DUANE FE. HAINES ~
TENTH EDITION
NEUROANATOMY
ATLAS
IN CLINICAL CONTEXT
Structures, Sections, Systems, and Syndromes
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10th Edition
NEUROANATOMY ATLAS
IN CLINICAL CONTEXT
Structures, Sections, Systems, and Syndromes
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10th Edition
NEUROANATOMY ATLAS
IN CLINICAL CONTEXT
Structures, Sections, Systems, and Syndromes
Duane E. Haines, PhD, FAAAS, FAAA
Professor, Department of Neurology, and Professor, Department of Neurobiology and Anatomy,
Wake Forest School of Medicine, Winston-Salem, North Carolina
And
Professor Emeritus, Department of Neurobiology and Anatomical Sciences and Professor,
Departments of Neurology and of Neurosurgery, University of Mississippi Medical Center,
Jackson, Mississippi
Special Contributions by:
Mary Alissa Willis, MD
Assistant Professor
Cleveland Clinic Lerner College of Medicine of Case Western Reserve University
Cleveland, Ohio
H. Wayne Lambert, PhD
Director of Anatomy Division
West Virginia University School of Medicine
Morgantown, West Virginia
Illustrators: W. K. Cunningham, BA, MSMI and M. P. Schenk, BS, MSMI, CMI, FAMI
Computer Graphics: C. P. Runyan, BS
Photographers: G. W. Armstrong, RBP; R.W. Gray, BA
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First Edition, 1983
Second Edition, 1987
Third Edition, 1991
Fourth Edition, 1995
Fifth Edition, 2000
Sixth Edition, 2004
Seventh Edition, 2008
Eighth Edition, 2012
Ninth Edition, 2015
Tenth Edition, 2019
Portuguese Translation, 1991
Japanese Translation, First Japanese Edition, 1996; Chinese (Taiwan) Translation, 1997
Japanese Translation, Second Japanese Edition, 2000; Chinese (Beijing) Translation, 2002;
Chinese (Nanjing) Translation 2002
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Library of Congress Cataloging-in-Publication Data
Names: Haines, Duane E., author. | Willis, M. Alissa (Mary Alissa),
contributor. | Lambert, Harold Wayne, 1972- contributor.
Title: Neuroanatomy atlas in clinical context : structures, sections,
systems, and syndromes / Duane E. Haines ; special contributions by Mary
Alissa Willis, H. Wayne Lambert ; illustrators, W.K. Cunningham and M.P.
Schenk ; computer graphics, C.P. Runyan ; photographers, G.W. Armstrong,
R.W. Gray.
Other titles: Neuroanatomy in clinical context
Description: 10th edition. | Philadelphia : Wolters Kluwer, 2019. | Preceded
by Neuroanatomy in clinical context / Duane E. Haines. Ninth edition.
2014. | Includes bibliographical references and index.
Identifiers: LCCN 2018022530 | ISBN 9781496384164
Subjects: |MESH: Central Nervous System—anatomy & histology | Atlases
Classification: LCC QP376 |NLM WL 17 | DDC 612.8/2-dce23
LC record available at https://Iccn.loc.gov/2018022530
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Preface
to the Tenth Edition
he first edition of this book contained several unique features,
one of which was a particular emphasis on clinical information,
emma COrrelations, terminology, and the integration of neuroanatomical concepts with clinical concepts. Morphologic concepts, it could be
argued, are not learned/understood for their own sake, but are learned
as the basis for understanding the impaired patient. These guiding principles have been followed through all subsequent editions.
The Tenth Edition continues and expands the approach of emphasizing clinical relevance. Clinical content has been revised and increased
throughout all chapters. Chapter 9 has been divided into a Part I (Herniation Syndromes of the Brain and Spinal Disc) and a Part II (Representative Stroke Syndromes). This further emphasizes the clinical application
of basic science concepts.
, This new edition of Neuroanatomy Atlas in Clinical Context continues to: (1) provide a sound anatomical base for integrating neuroscience and clinical concepts; (2) introduce new text, MRI, CT, and
artwork that emphasize information and concepts that are encountered
in the clinical setting; (3) utilize contemporary clinical and basic science terminology in its proper context; and (4) emphasize neuroscience
information, concepts, and images that collectively constitute a comprehensive, and clinically oriented, overview of systems neurobiology.
In addition, the revision of existing pages, the addition of new pages,
and the division of Chapter 9 into a Herniation Part and a Stroke Part
has resulted in an increase in the number of MRI, MRA, CT, CTA,
and angiograms from over 370 to over 430; this represents a significant
increase in clinically relevant examples. Understanding systems neurobiology is an absolutely essential element in the successful diagnosis of
the neurologically compromised patient.
Many comments, suggestions, insights, and ideas from my colleagues,
medical students, residents, and graduate students have been factored
into the modifications in this new edition; their candor is greatly appreciated. While minor corrections, or changes, have been made on almost
every page, the major improvements and new information introduced in
the Tenth Edition of Neuroanatomy Atlas in Clinical Context continue
as follows:
First, all clinical information throughout the Atlas appears in a light
blue screen. This: (1) makes it very easy to identify any and all clinical
comments, or examples, on every page; (2) does not reduce clinical concepts by trying to compress them into small summary boxes; (3) keeps
all clinical correlations and information in their proper neuroanatomical context; and (4) emphasizes the overall amount—and relevance—of
the clinical information presented in this Atlas. This approach allows
the user to proceed from a basic point to a clinical point or from a clinical point to a basic point, without a break in the flow of information,
or the need to go to a different page. This greatly expedites the learning
process.
Second, any new images of brain or spinal cord anatomy and any
new pieces of artwork in Chapters 2 and 3 have been prepared with
the utmost care, to be absolutely consistent with the existing images. A
special effort has been made to present color images of the best quality
as is reasonably possible.
Third, brain herniation is ubiquitous in cases of trauma to the head
and neck, particularly when there is an increase in intracranial pressure.
Sulci and cisterns may be obliterated, and the brain may be extruded
from one compartment into another. Herniation may be silent or, more
likely, may result in deficits reflecting the particular brain region damaged. Herniation syndromes have elegant anatomical correlates; in most
of these cases, there is a close correlation between the brain structures
injured and the deficits experienced by the patient. Stroke may share
features with herniation syndromes: sudden onset, need for immediate
medical attention, and in certain situations the likelihood of survival
may be remote. Recognizing these features, a new Part was added to
Chapter 9 on Stroke Syndromes and some of their ramifications. This
new Part of Chapter 9 introduces a variety of vascular lesions, their
correlations with vessel territories, and basic deficits.
Fourth, the line drawings of the color-stained sections of the spinal
cord and the brainstem in Chapter 6, have been revised, labels have
been corrected, more space has been made on the plate, and the colorcoding has been updated. In addition, a new cross section was added
to illustrate that the trochlear nucleus, decussation of the superior cerebellar peduncle, substantia nigra, and the crus cerebri are characteristic
features in a cross section of the brainstem at the level of the inferior
colliculus.
Fifth, the two line drawings that illustrate the functional components
of spinal cord and brainstem nuclei that previously appeared at the
beginning of Chapter 8 have been revised, recolorized, and now appear
as the two introductory pages for Chapter 6. The revised color scheme
used here and the corresponding color changes on the same nuclei in
the line drawings have proved to be very helpful and are continued in
this Tenth Edition. In addition, the line drawings on the page facing the
stained section in the forebrain portion of this Chapter (Figures 6-31 to
6-40) were recast and prepared in colors that complement the stained
section. The white matter (fiber bundles, pathways, etc.) appears in a
light black, and the gray matter (nuclei, cell bodies, etc.) appears in a
light tan/brown. This will greatly expedite the learning of and the correlation between the stained section and artwork on the facing page.
Sixth, many other minor adjustments have been made throughout;
these include, labeling changes and/or corrections, adding and/or relocating CT and MRI
(both normal and abnormal) for a better corre-
lation, clarifying clinical and neuroanatomical information, stressing a
better correlation between structure and function, bolding key terms
while retaining italics for emphasis of important points, and integrating
tidbits of information that are encountered in the initial educational
experience and that certainly energize the learning opportunity.
Two further issues continue to figure prominently in this new edition.
First, the question of whether, or not, to use eponyms in their possessive
form. To paraphrase one of my clinical colleagues, “Parkinson did not
die of his disease (so-called ‘Parkinson’ disease); he died of a stroke. It
V
was never his own personal disease.” There are rare exceptions, such as
Lou Gehrig disease, but the point is well taken. McKusick (1998a,b) also
has made compelling arguments in support of using the nonpossessive
form of eponyms. However, it is acknowledged that views differ on this
question—much like debating how many angels can dance on the head
of a pin. Consultation with my neurology and neurosurgery colleagues,
the style adopted by Dorland’s Illustrated Medical Dictionary (2012)
and Stedman’s Medical Dictionary (2006), a review of some of the more
comprehensive neurology texts (e.g., Rowland & Pedley, 2010; Ropper
& Samuels, 2009), the standards established in the Council of Biology
Editors Manual for Authors, Editors, and Publishers (1994), and the
American Medical Association’s Manual ofStyle (2007) clearly indicate
an overwhelming preference for the nonpossessive form. Recognizing
that many users of this book will enter clinical training, it was deemed
appropriate to encourage a contemporary approach. Consequently, the
nonpossessive form of the eponym is used.
The second issue concerns use of the most up-to-date anatomical
terminology. With the publication of Terminologia Anatomica (1998),
a new Official international list of anatomical terms for neuroanatomy is available. This new publication, having been adopted by the
International Federation of Associations of Anatomists, supersedes all
previous terminology lists. Every effort has been made to incorporate
any applicable new or modified terms into this book. In addition, the
well-reasoned modification in the Edinger-Westphal terminology that
reflects its functional characteristics is also adapted for this Atlas (Kozicz
et al., 2011). The Edinger-Westphal complex consists of an Edinger—
Westphal preganglionic nucleus (EWpg) that projects specifically to the
ciliary ganglion and an Edinger—Westphal centrally projecting nucleus
(EWcp) that projects to a variety of targets including the spinal cord,
spinal trigeminal, cuneate, gracile, facial, inferior olivary, and parabrachial nuclei, and to the reticular formation, but does not project to the
ciliary ganglion.
Lastly, the pagination of the Tenth Edition has been slightly modified
to accommodate changes which have increased integration, introduced
significant new clinical correlates and images, repositioned a few images
to enhance learning opportunities and the overall flow of information,
and to accommodate new pages and a new chapter on herniation syndromes. A sampling of Q&As are included in this print version with a
much larger sample available online through thePoint. All the Q&As
have been revised and updated to assist the user in practicing his or her
level of understanding, comprehension, and competence.
Duane E. Haines
Winston-Salem, North Carolina
REFERENCES
Council of Biology Editions Style Manual Committee. Scientific Style
and Format—The CBE Manual for Authors, Editors, and Publishers.
6th ed. Cambridge: Cambridge University Press; 1994.
Dorland’s Illustrated Medical Dictionary. 32nd ed. Philadelphia, PA:
Saunders/Elsevier; 2012.
Federative Committee on Anatomical Terminology. Terminologia
Anatomica: International Anatomical Terminology. New York:
Thieme; 1998.
Iverson C, Christiansen S, Flanagin A, et al. American Medical
Association Manual of Style—A Guide for Authors and Editors.
10th ed. New York: Oxford University Press; 2007.
Kozicz T, Bittencourt JC, May PJ, et al. The Edinger-Westphal nucleus:
a historical, structural, and functional perspective on a dichotomous
terminology. JComp Neurol 2011;519(8):1413-1434.
Vi
McKusick VA. On the naming of clinical disorders, with particular
reference to eponyms. Medicine (Baltimore) 1998a;77(1):1-2.
McKusick VA. Mendelian Inheritance in Man: A Catalog of Human
Genes and Genetic Disorders. 12th ed. Baltimore, MD: The Johns
Hopkins University Press; 1998b.
Ropper AH, Samuels MA. Adams and Victor’s Principles of Neurology.
9th ed. New York: McGraw-Hill Companies, Inc.; 2009.
Rowland LP, Pedley TA, eds. Merritt’s Neurology. 12th ed. Baltimore,
MD: Lippincott Williams & Wilkins; 2010.
Stedman’s Medical Dictionary. 28th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2006.
y basic science colleagues in the Department of Neurobiology and Anatomical Sciences (Dr. Michael Lehman, Chair)
and my clinical colleagues in the Department of Neurology (Dr. Alex Auchus, Chair), and the Department of Neurosurgery
(Dr. H. Louis Harkey, Chair), all at The University of Mississippi Medical Center, have been very gracious in offering suggestions and comments, both great and small, on the revisions for previous editions.
