically distinct groups of neurons: one innervating the eye movement, eye
ipsilateral lateral rectus muscles and the other projecting across the midline up the contralateral medial abduction
longitudinal fasciculus (MLF) to the ventral nucleus of the contralateral CNIII nuclear complex. These
internuclear connections produce the simultaneous activation of the contralateral medial rectus muscle
and the ipsilateral lateral rectus that ensures conjugate lateral horizontal gaze.
The CNVI fasciculus projects anteriorly and caudally to exit the inferior edge of the pons just medial to
the corticospinal tracts. The nerve ascends between the pons and the clivus within the pontine cistern.
It pierces the dura and then enters the lateral cavernous sinus below the trochlear nerve. It reaches the
orbit through the superior-orbital fissure.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 3

P late 1-2â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

5,9=,: (5+ 5<*3,0 =0,>,+ 05 7/(5;64 -964 ),/05+

7VZ[LYPVY WOHU[VT ]PL^ Oculomotor nerve (III)
Red nucleus

Superior colliculus Oculomotor nucleus
Mesencephalic nucleus of trigeminal nerve Accessory oculomotor (Edinger-Westphal) nucleus
Trochlear nucleus

Lateral geniculate body Trochlear nerve (IV)

Principal sensory nucleus of trigeminal nerve Motor nucleus of trigeminal nerve

Trigeminal nerve (V) and ganglion (gasserian) Trigeminal nerve (V) and ganglion
Facial nerve (VII) and geniculate ganglion
Abducens nucleus
Vestibulocochlear nerve (VIII)
Facial nucleus

Geniculum (geniculate ganglion) of facial nerve

Superior and inferior salivatory nuclei

Cochlear nuclei Anterior Nucleus ambiguus
Posterior
Dorsal nucleus of vagus nerve (X)

Vestibular nuclei Glossopharyngeal nerve (IX)
Glossopharyngeal nerve (IX)
Vagus nerve (X) ,MMLYLU[ MPILYZ
Vagus nerve (X) Accessory nerve (XI) (MMLYLU[ MPILYZ
Spinal tract and spinal nucleus of trigeminal nerve 4P_LK MPILYZ
Hypoglossal nucleus
Solitary tract nucleus Accessory nucleus

5HTL HUK U\TILY! 6YPNPU JV\YZL HUK KPZ[YPI\[PVU *OPLM M\UJ[PVUZ
;`WL VM MPILYZ Branchiomotor fibers arise from the MHJPHS U\JSL\Z in the lower pons and ascend to loop around the ab-
-HJPHS =00 ! ducens nucleus and then descend anterolaterally between the spinal trigeminal complex and the VII :WLJPHS TV[VY! Muscles of
:WLJPHS TV[VY nerve motor nucleus. The nerve emerges as two divisions through the recess between the inferior facial expression, stapedius,
.LULYHS ]PZJLYHS TV[VY cerebellar peduncle and the medulla; a larger TV[VY YVV[ and smaller ULY]\Z PU[LYTLKP\Z containing stylohoid, and posterior belly
:VTH[PJ ZLUZVY` mainly afferent special sensory fibers for taste and secretomotor fibers to the W[LY`NVWHSHU[PUL NHUNSPVU of the digastrics muscle
:WLJPHS ZLUZVY` (lacrimation and mucous membrane secretory function in the mouth and nose). Both divisions of the .LULYHS ]PZJLYHS TV[VY!
facial nerve, along with CN VIII, then pass through the internal acoustic meatus. At the level of the Parasympathetic innervations
geniculate ganglion secretomotor fibers (originating from the Z\WLYPVY SHJYPTHS ZHSP]H[VY` U\JSL\Z), of the submandibular, sub-
separate and proceed superiorly to the pterygopalatine ganglion. The chorda tympani (carrying lingual, lacrimal, and nasal/
secretomotor fibers to the submandibular ganglion and special sensory taste fibers from the anterior oral mucous membrane glands
two thirds of tongue and soft palate) separates distal to the geniculate nucleus and joins the lingual :VTH[PJ ZLUZVY! External aud-
nerve to the tongue. The branchiomotor fibers proceed through the boney facial canal and emerge itory meatus and skin over
in the face anterior to the mastoid process from the stylomastoid foramen. It enters the parotid mastoid
gland to divide into diverging branches toward the facial muscles and the platysma (Plate 1-24). :WLJPHS ZLUZVY`! Taste
anterior 2/3rds of the tongue

=LZ[PI\SVJVJOSLHY =000 ! The vestibulocochlear nerve emerges through the internal acoustic meatus at the pontomedullary angle /LHYPUN
:WLJPHS ZLUZVY` posterolateral to the facial nerve. The primary neurons are bipolar cells located in the vestibular and ,X\PSPIYP\T HUK IHSHUJL
.SVZZVWOHY`UNLHS 0? ! multiple spiral ganglia. Peripheral processes pass from special auditory (cochlea) and vestibular 9LMSL_P]L L`L TV]LTLU[Z
:WLJPHS TV[VY (ampullae, utriculus, and sacculus) receptors, while the central processes project to two cochlear, and four
.LULYHS ]PZJLYHS TV[VY vestibular brainstem nuclei, respectively. The ventral and dorsal cochlear nuclei are located at the level of
=PZJLYHS ZLUZVY` the inferior cerebellar peduncle in the superior medulla. Most cochlear nuclear fibers decussate through
:VTH[PJ ZLUZVY` the trapezoid body, after which third- and fourth-order neurons then ascend the lateral lemniscus to the
inferior colliculus with projections ultimately to the auditory cortex. The superior, inferior, medial, and
lateral vestibular nuclei lie in the anterolateral floor of the fourth ventricle and connect with the
cerebellum, the nuclei of CNs III, IV, and VI (through the medial longitudinal fasciculus) and to anterior
horn cells controlling muscles of head and neck (vestibulospinal tract).

Special branchiomotor fibers arise from cranial end of nucleus ambiguous and supply the stylopharyngeus :WLJPHS TV[VY! Stylopharyn-
muscle. Secretomotor fibers arise from inferior salivatory nucleus and proceed as parasympathetic fibers geus; elevation of pharynx
through the tympanic nerve to the otic ganglion; postganglion fibers (lesser petrosal nerve) innervate the .LULYHS ]PZJLYHS TV[VY!
parotid gland. Special sensory taste fibers from the posterior third of tongue have their cell bodies in the Parotid and mucous glands
petrosal ganglion and then project centrally to the solitary tract nucleus. “Visceral” sensory fibers from secretion
the posterior tongue, fauces, tonsil, tympanic cavity, eustachian tube, and mastoid cells end in a
combined dorsal glossopharyngeal vagal nucleus but with ordinary sensory fibers probably ending in the :WLJPHS ZLUZVY`! Taste pos-
spinal tract and nucleus of trigeminal nerve. Special visceral afferents from pressure receptors in the terior third of tongue, and
carotid sinus mediate decreased heart rate and blood pressure through vagus nerve connections. numerous taste buds in
The nerve emerges from the medulla above the vagus nerve and leaves the skull through the jugular vallate papillae
foramen. It runs forward between the internal carotid artery and internal jugular vein and curves over the .LULYHS ]PZJLYHS ZLUZVY`!
stylopharyngeus muscle, to end in branches for the tonsils, and mucous membrane and glands of pharynx General sensation from pos-
and pharyngeal part of tongue. The tympanic branch forms the main part of the tympanic plexus, which terior tongue, fauces, tonsil,
supplies the tympanic cavity and the lesser petrosal nerve carrying secretomotor fibers for the parotid tympanic cavity, eustachian
gland. tube, and mastoid cells.
Carotid body and sinus
:VTH[PJ ZLUZVY`! Outer ear
sensation

4 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-3â•… Cranial Nerve and Neuro-Ophthalmologic Disorders

NERVES AND NUCLEI IN LATERAL DISSECTION

Medial dissection Substantia nigra Accessory oculomotor (Edinger-Westphal) nucleus
Oculomotor nucleus
Red nucleus Trochlear nucleus
Cerebral aqueduct
Oculomotor nerve (III) Trochlear nerve (IV)

Mesencephalic nucleus of trigeminal nerve

Abducens nucleus

Trigeminal nerve (V) and ganglion (gasserian) Internal genu of facial nerve

Principal sensory nucleus of trigeminal nerve Facial nucleus
Motor nucleus of trigeminal nerve
Facial nerve (VII) Vestibular nuclei
Vestibulocochlear nerve (VIII)
Abducens nerve (VI) Anterior and posterior cochlear nuclei
Glossopharyngeal nerve (IX)
Hypoglossal nerve (XII) Superior and inferior salivatory nuclei
Vagus nerve (X)
Accessory nerve (XI) Solitary tract nucleus
Inferior olivary complex
Posterior (dorsal) nucleus of vagus nerve (X)
Spinal tract and spinal nucleus of trigeminal nerve
Median aperture (foramen of Magendie)
Efferent fibers
Hypoglossal nucleus

Nucleus ambiguus Afferent fibers
Accessory nucleus
Central canal
Mixed fibers

Name and number: Origin, course, and distribution Chief functions
Type of fibers
The dorsal vagal nucleus is a mixture of visceral efferent and afferent cells forming elongated column on Special Motor:
Vagus (X): each side of midline and extending through the length of the medulla, lateral to the hypoglossal nuclei. Intrinsic laryngeal muscles
Special motor From here, preganglionic parasympathetic fibers go to parasympathetic ganglia innervating cardiac and and contribute to pharyngeal
unstriated muscles in the thoracic and abdominal viscera. Motor fibers for striated muscles of larynx constrictors
General visceral motor and pharynx originate in the midportion of the nucleus ambiguous (ill-defined column of large cells General visceral motor:
Somatic sensory located in the reticular formation). Parasympathetic supply
Visceral sensory Afferent fibers from visceral receptors have their cell bodies in the inferior vagal (nodose) ganglion and end (movement and secretion) to
Special sensory in the mixed dorsal vagal nucleus. They convey sensation from the pharynx, larynx, trachea, and viscera. the heart, the great vessels,
However, a few special sensory taste fibers from the epiglottis and the adjacent tongue end in the solitary trachea, bronchi, and ali-
tract nucleus. General somatic afferents from auricular and meningeal branches with cell bodies in the mentary canal, and associated
jugular ganglion end in the spinal tract and nucleus of the trigeminal nerve. glands from pharynx almost to
The nerve is attached by a series of medullary rootlets located laterally between the olive and inferior left colic (splenic) flexure
cerebellar peduncle. The vagus nerve leaves the skull through the jugular foramen and is soon joined by Somatic sensory:
the cranial part of the accessory nerve to then descend in the neck within the carotid sheath. The vagus Parts of auricle, external
nerve continues through the thorax and contributes to cardiac, pulmonary, and esophageal plexuses. It acoustic meatus, and tympanic
enters the abdomen as the anterior and posterior vagal trunks. membrane meninges of
posterior cranial fossa
General visceral sensory:
Pharynx, larynx, trachea, and
abdominal viscera