A special thanks is due four colleagues for their important help with
the Tenth Edition. First, Dr. M. Alissa Willis and Dr. H. Wayne Lambert read all chapters with particular attention to clinical information,
examples, comments, and terminology. Second, Dr. Jian Chen (Neurology, Mississippi) and Dr. Quang Vu (Neurology, Wake Forest) were
absolutely essential to helping me locate clinical images both normal
and with particular lesions to illustrate a point. I greatly appreciate the
cooperation of all of these individuals; they did a wonderful job.
The modifications in this Tenth Edition focus on improving the integration of basic science concepts with the realities of their clinical applications, and offer several new innovations that make the learning of,
and the transition between, basic science and clinical concepts easier,
more fluid, and seamless. The color coding of all clinical information
throughout the text, addition of new clinically relevant information and
examples, and the upgrading of contemporary anatomical and clinical
concepts and terms are but some examples.
A thank you is due the following individuals for their contributions
to recent Editions: Drs. Bishnu Sapkota and David Sinclair, Drs. Robert
McGuire and William McCluskey, Drs. Louis Harkey and Andy Parent,
Dr. Alan Sinning, Mr. Ken Sullivan, and graduate student Mr. Martin O.
Bohlen, medical students Ms. Kelly Brister and Mr. Jarrett R. Morgan,
Dr. Tim McCowan, Dr. Jonathan Wisco (UCLA), Drs. Amy Jones and
Bridgett Jones, and Drs. Kim Simpson and Jim Lynch.
The external reviewers commissioned by Wolters Kluwer were faculty: Dr. James D. Foster, Dr. Eustathia L. Giannaris, Dr. Joerg R. Leheste,
Dr. Mary A. Matteliano, Dr. Todd A. Nolan, Dr. Omid B. Rahimi, and
students: John Brandt, Rachel Krieger, Avani Patal, Ronald Sahyouni,
Farooq Usmani, and Haley Zlomke. Their time, energy, and input represented an essential feature in this new edition.
Modifications, both great and small, to the existing artwork and
labeling scheme, and the generation of many new renderings, tables,
and compiling plates, were predominately the work of Mr. Walter (Kyle)
Cunningham (Medical Illustrator) and Mr. Michael Schenk. Mr. Chuck
Runyan (Biomedical Photography), Mr. Bill Armstrong (Manager of
Biomedical Photography), and Mr. Robert W. Gray (Biomedical Photography) photographed new brain and spinal cord specimens. I am
enormously appreciative of the time, energy, dedication, and professionalism of these individuals toward creating the best possible images, photographs, artwork, and finished plates for this book. Mr. Cunningham
|V
went out of his way to do an absolutely outstanding job to meet and
repeatedly exceed the expectations of the author. Thank you, Kyle!
Over the years, many colleagues, friends, and students (now faculty
or medical/dental practitioners) have made many helpful comments.
They are again acknowledged here, because these earlier suggestions
continue to influence this book: Drs. A. Agmon, A. Alqueza, B. Anderson, C. Anderson, R. Baisden, S. Baldwin, R. Borke, J. Brandt, P. A.
Brewer, A. S. Bristol, Patricia Brown, Paul Brown, A. Butler, T. Castro,
B. Chronister, C. Constantinidis, A. Craig, J. L. Culberson, P. DeVasto,
V. Devisetty, E. Dietrichs, L. Ehrlichman, J. Evans, E. M. Fallon, B. Falls,
C. Forehand, J. D, Foster, R. Frederickson, G. C. Gaik, E. Garcis-Rill, E.
L. Giannaris, G. Grunwald, B. Hallas, T. Imig, J. King, J. A. Kmiec, R.
Krieger, P. S. Lacy, A. Lamperti, J. R. Leheste, G. R. Leichnetz, E. Levine,
R. C. S. Lin, J. C. Lynch, T. McGraw-Ferguson, G. F. Martin, M. A.
Matteliano, A. Miam, G. A. Mihailoff, M. V. Mishra, B. G. Mollon, T. A.
Nolan, R. L. Norman, R. E. Papka, A. Patel, A. N. Perry, K. Peusner, C.
Phelps, B. Puder, O. B. Rahimi, H. J. Ralston, J. Rho, L. T. Robertson, D.
Rosene, A. Rosenquist, I. Ross, R. Sahyouni, J. D. Schlag, M. Schwartz,
J. Scott, V. Seybold, L. Simmons, K. L. Simpson, A. Singh, D. Smith, S.
Stensaas, C. Stefan, D. G. Thielemann, M. Thomadaki, $. Thomas, M.
Tomblyn, J. A. Tucker, D. Tolbert, F Usmani, F. Walberg, S. Walkley,
M. Woodruff, M. Wyss, R. Yezierski, H. Zlomke, and A. Y. Zubkov. I
have greatly appreciated their comments and suggestions. The stained
sections used in this Atlas are from the teaching collection in the Department of Neurobiology and Anatomy at West Virginia University School
of Medicine. The author, who was on the faculty at WVU from 1973 to
1985, expresses his appreciation to Mr. Bruce Palmer. This Tenth Edition would not have been possible without the interest and support of
the publisher, Lippincott Williams & Wilkins. I want to express thanks
to my editors, Crystal Taylor (Senior Acquisitions Editor), Amy Millholen
(Development
Editor), John Larkin
(Editorial Coordinator)
Michael
McMahon (Marketing Manager), Barton Dudlick (Production Project
Manager), Amanda Ingold (Editorial Assistant), and especially Kelly
Horvath (Freelance Development Editor) for their encouragement, continuing interest, and confidence in this project. Kelly was absolutely an
essential key in the process and I greatly appreciate her hard work and
wonderful cooperation. Their cooperation has given me the opportunity
to make the improvements seen herein.
Lastly, but clearly not least, I want to express a special thanks to my
wife, Gretchen. The significant changes made in this edition required
attention to many, and multiple, details. She carefully and critically
reviewed the text, patiently listened to more neurobiology than she
could have ever imagined, and gleefully informed me about rules of
grammar and punctuation that I am not sure I even knew existed. She
also got a kick out of arguing about the singular versus plural form of
Latin terms. I gladly dedicate this Tenth Edition to Gretchen.
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Table
—
Preface to the Tenth Edition
Acknowledgments
v
vii
Introduction and User’s Guide
1
External Morphology of the Central Nervous System
The Spinal Cord: Gross Views and Vasculature
8
The Brain: Lobes, Principle Brodmann Areas, Sensory—Motor Somatotopy
The Brain: Gross Views, Vasculature, and MRI
The Cerebellum: Gross Views and MRI
34
The Insula: Gross View, Vasculature,and MRI
Vascular Variations of Clinical Relevance
Cranial Nerves
36
38
43
Synopsis of Cranial Nerves
Cranial Nerves in MRI
14
44
46
Deficits of Eye Movements in the Horizontal Plane
53
Cranial Nerve Deficits in Representative Brainstem Lesions
Cranial Nerve Cross Reference
55
Meninges, Cisterns, Ventricles,
and Related Hemorrhages
57
The Meninges and Meningeal and Brain Hemorrhages
Meningitis
60
Epidural and Subdural Hemorrhage
62
Cisterns and Subarachnoid Hemorrhage
Meningioma
58
64
66
Ventricles and Hemorrhage into the Ventricles 68
The Choroid Plexus: Locations, Blood Supply, Tumors
72
Hemorrhage into the Brain: Intracerebral Hemorrhage
74
54
11
7
Internal Morphology of the Brain in Unstained Slices
75
andin MRI
Part I: Brain Slices in the Coronal Plane Correlated with MRI
Part II: Brain Slices in the Axial Plane Correlated with MRI
75
85
Internal Morphology of the Spinal Cord and Brain:
Functional Components, MRI, Stained Sections
Functional Components of the Spinal Cord and Brainstem
The Spinal Cord with CT and MRI
96
98
Arterial Patterns within the Spinal Cord with Vascular Syndromes
The Degenerated Corticospinal Tract
108
110
The Medulla Oblongata with MRI and CT
112
Arterial Patterns within the Medulla Oblongata with Vascular Syndromes
The Cerebellar Nuclei
95
124
126
The Pons with MRI and CT
130
Arterial Patterns within the Pons with Vascular Syndromes
The Midbrain with MRI and CT
138
140
Arterial Patterns within the Midbrain with Vascular Syndromes
The Diencephalon and Basal Nuclei with MRI
152
154
Arterial Patterns within the Forebrain with Vascular Syndromes
174
Internal Morphology of the Brain in Stained Sections:
Axial—Sagittal Correlations with MRI
177
Axial-Sagittal Correlations with MRI
178
Tracts, Pathways, and Systems in Anatomical and Clinical
Orientation
Orientation
189
Sensory Pathways
192
Motor Pathways
210
Cranial Nerves
|
190
226
Spinal and Cranial Nerve Reflexes
Cerebellum and Basal Nuclei
234
242
Optic, Auditory, and Vestibular Systems
262
Internal Capsule and Thalamocortical Connections
Limbic System: Hippocampus and Amygdala 280
Hypothalamus and Pituitary
288
276
Clinical Syndromes of the CNS
297
Part I: Herniation Syndromes of the Brain and Spinal Discs
Part II: Representative Stroke Syndromes
297
309
Anatomical-Clinical Correlations: Cerebral Angiogram,
MRA, and MRV_ 317
Cerebral Angiogram, MRA, and MRV_
318
Overview of Vertebral and Carotid Arteries
329
Q&As: A Sampling of Study and Review Questions, Many
in the USMLE Style, All with Explained Answers
331
Sources and Suggested Readings
Index
See online Interactive Atlas
343
xi
Duane E. Haines, PhD
Recipient of the 2008 Henry Gray/Elsevier Distinguished
Educator Award from The American Association of
Anatomists
Elected a Fellow of the American Association of
Anatomists and a Fellow of the American Association
for the Advancement of Science
Recipient of the 2010 Alpha Omega Alpha Robert J. Glaser
Distinguished Teacher Award from AOA and The Association
of American Medical Colleges
Xi
Neuroanatomy Consultant for Stedman’s Medical Dictionary
and for Dorland’s Illustrated Medica! Dictionary
Co-recipient, International Society for the History of
Neuroscience, 2017 Outstanding Articles Award, Journal of
the History of the Neurosciences
See
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©.
Introduction and User’s Guide
©
ales
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his new edition of Neuroanatomy Atlas in Clinical Context
continues to emphasize brain anatomy in a clinically relevant
format. This includes: (1) correlating the central nervous system
(CNS) anatomy with magnetic resonance images (MRIs) and computed
tomography (CT) throughout; (2) using clinical terms, phrases, and
examples in their proper context; (3) highlighting cerebrovascular anatomy with numerous clinical examples; (4) emphasizing internal vascular
territories throughout the CNS, and the myriad deficits resulting from
vascular lesions; and (5) presenting an extensive treatment of systems
neurobiology integrating connections, blood supply, and deficits at all
levels of the neural axis.
The presentation of all clinical information in a light blue screen continues throughout this edition. This: (1) makes it very easy to identify all
clinical information; (2) does not reduce clinical concepts to summary
boxes; (3) keeps all clinical correlations and information in their proper
context; and (4) emphasizes the amount—and relevance—of the clinical
information presented. This approach allows the user to proceed from
a basic point to a clinical point or from a clinical point to a basic point,
without a break in the flow of information.
The opportunity to view, study, and understand CNS anatomy in
both Anatomical and Clinical Orientations continues to be emphasized.
The style of presentation and emphasis on clinical application expedites
learning and the understanding that will be eminently useful in the clinical environment. This approach allows for learning concepts in a setting
that can be seamlessly transferred to, and applied within, the clinical
experience. A focused approach in this new edition is to continue the
emphasis on integration of basic science with clinical application.
Recognizing that about 50% of intracranial events that result in
neurologic deficits are vascular in nature, as broadly defined, vascular
anatomy, distribution territories, and vascular patterns and variations
thereof are covered in detail. Also, a new section on Stroke has been
added to Chapter 9. These vascular topics, and their clinical correlations are discussed and illustrated with computed tomography angiography (CTA), magnetic resonance angiography (MRA), and magnetic
resonance venography (MRV) in all chapters. Recognizing vascular
patterns, territories, and variations, is central to a successful diagnosis.
A thorough knowledge and understanding of systems, reflexes, pathways, their blood supply, and the results of lesions thereof, are essential to diagnosis of the neurologically compromised patient. Put simply,
deficits seen in many patients who present with neurologic deficits are
a direct reflection of damage to functional systems that convey information from the periphery to targets in the brainstem or forebrain,
or centrally generated signals that convey information that influences
motor activity. A thorough knowledge of systems neurobiology (sensory
and motor pathways, spinal and brainstem reflexes) is absolutely essential. A concurrent understanding of the appearance and relationships
of brain regions in MRI and CT is an integral part of the diagnostic
effort. Systems traverse regions; it is not possible to become competent
in one and not the other. The number of images (CT, CTA, MRI, MRA,
MRYV, angiograms, and venograms) has been increased from about 372
to about 433 in this new edition. The majority of these 61 new images
are found in Chapters 2, 8, 9, and 10. The use of these images in a contemporary educational setting is absolutely essential for preparing the
user for the realities of the clinical environment. In the clinical setting,
the user will not be studying gross brain or stained slices, but will rely
almost exclusively on CT, MRI, or variations of these modalities. The
goal is to give the user the knowledge base and skills needed to excel in
the clinical setting.