Special sensory:
Taste from epiglottis
and valleculae

Accessory (XI): The accessory nerve consists of cranial and spinal roots. Cranial roots arises from cells within the lower Special Motor
Special motor end of the nucleus ambiguous and supply intrinsic laryngeal muscles. The spinal roots arise from a group Internal branch (vagus n.):
of anterior horn cells in the upper five or six cervical segments (the spinal accessory nucleus) and supply Intrinsic muscles of
the sternocleidomastoid and trapezius muscles. the larynx via the recurrent
The cranial root fibers form the internal branch of the accessory nerve and arise as a series of rootlets on laryngeal nerve (except
the surface of medulla oblongata below, and in line with the glossopharyngeal and vagal nerve rootlets. cricothyroid-superior
The spinal rootlets emerge through the lateral white column of the spinal cord and ascend behind the laryngeal nerve) and soft
denticulate ligaments and unite to form the external branch of the accessory nerve entering the skull palate (except tensor veli
through the foramen magnum behind vertebral artery. Cranial and spinal roots unite for a short distance, palatine-mandibular division
before leaving the skull through the jugular foramen. The internal branch joins the vagus nerve. The of the trigeminal nerve)
external branch runs downward and backward through the sternocleidomastoid muscle, then crosses the
posterior triangle of neck and ends in the trapezius muscle. It also communicates with branches of spinal External branch:
nerves C2–C4. Sternocleidomastoid and
trapezius muscles

Hypoglossal (XII): Motor The hypoglossal nucleus is a medial column of cells situated in the lower floor of the fourth ventricle Somatic motor:
and extends the length of the medulla anterior to the central canal in the “closed” part of medulla Intrinsic and extrinsic muscles
oblongata. Axons from the nucleus course anteriorly and just lateral to the medial lemniscus and cross of the tongue
the most medial portion of the inferior olive to exit the brainstem in the anterolateral sulcus between the
pyramidal tract and the prominence of the inferior olive. The fibers emerge as 10-15 rootlets and fuse to
form two bundles that unite as they pass through the hypoglossal canal of the occipital bone. The
hypoglossal nerve then runs forward between the internal carotid artery and internal jugular vein and
inclines upward into tongue. It is joined by a filament from spinal nerve C1, but this soon leaves to
form the superior root (descendens hypoglossi) of the ansa cervicalis.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 5

Plate 1-4â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

OLFACTORY PATHWAYS

Olfactory bulb cells: schema

Efferent fibers to olfactory bulb

Afferent fibers from bulb
to central connections
and contralateral bulb

Granule cell (excited by Subcallosal (parolfactory) area
and inhibiting to mitral Septal area and nuclei
and tufted cells) Fibers from Contralateral
Mitral cell Fibers to olfactory bulb
Recurrent process
Tufted cell

Periglomerular
cell

Cranial Nerve I: Glomerulus Anterior commissure
Olfactory Nerve
Medial olfactory stria
ANATOMY
The olfactory nerves are concerned with the special Olfactory
sense of smell. The nerve fibers are the central pro- nerve fibers
cesses of bipolar nerve cells located in the olfactory
epithelium, which covers most of the superior-posterior Olfactory tract
nasal septum and the lateral wall of the nasal cavity. The
unmyelinated peripheral olfactory fibers aggregate into Olfactory cells Dura mater
approximately 20 slender olfactory bundles that make
up the olfactory nerve. The nerve traverses the eth- Olfactory mucosa Olfactory trigone
moidal cribriform plate surrounded by finger-like
extensions from the dura mater and arachnoid to end Olfactory nerves (I) and olfactory tubercle
in the “glomeruli” of the homolateral olfactory bulb.
Within the bulb, these fibers synapse with second-order Olfactory bulb Lateral olfactory stria Uncus
neurons called mitral and tufted cells whose axons con- Cribriform plate of ethmoid bone Hippocampal
stitute the olfactory tract that courses along the frontal Lateral olfactory tract nucleus fimbria
lobe base. It then divides into the medial and lateral
olfactory striae on either side of the anterior perforated Anterior olfactory nucleus Anterior perforated substance Dentate gyrus
substance and projects directly into the primary olfac-
tory cortex within the temporal lobe. This direct Amygdaloid body (WOHU[VT
pathway without a central sensory relay site (such as in
the thalamic nuclei) is unique among the cranial nerves. Piriform lobe Parahippocampal gyrus
Although most of the olfactory tract fibers have ipsilat-
eral central connections, some fibers decussate in the infection. Post-traumatic anosmia or hyposmia may be anosmia is unusual because of generally unilateral
anterior commissure, making the cortical representa- either unilateral or bilateral. Tumors of the olfactory involvement and slow tumor growth with slow decline
tion of smell bilateral. The human primary olfactory groove affect the olfactory bulb and tract. The most in olfactory function. Once such tumors are large
cortex includes the uncus, hippocampal gyrus, amygda- common are olfactory groove meningiomas, which are enough (> 4╯cm in diameter), they cause pressure on the
loid complex, and entorhinal cortex. usually histologically benign tumors causing mostly frontal lobes and the optic tracts, with symptoms of
unilateral, and occasionally bilateral, gradual olfactory headaches, visual disturbances, personality changes, and
OLFACTORY NERVE DISORDERS dysfunction. Other tumors include sphenoid and memory impairment. Very large olfactory groove
Anosmia is not always apparent to the patient, and due frontal osteomas, pituitary tumors, and nasopharyngeal tumors on rare occasion cause ipsilateral optic atrophy
to the close association of flavor perception and olfac- carcinomas. Unless specifically tested, a presentation of by exerting direct pressure on the optic nerve with
tion, may be reported as altered taste rather than loss
of smell. Bilateral anosmia is more common and usually
of benign nature, whereas unilateral anosmia should
raise suspicion for a more serious disorder, such as an
olfactory groove meningioma or frontal basal tumor.
The most common cause of anosmia is nasal and para-
nasal sinus infection with inflammation and is referred
to as transport or conductive olfactory disorders. Post-
traumatic olfactory dysfunction is the cause for 20% of
patients with anosmia and is the result of olfactory
nerve shearing as it passes through the cribriform plate.
In more substantial damage, the olfactory nerve is
torn by fractures involving the cribriform plate, with
cerebrospinal fluid rhinorrhea and possible meningeal

6 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

P late 1-5â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
OLFACTORY RECEPTORS

Cranial Nerve I: Olfactory Subfrontal meningioma. T1-weighted, gadolinium-enhanced sagittal and coronal MR images show
Nerve (Continued) a large enhancing skull-based mass displacing and compressing the olfactory apparatus.

contralateral papilledema from increased intracranial Distribution of olfactory Section through olfactory mucosa
pressure. The finding of ipsilateral optic atrophy, con- epithelium (blue area)
tralateral papilledema, and ipsilateral anosmia is known
as the Foster-Kennedy syndrome. Esthesioneuroblasto- Olfactory bulb
mas arise from the upper nasal cavity and manifest with
nasal obstruction and epistaxis. Rarely, they involve the Lateral nasal wall Cribriform plate
orbit and cause diplopia, visual loss, proptosis, and peri- Cribriform plate Schwann cell
orbital swelling. Anosmia is an early sign of neurode- of ethmoid bone Olfactory gland
generative processes, particularly Parkinson disease, Unmyelinated
Alzheimer disease, and Lewy body dementia. It fre- Septum olfactory axons
quently precedes other neurologic signs, such as motor Basement
findings or cognitive changes. Olfactory discrimination membrane
is affected by many medications thought to disrupt the Sustentacular
physiologic turnover of receptor cell and includes cells
opiates, antiÂc

Plate 1-6â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

OLFACTORY BULB AND NERVE

Internal nasal branch of anterior Olfactory bulb Olfactory tract
(lateral ramus) ethmoidal
nerve Olfactory nerves Lateral posterior superior
External nasal nasal branches
branch Cribriform plate
of ethmoid bone Maxillary nerve
Pterygopalatine
Lateral ganglion and branches
wall Nerve of pterygoid canal
Greater petrosal nerve
Deep petrosal nerve
Pharyngeal branch

Cranial Nerve I: Olfactory Cribriform plate of ethmoid bone Nasopalatine nerve
Nerve (Continued) (passing to septum)
Internal nasal branch (mediai Posterior inferior nasal branch
potential is converted to a digital action potential, ramus) of anterior ethmoidal nerve Lesser (minor) palatine nerves
which is conducted via the axon of the olfactory cell to Greater (major) palatine
the brain. Nasopalatine nerve nerve and branches
Olfactory bulb
Sense of Smell. As with taste fibers, which may Incisive canal Olfactory nerves
respond to a variety of taste stimuli, individual olfactory Olfactory tract
nerve fibers respond to a number of different odors. Nasal
Humans differentiate the odors of thousands of chemi- septum nucleus (a continuation of the granule cell layer
cals; nevertheless, it has not been possible to identify a throughout the olfactory tract) and olfactory tubercle,
set of primary odor qualities analogous to the four respond to groups of substances that evoke subjective the sites of origin of the efferent fibers projecting to
primary tastes. sensations. both the ipsilateral and contralateral olfactory bulbs.
OLFACTORY PATHWAY Other axons from the lateral stria reach the piriform
Olfactory Bulb. About 100 million olfactory afferent Olfactory Tract and Central Connections. The axons lobe of the temporal cortex and terminate in the amyg-
fibers enter the olfactory bulb, a flattened, oval mass of mitral and tufted cells form the olfactory tract, dala (amygdaloid body), the septal nuclei, and the
lying near the lateral margin of the cribriform plate of through which they project to the olfactory trigone and hypothalamus.
the ethmoid bone. The incoming olfactory fibers into the lateral and medial olfactory striae, establishing
coalesce in the outermost layer of the olfactory bulb to a complex pattern of central connections. Some mitral
form presynaptic nests, or glomeruli. Each glomerulus and tufted cell axons terminate in the anterior olfactory
is composed of about 25,000 receptor cell axon termi-
nals. The terminals synapse and excite the dendrites of
mitral and tufted cells, which are the second-order
neurons in the olfactory bulb. Each mitral cell sends its
dendrite to only a single glomerulus, while each tufted
cell sends dendrites to several glomeruli. Olfactory
afferents within the glomeruli also activate periglomer-
ular cells, which then inhibit mitral and tufted cells.
Further inhibition arises at the dendrodendritic con-
tacts between mitral and tufted cells and the processes
of granule cells, which lie deeper still within the olfac-
tory bulb. These contacts are an example of two-way
synaptic feedback connections: the granule cells are
excited by mitral and tufted cells and, in turn, inhibit
them. Integration of olfactory information occurs when
excitation is spread throughout the multiple-branched
granule cell processes, and also when granule cells are
excited by the centrifugal efferent fibers that reach the
olfactory bulb from higher centers. Another factor in
this highly complex integrative process is the recurrent
collaterals of mitral cells that appear to excite mitral,
tufted, and granule cells.

There is a dramatic transformation in the response
to odors between the glomeruli and the mitral cells.
The glomeruli respond to different substances based on
their physiochemical properties, whereas mitral cells

8 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-7â•… Cranial Nerve and Neuro-Ophthalmologic Disorders

EYE

Horizontal section Tendon of medial
Zonular fibers (suspensory ligament of lens) rectus muscle

Perichoroidal space Hyaloid canal Ciliary part of retina
Ciliary body
Choroid and ciliary muscle
Bulbar conjunctiva
Sclera Scleral spur
Scleral venous
Fascial sheath sinus (canal of
of eyeball Schlemm)
(Tenon’s capsule) Iris
Episcleral space Lens

Fovea centralis Capsule
in macula (lutea) of lens
Meningeal sheath
of optic nerve Cornea
Subara-
chnoid Anterior
space chamber

Central retinal Vitreous body Posterior
artery and vein chamber
Iridocorneal
Optic nerve (II) angle
Lamina cribrosa of sclera Ciliary processes
Ora serrata
Tendon of lateral
rectus muscle

Section through retina Inner limiting membrane
Axons at surface of retina passing via optic nerve,
Cranial Nerve II: chiasm, and tract to lateral geniculate body
Optic Nerve
Ganglion cell

HUMAN EYE Müller cell (supporting glial cell)
The human eye is a highly developed sense organ con- Amacrine cell
taining numerous accessory structures that modify Bipolar cell
visual stimuli before they reach the photoreceptors. Horizontal cell
The extraocular muscles move the eyeball, thus causing Rod
the image of the object viewed to fall on the fovea, the Cone
retinal area of highest visual acuity. The shape of the Pigment cells of choroid
eyeball, its surfaces, and the refractive properties of
the tear film, cornea, lens, and aqueous and vitreous signals from the inner to the outer plexiform layer of reaching the surrounding area. Neither bipolar nor
humors assist in focusing the image on the retina. To the retina; horizontal cells are interneurons activated by horizontal cells generate action potentials; all informa-
allow viewing of near and far objects, this focus can be rods and cones and send their axons laterally to act on tion is transferred by changes in membrane potential,
adjusted by the action of the ciliary muscle, which neighboring bipolar cells. As a result of the actions of which spread passively through the cell bodies and
changes the shape of the lens. The intensity of the light horizontal cells, bipolar cells have concentric receptive axons.
reaching the retina is controlled by the muscles of the fields; that is, their membrane potentials are shifted in
iris, which vary the size of the pupillary aperture. Inci- one direction by light reaching the center of their The processes of bipolar cells that reach the outer
dent light must traverse most of the retinal layers before receptive field, and in the opposite direction by light plexiform layer form synapses with ganglion cells and
it reaches the photoreceptor cells lying in the outer part amacrine cells. Ganglion cells are output neurons whose
of the retina. Beyond the photoreceptors is a layer
of pigment cells, which eliminates back reflections by
absorbing any light passing through the photoreceptor
layer.

RETINA
The retina has several distinct layers. Rods and cones
form synaptic connections with bipolar and horizontal
cells. Bipolar cells are relay neurons that transmit visual

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 9

Plate 1-8â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
CRANIAL NERVE II AND VISUAL PATHWAYS

Visual system lesions Visual fields
Overlapping Ipsilateral optic nerve
visual fields lesion

Projection on Chiasm lesion
left retina (bitemporal hemianopia)

Projection on left Optic (II) Optic tract lesion
dorsal lateral nerves (left homonymous hemianopia)
Optic
geniculate nucleus chiasm

Meyer’s Optic Meyer’s
loop tracts loop
Lateral
geniculate Optic radiations (temporal lobe)
bodies (superior hemianopic defect)

Ipsilateral Optic radiations (parietal lobe)
6 (inferior hemianopic defect)
5
Cranial Nerve II: Optic 4
Nerve (Continued) 3
21

Contralateral

axons comprise the optic nerves and optic tracts; ama- Projection on left Optic radiations (complete)
crine cells are interneurons. Unlike other retinal neurons, occipital lobe (left homonymous hemianopia)
both amacrine and ganglion cells generate action
potentials. Localization Occipital lobe lesion
1. Unilateral vision loss: lesion of eye or optic sparing occipital pole
The photoreceptor cells are called rods and cones (macular-sparing
because of the shapes of their outer segments. Rods nerve homonymous hemianopia)
function as receptors in a highly sensitive, monochro- 2. Temporal visual field loss of both eyes:
matic visual system, whereas cones serve as receptors in with
the color vision system, which is less sensitive but more lesion at the chiasm
acute. Both receptors, however, are activated in a 3. Homonymous visual field loss of both eyes:
similar manner—they are hyperpolarized by photons of
light falling directly upon them. For example, the lesion posterior to the chiasm
detection of light in the rod begins with the absorption
of photons by the visual pigment, rhodopsin. Rhodopsin Calcarine fissure
is a combination of the protein, opsin and the cis isomer
of retinine, a compound derived from vitamin A. It is segment. The change in the receptor membrane trig- entire rod in a depolarized state). When light absorp-
located within the membranous lamellae of the rod’s gered in the rod by light absorption is not the typical tion provokes a decrease in Na+ permeability, the dark
outer segment, a highly modified cilium associated with increase in ion permeability most sensory receptors current is cut off and the rod becomes more hyper-
a typical basal body. Upon the absorption of a photon, undergo when activated; rather, there is a decrease in polarized. This hyperpolarization influences the synap-
rhodopsin is converted to lumirhodopsin, which is unsta- the permeability of the outer segment membrane to tic action of the rod on horizontal and bipolar cells.
ble and changes spontaneously to metarhodopsin, which sodium ions (Na+). In the absence of light, this perme- Polarization changes in one rod may also spread to
is then degraded by a chemical reaction known as ability is relatively high, and there is a steady inward neighboring receptors via electrical synapses. Any
bleaching. Rhodopsin lost by this bleaching process is flow of Na+ (the current flow resulting from this ionic photon that is successfully absorbed by photopigment
restored to its active form by enzymatic reactions that movement, known as the “dark current,” keeps the produces the same electrochemical result, regardless of
require metabolic energy and vitamin A. After a brief
time lag, the absorption of a photon leads to changes
in the ionic permeability of the membrane of the outer

10 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-9â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
OPTIC NERVE APPEARANCE

Normal optic nerve

Swollen optic nerve

Cranial Nerve II: Optic
Nerve (Continued)

the wavelength of that photon. However, the probabil- Pale optic nerve
ity that a photon will be absorbed by photopigment
varies considerably with the wavelength of the incident
light, and rhodopsin has a maximal absorbency for light
with a wavelength of 500╯nm. Cones may contain one
of three different photopigments, with a maximum
absorbency at 445╯nm (blue), 535╯nm (green), and
570╯nm (red). Cone pigments all contain cis retinine but
have different forms of opsin, which modify the light
absorption pattern. By analyzing the relative activity
produced by the three types of cones, the central
nervous system (CNS) is able to determine the wave-
length of the incident light, and a sensation of color
vision results.

RETINOGENICULOSTRIATE VISUAL PATHWAY in the right half of the visual field activate neurons in visual cortex. The upper field is represented in the
In mammals, most retinal ganglion cells send excitatory the left half of each retina. Ganglion cells from these lateral parts of the lateral geniculate nuclei and the
or inhibitory impulses via the optic nerves and tracts to areas project to the left lateral geniculate body, which inferior portions of the visual cortex, and the lower
the dorsal lateral geniculate nucleus of the lateral genicu- then projects to the left visual cortex. Input from both visual field is represented in the corresponding medial
late body of the thalamus, from where retinal informa- eyes is relayed by neurons in different layers of the and superior regions. The macula (central visual field)
tion is relayed to the primary visual cortex via the lateral geniculate body. Similarly, stimuli in the left half is represented in the central parts of the lateral genicu-
geniculostriate projection, or optic radiations. In man, this of the visual field are relayed to the right visual cortex. late nuclei and the posterior visual cortex, and in the
cortical area covers both walls of the posterior calcarine peripheral retina, in the peripheral parts of the lateral
fissure and adjacent parts of the occipital pole (Brod- The upper and lower visual fields are also topograph- geniculate nuclei, and the anterior visual cortex. The
mann’s area 17). The transmission of information from ically mapped onto the lateral geniculate body and
retina to visual cortex is topographically organized. Stimuli

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 11

Plate 1-10â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

RETINAL PROJECTIONS TO THALAMUS, MIDBRAIN, AND BRAINSTEM

Optic radiation To visual cortex
Optic tract From visual cortex
Optic chiasm
Optic (II) nerve Pulvinar
Pretectum
Brachium of
superior colliculus

Superior colliculus

Lateral geniculate body Accessory optic
(dorsal and ventral lateral tract
geniculate nuclei) Brachium
Nucleus of transpeduncular tract of inferior
colliculus
Cerebral peduncle Inferior
Transpeduncular tract colliculus
Nucleus reticularis tegmenti pontis Nucleus of
accessory
Pons optic tract
Superior
To thalamus Superior cerebellar
Mesencephalic colliculus peduncle
reticular formation

Cranial Nerve II: Optic Oculomotor nucleus Middle
Nerve (Continued) cerebellar
peduncle
fovea, the central spot of the macula, is represented by Medial pontine Inferior
a proportionally larger cortical area than the periphery reticular formation cerebellar
of the retina. peduncle
Pons Inferior olive

NEUROLOGIC DEFICITS OF THE RETINA Reticular formation Tectospinal tract
AND OPTIC NERVE Medulla
the optic radiations or striate cortex will cause partial
Neurologic deficits in the visual system can be localized CHIASMAL AND POSTCHIASMAL or complete contralateral homonymous hemianopic
by determining the type and extent of the resultant NEUROLOGIC DEFICITS defects.
visual field deficit. Retinal and optic nerve damage pro- Lesions at the optic chiasm will result in bitemporal VISUAL SYSTEM: RETINAL PROJECTIONS
duces vision loss in the affected eye. Most retinal lesions hemianopsia, caused by damage to the fibers from the The main retinal projection is to the dorsal lateral
will be visible on ophthalmoscopy of the ocular fundus. nasal segment of both retinas. Interruption of the optic geniculate nucleus, which then projects to the visual
Optic nerve lesions will produce central scotomas and tract (that portion of the visual pathways between the cortex. The retinogeniculostriate system thus formed is
visual field defects that might respect the horizontal chiasm and lateral geniculate body) results in a contra-
meridian. If the optic nerve is affected in its anterior lateral homonymous hemianopsia. Similarly, lesions of
portion (i.e., where it is visualized on ocular fundus-
copy), one may see swelling of the optic nerve head
during the acute phase of injury. If the retrobulbar
portion of the optic nerve is the site of injury, then the
optic nerve head (so-called “optic disc”) will look
normal acutely. After several weeks, injury to the optic
nerve anywhere along its course will manifest as relative
pallor of the optic nerve head. Unilateral or asymmetric
bilateral optic nerve damage will cause a relative affer-
ent pupillary defect (less transmission of light along the
more damaged optic nerve to the brain centers control-
ling pupillary constriction).

12 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-11â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
3LM[ YLSH[P]L HMMLYLU[ W\WPSSHY` KLMLJ[
7\WPSSHY` SPNO[ YLMSL_

Light

No light; both pupils dilate

Optic nerves Short
Optic chiasm ciliary
nerves
Ciliary
ganglion

Optic tract CN III Light in right eye; both pupils constrict
Red nucleus Light in left eye; both pupils dilate

Edinger-
Westphal

nucleus

Pretectal nucleus

Superior colliculus

Cranial Nerve II: Optic midline and runs caudally, sending terminals to the (which controls the degree of curvature of the lens).
Nerve (Continued) brainstem reticular formation and then continuing on The former is a subcortical reflex and relays in the
to cervical and thoracic levels as the tectospinal tract; accessory oculomotor (Edinger-Westphal) nucleus,
the basis for essentially the entire visual consciousness these fibers are probably involved in the orienting whereas the latter involves pathways through the cere-
in man. movements of the head and body. A second group of bral cortex. In the pupillary light reflex, afferent pupil-
fibers projects to the posterior thalamus (pulvinar), lary fibers leave the optic tract before the lateral
Other optic nerve fibers terminate within the superior which then projects to the cortical association areas. geniculate bodies, travel in the brachium of the superior
colliculus. This multilayered structure plays an impor- Fiber projections responsible for eye movements relay colliculus, and synapse in the pretectal nuclei (explain-
tant role in orienting the reactions that shift the head in the mesencephalic reticular formation below the ing why lesions of the geniculate bodies, the optic radia-
and eyes in order to bring an object of interest into the superior colliculus (vertical eye movements), and in the tions, or the visual cortex do not affect the pupillary
center of the visual field. In addition to direct optic paramedian pontine reticular formation (horizontal eye reactivity, and why lesions of the brachium of the supe-
nerve input, the superior colliculus receives indirect movements). rior colliculus can cause a relative afferent pupillary
visual input via the visual cortex. As is the case through- defect without causing a visual field defect). Both pre-
out the visual system, this input is topographically orga- PUPILLARY LIGHT REFLEX AND tectal nuclei receive input from both eyes, and each
nized so that each point within the colliculus corresponds THE ACCOMMODATION REFLEX sends axons to both Edinger-Westphal nuclei. Parasym-
to a particular region within the visual field. Collicular The pretectum, like the superior colliculus, receives pathetic fibers for pupillary constriction leave the
neurons tend to respond best to interesting or moving visual information from optic nerve fibers not destined Edinger-Westphal nucleus and travel along the ipsilat-
stimuli, and the discharge of neurons in the deeper to synapse in the lateral geniculate bodies. This area is eral third cranial nerve to the ipsilateral ciliary ganglion
layers of the colliculus is closely related to the orienting involved in the pupillary light reflex (which regulates within the orbit. The postganglionic parasympathetic
movements of the eyes evoked by such stimuli. the size of the pupil) and the accommodation reflex fibers innervate the pupillary constrictor muscle and the
ciliary muscle for accommodation.
The deeper collicular layers are the source of several
efferent projections. One group of fibers crosses the