Imaging the Brain (CT and MRI)
Imaging the brain in vivo is now commonplace for the patient with
neurologic deficits. With this in mind, it is appropriate to make a few
general comments on these imaging techniques and what is routinely
seen, or best seen, in each. For details, consult sources such as Buxton,!
Grossman,” Harnsberger et al.,° Lee et al.,* or Osborn et al.°
Computed Tomography (CT)
In CT, the patient is passed between a source of x-rays and a series of
detectors. Tissue density is measured by the effects of x-rays on atoms
within the tissue as x-rays pass through the tissue. Atoms of higher numbers have a greater ability to attenuate (stop) x-rays, whereas those with
lower numbers are less able to attenuate x-rays. The various attenuation intensities are computerized into numbers (Hounsfield units or
CT numbers). Bone is given the value of +1,000 and is white, whereas
air is given a value of -1,000 and is black. In this respect, a lesion or
defect in a CT that is hyperdense is shifted toward the appearance of
bone; it is more white. For example, acute subarachnoid blood in CT
is hyperdense to the surrounding brain; it is more white than the brain
and is shifted more to the appearance of bone (Figure 1-1). A lesion in
CT that is hypodense is shifted toward the appearance of air or cerebrospinal fluid; it is more black than the surrounding brain (Figure 1-2).
In this example, the territory of the middle cerebral artery is hypodense
(Figure 1-2). Isodense in CT refers to a condition in which the lesion
and the surrounding brain have textures and/or shades of gray that are
essentially the same. Iso- is Greek for equal: “equal density.” Extravascular blood, an enhanced tumor, fat, the brain (gray and white matter),
and cerebrospinal fluid form an intervening continuum from white to
black. In general, Table 1-1 summarizes the white to black intensities
seen for selected tissues in CT.
The advantages of CT are: (1) it is done rapidly, which is especially
important in trauma; (2) it clearly shows acute and subacute hemor-
rhages into the meningeal spaces and brain; (3) it is especially useful
for children in trauma cases; (4) it shows bone (and skull fractures) to
advantage; and (5) it is less expensive than MRI. The disadvantages
of CT are: (1) it does not clearly show acute or subacute infarcts or
ischemia, or brain edema; (2) it does not clearly differentiate white from
gray matter within the brain nearly as well as MRI; and (3) it exposes
the patient to ionizing radiation.
CT in the axial plane of a patient with subarachnoid hemorrhage. Bone is white, acute blood (white) outlines the sub-
arachnoid space, brain is gray, and cerebrospinal fluid in the third and
lateral ventricles is black.
Magnetic Resonance Imaging (MRI)
The tissues of the body contain proportionately large amounts of protons (hydrogen). Protons have a positive nucleus, a shell of negative
electrons, and north and south poles; they function like tiny spinning
bar magnets. Normally, these atoms are arranged randomly in relation
to each other because of the constantly changing magnetic field produced by the electrons. MRI uses this characteristic of protons to generate images of the brain and body.
When radio waves are sent in short bursts into the magnet containing
the patient, they are called a radiofrequency pulse (RP). This pulse may
vary in strength. When the frequency of the RP matches the frequency of
the spinning proton, the proton will absorb energy from the radio wave
(resonance). The effect is twofold. First, the magnetic effects of some
protons are canceled out; second, the magnetic effects and energy levels
in others are increased. When the RP is turned off, the relaxed protons
release energy (an “echo”) that is received by a coil and computed into
an image of that part of the body.
The two major types of MRI images (MRI/T1 and MRI/T2) are related
to the effect of RP on protons and the reactions of these protons (relaxation) when the RP is turned off. In general, those canceled-out protons
return slowly to their original magnetic strength. The image constructed
from this time constant is called T1 (Figure 1-3). On the other hand, those
protons that achieved a higher-energy level (were not canceled out) lose
Axial CT showing a hypodense area within the territory of the
middle cerebral artery on the right side of the patient. This is
indicative of a lesion in this region which would result in substantive
deficits.
their energy more rapidly as they return to their original state; the image
constructed from this time constant is T2 (Figure 1-4). The creation of a
T1-weighted image versus a T2-weighted image is based on a variation in
the times used to receive the “echo” from the relaxed protons.
The terms hyperintense, hypointense, and isointense apply to T1- and
T2-weighted MRI. Hyperintense in T1 is a shift toward the appearance
of fat, which is white in the normal patient; a hyperintense lesion in T1 1s
more white than the surrounding brain (Figure 1-5A; Table 1-2). A meningioma, and the surrounding edematous areas, are hyperintense: more
white than the surrounding brain (Figure 1-5A). In T2, hyperintense is a
shift toward the appearance of cerebrospinal fluid, which is also white
in the normal individual (Figure 1-4); a hyperintense condition in T2 is
also more white than the surrounding brain (Table 1-2). Hypointense in
both T1 and T2 is a shift toward the appearance of air or bone in the
normal patient; this is a shift to more black than the surrounding brain.
In this example, there are hypointense areas (arrows) adjacent to the
lateral ventricles in the frontal and occipital areas (Figure 1-5B). Isointense refers to a situation in which a lesion and the surrounding brain
have shades of gray and/or textures that are basically the same. In this
example of a pituitary tumor in a T1 MRI, the color and texture of the
tumor is essentially the same as the surrounding brain; it is isointense
(Figure 1-SC). Iso- is Greek for equal: “equal intensity.”
Table 1-1 The Brain and Related Structures in CT
STRUCTURE/FLUID/SPACE
Gray SCALE
Bone, acute blood
Very white
Enhanced tumor
Very white
Subacute blood
Light gray
_ Muscle
Light gray
Gray matter
Light gray
White matter
| Medium gray
Cerebrospinal fluid
Medium gray to black
Air, fat
Very black
|
_ A sagittal T1-weighted MRI. Brain is gray, and cerebrospinal
fluid is black.
A sagittal T2-weighted MRI. Brain is gray, blood vessels frequently appear black, and cerebrospinal fluid is white.
Table 1-2 summarizes the white to black intensities seen in MRI
images that are T1-weighted versus T2-weighted. It should be emphasized that a number of variations on these two general MRI themes are
routinely seen in the clinical environment.
The advantages of MRI are: (1) it can be manipulated to visualize a
wide variety of abnormalities or abnormal states within the brain; and
(2) it can show great detail of the brain in normal and abnormal states.
The disadvantages of MRI are: (1) it does not show acute or subacute
subarachnoid hemorrhage or hemorrhage into the substance of the
, brain in any detail; (2) it takes much longer to do and, therefore, is not
useful in acute situations or in some types of trauma; (3) it is comparatively more expensive than CT; and (4) the scan is extremely loud and
may require sedation in children. The ensuing discussion briefly outlines
the salient features of individual chapters.
CHAPTER
Axial MRIs showing a hyperintense lesion, meningioma, and
edema (A), hypointense areas in the white matter of the hemisphere (B, arrows), and a pituitary tumor (PT) that is isointense (C).
2
This chapter presents: (1) the gross anatomy of the spinal cord and its
arteries; and (2) the external morphology of the brain from all views,
including the insular cortex, accompanied by MRIs and drawings of the
vasculature patterns from the same perspectives. All gross brain images
appear in color, two new images have been included but none eliminated,
and clinical terminology such as that used for segments of the cerebral
vessels (A,;—-A;, M,;—Mg, and P,—-P,), continues to be emphasized. Line
drawings and accompanying CT that focus on vascular variations that
have important clinical implications are featured in this chapter.
Table 1-2 The Brain and Related Structures in MRI
NORMAL
T1
ae
Bone
Very black
Very black
Air
Very black
Very black
[ Dark gray
Dark gray
White matter
Muscle
Light gray
Dark gray
Gray matter
Dark gray
Light gray
Fat
White
Gly
Cerebrospinal fluid
Very black
Very white
ABNORMAL
9
A192
Edema
Dark gray
Light gray to white
| Tumor
Variable
Variable
.
CHAPTER 3
This chapter focuses on: (1) the relationships of cranial nerves; (2) their
exits from the brainstem; (3) their appearance in representative MRI;
and (4) examples of cranial nerve deficits seen in cases with lesions of
the brainstem. A new image has been added emphasizing the arrangement of cranial nerve exits and their relationship to functional cell columns. The detailed cross-reference to other sections or pages in the Atlas
where additional cranial nerve information is found was also revised.
CHAPTER 4
The structure of the meninges, and their appearance in MRI or CT,
is affected by a wide variety of events such as infections (meningitis),
trauma, vascular incidents (epidural, subdural, subarachnoid hemor-
[ White
(Rarely done)
rhage), and tumor
| Dark gray
Light gray to white
Subacute infarct
Dark gray
Light gray to white
Acute ischemia
Dark gray
Light gray to white
eaivere ischemia
| Dark gray
Light gray to white
this chapter. In addition, they are a central element in cases of increased
intracranial pressure and consequent herniation. The size, shape, and
relations of the ventricular system are clearly correlated with the distribution of intraventricular blood and tumors of the choroid plexus; all
of which are illustrated and described in this chapter.
Enhanced tumor
[ Acute infarct
(meningioma), examples of which are featured in
CHAPTER 5
sections to clarify anatomical points or possibly confusing issues; and
(5) most importantly, emphasizing how easily the Anatomical Orientation can be flipped into the Clinical Orientation (Figure 1-7). Knowing
external and internal brain and spinal cord structures in a Clinical
The general morphology of the forebrain and brainstem is continued
into the two sections of Chapter 5. Part I consists of brain slices and
MRI in the coronal plane; Part II consists of slices and MRI in the axial
plane. The coronal and axial brain slices in this chapter were prepared,
and oriented, such that the R/L sides of the MRI correlate exactly with
the corresponding R/L sides of the brain slice. The orientation drawings
(upper left) illustrate the direction, and hence laterality, of the view of
the respective slices.
:
The MRIs have been reorganized, and in several cases new ones
inserted, so as to maintain the remarkably close correlation between
structures identified in the brain slice and the same structures seen in
the corresponding MRIs. The MRI and the brain slice appear on the
same page so the correlation can be instantly made. Since brain sections
at autopsy or in clinic—pathologic conferences are viewed as unstained
specimens, the preference here is to present this material in a format that
will most closely parallel what is seen in these clinical settings.
Innovations that were introduced in recent editions are further
emphasized in this new edition. First, the ability to flip an image from
an Anatomical Orientation to a Clinical Orientation places everything
in the image (line drawing or stained section) into a clinical format: (1)
the images match exactly the corresponding MRI or CT; (2) the image
has right and left sides; and (3) the topography of all tracts and nuclei in
flipped images matches that as seen in CT or MRI. All images in Chapter 6 that can be flipped to a Clinical Orientation are identified by this
symbol in the lower left of the image.
CHAPTER 6
image V}| ebeuy
Orientation is absolutely essential to successful, and correct, diagnosis
and for planning an approach for treatment. Emphasizing cisterns,
their locations, names, relationships, and contents (arteries, veins,
structures, cranial nerves) remains an essential element in the learning/
review process (Figures 1-7 and 1-8).
Clinical Orientation
y
Online
Numerous improvements and updates have been made in Chapter 6
over the years of previous editions. These have been directed at addressing suggestions and improving the educational value and relevance
to the user. This has included: (1) revising functional components to
reflect a contemporary view; (2) moving the longitudinal representations of these nuclei to those pages where they are most relevant;
(3) revising the color coding of the longitudinal view and crosssectional artwork so they consistently match throughout the chapter
(Figures 1-6 and 6-3A,B); (4) adding new artwork and colored stained
Second, the inherent value of viewing brain anatomy and line drawings in a Clinical Orientation is stressed throughout this chapter, particularly in relation to somatotopy, vascular supply and territories,
clinical examples, and the MRI or CT, most of which are featured on the
same page as the line drawing or stained section. Third, the color keys
have been revised to reflect the modified color palate for the sensory
Anatomical orientation
MRI, T2-weighted image
6-4B
Medial motor cell
column, SE cells
Posterior horn,
SA input
6-4A, 6-4B
Lateral motor cell
column, SE cells
A stained section of the lumbar spinal cord (lower) and the
overview on spinal cord and brainstem cell columns showing
the level of this section and of the line drawing on the facing page. For
convenience only, these examples from 6-4A and 6-4B are reduced here
to fit in a single column.
CT cisternogram
An example of the brainstem showing anatomical and clinical
orientations at about the caudal one-third of the medulla and
the corresponding T1-weighted MRI (with especially important struc-
tures labeled), T2-MRI, and CT cisternogram. The abbreviations
are
keyed to the full label on the facing page in Chapter 6. For addition
al
examples and details of brainstem and spinal cord, see Chapter 6.