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 13

P late 1-12â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

OCULOMOTOR (III), TROCHLEAR (IV), AND ABDUCENS NERVES (VI)

Cranial Nerves III, IV, and VI Long ciliary nerve Ciliary ganglion Abducens nucleus
(Oculomotor, Trochlear, Posterior ethmoidal nerve
and Abducens) Short ciliary nerves
Sensory root of ciliary ganglion Trochlear nucleus
OCULOMOTOR NERVE Anterior ethmoidal nerve
The oculomotor nerve carries somatic motor fibers to Superior oblique muscle Sympathetic root of ciliary ganglion Oculomotor nucleus
the levator palpebrae superioris muscle and to the Superior division of
medial, superior, and inferior rectae muscles, and to the Levator palpebrae oculomotor nerve Accessory oculomotor
inferior oblique muscle. It also conveys important para- superioris muscle (Edinger-Westphal)
sympathetic fibers to intraocular structures, such as the Superior Frontal nerve (cut) nucleus (parasympathetic)
sphincter pupillae and ciliary muscles, and is joined by rectus muscle
sympathetic fibers from the internal carotid plexus,
which are distributed with its branches. Some oculoÂ

Plate 1-13â•… Cranial Nerve and Neuro-Ophthalmologic Disorders

NERVES OF ORBIT AND CAVERNOUS SINUS

Superior view Medial branch Supraorbital nerve
Supratrochlear nerve Lateral branch
Medial rectus muscle
Cranial Nerves III, IV, and VI Superior oblique muscle Levator palpebrae superioris muscle
(Oculomotor, Trochlear, Infratrochlear nerve Superior rectus muscle
and Abducens) (Continued) Lacrimal gland
Nasociliary nerve Lacrimal nerve
ciliary nerves that penetrate the sclera around the optic Trochlear nerve (IV) Lateral rectus muscle
nerve and continue forward in the perichoroidal space Common tendinous ring (of Zinn) Frontal nerve
to supply the ciliaris and sphincter pupillae muscles and Ophthalmic nerve (V1) Maxillary nerve (V2)
the intraocular vessels.
Optic nerve (II) Meningeal branch of maxillary nerve
The sensory and sympathetic roots of the ciliary ganglion Internal carotid artery
are derived from the nasociliary nerve and the internal and nerve plexus Mandibular nerve (V3)
carotid vascular nerve plexus, but they do not always Oculomotor nerve (III) Lesser petrosal nerve
join the ganglion. Instead, their fibers may reach the Meningeal branch of mandibular nerve
eye by joining the ciliary nerves directly, while the sym- Trochlear nerve (IV) Greater petrosal nerve
pathetic fibers (already postganglionic after relaying in Abducens nerve (VI)
the superior cervical trunk ganglia) may follow the oph- Tentorium cerebelli Trigeminal (semilunar) ganglion
thalmic artery and its branches to their destinations. Tentorial (meningeal) branch of ophthalmic nerve
The sensory fibers convey impulses from the cornea, iris, Superior view: levator palpebrae superioris, superior
and choroid and the intraocular muscles. rectus, and superior oblique muscles partially cut away Long ciliary nerves
TROCHLEAR NERVE Short ciliary nerves
The trochlear nerve is slender, and its nucleus of origin Supratrochlear nerve J\[ Lacrimal nerve
is located in the midbrain just caudal to the oculomotor Supraorbital nerve branches J\[ Ciliary ganglion
nuclei. The trochlear fibers curve posterolaterally and Parasympathetic root of ciliary ganglion
slightly caudally around the cerebral aqueduct to reach Infratrochlear nerve (from inferior branch of oculomotor nerve)
the upper part of the superior medullary velum; here Anterior ethmoidal nerve Sympathetic root of ciliary ganglion
the nerve fibers from opposite sides decussate before (from internal carotid plexus)
emerging on either side of the frenulum veli, below the Optic nerve (II) Sensory root of ciliary ganglion
inferior colliculi. No other cranial nerves emerge from Posterior ethmoidal nerve (from nasociliary nerve)
the dorsal aspect of the brainstem. Superior branch of Branches to inferior and medial
oculomotor nerve (III) J\[ rectus muscles
Each trochlear nerve winds forward around the mid- Abducens nerve (VI)
brain below the free edge of the tentorium cerebelli, Nasociliary nerve Inferior branch of oculomotor nerve (III)
passes between the superior cerebellar and posterior Internal carotid plexus Lacrimal nerve
cerebral arteries and above the trigeminal nerve, and Trochlear nerve (IV) (J\[) Meningeal branch (V2)
pierces the inferior surface of the tentorium near its Oculomotor nerve (III)
attachment to the posterior clinoid process to run Frontal nerve (J\[)
forward in the lateral wall of the cavernous sinus Abducens nerve (VI) Ophthalmic nerve (V1)
between the oculomotor and ophthalmic nerves. The
nerve enters the orbit through its superior fissure, Internal carotid artery Meningeal branch (V3)
immediately lateral to the common annular tendon,
and passes medially between the orbital roof and the Oculomotor (III) nerve Optic chiasm
levator palpebrae superioris to supply the superior Diaphragma sellae
oblique muscle. Proprioceptive fibers are transferred Trochlear (IV) nerve Pituitary gland
through a communication with the ophthalmic nerve
to the trigeminal nerve. The trochlear nerve usually Internal carotid artery
receives sympathetic filaments from the internal carotid
nerve plexus. Abducens (VI) nerve

Ophthalmic nerve

Cavernous sinus

Maxillary nerve

ABDUCENS NERVE upward in front of the pons, usually behind the inferior orbit through the superior orbital fissure, within the
The abducens nerve arises from the abducens nucleus, cerebellar artery. Near the apex of the petrous part of common annular tendon, and ends by supplying the
which is located in the pons, subjacent to the facial the temporal bone, the nerve bends sharply forward lateral rectus muscle.
colliculus in the upper half of the floor of the fourth above the superior petrosal sinus to enter the cavernous
ventricle. The nucleus is encircled by fibers of the sinus, where it lies adjacent to the internal carotid The abducens has a relatively long intracranial
homolateral facial nerve. The abducens nerve fibers artery. There the abducens may transfer proprioceptive route in the posterior cranial fossa and cavernous
pass forward to emerge near the midline through the fibers to the ophthalmic branch of the trigeminal nerve sinus. Consequently, it is vulnerable to increases in
groove between the pons and the pyramid of the and receive sympathetic filaments from the internal intracranial pressure and to pathologic or traumatic
medulla oblongata. Each abducens nerve then inclines carotid nerve plexus. The abducens nerve enters the lesions affecting nearby parts of the brain, skull, or
sinus.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 15

Plate 1-14â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
CONTROL OF EYE MOVEMENTS

Excitatory endings
Inhibitory endings

Frontal eye fields Parieto-
occipito-
temporal
eye fields

Interstitial Superior oblique
nucleus of muscle
Cajal

Superior Superior
colliculus rectus
Oculomotor muscle

nucleus Medial

Control of Eye Movements Abducens longitudinal
internuclear fasciculus
projections

Oculomotor (III) nerve

The extraocular muscles responsible for eye move- Trochlear (IV) nerve
ments are controlled by motor neurons located in Medial rectus muscle
various nuclei. Thus the lateral rectus is controlled by Cortical projections Lateral
the abducens nucleus, the superior oblique by the Trochlear rectus
trochlear nucleus, and the superior, inferior, and medial nucleus Medial muscle
longitudinal
recti and the inferior oblique muscles by the oculomo- fasciculi
tor nucleus. Both smooth (pursuit) and rapid (saccadic) Medial Ascending tract
eye movements depend on patterns of activity produced longitudinal of Dieters
in these muscles by direct projections from the vestibu- fasciculi
lar nuclei and the reticular formation, and by indirect
activation from the superior colliculus and the cerebral Abducens nucleus
cortex.
The medial and lateral rectus muscles move the eyeball Superior Vestibular Inferior Inferior
Medial nuclei oblique rectus
horizontally, causing the cornea to look medially or Lateral muscle muscle
laterally. The actions of the superior and inferior rectus Inferior
muscles and those of the oblique muscles are more
complicated. The superior and inferior rectus muscles
move the eyeball upward and downward, respectively.
Because they are disposed at an angle of about 20
degrees to the sagittal plane (due to the long axis of each Vestibular nerve
orbit being directed slightly outward), they also impart
a minor degree of rotation to the eyeball (intorsion for
the superior rectus and extorsion for the inferior rectus). Abducens (VI) nerve

When the eyeball is abducted, the superior and inferior Paramedian pontine
rectus muscles purely elevate and depress the eyeball. reticular formation
The inferior oblique muscle rotates the eyeball outward
(excyclotorsion) and elevates the eyeball when it is
adducted. However, an exact idea of the actions of the
extrinsic eye muscles cannot be obtained by considering
each muscle separately because, under normal circum- action of turning the head excites vestibular afferent fibers
stances, none of the six extraocular muscles acts alone. VESTIBULAR PROJECTIONS IMPORTANT FOR from semicircular canal receptors. Fibers from an indi-
Consequently, all eye movements are the result of VISUAL FIXATION vidual semicircular canal excite two specific groups of

highly integrated and delicately controlled agonist and The vestibular projection is important for the mainte- relay neurons in the vestibular nuclei. One group excites
antagonist activities. The actions of individual muscles nance of visual fixation during head movements. To the extraocular motor neurons that cause the eyes to
have been determined from studies of congenital effect smooth movement, tracking, and proper visual- move in the direction opposite to the head movement,
defects or from functional disturbances caused by ization, the contraction of one eye muscle must be and the other group inhibits motor neurons that acti-
disease or injury to the nerve supply. accompanied by the relaxation of its antagonist. The vate movement of the eyes in the same direction as the

16 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-15â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
CONTROL OF EYE MOVEMENTS—PATHOLOGY

Right abducens nucleus lesion: Right MLF lesion:
right horizontal gaze palsy right internuclear ophthalmoplegia
XX
X

Right R Left L R Right L Left
lateral medial medial Lateral
rectus rectus rectus rectus
muscle muscle muscle muscle

Cortical projection
/VYPaVU[HS ZHJJHKLZ

Oculomotor (III)
nerve and nucleus

Abducens Abducens internuclear projections
(VI) nerve
Medial Lesion in
Facial longitudinal
(VII) nerve fasciculus (MLF) right MLF

Control of Eye Movements fascicles Cortical projection VI nerve
Lesion in /VYPaVU[HS W\YZ\P[ Abducens
(Continued) (VI) nucleus
right VI Vestibular nucleus
head. For example, turning the head to the right will nucleus /VYPaVU[HS =69
excite fibers from the right horizontal semicircular
canal, which, in turn, will activate neurons in the right Paramedian pontine
medial and lateral vestibular nuclei. Some of these ves- reticular formation
tibular neurons will then excite motor neurons control- /VYPaVU[HS ZHJJHKLZ
ling the right medial and left lateral rectus muscles.
Other vestibular neurons will inhibit motor neurons Right abducens nucleus lesion: Right MLF lesion:
controlling the right lateral rectus and internuclear right horizontal gaze palsy right internuclear ophthalmoplegia
neurons controlling the left medial rectus. The result
will be a compensatory movement of both eyes to the Absent right
left. The vestibulocerebellum modulates the vestibulo– gaze in
extraocular reflex in such a way that the resulting eye both eyes
movement precisely compensates for the head move-
ment and thus keeps the gaze fixed on the same point. Nystagmus
of abducting
The connections of the right vestibular nuclei to the left eye
abducens, trochlear, and oculomotor nuclei can be divided
into two sections. The first section comprises vestibular No adduction
projections to motor neurons supplying the superior of right eye
and inferior rectus and superior and inferior oblique
muscles. These motor neurons all receive excitatory and pursuit eye movements that do not involve the crossed pathway. Pathways from the frontal and parietal
input from the contralateral medial nucleus and inhibi- vestibular nuclei. These pathways ultimately converge eye fields descend via the superior colliculus into the
tory input from the ipsilateral superior nucleus. The on the final common pathways for horizontal and verti- brainstem and cross at the level of the midbrain–pontine
innervation of medial and lateral rectus motor neurons, cal ocular motor control also used in the vestibulo- junction to synapse on the contralateral paramedian
which mediate horizontal eye movements, is organized ocular system, but initially via different anatomic pontine reticular formation. The paramedian pontine
differently. The medial vestibular nucleus sends excit- pathways. For example, saccadic eye movements (fast reticular formation projects to the ipsilateral abducens
atory fibers to the contralateral abducens nucleus and conjugate eye movements to a fixed target, either vol- nucleus, from which abducens neurons project to the
inhibitory fibers to the ipsilateral abducens nucleus. untary or reflex in origin) are initiated in the frontal and ipsilateral lateral rectus muscle, whereas abducens
These fibers excite or inhibit the lateral rectus motor parietal lobes. The horizontal saccade pathway is a interneurons project cross the midline to ascend in the
neurons and another group of neurons within the abdu-
cens nucleus, the internuclear neurons, which project
to the opposite oculomotor nucleus to excite the medial
rectus motor neurons. The latter neurons are also
excited by fibers that originate in the lateral vestibular
nucleus and pass upward in the ascending tract of
Deiters.

In addition to the pathways described above, each
ocular motor nucleus also receives input for saccadic

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 17

Plate 1-16â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
CONTROL OF EYE MOVEMENTS—PATHOLOGY (CONTINUED)

Pineal mass
Superior
colliculus

Control of Eye Movements

(Continued)

contralateral medial longitudinal fasciculus and synapse Upgaze deficit
on the medial rectus subnucleus of the contralateral
oculomotor nucleus. The pathways for vertical saccades
involve the rostral interstitial nucleus of the medial
longitudinal fasciculus, the interstitial nucleus of Cajal,
the posterior commissure, and the nucleus of the pos-
terior commissure.

In contrast to the saccadic pathways, the pathways for
horizontal smooth pursuit (conjugate maintenance of
fixation of the eyes while following a moving target)
descend ipsilaterally from cortical centers of eye move-
ment control to synapse directly on the abducens
nucleus, and from there to the ipsilateral abducens
nerve and lateral rectus and the contralateral oculomo-
tor nerve and medial rectus. This internuclear connec-
tion between the abducens nucleus and the contralateral
oculomotor nucleus via the medial longitudinal fascicu-
lus is the final common pathway responsible for conju-
gate horizontal gaze, whether initiated reflexively via
the vestibulo-ocular system or voluntarily via the sac-
cadic or pursuit systems.

NEUROLOGIC DEFICITS Posterior midbrain syndrome (with upgaze palsy and lid retraction) secondary to a pineal mass
Eye movement disorders from brainstem involvement
of the pathways subserving horizontal and vertical gaze fasciculus will disrupt only the abducens interneuron with pineal tumors. If the posterior commissure is pri-
are usually exquisitely localizing. For example, a lesion projections, and therefore the patient will have all eye marily involved, these patients may have selective
in the right abducens nucleus will cause a complete loss movements intact except for poor adduction of the absence of upward eye movements with preservation of
of gaze of either eye toward the right (usually with an right eye (poor movement of the right eye toward the all other eye movements. Associated clinical abnormali-
associated ipsilateral lower motor neuron facial palsy nose), a so-called internuclear ophthalmoplegia. ties include upper lid retraction and nonreactive pupils
because the fascicles of the facial nerve wrap around the to light with intact pupillary constriction when viewing
abducens nucleus before exiting the brainstem), whereas Vertical gaze may be selectively abnormal, with a near target (all part of the so-called dorsal midbrain
a lesion of just to the right paramedian pontine reticular lesions in the midbrain and pretectal area, especially syndrome).
formation will cause an absence of voluntary and reflex from compression from above, such as typically seen
saccades to the right, with relative preservation of the
vestibulo-ocular reflex (VOR) and pursuit eye move-
ments. A lesion of the right medial longitudinal

18 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-17â•… Cranial Nerve and Neuro-Ophthalmologic Disorders

CILIARY GANGLION

Sphincter pupillae muscle Short ciliary nerves Oculomotor Accessory oculomotor
Dilator pupillae muscle (parasympathetic) (Edinger-Westphal)
Ciliary muscle Ciliary root of ciliary ganglion nucleus (parasympathetic)
ganglion

Superior colliculus

Lateral
geniculate body

Autonomic Innervation Optic nerve (II) Ophthalmic Tympanic
of the Eye nerve (V1) plexus
Nasociliary nerve Tectospinal tract
Sympathetic Fibers. The sympathetic preganglionic Long ciliary nerve Trigeminal Thoracic part
fibers for the eye emerge in the ipsilateral first and Nasociliary (sensory) ganglion of spinal cord
second, and occasionally in the third, thoracic spinal root of ciliary ganglion Internal
nerves. They pass through white or mixed rami com- Sympathetic root of ciliary ganglion carotid plexus Preganglionic
municantes to the sympathetic trunks in which the Internal sympathetic
fibers ascend to the superior cervical ganglion, where Ophthalmic artery carotid artery cell bodies
they relay, although a proportion may form synapses in inter-
higher up in the internal carotid ganglia. The postgan- Superior cervical sympathetic ganglion mediolateral
glionic fibers run either in the internal carotid plexus and Dorsal root ganglion nucleus
reach the eye in filaments that enter the orbit through (lateral
its superior fissure, or else they run alongside the oph- First thoracic sympathetic trunk ganglion horn) of gray
thalmic artery in its periarterial plexus. matter
Preganglionic Gray ramus communicans
Some of the filaments passing through the superior Postganglionic White ramus communicans
orbital fissure form the sympathetic root of the ciliary
ganglion; their contained fibers pass through it without T1 spinal nerve
relaying to become incorporated in the 8 to 10 short
ciliary nerves. Other filaments join the ophthalmic nerve Sympathetic
or its nasociliary branch and reach the eye in the two fibers
to three long ciliary nerves that supply the radial muscu-
lature in the iris (dilator pupillae). Both long and short Preganglionic Parasympathetic
ciliary nerves also contain afferent fibers from the Postganglionic fibers
cornea, iris, and choroid. Fibers conveyed in the short Afferent fibers
ciliary nerves pass through a communicating ramus Visual pathway
from the ciliary ganglion to the nasociliary nerve; this Descending pathway
ramus is called the sensory root of the ciliary ganglion. The
parent cells of these sensory fibers are located in the Interruption of the sympathetic fibers causes Left dilated pupil with no other sign
trigeminal (semilunar) ganglion, and their central pro- ipsilateral ptosis, anhidrosis, and miosis without
cesses end in the sensory trigeminal nuclei in the brain- abnormal ocular motility (Horner syndrome)
stem. The sensory trigeminal nuclei have multiple
interconnections with other somatic and autonomic ciliary nerves and are distributed to the constrictor fibers the sympathetic chain is disrupted, there may also be
centers and thus influence many reflex reactions. Other of the iris (sphincter pupillae), to the ciliary muscle, and loss of sweating on the ipsilateral face. A lesion of the
sympathetic fibers from the internal carotid plexus to the blood vessels in the coats of the eyeball. ciliary ganglion will cause disruption of the parasympa-
reach the eye through the ophthalmic periarterial thetic fibers to the pupillary constrictor muscle, and
plexus and along its subsidiary plexuses around the Neurologic Disorders. Disruption of the sympathetic there will be isolated enlargement of the ipsilateral
central retinal, ciliary, scleral, and conjunctival innervation to the eye at any level along the sympa- pupil, especially notable in lighted conditions, but no
arteries. thetic pathways will result in a Horner syndrome, in findings such as ptosis or extraocular muscle weakness
which the pupil on the involved side is smaller and to suggest a lesion along the course of the oculomotor
Parasympathetic Fibers. The parasympathetic pre- dilates poorly, especially notable in the dark, and the nerve.
ganglionic fibers for the eye are the axons of cells in upper lid droops slightly (ptosis). Depending on where
the accessory, or autonomic, (Edinger-Westphal) oculomotor
nucleus. They run in the third cranial nerve and exit in
the motor root of the ciliary ganglion, where they relay.
The axons of these ganglionic cells are postganglionic
parasympathetic fibers, which reach the eye in the short

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 19

Plate 1-18â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

Efferent fibers TRIGEMINAL NERVE (V) Trigeminal nerve (V) ganglion and nuclei
Afferent fibers Motor nucleus
Proprioceptive fibers Ophthalmic nerve (V1) Mesencephalic nucleus
Parasympathetic fibers Tentorial (meningeal) branch Principal sensory nucleus
Sympathetic fibers Spinal tract and nucleus
Nasociliary nerve
Lacrimal nerve
Sensory root of ciliary ganglion
Frontal nerve
Ciliary ganglion
Posterior ethmoidal nerve
Long ciliary nerve
Short ciliary nerves
Anterior ethmoidal nerve
Supraorbital nerve
Supratrochlear nerve
Infratrochlear nerve
Internal nasal branches and
External nasal branches
of anterior ethmoidal nerve

Maxillary nerve (V2) Facial nerve (VII)
Chorda
Meningeal branch tympani nerve
Zygomaticotemporal nerve
Zygomaticofacial nerve Submandibular Inferior Superficial
ganglion alveolar nerve temporal branches
Zygomatic nerve Nerve to mylohyoid Articular branch
Infraorbital nerve Otic ganglion and anterior
Pterygopalatine ganglion Mandibular nerve (V3) Tensor tympani nerve auricular nerves
Superior alveolar branches of infraorbital nerve Auriculotemporal nerve
Nasal branches (posterior superior lateral, Parotid branches
nasopalatine, and posterior superior medial) Meningeal branch
Nerve (vidian) of pterygoid canal Lesser petrosal nerve (from
(from facial nerve [VII] and carotid plexus) glossopharyngeal nerve [IX])

Pharyngeal branch
Greater and lesser palatine nerves

Deep temporal nerves (to temporalis muscle)
Lateral pterygoid and masseteric nerves