CHAPTER 8
This chapter illustrates a wide variety of clinically relevant CNS tracts/
pathways in both Anatomical and Clinical Orientations, includes 15
illustrations of pathways of spinal and brainstem reflexes that may be
tested during a comprehensive neurologic examination, and contains
literally dozens of clinical correlations and/or examples. The following
features enhance the user's comprehension of concepts that are directly
relevant to diagnosing the impaired patient. First, inclusion of comprehensive pathways in an atlas format allows for the learning of clinically relevant concepts in a wide variety of educational settings. Second,
pathways that are most important to developing diagnostic skills are
presented in Anatomical and Clinical Orientations which show: (1) its
origin, extent, course, and termination; (2) laterality, an enormously
1
©
CT of a patient following injection of a radiopaque contrast
media into the lumbar cistern. In this example, at the medullary level (a cisternogram), neural structures appear gray and the subarachnoid space appears light.
and motor nuclei of the spinal cord and brainstem. Fourth, continuity
from Anatomical Orientation to Clinical Orientation is again illustrated
in a series of line drawings and MRI and CT on odd-numbered pages
showing spinal cord and brainstem levels (Figure 1-7). This new edition
continues to utilize CT cisternograms as an integral part of the learning
experience (Figure 1-8).
The new innovations introduced in this chapter are designed to
enhance its educational value, help the first-time user master the topic,
modify misplaced leader lines, and recast a couple of line drawings to
enhance their clinical relevance. Three particularly significant changes
offer marked improvements. First, the line drawings for Figures 6-31A
through 6-40A have been recast and prepared in color to match, as
closely as is reasonably possible, the stained section on the facing page.
This represents a major change in this chapter and will greatly enhance
learning and integrating internal brain structures. Second, the artwork
page has been revised to create more useable space on each page of
the chapter. Third, this extra space has allowed for revising each figure
description to include additional clinical information and anatomical
correlation relevant to that particular brain/spinal cord section. The
emphasis in this, and in all chapters, is to provide CNS morphology in
a format that will be most useful and relevant to what the user will see
in the clinical setting.
important clinical concept; (3) position throughout the neural axis and
its decussation, if applicable; (4) somatotopy within tracts; and (5) the
blood supply at all levels. Third, a brief summary of the principal neuroactive substances associated with many pathways, whether they result
in excitation (+) or inhibition (—) at their receptor sites, and deficits that
may correlate with the loss of particular neurotransmitters is included.
Fourth, clinical correlations accompany each pathway drawing; these
describe deficits, lesions, clinical terminology, and laterality of deficits
at different levels of the pathway. In toto, the drawings in Chapter 8
provide a maximal amount of clinically relevant information, each in a
single easy-to-follow illustration.
Interspersed within this chapter are illustrations presented in Clinical
Orientation that immediately follow, and complement, the corresponding pathway presented in Anatomical Orientation (Figures 1-9 and
1-10). These clinical illustrations overlay MRIs, focus on cranial nerves
and long tracts that are especially important to the diagnosis of the
impaired patient. This approach recognizes that, in some educational
settings, pathways are taught anatomically, while in others the emphasis
is on a Clinical Orientation; both approaches are accommodated in this
atlas. It is essential to emphasize that when viewing MRI or CT of a
rus cerebri
ML in midbrain
ALS in midbrain
Red nucleus
CHAPTER 7
The arrangement of pages in this chapter remains basically the same as
in previous editions: axial brain images in color and the corresponding
axial MRI are on left-hand pages and sagittal brain images in color and
the corresponding sagittal MRI are on right-hand pages. The heavy red
line on the axial images (odd-numbered Figures 7-1 to 7-9) indicates
the plane of section of the sagittal image on the facing page; similarly,
the heavy red line on the sagittal images (even numbered Figures 7-2
to 7-10) indicates the plane of section of the axial image on the facing page. Correlations between stained slices and between structures in
MRI can be easily made.
The ability to compare different planes of section (stained section
and MRI) on facing pages allows the user to build a three-dimensional
view of a variety of internal structures in images that are commonly
available in the clinical environment. However, these images can also
be viewed as an axial series (all left-hand pages) or a sagittal series
(all right-hand pages). Educational flexibility is inherent within these
arrangements.
Substantia nigra
idbrain tegmentum
Inferior colliculus
erebral aqueduct
Basilar pons
ML in pons
Pot
Adon
ML in medulla
Anterolateral system
(ALS) in medulla
Spinal trigeminal
tract and nucleus
ontine tegmentum
Fourth ventricle
uperior cerebellar
peduncle
yramid
Inferior olive
estiform body
ourth ventricle
Medial lemniscus (ML)
| The medulla, pons, and midbrain portions of the posterior col| umn-medial lemniscus pathway (see Figure 8-3A for the entire
pathway) superimposed on MRI and shown in a Clinical Orientation.
For convenience only, this example from Figure 8-3A is reduced here to
fit in a single column.
ML in midbrain
* Loss of proprioception, discriminative
touch, and vibratory sense on right LE
(+ UE if medial part of ML involved)
+ Loss of pain and thermal sensation
on right UE and LE
ALS in midbrain
Red nucleus
eS
Mid-to-rostral pons
ae
* Loss of proprioception, discriminative
touch, vibratory, pain, and thermal
senses on right UE and LE
* Loss of discriminative touch, pain, and
thermal sense on left side of face;
paralysis of masticatory muscles
ML in pons
(trigeminal nuclei involved)
Caudal pons
+ Proprioception and pain/thermal loss as
in mid-to-rostral pons
+ Left-sided facial and lateral rectus
paralysis (facial/abducens nucleus/nerve)
* Left-sided loss pain/thermal sense on
face
[ + Left ptosis, miosis, anhidrosis (Horner)
ALS in pons
ML in medulla
Anterolateral system
(ALS) in medulla
* Loss of proprioception, discriminative
touch, and vibratory sense on right UE/LE
* Tongue weakness: deviates to left on
attempted protrusion
* Hemiplegia of right UE and LE
a9”
——==
Spinal trigeminal
tract and nucleus
Medial lemniscus (ML)
The medulla, pons, and midbrain portions of the posterior
~ column-medial lemniscus pathway (see Figure 8-3B for the
entire pathway) superimposed on MRI in a Clinical Orientation, with
lesions and corresponding deficits at representative levels. For convenience only, this example from Figure 8-3B is reduced here to fit in a
single column.
patient compromised by neurologic lesion or disease, all of the internal
brain anatomy and all tracts, including their somatotopy, are seen in a
Clinical Orientation. It is absolutely essential that the user recognize
and understand this fact of clinical reality.
Since all possible pathways that may be taught in a given neurobiology course cannot be anticipated, flexibility is designed into this
chapter. The last figure in each section is a blank master drawing that
follows the same format as the preceding figures. These may be used for
learning, review, practicing pathways, in an instructional setting, and as
a substrate for examination questions.
CHAPTER 9
The emphasis of Chapter 9 is on clinical concepts. In this edition, the
title of Chapter 9 has been modified to reflect its expanded treatment of
a wider range of clinical cases and examples; the revised title is Clinical
Syndromes of the CNS. In addition, this chapter has been organized
into two parts, a Part I, Herniation Syndromes of the Brain and Spinal
Discs, and a Part II, Representative Stroke Syndromes. This significantly
broadens the clinical information and follows a suggestion to include
more stroke examples, but in a consistent context. In addition to stroke
images in other chapters, this revised Chapter 9 has 36 new images
focusing on stroke.
Recognizing that brain herniations share general features in common
with intervertebral disc extrusions, selected spinal cord syndromes are
included to offer a more complete picture of this general phenomenon.
There is a finite amount of space in the cranial cavity; small space-taking events may temporarily be accommodated, while large and especially
rapidly occurring events are not tolerated. Anything that compromises
this finite amount of space, may result in increased intracranial pressure (ICP) and a cascade of events that leads to herniation of the brain
from one location/compartment to another, commonly called a herniation syndrome. A herniation may be silent, or may result in sudden and
potentially catastrophic deficits; in some cases, and if untreated, death
may follow within minutes.
.
Increased ICP may be signaled by effacement of sulci or cisterns OF a
shift in brain structures that may be subtle, particularly in an isodense
CT, or obvious, as in an edematous tumor. Once evidence of ICP has
been determined, a course of treatment is put in motion to guard against
further clinical deterioration. Blood within the cranial cavity may result
from trauma (common), aneurysm rupture, arteriovenous
tion (AVM) bleed, and a variety of other causes.
CHAPTER
malforma-
10
This chapter contains a series of angiograms (arterial and venous phases),
MRA images, and MRV images. Fourteen new images showing a variety
of vascular lesions correlated with the normal vascular patterns have been
added. The angiograms are shown in lateral and anterior—posterior projections—some as standard views with corresponding digital subtraction
images. MRA and MRV technology are noninvasive methods that allow
for the visualization of arteries (MRA) and veins and venous sinuses
(MRV). However, there are many situations when both arteries and veins
are seen with either method. Use of MRA and MRV is commonplace, and
this technology is an important diagnostic tool.
CHAPTER
11
The questions and corresponding answers of Chapter 11 recognize that
examinations are an essential part of the educational process; these
elements should prepare, as much as reasonably possible, the user for
future needs and expectations. Many are prepared as a patient vignette
and in the USMLE Step-1 style (single best answer) which emphasize:
(1) anatomical and clinical correlations; (2) application of basic neurobiology concepts to clinical practice; (3) integration of regional neurobiology, systems neurobiology, neurovascular patterns, and disease
processes; and (4) the topographical maps within motor and sensory
systems.
While generally grouped by chapter, questions may draw on information from more than one chapter thus reflecting the reality of many
major examinations. Correct answers are given, incorrect answers are
explained. A sampling of questions and answers is provided in this chapter with over 300 provided online. While not exhaustive, these questions
represent a broad range of clinically relevant topics.
REFERENCES
1. Buxton RB. Introduction to Functional Magnetic Resonance Imag-
ing, Principles and Techniques. 1st ed. Cambridge, UK: Cambridge
University Press; 2002.
2. Grossman CB. Magnetic Resonance Imaging and Computed
Tomography of the Head and Spine. 2nd ed. Baltimore, MD:
Williams & Wilkins; 1996.
3. Harnsberger HR. Suprahyoid and infrahyoid neck. In: Harnsberger
HR, Osborn AG, Macdonald AJ, et al., eds. Diagnostic and Surgical
Imaging Anatomry: Brain, Head & Neck, Spine. Salt Lake City, UT:
Amirsys Publishing Inc; 2011.
4. Lee SH, Rao KCVG, Zimmerman RA. Cranial MRI and CT. 4th ed.
New York: McGraw-Hill Health Professions Division; 1999,
5. Osborn AG, Salzman KL, Barkovich AJ, et al. Diagnostic Imaging:
Brain. 2nd ed. Salt Lake City, UT: Amirsys Publishing Inc; 2010,
Q&A for this chapter is available online on TC POiNt.
Z|
External Morphology
of the Central Nervous System
The adult central nervous system (CNS) consists of the forebrain (telencephalon and diencephalon), the brainstem (mesencephalon, meten-
cephalon, and myelencephalon), the cerebellum, and the spinal cord.
The cerebellum is not part of the brainstem but is a suprasegmental
structure located within the posterior fossa but superior to the long
axis of the brainstem. Generally speaking, lesions in a specific CNS
region may result in deficits that are unique to that region, in deficits
that may reflect damage to tracts or pathways traversing that region,
or to combinations of these. CNS divisions, representative structures
located therein, and cranial nerves (CN) associated with each are sum-
marized below.
COMPARTMENTS
The cranial cavity is lined by the meninges; the inner portions (meningeal dura + arachnoid matter) of which form dural reflections. These
larger reflections, as the falx cerebri, separate the right cerebral hemisphere from the left, and as the tentorium cerebelli, separate the two
cerebral hemispheres (which are supratentorial) from the brainstem
and the cerebellum (which are infratentorial). The contents of the
right and left supratentorial compartments are continuous with the
contents of the single infratentorial compartment via the midbrain
which occupies the tentorial notch (incisura). Increases in intracranial
pressure (ICP) within one supratentorial compartment may result in
herniation of CNS structures across the midline and/or downward
through the tentorial notch. In similar manner increased ICP in the
infratentorial compartment may result in upward herniation through
the tentorial notch or downward herniation through the foramen
magnum (see Chapter 9).
chapter
MAIN BLOOD VESSELS
The blood supply to the spinal cord arises from the anterior spinal artery,
a branch of the vertebral artery, and from the posterior spinal arteries
usually branches of the posterior inferior cerebellar arteries. This is supplemented by segmental arteries (cervical, posterior intercostal, and lumbar arteries). Branches of segmental arteries are the anterior and posterior
radicular arteries, found at every spinal root level, and anterior and posterior spinal medullary arteries, found at about 6—18+ spinal levels; their
numbers are variable. The radicular arteries serve each set of spinal roots
and the corresponding posterior root ganglion (there are radicular arteries
at each spinal level), while spinal medullary arteries are principally a supplemental supply to the anterior and posterior spinal arteries and to the
arterial vasocorona (spinal medullary arteries are not found at each spinal
level). The artery of Adamkiewicz, an especially large anterior spinal medullary artery, arises from lower thoracic or upper lumbar levels (usually
T8-L2, ~80%-85%) and is more commonly (75+%) seen on the left side.
The blood supply to the brain is from the two internal carotid arteries and the two vertebral arteries, the latter join to form the basilar
artery. The former is commonly referred to as the internal carotid system, the latter as the vertebrobasilar system. These two systems are connected with each other by the posterior communicating arteries. Each
internal carotid artery divides into middle (segments M,;—M,) cerebral
and anterior (segments A;—-A;) cerebral arteries which generally serve
superficial and deep structures in lateral and medial regions of the hemisphere, respectively. The two vertebral arteries join to form the basilar
artery; the basilar bifurcates to form the posterior cerebral (P;—P,4) arter-
ies; proximal PCA branches primarily serve the thalamus and rostral
midbrain, its distal branches serve temporal and occipital cortices.
eee
ee
Divisions of the CNS, Representative Structures, and Associated Cranial Nerves (CNs)
ee
Forebrain
Telencephalon: cerebral cortex, lobes, gyri, sulci, subcortical white matter, internal capsule, basal nuclei, CN I
Diencephalon: various divisions of the dorsal thalamus, hypothalamus, subthalamus, epithalamus, metathalamus, CN II
Brainstem
Mesencephalon: midbrain, tectum, tegmentum, crus cerebri, substantia nigra, red nucleus, CNs III, IV
Metencephalon: pons, basilar and tegmental areas, cerebellar peduncles, CN V
as the nerves
Myelencephalon: medulla, pyramid, inferior olive, restiform body; CNs IX, X, XII; CNs VI, VIL, and VIII, which are regarded
of the pons-medulla junction; CN XI arises from C1—C5/6 cervical levels of the spinal cord, ascends through the foramen
magnum, joins with CNs IX and X to exit the cranial cavity via the jugular foramen
Cerebellum
Anterior, posterior, flocculonodular lobes; cerebellar peduncles, cortex, nuclei
Spinal cord
white and gray matter, spinal laminae
Anterior and posterior roots, posterior root ganglia, cervical and lumbosacral enlargements, spinal
of Rexed, anterior and posterior horns
TD
Accessory nerve (AccNer)
C2 PR
AccNer
Dura
CoRR
AccNer
CARR
C5 Posterior
AccNer
root (PR)
C6 PR
Pent
Denticulate
ligament (DenLi
9
(Bentig)
Fasciculus cuneatus
Sulci:
Posterior median
Posterior intermediate
Posterolateral
Fasciculus gracilis
C7 PR
C8 PR
T1 PR
Overview of a posterior aspect of the spinal cord from C2-T1
(A) and details from the same specimen showing the C2—C4
and C7-T1 levels (B, C).
The denticulate ligaments anchor the spinal cord within the dural
sac; they are pial tissue sheets that extend laterally to attach to the
arachnoid on the inner surface of the dura. The accessory nerve
(CN XI) arises from spinal cervical levels C1-—C5/6 and courses rostrally
between the anterior and posterior roots (B). The posterior surface of
the cord clearly shows structures and sulci characteristic of the posterior column system, the location of the posterolateral sulcus, which is
well delineated, and the entrance point for posterior (sensory, dorsal)
supply their respective roots. The posterior spinal artery is located
medial to the posterior root entry zone and the anterior spinal artery
lies within the anterior median sulcus (Figure 2-3 on facing page).
Radiculopathy results from spinal nerve root damage, and gives
rise to what is commonly called sciatica. The most common causes are
intervertebral disc disease/protrusion, spondylolysis, and motor and/or
sensory deficits that correlate with the level affected. The main symptoms are pain radiating in a root or dermatomal distribution, weakness,
hyporeflexia, and/or paresthesia of the muscles served by the affected
root. The discs most commonly involved at cervical (C) and lumbar
roots (C).
45%), and LS-S1 (40%-45%). Thoracic disc problems are rare, well
Posterior and anterior spinal medullary arteries accompany their
respective roots (Figure 2-3 on facing page) and the radicular arteries
(L) levels are C6-C7 (65%-70%), C5-C6 (16%-20%), L4-L5 (40%—
under 1% of all disc protrusions. For additional information on spinal
disc extrusions, see Chapter 9.
Fasciculus gracilis
baer
ater rcol(PR)
Fasciculus cuneatus
C3 Anterior
root (AR)
Anterior
funiculus
Denticulate
ligament
(DenLig)
Anterior spinal
medullary
C5 AR
:
arter
u
Anterolateral sulcus
Welle)
Thoracic
anterior roots
ALSul
Anterior spinal artery
C7 AR
ALSul
Anterior
median fissure
ee)
Anterior aspect of the spinal cord from C3—C7 (A), the C7 segshowing the anterior spinal artery and the comparatively diminutive
ment showing the posterior and anterior roots and the posteri- __size of the thoracic roots (C). The anterolateral sulcus, the exit point for
or root ganglion (B), and a view of the anterior surface at thoracic levels
anterior (motor) roots, is irregular in appearance (A).
Posterior spinal arteries
Fasciculus
gracilis
Arterial
vasocorona
Basilar artery
Fasciculus
cuneatus
—~ Posterior inferior
cerebellar arteries
Lateral corticospinal
=~
tract
Vertebral arteries
Anterior spinal artery
Posterior spinal
Anterolaterai
medullary artery
system
Posterior radicular
artery (on posterior root)
Sulcal arteries
Anterior spinal
medullary artery
Anterior radicular artery
(on anterior root)
Segmental artery
arteries) arise at intermittent levels, not at every level, and serve to augment
Semi-diagrammatic representation showing the origin and genis an uneral location of principal arteries supplying the spinal cord. The _ the blood supply to the spinal cord. The artery of Adamkiewicz
2-3
in lower
left
the
on
usually
arising
artery
medullary
spinal
large
usually
anterior and posterior radicular arteries arise at every spinal level and serve
arterial
The
cases).
of
~85%
in
(T9-L2,
levels
lumbar
upper
thoracic or
their respective roots and ganglia. The anterior and posterior spinal medulsurface.
cord
the
covering
plexus
anastomotic
diffuse
a
is
vasocorona
lary arteries (also called medullary feeder arteries or segmental medullary
External Morphology of the Central Nervous System
‘fy
if
)
———
Dura and
arachnoid
Thoracic
cord
We
Posterior root
Lumbar and
sacral cord
(LuSaCd)
LuSaCd
L1
SaCoCd
Sacral and
coccygeal
cord
(SaCoCd)
Conus
medullaris
Lumbar
cistern
FTInt
CaEq
Cauda
equina
(CaEq)
L5
Filum terminale
internum (FTInt)
S1
Dura and
arachnoid
Overall posterior (A, B) and sagittal MRI (C, T2-weighted)
views of the lower thoracic, lumbar, sacral, and coccygeal spinal cord segments and the cauda equina.
The dura and arachnoid are retracted in A and B. The cauda equina
is shown in situ in A, and in B the nerve roots of the cauda equina have
been spread laterally to expose the conus medullaris and filum terminale
internum. This latter structure is also called the pial part of the filum
terminale. See Figures 6-3 and 6-4 for cross-sectional views of the cauda
equina.
In the sagittal MRI (C), the lower portions of the cord, the filum
terminale internum, and cauda equina are clearly seen. In addition, the
intervertebral discs and the bodies of the vertebrae are clear. The lumbar
cistern is an enlarged part of the subarachnoid space caudal to the end of
the spinal cord. This space contains the anterior and posterior roots from
the lower part of the spinal cord that collectively form the cauda equina.
The filum terminale internum also descends from the conus medullaris
through the lumbar cistern to attach to the inner surface of the dural sac.
The dural sac ends at about the level of the $2 vertebra and is attached to
Coccyx
the coccyx by the filum terminale externum (also see Figure 4-1). A lumbar puncture is made by inserting a large-gauge needle (18-22 gauge)
between the L4 and LS (preferred) vertebrae or the L3 and L4 vertebrae
and retrieving a sample of cerebrospinal fluid from the lumbar cistern.
This sample may be used to evaluate for infection, inflammation, malignancy, or elevated intracranial pressure.
A cauda equina syndrome may be seen when an extruded disc (L4—
LS more common level) impinges on the cauda equina or in patients
with tumor, trauma, or other conditions that damage these nerve roots.
The symptoms are usually bilateral and may include (1) significant
weakness (paraplegia is a possible outcome) and hypo- or areflexia of
the lower extremity; (2) saddle anesthesia (commonly seen), which presents as sensory deficits on the buttocks, medial and posterior aspects
of thighs, genitalia and anus, and perineum; (3) urinary retention (commonly seen) or incontinence, decreased sphincter tone, and fecal incontinence; and (4) decrease in sexual function (may appear later if cause is
left untreated). Although sensory loss is common, these patients may or
may not experience low back pain or sciatica.
Central sulcus
Precentral sulcus
Postcentral sulcus
Parietooccipital
Lobes
sulcus
Frontal
Parietal
Temporal
Occipital
Preoccipital
notch
Lateral sulcus
Limbic
|eee
|
Insular
Central sulcus
Paracentral sulcus
Marginal sulcus (marginal
ramus of the cingulate
sulcus)
Cingulate sulcus
Corpus callosum
Parietooccipital
sulcus
Fornix
Diencephalon
Calcarine
Preoccipital notch
sulcus
Optic nerve
Collateral sulcus
os
Lateral (A) and medial (B) views of the cerebral hemisphere show-
~)
ing the landmarks used to divide the cortex into its main lobes.
On the lateral aspect, the central sulcus (of Rolando) separates frontal and parietal lobes. The lateral sulcus (of Sylvius) forms the border
between temporal lobe inferiorly and between frontal and parietal lobes
superiorly. The occipital lobe is located caudal to an arbitrary line drawn
between the terminus of the parietooccipital sulcus and the preoccipital
notch. A horizontal line drawn from the upper end of the lateral fissure
to the rostral edge of the occipital lobe represents the border between
parietal and temporal lobes. The insular lobe, commonly referred to as
the insular cortex (see also Figures 2-40 and 2-41), is located internal to
the lateral sulcus in the general area that is shaded gray (A). This part of
the cortex is made up of long and short gyri that are separated from each
other by the central sulcus of the insula (see Figure 2-40). The insula, as
a whole, is separated from the adjacent portions of the frontal, parietal,
and temporal opercula by the circular sulcus, hence the designation of the
insula as a lobe. This sulcus is generally located at the circumference of
the gray area (A).
On the medial aspect, the cingulate sulcus separates medial portions of
frontal and parietal lobes from the limbic lobe. An imaginary continuation of the central sulcus intersects with the cingulate sulcus and forms the
border between frontal and parietal lobes. The parietooccipital sulcus and
an arbitrary continuation of this line to the preoccipital notch separate
the parietal, limbic, and temporal lobes from the occipital lobe.
Postcentral gyrus
Precentral gyrus
E
E
Supramarginal
gyrus
Pars opercularis
Lobes
————ae
Frontal
Parietal
;
Pars triangularis
Temporal
of
A
te
é
Ee
Occipital
Limbic
Anterior paracentral gyrus
Posterior paracentral gyrus
Calcarine sulcus
B
18
Optic nerve
Lateral (A) and medial (B) views of the cerebral hemisphere
2-6
showing the more commonly described Brodmann areas.
In general, area 4 comprises the primary somatomotor cortex, areas
3, 1, and 2 the primary somatosensory cortex, and area 17 the primary
visual cortex. Area 41 is the primary auditory cortex, and the portion of
area 6 in the caudal part of the middle frontal gyrus is generally recognized as the frontal eye field in humans.
The somatomotor cortex is the precentral plus the anterior paracentral gyri; the total representation of the body extends from one gyrus
into the other. The term precentral gyrus should not be equated with the
term somatomotor cortex, without qualification, as this excludes the
lower extremity. The same reasoning applies to the term somatosensory
cortex as related to the postcentral and posterior paracentral gyri.
The inferior frontal gyrus has three portions: a pars opercularis, a
pars triangularis, and a pars orbitalis. A lesion that is located primarily in areas 44 and 45 (shaded) will give rise to what is called a Broca
aphasia, also called motor, expressive, or nonfluent aphasia; it is also
Lingual gyrus
sometimes considered an apraxia. These patients do not have paralysis
of the vocal apparatus, but rather have great difficulty turning ideas into
meaningful speech. They have significant difficulty producing words
in a meaningful tone and sequence. These patients may have mutism
or slow, labored speech that consists of familiar single words or short
phrases with words left out (telegraphic speech). These patients are well
aware of their deficits.