Tensor veli palatini and medial pterygoid nerves
Buccal nerve
Mental nerve

Inferior dental plexus
Lingual nerve

Cranial Nerve V: mastication and sensory innervation to the face and and facial muscles. The smaller medial motor root sup-
Trigeminal Nerve mucous membranes of the nasal and oral cavities. plies muscles derived from the first branchial arch: the
masticatory muscles, the mylohyoid, the anterior belly
ANATOMY The trigeminal nerve emerges from the anterolateral of the digastric, the tensor veli palatine, and tensor
The trigeminal nerve is the largest cranial nerve and aspect of the upper pons. The large sensory root tympani. Numerous parasympathetic and sympathetic
gives rise to three major branches: the ophthalmic, conveys sensation from most of the face and scalp; parts fibers join branches of the trigeminal nerve through
maxillary, and mandibular nerves. It is a mixed nerve of the auricle; and the external acoustic meatus, the interconnections with the oculomotor (III), trochlear
that provides motor innervation to the muscles of nasal, and oral cavities; teeth; temporomandibular joint; (IV), facial (VII), and glossopharyngeal (IX) nerves.
nasopharynx; and most of the meninges in the anterior The sensory and motor roots emerge from the pons and
and middle cranial fossae. It carries proprioceptive travel over the superior border of the petrous temporal
impulses from masticatory and, likely, from extraocular

20 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-19â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
TRIGEMINAL NUCLEI: AFFERENT AND CENTRAL CONNECTIONS
Internal
capsule Cerebral cortex:
postcentral gyrus
Centromedian nucleus (intralaminar)
Ventral posteromedial (VPM )
nucleus of thalamus

Cranial Nerve V: Trigeminal Midbrain Trigeminal mesencephalic nucleus
Nerve (Continued) Dorsal trigeminal Trigeminal motor nucleus
lemniscus (dorsal
bone near its apex. The sensory root expands into the trigeminothalamic tract) Principal sensory trigeminal nucleus
semilunar-shaped trigeminal ganglion (gasserian gan- Ventral trigeminal Touch, pressure
glion) and contains pseudounipolar cells with periph- lemniscus (ventral Pain, temperature
eral processes conveying sensory impulses from the face trigeminothalamic tract) Proprioception: from muscle spindles
and head structures through the three major trigeminal Trigeminal (semilunar) ganglion
divisions. Pontine Ophthalmic n.
reticular Maxillary n.
The central processes coalesce to form the sensory formation Sensory root and
root, which enters the brainstem to end in one of three Pons motor root of
major nuclear complexes, the spinal (inferior) trigemi- mandibular n.
nal nucleus, the principal sensory (pontine) nucleus, or Medullary reticular formation:
the mesencephalic nucleus. The spinal tract of the tri- Lateral reticular formation Facial
geminal nucleus descends from the pons, through the Medial reticular formation (VII) n.
medulla, and into the spinal cord, where it is contiguous
with Lissauer’s tract. The spinal tract gives off fibers to Ventral trigeminal Glosso-
the medially located nucleus of the spinal tract of the lemniscus pharyngeal
trigeminal nerve. The spinal nucleus of the trigeminal (IX) n.
nerve receives pain, temperature, and soft touch input Spinal (descending)
from the face and mucous membranes. From the spinal trigeminal tract
nucleus, the ascending fibers travel ipsilaterally in the
trigeminothalamic tract to the ventral posteromedial Spinal (descending)
(VPM) and intralaminar nucleus of the thalamus. Pro- trigeminal nucleus
jections ascend to the proximal sensory cortex for pain Dorsolateral fasciculus
and temperature perception.
(of Lissauer)
The principal sensory nucleus, which is located in the
lateral pons, receives tactile and proprioceptive sensa- Cervical spinal cord
tion. It gives off fibers that travel in the trigeminal
lemniscus and the uncrossed dorsal trigeminothalamic Vagus (X) n.
tract, both of which terminate in the VPM nucleus of Substantia gelatinosa (lamina II)
the thalamus. It is represented bilaterally in the cortex.
extends from the main sensory nucleus to the superior The ophthalmic nerve (V1) collects pain, tempera-
The mesencephalic nucleus contains cell bodies that colliculus of the mesencephalon. ture, touch, and proprioceptive information from the
carry proprioceptive input from masticatory and extra- upper third of the face, top of the nose, scalp regions,
ocular muscle spindles. It is the only place in the central The motor fibers originate in the trigeminal motor and adjacent sinuses. It is joined by filaments from the
nervous system (CNS) where cell bodies of primary nucleus. The sensory and motor roots of the trigeminal internal carotid sympathetic plexus and communicates
sensory afferents are found in the CNS and not in nerve leave the pons and pass through Meckel’s cave with the oculomotor, trochlear, and abducens nerves as
sensory ganglia. The trigeminal mesencephalic nucleus to form the trigeminal ganglion. This ganglion then it runs forward in the lateral wall of the cavernous sinus.
divides into the three nerve trunks: the ophthalmic, Near its origin, it gives off a small recurrent tentorial
maxillary, and mandibular nerves. The small motor root (meningeal) branch to the tentorium cerebelli and then
passes under the ganglion to join the mandibular nerve.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 21

Plate 1-20â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
TRIGEMINAL NUCLEI: CENTRAL AND PERIPHERAL CONNECTIONS

Postcentral gyrus Thalamus
Precentral gyrus
Mesencephalic nucleus of V
Principal sensory nucleus of V

Ophthalmic Divisions
of trigeminal
Maxillary
Mandibular nerve V

Cranial Nerve V: Trigeminal Motor nucleus of V From cheek
Nerve (Continued) Nucleus of VII From upper teeth,
jaw, gum, palate
divides into the lacrimal, frontal, and nasociliary Nucleus of C1 VII To temporalis,
branches, which enter the orbit through the superior tractus solitarius C2 IX masseter,
orbital fissure. pterygoids
Nucleus of XII X
The maxillary nerve (V2) is larger than the ophthal- XII From tongue
mic nerve and is also sensory. It supplies the side of the Spinal tract and nucleus of V (anterior part)
forehead, medial cheek, side of the nose, upper lip, To muscles of tongue (lingual nerve)
palate, upper teeth, nasopharynx, anterior and medial
cranial fossae, meninges, and the skin overlying the To infrahyoid muscles To mylohyoid and digastric
maxilla. As with the other branches of the trigeminal (fix hyoid bone) (anterior belly)
nerve, it serves as a vehicle for the distribution of auto-
nomic fibers to the skull structures. The maxillary nerve From tongue (posterior part) From lower teeth, jaw, gum
gives off a small meningeal branch to the meninges of (inferior alveolar nerve)
the middle cranial fossa before passing through the
lower part of the lateral wall of the cavernous sinus. It To buccinator and orbicularis oris
then leaves the skull through the foramen rotundum
and enters the pterygopalatine fossa, where it commu- Somatic efferents
nicates with the pterygopalatine ganglion before
branching into different directions. In the pterygopala- Afferents and
tine fossa, the maxillary nerve superiorly gives off the CNS connections
zygomatic nerve (with the zygomaticotemporal and
zygomaticofacial branches), and inferiorly the superior Indefinite paths
posterior alveolar nerves. The superior middle and
superior anterior alveolar nerves arise from the infraor- Proprioception
bital part of the nerve that descend in the wall of the
maxillary sinus between the bone and the mucous mem- The mandibular nerve (V3) is the largest branch of through the foramen ovale and unite to form a short
brane, with dental and gingival rami uniting to form the the trigeminal nerve and consists of a large sensory root nerve that lies between the lateral pterygoid and tensor
superior dental plexus of the upper teeth and gums. The and a small trigeminal motor root. The sensory portion veli palatine muscles, anterior to the middle meningeal
maxillary nerve ultimately moves anterolaterally across innervates the cheeks, chin and lower lip, gums, inferior artery. The small otic ganglion closely adheres to the
the upper part of the posterior surface of the maxilla to teeth, mucous membranes of the mouth, anterior two medial side of the nerve. Just below the foramen, the
traverse the inferior orbital fissure on the way to the thirds of the tongue, side of the head, lower jaw, ante- mandibular nerve gives off a meningeal branch (nervus
orbit. It then passes through the infraorbital groove as rior wall of the external auditory meatus, external wall spinosus). It supplies the meninges of the middle and
the infraorbital nerve, with the external and internal of the tympanic membrane, and the temporomandibu- anterior cranial fossae and calvaria, and the mucous
nasal, inferior palpebral, and superior labial branches, lar joint. The sensory and motor parts leave the skull membrane of the mastoid air cells. The nerve to the
which supply the nasal alae, lower lid, upper lip skin,
and mucous membranes, respectively.

22 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-21â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
OPHTHALMIC (V1) AND MAXILLARY (V2) NERVES

Communicating branch Anterior ethmoidal nerve
Posterior ethmoidal nerve Supraorbital nerve
Long and short ciliary nerves Supratrochlear nerve
Ciliary ganglion Lacrimal gland
Lacrimal nerve Infratrochlear nerve
Nasociliary nerve (from nasociliary nerve)
Frontal nerve Cutaneous branch
Meningeal branch of lacrimal nerve
Tentorial branch
Ophthalmic Zygomaticotemporal
nerve (V1) nerve
Zygomaticofacial
Trigeminal (semi- nerve External nasal
lunar) ganglion
Trigeminal branch of
nerve (V) anterior
ethmoidal
nerve

Cranial Nerve V: Trigeminal Foramen Infraorbital nerve
Nerve (Continued) rotundum

medial pterygoid muscle sends fibers through the otic Foramen ovale Anterior superior
ganglia without relay to supply the tensor veli palatine Mandibular nerve (V3) alveolar nerve
and tensor tympani muscles. The main mandibular
nerve divides into a small anterior and a larger posterior Maxillary nerve (V2) Nasal branch
part. The anterior part contains primarily motor fibers Nerve (vidian) of pterygoid canal
through the nerve to the lateral pterygoid and two or Mucous membrane
three deep temporal nerves that innervate the tempo- Zygomatic nerve of maxillary sinus
ralis muscle. The anterior portion has one sensory Dental and gingival branches
branch, the buccal nerve, which innervates the areas of
skin overlying the buccinators muscle and the mucous Pterygopalatine ganglion Superior dental plexus
membranes beneath. The posterior part of the man-
dibular nerve is primarily sensory and divides into the Greater and lesser palatine nerves Infraorbital nerve entering
auriculotemporal, lingual, and inferior alveolar nerves. Ganglionic branches to pterygopalatine ganglion infraorbital canal
The mylohyoid muscle and the anterior belly of the Middle superior alveolar nerve
digastrics are supplied by a few motor fibers that are
distributed in the mylohyoid branch of the inferior Posterior superior alveolar nerve
alveolar nerve. At its origin, the auriculotemporal nerve
divides in two around the middle meningeal artery. It including the lingual surfaces of the lower gums. The gingival rami, which arise from the nerve as it passes
ends in the superficial temporal branches that supply branches communicate with the terminal branches of through the mandibular canal. The latter are delicate
the skin and fascia of the temple and adjacent areas the glossopharyngeal and hypoglossal nerves. The infe- nerves that unite to form the inferior dental plexuses
of the scalp. The auriculotemporal nerve also gives rior alveolar nerve descends behind the lingual nerve. supplying the lower teeth and gums. They may be
branches to the temporomandibular joint, the external It gives off its only motor branch, the mylohyoid nerve, joined by branches of the buccal and lingual nerves or
acoustic meatus, and the tympanic membrane, and an before entering the canal. The mylohyoid nerve sup- by filaments from nerves supplying the muscles attached
anterior auricular branch to the skin of the tragus and plies the mylohyoid muscle and the anterior belly of the to the mandible. These branches may carry sensory
part of the helix. It supplies filaments containing secre- digastric. The other branches of the inferior alveolar fibers, which explains why blocking the inferior alveolar
tomotor and vasomotor fibers to the parotid gland, nerve are the mental nerve and inferior dental and nerve alone does not always anesthetize the lower teeth.
which reach the nerve through the otic ganglion. Sensa-
tion to the anterior two thirds of the tongue and floor
of the mouth is carried by the lingual nerve. It is joined
near its origin by the chorda tympani, a branch of the
facial nerve, which conveys taste from the part of the
tongue anterior to the V-shaped sulcus terminalis.
The lingual nerve supplies the mucous membrane of
the anterior two thirds of the tongue, lower part of the
isthmus of the fauces, and the floor of the mouth,