The inferior parietal lobule consists of supramarginal (area 40) and
angular (area 39) gyri. Lesions in this general area of the cortex (shaded),
and sometimes extending into area 22, will give rise to what is known
as Wernicke aphasia, also sometimes called sensory, receptive, or fluent
aphasia. Words may be of appropriate meaning, tone, and strength but
have little correct sequencing; therefore, sentences have little or no meaning. Patients with a sensory aphasia speak freely and without hesitation,
but what is said may make little sense due to the use of inappropriate
words at inappropriate places in the sentences (paraphasia, or sometimes
called word salad). These patients may be unaware of their deficits.
Precentral gyrus (primary somatomotor cortex)
Postcentral gyrus (primary somatosensory cortex)
Hip area
Hip area
Trunk area —
Upper extremity
A
ees area
Lobes
Upper extremity_
—“ca
Hand area -
:
Face area
yf
/
Fi
ae
:
é
la
Parietal
/
!
f
!
{
\
\
Temporal
Occipital
er
ieLimbic
Anterior paracentral gyrus (somatomotor)
Lower extremity
Foot area
B
Posterior paracentral gyrus (somatosensory)
Lower extremity
7 Foot area
Genitalia
Left
ae inferior
visual
quadrant
:
Optic nerve
Lateral (A) and medial(B) views of the cerebral hemisphere
2-7
showing the general somatotopic organization of the primary
somatomotor and somatosensory cortices.
The lower extremity and foot areas are located on medial aspects
of the hemisphere in the anterior paracentral (motor) and the posterior
paracentral (sensory) gyri. The remaining portions of the body extend
from the margin of the hemisphere over the convexity to the lateral sulcus in the precentral and postcentral gyri. Using the appropriate terminology to specify these structural and functional regions of the cerebral
cortex is particularly useful.
An easy way to remember the somatotopy of these important
cortical areas is to divide the precentral and postcentral gyri generally into thirds: a lateral third that represents the face area, a middle
third that represents the upper extremity and hand with particular
Left superior
visual quadrant
emphasis on the hand, and a medial third that represents the trunk
and hip. The rest of the body representation, lower extremity and foot,
is on the medial aspect of the hemisphere in the anterior (motor) and
posterior (sensory) paracentral gyri. Lesions of the somatomotor cortex
result in motor deficits on the contralateral side of the body, whereas
lesions in the somatosensory cortex result in a loss of sensory perception from the contralateral side of the body. The medial surface of the
right hemisphere (B) illustrates the position of the left portions of the
visual field. The inferior visual quadrant is located in the primary visual
cortex above the calcarine sulcus, whereas the superior visual quadrant
is found in the cortex below the calcarine sulcus. Lesions of visual structures posterior to the optic chiasm may result in a contralateral (either
left or right based on the side of the lesion) homonymous hemianopia or
may present in other situations as a quadrantanopia.
External Morphology of the Central Nervous System—The Brain: Gross Views, Vasculature, and MRI nie
Longitudinal fissure
Superior frontal
gyrus (SFGy)
Middle frontal
We gyrus (MFGy)
Superior frontal
sulcus (SFSul)——Saee
Precentral
sulcus (PrCSul)
t
Precentral
gyrus (PrCGy)
Precentral
Central
sulcus (CSul)
gyrus (PrCGy)
Central
sulcus (CSul)
Postcentral
gyrus (PoCGy)
Supramarginal
gyrus
Postcentral sulcus
Superior parietal lobule
Anterior
cerebral
arteries
MFGy
SFGy
ACA
SFSul
territory
- PrCSul
CSul
PrCGy
PoCGy
cerebri
Falx
Superior (dorsal) view of the cerebral hemispheres showing the main gyri and sulci and an MRI (inverted inversion
recovery—lower left) and a CT (lower right) identifying structures
from the same perspective. Note the area of infarction representing
the territory of the anterior cerebral artery (ACA). The infarcted area
involves lower extremity, hip, and, possibly, lower trunk cortical areas;
because the lesion is in the left hemisphere, the deficits are on the
patient’s right side.
ee Watershed zone
Orbitofrontal branches
of MCA (Ma)
Callosomarginal branches
(from ACA)
Branches of MCA (M4)
Prerolandic
Paracentral branches
(from ACA)
Angular branches
of MCA (Mag)
Internal parietal branches
(from ACA)
Parieto-occipital sulcus
>
i
Branches of PCA
Parieto-occipital (P4)
Calcarine (P4)
9
Superior (dorsal) view of the cerebral hemispheres showing the
location and general branching patterns of the distal branches
of anterior (ACA), middle (MCA), and posterior (PCA) cerebral arteries.
Compare the distribution of ACA branches with the infarcted area in
Figure 2-8. The watershed zone represents an overlap of the distal territories of the MCA (laterally) and ACA (medially).
Joins superficial middle
cerebral vein (to enter
cavernous sinus) and
inferior anastomotic
vein (of Labbé)
Superior anastomotic
vein (of Trolard)
Superior anastomotic
vein (of Trolard)
Superior sagittal
sinus (SSS)
Superior cerebral veins
SSS toward sinus confluens
Superior (dorsal) view of the cerebral hemispheres showing the location of the superior sagittal sinus (SSS) and
the locations and general branching patterns of veins. The SSS is a
common location (~70%) of dural venous thrombosis. See Figures 10-4
and 10-5 for comparable angiograms (venous phase) of the superior
sagittal sinus.
External Morphology of the Central Nervous System
Precentral gyrus (PrCGy)
Central sulcus (CSul)
Precentral sulcus (PrCSul)
Superior frontal gyrus
Superior frontal sulcus
Postcentral gyrus (PoCGy)
Postcentral sulcus (PoCSul)
Superior parietal lobule
Intraparietal sulcus
Precentral sulcus (PrCSul)
Supramarginal gyrus
Middle frontal gyrus (MFGy)
Inferior frontal sulcus (IFSul)
Inferior frontal gyrus:
Pars opercularis (PoP)
Occipital
gyri (OGy)
Pars triangularis (PTr
Pars orbitalis (POrb
Lateral sulcus (LatSul)
~
Olfactory bulb
Preoccipital notch
Superior temporal gyrus (ST Gy)
Superior temporal sulcus (STSul)
Midd!e temporal gyrus (MT Gy)
Pr€Sul
PrOGy
— CSul
PoCSul
MFGy
PoCGy
IFSul
LatSul
OGy
PoP
PTr
MTGy
POrb
sTGy
STSul
Lateral view of the left cerebral hemisphere showing the prin- _the lower extremity), the parts of the inferior frontal gyrus
(partes opercucipal gyri and sulci and a T1 MRI on which many of these
__laris, triangularis, and orbitalis, sometimes called the Broca convolution)
structures can be identified from the same perspective. Especially importand the supramarginal and angular gyri that collectively form the hie
ant cortical areas are the precentral and postcentral gyri (primary somato- __parietal lobule. The frontal eye field is located
primarily in the caudal are
motor and somatosensory cortices, respectively, for the body, excluding
of the middle frontal gyrus adjacent to the precentral gyrus.
;
|
Watershed zone
/—
Rolandic branches
Prerolandic branches
Central sulcus
Anterior and posterior
|
parietal branches of MCA
Angular branches
of MCA
Temporal branches of MCA
Anterior
Middle
Posterior
Lateral view of the left cerebral hemisphere showing the
branching pattern of the middle cerebral artery. The middle cerebral artery (MCA) initially branches in the depths of the lat-
PCA. The individual branches of the overall My segment are named
usually according to their relationship to gyri, sulci, or position on
a lobe. Terminal branches of the posterior and anterior cerebral
eral sulcus (as M, and M; segments); these branches, when seen on
arteries course over the edges of the temporal and occipital lobes,
the surface of the hemisphere, represent the M, segment. Distal MCA
branches (upper) form a watershed zone with the distal ACA, and
other distal MCA branches form a comparable zone (lower) with the
and parietal and frontal lobes, respectively (see Figure 2-9). See
Figure 10-1 for an angiogram of the middle and anterior cerebral
arteries.
Superior anastomotic vein (of Trolard)
Rolandic vein
Superior sagittal sinus
Superior sagittal sinus
Superficial cerebral
veins
Superior cerebral veins
Straight sinus
Superficial middle
Position of
sinus confluens
cerebral vein
=
=
=,
—lransverse sinus
y/
Occbial anus
Inferior anastomotic vein (of Labbé)
Superior petrosal sinus
Inferior petrosal sinus
Sigmoid sinus
Cerebellar veins
Internal jugular vein
Lateral view of the left cerebral hemisphere showing the
locations of sinuses and the locations and general patterns of
superficial veins. Communication between veins and sinuses or between
sinuses also is shown. See Figures 10-2 and 10-11 for comparable angio-
gram and MRV of the sinuses and superficial veins. Sinus thromboses
are commonly seen in the superior sagittal and/or the transverse sinuses
(~70% each) but are less frequently seen in superficial veins on the cortex,
and are rarely seen in inferior sagittal or cavernous sinuses.
External Morphology of the Central Nervous System
wee Frontal pole
Olfactory sulcus (OlfSul)
Olfactory bulb
Gyrus rectus (GyRec)
Orbital gyri (OrbGy)
Olfactory tract
Temporal pole
Optic nerve
Infundibulum
Optic chiasm
Uncus (Un)
Optic tract (OpTr)
Mammillary
Interpeduncular
fossa (IPF)
body (MB)
Parahippocampal
gyrus
Inferior temporal
gyrus
Collateral sulcus
Crus cerebri (CC)
Substantia nigra
Occipitotemporal
gyri
Cerebral
aqueduct (CA)
Lingual gyrus
Superior
colliculi (SC)
Occipital gyri
Occipital pole
GyRec
OrbGy
——
Anterior
cerebral
artery
piu
Middle
cerebral
Optr
artery
OpTr
Hypothalamus
Un
Un
CC
IPF
a
emporal lobe
CA
SC
Cerebellum
Inferior (ventral) view of the cerebral hemispheres
and diencephalon with the brainstem caudal to midbrain removed and two MRIs (inversion recovery—lower left; T2
weighted—lower right) showing many structures from the same
e
1
¢
1
’
perspective. Note the relationships of the midbrain to surrounding
structures (cerebellum, medial aspect of the temporal lobe, uncus
[as related to uncal herniation], and hypothalamus and optic tract)
and to the cisterns.
:
Orbital Branches of ACA
Orbitofrontal branches
of MCA (Mg)
Anterior cerebral
artery (ACA, Ap)
Internal carotid
_ |nternal carotid
aitery
“
Posterior communicating
artery
Superior
trunk of MCA
FZ
cae segment of MCA
a
Inferior
Anterior Temporal
branch of PCA
trunk of MCA
(P., Segment)
Lenticulostriate
arteries
Posterior
communicating artery
P. segment of PCA
Posterior temporal
branch of PCA
°
(P, segment)
Parieto-occipital branch
of PCA (P,, segment)
Calcarine branch of
PCA (P, segment)
Inferior (ventral) view of the cerebral hemisphere, with
the brainstem caudal to the midbrain removed, showing segments P,-P, of the posterior cerebral artery (PCA), a small
portion of the anterior cerebral artery, and the initial branching
of the M, segment of the middle cerebral artery into superior
and inferior trunks. The correlation between the superior and
inferior trunks of the MCA and segments M,—My, are shown in
Figure 2-42.
Anterior cerebral vein
Sphenoparietal sinus
Ophthalmic vein
Sphenoparietal sinus
wren,
Superficial middle
§\cerebral vein
Intercavernous sinuses
Anterior
Deep middle
Posterior
Inferior petrosal sinus
Superior petrosal sinus
, cerebral vein
ae
a,
Yj
Ww
nent
/~Cavernous sinus
Basal vein
/
(of Rosenthal)
~
Sigmoid sinus
Internal jugular vein
Internal cerebral vein
Y Great cerebral vein (of Galen)
Straight sinus
Transverse sinus
Sinus confluens
Transverse sinus
Inferior (ventral) view of the cerebral hemisphere, with the brainstem removed, showing the relationships of the main sinuses and
the anterior cerebral vein, the deep middle cerebral vein, and the superficial
middle cerebral vein. See Chapter 10 for comparable views of these veins and
sinuses. Dural venous thromboses are rarely found in the cavernous sinuses
and are infrequently located in the straight sinus and internal cerebral veins.