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 23

Plate 1-22â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II

MANDIBULAR NERVE (V3)

Lateral view

Anterior division Temporal fascia Posterior Deep temporal nerves
Posterior division and temporalis muscle Anterior
Foramen ovale
Masseteric nerve

Meningeal branch Lateral pterygoid
nerve and muscle
Foramen spinosum
Buccal nerve
Middle and buccinator
meningeal artery muscle (cut)
Auriculo- Submandibular
temporal ganglion
nerve Sublingual
Posterior gland
auricular nerve Mylohyoid
Facial nerve (VII) muscle (cut)
Mental nerve
Chorda tympani nerve
Inferior alveolar nerve (cut)
Lingual nerve Digastric muscle (anterior belly)
Inferior alveolar nerve (cut)

Nerve to mylohyoid
Medial pterygoid muscle (cut)
Digastric muscle (posterior belly)

Stylohyoid muscle

Cranial Nerve V: Trigeminal Hypoglossal nerve (XII)
Nerve (Continued) Submandibular gland

Sublingual nerve

TRIGEMINAL NERVE DISORDERS Medial view Motor root Geniculum (geniculate
Patients with trigeminal neuropathy frequently have Sensory root ganglion) of facial nerve
facial numbness. The examination of touch, pain, and Trigeminal (semilunar) ganglion
temperature in the three divisions of the trigeminal Ophthalmic nerve (V1) Tympanic cavity
nerve, as well as the blink reflex, is routinely checked. Maxillary nerve (V2) Chorda tympani nerve
Although the muscles of mastication are frequently dif- Mandibular nerve (V3) Facial nerve (VII)
ficult to assess, jaw deviation toward the paretic anterior Anterior division
pterygoid muscle on forward protrusion may help to Tensor veli palatini Tensor tympani
indicate trigeminal motor weakness or isolated V3 divi- nerve and muscle muscle and nerve
sion involvement. Impairment of general sensation Otic ganglion Lesser petrosal nerve
from the tongue and palate carried by the trigeminal Chorda tympani nerve Auriculotemporal nerve
nerve can, at times, result in mild taste disturbances, Medial pterygoid Middle meningeal artery
even though the special sensory fibers providing nerve and muscle (cut) Maxillary artery
primary taste sensation, supplied by the facial and glos- Nerve to mylohyoid
sopharyngeal nerves, are not involved. Facial trauma or, Pterygoid hamulus Inferior alveolar nerve
rarely, invasive dental treatments account for the major- Lingual nerve entering mandibular foramen
ity of trigeminal nerve injuries with sensory loss
depending on the involved site. Herpes zoster is a Trigeminal ganglionopathy in association with connec- typically part of a more widespread sensory
common viral cause of a trigeminal neuropathy and tive tissue disease is likely caused by circulating autoan- ganglionopathy.
occurs when latent varicella-zoster virus within the tri- tibodies to ganglion cell bodies. This is particularly
geminal ganglion becomes reactivated. A vesicular rash seen in scleroderma or Sjögren syndrome. Numbness Metastatic neoplasm or tumors involving the face,
and neuralgic pain along the involved division are char- begins around the mouth and spreads slowly over such as squamous cell carcinoma, microcystic adnexal
acteristic, with a chronic postherpetic neuralgia persist- months to involve all trigeminal divisions. Frequently, carcinomas, and keratoacanthoma, may invade cutane-
ing for months to years. Herpes zoster ophthalmicus the ophthalmic division is less involved or spared. ous nerve branches, especially at their exit point from
occurs when the ophthalmic division is involved. If not In Sjögren syndrome, trigeminal ganglionopathy is the skull (mental and infraorbital neuropathies), and
promptly addressed, corneal scarring and visual loss is exhibit focal sensory loss. The numb chin syndrome (or
the most serious potential complication. Rarely, ipsilat-
eral carotid and middle cerebral artery granulomatous
angiitis with infarctions may occur as the virus travels
retrograde from the ganglion along the trigeminal
nerve. Worldwide leprosy or Hansen disease is the most
common cause of trigeminal neuropathy. It affects with
coolest areas of the skin, and sensory loss confined to
the pinna of the ear or tip of the nose raises Hansen
disease as a consideration.

24 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-23â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
TRIGEMINAL NERVE DISORDERS
Varicella-zoster with probable keratitis

Herpes zoster

Progressive systemic sclerosis (scleroderma)

Cranial Nerve V: Trigeminal Typical skin
Nerve (Continued) changes in
scleroderma.
isolated mental neuropathy) consists of unilateral Extensive
numbness of the chin and adjacent lower lip and may collagen
be an ominous sign of primary or metastatic cancer deposition
involving the mandible, skull base, or leptomeninges. and some
The most common etiologies are metastatic breast epidermal
cancer and lymphoproliferative malignancies. atrophy.

Trigeminal neuralgia, also known as tic douloureux, is Characteristics. Thickening, tightening, and rigidity Sclerodactyly. Fingers partially fixed in semiflexed
an often severe and disabling lancinating or electrical of facial skin, with small, constricted mouth and position; terminal phalanges atrophied; fingertips
facial pain syndrome occurring in the trigeminal nerve narrow lips, in atrophic phase of scleroderma pointed and ulcerated
distribution (typically maxillary or mandibular) without
associated neurologic deficits. It characteristically neuralgia. Bilateral symptoms, trigeminal sensory find- higher doses alone are inadequate or cause side effects.
affects middle-aged people, women more than men, ings, and loss of corneal reflexes are strong indicators Tricyclic antidepressants and other anticonvulsants,
and involves the right side more than the left. It is rare of secondary trigeminal neuropathy and should raise such as phenytoin, gabapentin, lamotrigine, topiramate,
to have bilateral attacks of trigeminal neuralgia except concern. Anticonvulsants are the primary medical and pregabalin, may also be useful as adjuvant drugs or
in the setting of multiple sclerosis. The attacks are therapy for trigeminal neuralgia, with most patients monotherapy. Several surgical approaches are available
mostly unilateral and brief, lasting for seconds to several responding to carbamazepine and, more recently, for patients who do not respond to medical therapy.
minutes, and rarely occur during sleep. Paroxysms of oxcarbazepine. Baclofen, an antispasmodic, is advocated Trigeminal neuralgia can recur after any procedure at
pain are frequently provoked by non-nociceptive trig- by some as an adjuvant treatment to carbamazepine if a lifetime rate of about 20%.
gers, including talking, chewing, shaving, drinking hot
or cold liquids, or any form of sensory facial stimula-
tion. Between paroxysms, a constant dull ache can
persist, often leading patients to believe the problem is
of dental origin. The frequency of attacks fluctuates
markedly, disabling a patient for weeks and then remit-
ting for months to years. The etiology is thought to
involve loss of myelin insulation within the posterior
root of the trigeminal nerve. It may be idiopathic or due
to compression at the entry zone of the trigeminal
nerve root by the ectatic artery, (branch of the superior
cerebellar artery), multiple sclerosis plaque, infarction,
vascular malformation, cerebellopontine angle tumor,
or rarely, posterior communicating or distal anterior
inferior cerebellar artery (AICA) aneurysm. Magnetic
resonance imaging (MRI) scanning of the brain with
gadolinium is indicated for all patients with trigeminal

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 25

Plate 1-24â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
FACIAL NERVE (VII)

Greater petrosal nerve Geniculate ganglion Facial nerve (VII)
Deep petrosal nerve (from Internal carotid Internal acoustic meatus
internal carotid plexus) plexus (on internal Intermediate nerve
Lesser petrosal nerve carotid artery) Motor nucleus of facial nerve
Nerve (vidian) of pterygoid canal Superior salivatory nucleus
Otic ganglion Solitary tract nucleus
Pterygopalatine ganglion

Facial muscles Temporal branches

Cranial Nerve VII: Frontal belly (frontalis)
Facial Nerve of occipitofrontalis
Orbicularis oculi
ANATOMY Corrugator supercilii
The facial nerve is a mixed nerve containing special Zygomaticus major
motor, special sensory, general sensory, and parasympa- Zygomaticus minor
thetic fibers. The facial nerve comprises two roots: a Procerus
larger motor root, which supplies the facial mimetic Levator labii
musculature, the stapedius, the stylohyoid, and the pos- superioris
terior belly of the digastric, and a smaller sensory root Levator labii
called the nervus intermedius, which carries sensation superioris
and parasympathetic fibers. alaeque nasi
Levator
THE MOTOR DIVISION anguli oris
Fibers arise from the motor facial nucleus, located in Nasalis
the reticular formation of the lowest part of the pons.
The nucleus is posterior to the superior olive, medial Depressor Taste: anterior 2⁄3 Zygomatic Occipital
to the nucleus of the spinal tract of the trigeminal nerve, septi nasi of tongue branches belly
and anterolateral to the nucleus of the abducens nerve. Orbicularis (occipitalis)
The supranuclear control of facial movements occurs oris Buccal of occipito-
through the corticonuclear fibers originating in the pre- Depressor branches frontalis
central gyrus. These fibers course through the corona anguli oris muscle
radiata, genu of the internal capsule, and the medial Depressor labii Cervical branch Occipital
portion of the cerebral peduncle to the pons. The pos- inferioris branch of
terior portion of the facial nucleus controls the upper Mentalis posterior
facial musculature and receives bilateral supranuclear (Risorius) auricular
input, while the anterior facial nucleus controls the (not shown) nerve
lower facial muscles and receives predominantly con- Buccinator
tralateral input. Supranuclear lesions, such as with Platysma Mbraanndcihbular Branches to auricular muscles
stroke, would therefore produce a pattern of contralat- Posterior auricular nerve
eral predominantly lower facial weakness. The efferent
fibers of the motor nucleus form a motor root and Sublingual gland Nerve to stapedius muscle
course around the abducens nucleus superiorly and Stylomastoid foramen
exit the brainstem laterally in the cerebellopontine
angle. The motor root travels with the nervus interme- Submandibular gland Tympanic plexus
dius and CN VIII in the cerebellopontine angle and
enters the internal auditory meatus of the temporal Submandibular ganglion Tympanic nerve (of Jacobson)
bone. Within the temporal bone, there are four por- (from glossopharyngeal nerve)
tions of the facial nerve. (1) In the meatal (canal)
Lingual nerve (from trigeminal nerve) Glossopharyngeal nerve (IX)

Chorda tympani nerve Digastric muscle (posterior belly)

Stylohyoid muscle

Caroticotympanic nerve (from internal carotid plexus)

Efferent fibers
Afferent fibers
Parasympathetic fibers
Sympathetic fibers

segment, the motor division is on the superoanterior petrosal nerve arises from the geniculate ganglion. This
surface of CN VIII, and the nervus intermedius is in nerve is composed of preganglionic parasympathetic
between them. (2) In the labyrinthine segment, the efferents that innervate the nasal, lacrimal, and palatal
motor root, and nervus intermedius enter the facial glands via the pterygopalatine ganglion. The greater
canal in the petrous bone. The labyrinthine segment superficial petrosal nerve also carries sensory fibers
passes above the labyrinth and reaches the geniculate from the external auditory meatus, lateral pinna, and
ganglion, which contains the sensory fibers of the mastoid. (3) The horizontal (tympanic) segment con-
nervus intermedius. Here the greater superficial tains the facial nerve as it runs horizontally backward

26 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-25â•… Cranial Nerve and Neuro-Ophthalmologic Disorders
MUSCLES OF FACIAL EXPRESSION: LATERAL VIEW

Scalp Skin and subcutaneous tissue
Epicranial aponeurosis (galea aponeurotica)

Temporal fascia Auricularis anterior muscle
Orbicularis Orbital part Auricularis superior muscle
oculi muscle Palpebral part Auricularis posterior muscle
Occipital belly
Frontal belly (frontalis) (occipitalis) of
of epicranius muscle epicranius muscle

Corrugator supercilii muscle Parotid
(frontalis and orbicularis fascia
oculi, WHY[PHSS` J\[ H^H`) Masseteric
fascia
Procerus muscle Investing layer
Levator labii of (deep)
superioris muscle cervical fascia

Levator labii superioris
alaeque nasi muscle
(WHY[PHSS` J\[ H^H`)

Cranial Nerve VII: Facial Nasalis Transverse part
Nerve (Continued) muscle Alar part
Depressor septi
nasi muscle

below and medial to the horizontal semicircular canal. Orbicularis oris muscle
(4) In the mastoid (vertical) segment the facial nerve Zygomaticus
bends inferiorly. The nerve to the stapedius muscle minor muscle
branches off in this segment. The chorda tympani also Zygomaticus
branches off here and joins the lingual nerve. It contains major muscle
the preganglionic parasympathetic fibers from the supe-
rior salivatory nucleus and innervates the submandibu- Orbicularis oris muscle
lar and sublingual glands via the submaxillary ganglion.
The chorda tympani also contains afferent taste fibers Mentalis muscle
from the anterior two thirds of the tongue that then Depressor labii inferioris muscle
continue on to the nucleus of the solitary tract. CN VII
exits the facial canal through the stylomastoid foramen Depressor anguli oris muscle
and gives off the posterior auricular nerve (to the Buccinator muscle
posterior auricular, transverse and oblique auricular Risorius muscle
muscles, and occipitalis) and digastric and stylohyoid
branches. The facial nerve pierces the parotid gland and Platysma muscle
divides into temporofacial and cervicofacial branches,
which further divide into temporofrontal, zygomatic,
buccal, marginal mandibular, and cervical branches.

THE SENSORY AND PARASYMPATHETIC Sternum cranial fossa likely reach the facial nerve through the
DIVISION (NERVUS INTERMEDIUS) Clavicle greater petrosal branch.

The nervus intermedius is the parasympathetic and controlling lacrimation. The gustatory afferents end in FACIAL NERVE DISORDERS
sensory division of the facial nerve. It carries the pre- the nucleus of the tractus solitarius in the medulla. Facial weakness is caused by both central and peripheral
ganglionic parasympathetic fibers to the submaxillary Fibers conveying general sensations from the external lesions, and differentiating between the two frequently
ganglion (and then postganglionic fibers travel to the auditory meatus, lateral pinna, and mastoid likely come requires close examination. Peripheral facial weakness
submandibular and sublingual glands) and to the ptery- through interconnections between the chorda tympani
gopalatine ganglion (postganglionic fibers travel to the and the auricular branch of the vagus and terminate in
lacrimal, nasal, and palatal glands). The nervus inter- the spinal nucleus of the trigeminal nerve. The afferents
medius receives sensory fibers from the geniculate gan- from the meninges and their arteries in the middle
glion. This ganglion receives afferents from the mucosa
of the pharynx, nose, palate, and skin of the external
auditory meatus, lateral pinna, and mastoid, and it
carries taste sensation from the anterior two thirds of
the tongue. The superior salivatory nucleus of the
pontine tegmentum gives rise to the parasympathetic
fibers. The lacrimal nucleus contains the fibers

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 27

Plate 1-26â•… Spinal Cord and Peripheral Motor and Sensory Systems: PART II
CENTRAL VERSUS PERIPHERAL FACIAL PARALYSIS
Hyperacusis

This may be an early or initial symptom
of a peripheral VII nerve palsy: patient
holds phone away from ear because
of hyperacusis, an uncomfortable
sensitivity to sound. Loss of taste also
may occur on affected side.

Left peripheral VII facial weakness Left central facial weakness
Attempt to close eye results in
eyeball rolling superiorly exposing
sclera (Bell phenomenon) but no
closure of the lid per se

Cranial Nerve VII: Facial
Nerve (Continued)

involves both the upper and lower part of the face to Patient unable to wrinkle forehead; Incomplete smile with very subtle
the same degree, whereas upper motor neuron lesions eyelid droops very slightly; cannot flattening of affected nasolabial fold;
typically manifest with a gradient of weakness, with show teeth at all on affected side in relative preservation of brow and
relative preservation of movement in the brow and attempt to smile; and lower lip forehead movement
forehead (e.g., frontalis muscles). Supranuclear lesions, droops slightly the anterior two thirds of the tongue, and affected
such as in suprabulbar palsies, may result in an absence unilateral facial anesthesia and loss of corneal reflex. A somatic sensation for the external auditory canal and
of voluntary facial movements but retention of reflexive proximal pregeniculate, intracanicular facial nerve lesion mastoid area. Lesions between the geniculate ganglion and
movements (e.g., smiling) in response to emotional characteristically also causes diminished lacrimation the stapedius nerve spare lacrimation, because the greater
stimuli. from greater petrosal nerve involvement, as well as petrosal nerve has already exited. Damage between the
hyperacusis (i.e., increased sensitivity to sound) due to branch points of the stapedius nerve and the chorda tympani
Intrapontine lesions that affect the facial motor associated stapedius muscle paresis. These lesions also results in hyperacusis and impaired salivation and taste,
nucleus or its exiting fibers will often involve neighbor- lead to diminished salivation, absent or altered taste for
ing brainstem structures; for instance, a paramedian
pontine reticular formation lesion causing ipsilateral
conjugate gaze palsy, an associated sixth cranial nerve
tract lesion with limited ipsilateral lateral rectus palsy,
or contralateral hemiparesis of the arm and leg.

The facial nerve can be damaged at any level along
its course (Plate 1-27). Facial musculature paralysis is
the hallmark of seventh cranial nerve lesions. The pres-
ence or absence of symptoms related to the various
other components of the facial nerve are important for
further localization. The patient with a peripheral facial
nerve palsy, with the exception of an early very distal
branch lesion within the parotid gland, has weakness of
the entire ipsilateral side of their face, with asymmetric
smile, inability to close the eye (orbicularis oculi), or
wrinkle the forehead (frontalis). Intracranial, extramed-
ullary lesions affecting the seventh nerve typically occur
within the cerebellopontine (CP) angle, most com-
monly caused by large acoustic neuromas, and often
involve the vestibulocochlear nerve. In these cases,
diminished hearing, at times initially presenting with
tinnitus, usually precede the onset of peripheral facial
paresis. Rarely, very large tumors may also involve the
ipsilateral trigeminal cranial nerve with accompanying

28 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS

Plate 1-27â•… Cranial Nerve and Neuro-Ophthalmologic Disorders

Occipitofrontalis muscle FACIAL PALSY Facial Acoustic (VIII) nerve
Corrugator Sites of facial (VII) nerve injury (VII) Abducens
supercilii muscle nerve nucleus
Temporal branch Orbicularis
oculi muscle
Lacrimal gland

Pterygopalatine Geniculate
ganglion ganglion
Pons
Greater 1
petrosal
nerve 2

3 Facial
nucleus
Stapedius muscle
4
Tympanum Stylo-

Lingual nerve mastoid
foramen

Tongue Posterior
auricular nerve
5 Chorda tympani

Cranial Nerve VII: Facial Orbicularis Parotid gland
Nerve (Continued) oris muscle Buccal branch

but not change in lacrimation. Lesions distal to the Marginal mandibular branch
chorda tympani branch point result in pure ipsilateral
facial weakness. Distal lesions that affect individual Levator anguli oris muscle Sublingual Cervical branch
motor branches result in weakness that may be restricted Depressor anguli oris muscle gland
to individual facial muscles. Zygomatic branch
Risorius muscle Platysma muscle
BELL PALSY (“IDIOPATHIC” FACIAL PALSY) Submandibular ganglion
Bell palsy is a common cause of unilateral facial weak- Submandibular gland
ness. Onset of weakness is acute to subacute, evolving Buccinator muscle
over hours to a few days. The lesion burden is usually
proximal, with loss of total motor function on one side Sites of lesions and their manifestations
of the face, hyperacusis, disturbed taste, and decreased 1. Intrapontine lesions: Peripheral motor facial paralysis associated with eye movement abnormalities
lacrimation. A preceding dull ache behind the ipsilateral (ipsilateral abducens or horizontal gaze palsies) and contralateral motor paralysis.
ear is a common initial symptom. Nerve edema with 2. Intracranial and/or internal auditory meatus: All symptoms of 3, 4, and 5, plus deafness
subsequent compression and ischemia within the facial due to involvement of eighth cranial nerve.
canal has been noted pathologically. The cause is 3. Geniculate ganglion: All symptoms of 4 and 5 with diminished lacrimation, plus pain behind ear.
believed to be reactivation of latent herpes simplex or Herpes of tympanum and of external auditory meatus may occur.
varicella-zoster virus. A short course of corticosteroids, 4. Facial canal: All symptoms of 5, plus loss of taste in anterior tongue and decreased salivation on
if given early in the course, reduces the duration of affected side due to chorda tympani involvement. Hyperacusis due to effect on nerve branch to
paralysis and risk of permanent impairment. The long- stapedius muscle.
term prognosis is generally good, but severe cases may 5. Below stylomastoid foramen (parotid gland tumor, trauma): Facial paralysis (mouth draws to
result in permanent partial facial paresis. Facial synki- opposite side) on affected side with patient unable to close eye or wrinkle forehead; food collects
nesis, caused by aberrant regeneration of nerve, may between teeth and cheek due to paralysis of buccinator muscle.
manifest as ipsilateral eye closure occurring with
smiling or ipsilateral lip and chin muscle activation Symptoms typically include systemic symptoms (e.g., may rarely inflame and damage the facial nerve where
during blinking. Excessive lacrimation when eating arthralgia, fever, rash), as well as other neurologic it travels through the petrous bone. Leprosy may lead
results from aberrant regeneration of salivatory fibers symptoms (e.g., headache, radiculitis, encephalopathy). to bilateral facial nerve lesions. Unilateral or bilateral
to the lacrimal glands (“crocodile tears”). Herpes zoster infection within the external auditory facial neuropathy is a common neurologic manifesta-
canal (Ramsay-Hunt syndrome), may cause facial paral- tion of sarcoidosis. Bilateral facial weakness is common
OTHER ETIOLOGIES OF ysis that may precede the appearance of typical herpetic in Guillain-Barré syndrome (acute inflammatory demy-
FACIAL NEUROPATHY vesicles in the auditory canal. Extension of otitis media elinating polyradiculopathy).
Lyme disease is a relatively common infectious cause
of an acute unilateral or bilateral facial neuropathy.

THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 29