External Morphology of the Central Nervous System
Longitudinal a
a
Frontal pole
ae
Olfactory bulb
Olfactory sulcus (OlfSul)
Orbital sulci
Orbital gyri (OrbGy)
Gyrus rectus (GyRec)
Olfactory tract
Temporal pole (TPole)
Basilar pons (BP)
Occipitotemporal
sulcus
Parahippocampal
gyrus
Occipitotemporal
gyri
Collateral
sulcus
Middle cerebellar
peduncle (MCP)
Trigeminal nerve (TriNer)
Glossopharyngeal
nerve
Flocculus
es
+
:
oT
~~
3
>
:
Facial
acial ner nerve
Vestibulocochlear
Aerie
Vagus nerve
Abducens nerve
Olive (inferior);
olivary eminence
Decussation
“Cerebellum (Cbl)
of pyramids
TriNer
MCP
Fourth
ventricle
Chl
Inferior (ventral) view of the cerebral hemispheres, diencephalon, brainstem, and cerebellum, and two MRIs
(both T1-weighted images) that show structures from the same perspective. Note the slight differences in the sizes of the fourth ventricle. The larger midline space seen in the right MRI is representative
of a slightly lower axial plane through the pons when compared to
the left MRI, which represents a slightly more superior plane. What
appear to be two foramina on either side of the fourth ventricle
(right MRI) is actually a small depression (a blind sac or
foramen
caecum) between the superior cerebellar peduncles and
the middle cerebellar peduncles. See Figure 2-31 for a view from
the same
perspective.
Olfactory tract and bulb
Anterior
y communicating artery
Ao segment of ACA
Ophthalmic artery
A; segment of ACA
Internal carotid artery
Anterior, polar temporal,
and uncal branches of M,
Superior trunk of MCA Mp
Posterior communicating
M, segment of MCA
artery:
Inferior trunk of MCA Mo
Superior cerebellar artery.
Lenticulostriate arteries
Basilar artery
Posterior cerebral artery
Anterior inferior
cerebellar artery
Posterior inferior
cerebellar artery
Vertebral artery
Inferior (ventral) view of the cerebral hemispheres, diencephalon, brainstem, and cerebellum, which shows the ar-
terial patterns created by the internal carotid and vertebrobasilar systems. Note the arterial structures forming the cerebral arterial circle (of
Willis). Details of the cerebral arterial circle and the vertebrobasilar
arterial pattern are shown in Figure 2-21; see Figures 10-9 and 1010 for comparable MRAs of the cerebral arterial circle and its major
branches.
Olfactory tract and bulb
Anterior cerebral vein
Sphenoparietal sinus
Ophthalmic vein
\
Dr
Anterior intercavernous
))
sinus
Cavernous sinus
Posterior intercavernous
sinus
=
foe
,
~~
| Superficial middle
cerebral vein
Cen,
;,
£4
+—__;++—Deep middle
]cerebral vein
nae
Superior petrosal
sinus
Inferior petrosal
sinus
Internal jugular
vein
Sigmoid sinus
Basilar plexus
Transverse sinus
Transverse sinus
Anterior vertebral
venous plexus
Occipital sinus
2-19
Inferior (ventral) view of the cerebral hemispheres, diencephalon, brainstem, and cerebellum showing the locations
and relationships of principal sinuses and veins. Venous thromboses are
infrequently located in the petrosal sinuses and the cavernous sinus.
External Morphology of the Central Nervous System
Olfactory tract
Gyrus rectus
Optic nerve
(cranial nerve II)
Internal carotid
artery
Optic chiasm
Optic tract
Infundibulum
Mamamillary bodies
Middle cerebral
artery (Mj)
Posterior
communicating
artery
—-Oculomotor nerve
_ (cranial nerve III)
Crus cerebri
Basilar artery
Trochlear nerve
(cranial nerve IV)
Uncus
Posterior cerebral
artery (P1)
Superior cerebellar
artery
-___ Parahippocampal
Basilar pons
gyrus
Trigeminal nerve
(cranial nerve V)
Abducens nerve
(cranial nerve V1)
Middle cerebellar peduncle
(brachium pontis)
Facial nerve
(cranial nerve VII)
Intermediate nerve (with VII)
Flocculus
Olive (inferior);
olivary eminence
Retroolivary sulcus
(postolivary sulcus)
~Vestibulocochlear nerve
(cranial nerve VIII)
Glossopharyngeal nerve
(cranial nerve IX)
Vagus nerve
(cranial nerve X)
Choroid plexus
Preolivary sulcus
(exit of twelfth nerve)
Hypoglossal nerve
(cranial nerve XII)
Pyramid
Branches of posterior
Anterior median fissure
inferior cerebellar artery
Accessory nerve
(cranial nerve Xl)
Motor decussation
(decussation of pyramids)
Detailed view of the inferior (ventral) aspect of the diencephalon and brainstem with particular emphasis on exit
and/or entrance points of cranial nerves (CNs II-XII) and the general
relationships of the optic nerve, chiasm, and tract.
Note an important relationship: the oculomotor nerve exits between
the superior cerebellar and the posterior cerebral (P, segment of PCA)
arteries. In this location, it is particularly susceptible to damage from
aneurysms arising from the basilar bifurcation or from the posterior
communicating artery/PCA intersection. Aneurysms of the basilar tip
are the most common of those found within the vertebrobasilar system
and comprise about 5% of all intracranial aneurysms. Such lesions may
give rise to deficits (seen individually or in combinations) characteristic
of a CN III injury, such as dilated pupil, loss of most eye movement, and
diplopia. Other important relationships also include the cranial nerves
of the pons-medulla junction (VI, VII, VIII) and the cranial nerves associated with the cerebellopontine angle (VII, VIII, LX, X). In this view, it
is easy to appreciate the fact that cranial nerves VI-XII occupy a compact area at the caudal aspect of the pons and lateral medulla. Lesions
in these areas may result in a variety of cranial nerve, long tract, and
potentially additional, deficits.
Vessels
Structures
Anterior communicating artery
Olfactory tract
Medial striate artery
Anterior cerebral artery {e
1
—
Optic chiasm
Optic nerve
Posterior communicating artery
Opthalmic artery
Internal carotid artery.
Anterior and polar
temporal arteries
Uncal artery
Middle cerebral
\
artery
M4
Mo
<<
Xa)
SS
ENG
—
—————
ae
;
Anterior perforated substance
/
Lenticulostriate arteries
PIL
AL I fA
Anterior choroidal artery
x
Posterior cerebral artery] a
2
GT
ww,
-
Optic tract
Mammillary body
Infundibulum
Crus cerebri
A
Posterior choroidal arteries ———
Quadrigeminal Shik ae
Oculomotor nerve (II!)
Trochlear nerve (IV)
Basilar pons
Superior cerebellar artery
Trigeminal nerve (V)
Trigeminal nerve (V):
Motor root
Sensory root —
Abducens nerve (VI)
—=.Facial nerve (VII)
Middle cerebellar
peduncle
Pontine arteries
Basilar artery
Vestibulocochlear
nerve (VIII)
Anterior inferior
cerebellar artery
Choroid plexus
\
Glossopharyngeal nerve (IX)
Vagus nerve (X)
Labyrinthine artery
Posterior inferior
Accessory nerve (XI!)
cerebellar artery
Hypoglossal nerve (XII)
Posterior spinal artery
Olive (inferior);
olivary eminence
Vertebral artery
Cerebellum
— Pyramid
Anterior spinal artery
Inferior (ventral) view of the brainstem showing the rela2-21
tionship of brain structures and cranial nerves to the arteries
forming the vertebrobasilar system and the cerebral arterial circle (of
Willis).
The posterior spinal artery usually originates from the posterior
inferior cerebellar artery (left, about 75% of cases), but it may arise
from the vertebral artery (right, about 25% of individuals). Although
the labyrinthine artery may occasionally branch from the basilar (right,
about 15% of the time), it most frequently originates from the anterior
inferior cerebellar artery (left, about 85% of cases).
Many vessels that arise ventrally course around the brainstem to
serve dorsal structures; they may be generally classified as circumferential vessels. The anterior cerebral artery consists of A; (between the
internal carotid bifurcation and the anterior communicating artery) and
segments A,—-As, which are distal to the anterior communicating artery.
Lateral to the internal carotid bifurcation is the M, segment of the middle cerebral artery (MCA), which usually divides into superior and inferior trunks that continue as the M, segments (branches) on the insular
cortex. The M; branches of the MCA are those located on the inner
surface of the opercula, and the My, branches are located on the lateral
aspect of the hemisphere.
Between the basilar bifurcation and the posterior communicating artery is the P, segment of the posterior cerebral artery;
P, is between the posterior communicator and the first temporal
branches; and P3-P, are distal to this segment. See Figures 10-9,
10-10, and 10-12 for comparable MRA of the cerebral arterial circle
and vertebrobasilar system. See Figure 4-10 for the blood supply of
the choroid plexus.
External Morphology of the Central Nervous System
Choroid plexus in
foramen of Luschka
Glossopharyngeai nerve (IX)
x
%
‘ie
fice
ee
Vagus nerve (X)
Fee
Cerebellum
Flocculus
Vestibulocochlear nerve (VIII)
a
Hypoglossal nerve (XII)
>
Intermediate nerve (with VII)
Facial nerve (VII)—=
Inferior olive
Trigeminal nerve (V)
(olivary eminence)
Pyramid
Trochlear nerve (IV)
Rees
Oculomotor nerve (III)
nerve (V1)
4
Basilar pons
Lateral view of the left side of the brainstem where the infeVII and VIII; less so IX, X, and XI. Although not technically a nerve of
rior aspects of the cerebellum, medulla, and pons converge; _the CPA, especially large lesions (generally larger than 2.0 cm) in this
this area is commonly called the cerebellopontine angle (CPA).
area may extend forward and involve CN V with appropriate sensory
The cranial nerves (CNs) related to the CPA in decreasing order,
based on the deficits seen following lesions/tumors in the CPA, are CNs
;
deficits. Vestibular schwannoma is the most common CPA lesion (about
80%-90%), with meningioma a distant second at about 5%-10%.
Crista galli
Anterior fossa
i
Ce
Cribriform plate of ethmoid bone
Ethmoid foramina (CN 1)
Middle fossa
Anterior clinoid
Optic canals (CMD
process
Superior orbital fissure
(CNs Ill, IV, VI, V,-Ophthalmic br.)
Posterior fossa
Position of internal carotid artery
Posterior clinoid process
Foramen rotundum
(V>-Maxillary br.)
Clivus
Foramen lacerum
Foramen ovale
(V3-Mandibular br. + motor root)
Groove for superior petrosal sinus
Foramen ovale
Groove for sigmoid sinus
Internal acoustic meatus
(CNs VII, VIII)
Endolymphatic sac opening
Groove for inferior petrosal sinus
Jugular foramen (CNs IX, X, Xl)
Condylar canal for emissary vein
Hypoglossal canal (CN XII)
=
Foramen magnum (CN XI)
Views of the internal aspects of the skull with particular emphasis on the foramina through which the cranial nerves pass.
The color boxes on the drawing of the skull base correlate with
the color outline of each of the detailed views. Correlate the cranial
nerves as seen in Figure 2-22 (above) with their respective foramina.
Examples of lesions generally associated with the contents of foramina
include tumors of the jugular foramen (mainly CNs IX, X, and
XI)
and vestibular schwannoma (mainly CNs VII and VIII). Meningi
omas
of the skull base are infrequent and may involve a number
of cranial
nerves in different combinations.
Choroid plexus, third ventricle
Fornix
Optic tract
Posterior choroidal arteries
Thalamogeniculate artery
Posterior cerebral artery
Lateral geniculate body
Mammillary body
Medial geniculate body
Quadrigeminal artery
Superior colliculus
Posterior communicating
Crus cerebri
artery
Internal carotid artery
Brachium of inferior colliculus
Oculomotor nerve
Superior cerebellar artery
Inferior colliculus
Trochlear nerve
Trigeminal nerve
Motor root
Sensory root
Superior cerebellar peduncle
Basilar artery
—
Anterior medullary velum
Middle cerebellar peduncle
Anterior inferior
cerebellar artery
Vestibulocochlear nerve
Labyrinthine artery
Abducens nerve
Glossopharyngeal nerve
Vagus nerve
Hypoglossal nerve
Accessory nerve
Posterior inferior cerebellar artery
Anterior spinal artery
Facial nerve
Posterior inferior
cerebellar artery
Choroid plexus,
fourth ventricle
Restiform body
Cuneate tubercle
Gracile tubercle
Posterior spinal artery
Vertebral artery
Lateral view of the left side of the brainstem and thalamus
showing the relationship of structures and cranial nerves to arteries. Arteries that serve dorsal structures (generally called circumferential
arteries) originate from ventrally located parent vessels and arch around
the brainstem and forebrain. The approximate positions of the posterior
Optic nerve
spinal and labyrinthine arteries, when they originate from the vertebral
and basilar arteries, respectively, are shown as dashed lines. Compare with
Figure 2-22 on the facing page. See Figure 10-7 for comparable angiogram
of the vertebrobasilar system. See Figure 4-10 for another view of the blood
supply to the choroid plexus of the third and fourth ventricles.
Olfactory tract
Optic chiasm
Infundibulum
Anterior perforated substance
Mammillary body
Optic tract
Interpeduncular fossa
Optic tract
Crus cerebri
Medical geniculate body
Brachium of
superior colliculus
Lateral geniculate body
Red nucleus
Lateral geniculate body
Medial geniculate nucleus
Pulvinar
Vein of Galen—=
Splenium of corpus callosum
— 7
en
and lateral geniculate body. Also note the characteristic position of
Inferior (ventral) view of the diencephalon and a crossbrachium of the superior colliculus to the medial geniculate body/
the
midbrain—
the
of
level
the
at
midbrain
the
of
section
2-25
nucleus. Deficits of the anterior choroidal artery syndrome include a
diencephalon junction.
contralateral hemiplegia (crus cerebri damage) and a contralateral hemiNote the structures of the hypothalamus, those related to cranial
anopia (optic tract damage).
nerve II, and the close relationship of the optic tract to the crus cerebri
External Morphology of the Central Nervous System
CMS SERRESRS
Anterior paracentral gyrus (APGy)
Central sulcus (CSul)
Paracentral sulcus (ParCSul)
Posterior paracentral gyrus (PPGy)
Precentral sulcus (PrCSul)
Marginal sulcus (MarSul)
7 Precuneus (PrCun)
Cingulate gyrus (CinGy)
Superior frontal
gyrus (SFGy)
Parieto-occipital
sulcus (POSul)
Cingulate sulcus
(CinSu!)
Cuneus (Cun)
Calcarine sulcus
(CalSul)
Lingual gyrus
(LinGy)
Sulcus of corpus
callosum (SulCC)
Olfactory bulb
Isthmus of cingulate gyrus
Paraterminal gyri
Occipitotemporal gyri
Parolfactory gyri (ParolfGy)
semnoes:
| pole
P
Parahippocampal gyrus
Uncus
Rhinal sulcus
APGy
PrCSul
ParCSul
CSul
PPGy
MarSul
SulCC
CinGy
PrCun
CinSul
ParolfGy
POSul
Cun
CalSul
LinGy
SFGy
MarSul
Corpus callosum
POSul
Colloid cyst
CalSul
Internal cerebral
vein
Midsagittal view of the right cerebral hemisphere and diencephalon, with brainstem removed, showing the main
gyri and sulci and two MRIs (both T1-weighted images) showing these
structures from the same perspective. The lower MRI is from a patient
with a small colloid cyst in the interventricular foramen. When compared
with the upper MRI, note the enlarged lateral ventricle with resultant
thinning of the corpus callosum.
A colloid cyst (colloid tumor, neuroepithelial cyst) is a congenital
growth usually discovered in adult life once the flow of CSF through the
interventricular foramen/foramina is compromised (obstructive hydrocephalus). These lesions are relatively rare (<1% of intracranial lesions);
are slow-growing; become a clinical issue when enlarging to about 1.5 cm,
or greater, in diameter; and are usually located in the rostral portions of
the third ventricle particularly at the level of the intraventricular foramen.
The patient may present with headache (evidence of increased intracranial
pressure), unsteady gait, weakness of the lower extremities, visual or somatosensory disorders, and/or personality changes or confusion. Treatment
is
usually by surgical removal; in select cases shunting may be recommend
ed.
A4 segment of ACA
Paracentral branches (of ACA)
Internal frontal branches
As segment of ACA
Callosomarginal branch
Internal parietal
branches (of ACA)
Ag segment of ACA
Zo
co
Parieto-occipital
branches of PCA (P,4)
Frontopolar branches
Orbital branches of ACA
Z=
Olfactory bulb
AK
Calcarine branches
Sl w a
of PCA (Pa)
Ao segment of ACA
Posterior
temporal
branches
of PCA (P3)
Anterior communicating artery
=
ier
fal ip’ "—~Anterior temporal branch of PCA (P3)
Az segment of ACA
Posterior cerebral artery (PCA)
Internal carotid artery
Anterior temporal branch of PCA
Posterior communicating artery:
=
Midsagittal view of the right cerebral hemisphere and
diencephalon showing the locations and branching patterns of anterior (ACA) and posterior (PCA) cerebral arteries. The
positions of gyri and sulci can be easily extrapolated from Figure
2-26 (facing page). Terminal branches of the anterior cerebral artery
(primarily Ay and As) arch laterally over the edge of the hemisphere
to serve medial regions of the frontal and parietal lobes, and the
same relationship is maintained for the occipital and temporal lobes
Inferior sagittal sinus
by branches of the posterior cerebral artery. The ACA is made up
of segments A; (precommunicating), A, (infracallosal), A3 (precallosal), and Ay + A; (supracallosal + postcallosal). See Figures 10-1
and 10-7 for comparable angiograms of anterior and posterior cerebral arteries. The junctions of the distal territories of large, and
in some cases smaller, arteries are called watershed zones. Vascular
insufficiency in a particular watershed zone results in characteristic
deficits.
Posterior vein of the corpus callosum
Superior thalamostriate (terminal) vein
Inferior sagittal sinus
Superior sagittal sinus
Internal occipital veins
Veins of the caudate
nucleus and septum
pellucidum
Venous angle
Septal veins
Straight sinus
Superior cerebellar
Olfactory bulb
vein
Great cerebral vein
(of Galen)
Anterior cerebral vein
Optic nerve
Basal vein (of Rosenthal)
#£/
Transverse sinus
Occipital sinus
Internal cerebral vein
| Midsagittal view of the right cerebral hemisphere and
diencephalon showing the locations and relationships of
sinuses and the locations and general branching patterns of veins.
The continuation of the superior thalamostriate vein (also called the
terminal vein due to its proximity to the stria terminalis) with the
internal cerebral vein is the venous angle. This venous landmark sig-
nifies the location of the interventricular foramen of Monro through
which the choroid plexus extends from lateral into third ventricles.
Dural venous thromboses are rarely seen in the inferior sagittal sinus,
internal cerebral vein, or their tributaries. See Figures 10-2 and 10-11
for comparable angiogram (venous phase) and MRV showing veins
and sinuses.
Anterior paracentral gyrus (APGy)
Central sulcus (CSul)
Paracentral sulcus (PCSul)
Posterior paracentral gyrus (PPGy)
Marginal sulcus (MarSul)
Superior frontal gyrus (SFGy)
Precuneus (PCun)
Body of corpus callosum (BCorC)
Sulcus of the
corpus callosum (SulCorC)
Splenium of corpus
callosum (SpICorC)
Cingulate gyrus (CinGy)
Parieto-occipital
sulcus (POSul)
Cingulate sulcus
(CinSul)
Cuneus (Cun)
Calcarine sulcus
(CalSul)
Genu of corpus
callosum (GCorC)
Septum
Lingual gyrus
(LinGy)
Rostrum of corpus
Tectum
callosum (RCorC)
Cerebellum (Cbl)
Midbrain tegmentum (MidTeg)
Basilar pons (BP)
al
Tonsil of cerebellum (Ton)
Pontine tegmentum (PonTeg)
Medulla (Med)
SFGy
PCSul
APGy
CSul
PPGy
MarSul
PCun
SplCorC
POSul
Cun
CalSul
LinGy
Chl
i
MidTeg
BP
PonTeg
A midsagittal view of the right cerebral hemisphere and diencephalon with the brainstem and cerebellum in situ. The MRI
(T1-weighted image) shows many brain structures from the same perspective. Important cortical relationships in this view include the cingulate,
parietooccipital, and calcarine sulci; the primary visual cortex is located
on either bank of the calcarine sulcus. The cingulate gyrus, medial aspect
Med
Ton
of the superior frontal gyrus, and precuneus occupy much of the medial
surface of the hemisphere. Note that the medial terminus of the central sulcus is above the splenium of the corpus callosum, which clearly illustrates
the fact that the primary somatomotor (anterior paracentral gyrus) and
somatosensory (posterior paracentral gyrus) cortices for the lower extremity are located somewhat caudally on the medial aspect of the hemispher
e.
Body of fornix (For)
Septum pellucidum (Sep)
Dorsal thalamus (DorTh)
Massa intermedia
Interventricular foramen
Choroid plexus of third ventricle
Stria medullaris thalami
Column of fornix
Anterior
commissure (AC)
Habenula
Suprapineal
recess
Lamina terminalis
Posterior
commissure
Pineal (P)
Supraoptic recess
—— Superior
colliculus (SC)
Optic chiasm
(OpCh)
Quadrigeminal
cistern (QCis)
Inferior
Optic nerve
colliculus (IC)
Cerebral
aqueduct (CA)
Anterior medullary
velum (AMV)
Fourth ventricle
Infundibulum (In)
(ForVen)
Infundibular recess
;
Mammillary body (MB)
Basilar artery’
Hypothalamic sulcus
Posterior inferior
cerebellar artery
Oculomotor nerve
Interpeduncular fossa (lpedFos)
Basilar pons (BP)
DorTh
Sep
Internal cerebral vein
P
AC
Tentorium cerebelli
Hypothalamus
QCis
OpCh
SC
In
Pituitary
gland:
Adenohypophysis
Neurohypophysis
IC
AMV
MB
ForVen
lpedFos
BP
A midsagittal view of the right cerebral hemisphere and
diencephalon with the brainstem in situ focusing on the
details primarily related to the diencephalon and third ventricle.
The MRI (T1-weighted image) shows these brain structures from the
same perspective. Note the recesses of the third ventricle in the vicinity of the
CA
hypothalamus, the position of the lamina terminalis, the relationships of the
interpeduncular fossa, and the general positions of the ventricular system and
cisterns in the midsagittal plane. These relationships are important to understanding images of patients with subarachnoid hemorrhage (e.g., see Figure
4-7) and numerous other clinical conditions. Hyth, hypothalamus.
External Morphology of the Central Nervous System
Pineal
Inferior colliculus (IC)
Frenulum
Internal cerebral vein
Superior colliculus (SC)
Pulvinar
nuclear
complex
Medial
geniculate
body (MGB)
Brachium of
Lateral
geniculate
body (LGB)
superior
é
i?
colliculus
Brachium of
inferior
colliculus
Crus cerebri
Crus cerebri
==" —Trochlear nerve
Trochlear nerve
(cranial nerve IV)
(cranial nerve IV)
Superior cerebellar
peduncle
Anterior medullary velum
Facial colliculus
Middle cerebellar
peduncle
Sulcus limitans
Superior fovea
Striae medullares of
fourth ventricle
Inferior cerebellar peduncle
(juxtarestiform body and
restiform body)
Lateral recess of
fourth ventricle
Vestibular area
Restiform body
Tela choroidea (cut edge)
Level of obex
Hypoglossal trigone
a.
uberculum cuneatum (cuneate tubercle)
Tuberculum gracile
(gracile tubercle)
ea
Posterior intermediate sulcus
Posterolateral sulcus
___ Trigeminal tubercle (tuberculum cinereum)
;
Cuneate fasciculus
Gracile fasciculus
Posterior median sulcus
Detailed superior (dorsal) view of the brainstem, with cerebellum removed, providing a clear view of the rhomboid fossa (and floor of the fourth ventricle) and contiguous parts of the caudal
diencephalon. The dashed line on the left represents the position of the
sulcus limitans, and the area of the inferior cerebellar peduncle is outlined by the dashed line on the right. This structure is composed of the
restiform body plus the juxtarestiform body, the latter of which contains
fibers (vestibulocerebellar and cerebellovestibular) interconnecting the
vestibular area in the lateral floor of the fourth ventricle and cerebellar
structures (cortex and nuclei). The former contains a number of cerebellar
afferent fibers (dorsal spinocerebellar, reticulocerebellar, olivocerebellar,
and others). The tuberculum cinereum is also called the trigeminal tubercle (tuberculum trigeminale) because it is the surface representation of
the spinal trigeminal tract and its underlying nucleus in the lateral aspect
of the medulla just caudal to the level of the obex (see also Figure 2-32).
The facial colliculus is formed by the underlying abducens nucleus and
internal genu of the facial nerve, the hypoglossal trigone by the underlying
hypoglossal nucleus, and the vagal trigone by the dorsal motor nucleus of
the vagal nerve. Tumors invading the fourth ventricle, radiation, surgical
procedures targeting these areas, or demyelinating lesions in these locations may result in signs/symptoms reflecting damage to nuclei and/or
tracts forming these elevations. Also see Figure 2-34.
Vessels
Structures
Choroid plexus, third ventricle
Pineal
Habenula
Medial thalamus
Thalamogeniculate arteries
Brachium of superior colliculus
Superior
Lateral thalamus
colliculus
Pulvinar nucleus
Internal capsule
me
Choroid plexus,
Nee d lateral ventricle
cer
Posterior choroidal artery:
Lateral
Medial geniculate body
Medial
Brachium of inferior colliculus
Quadrigeminal artery
Superior cerebellar artery:
Crus cerebri
Medial branch
Laterai branch
Trochlear nerve (IV)
Inferior colliculus
Superior cerebellar peduncle
Anterior medullary velum
Facial colliculus
Vestibular area
Inferior cerebellar peduncle
Middle cerebellar peduncle
Choroid plexus, fourth ventricle
te
Anterior inferior
cerebellar artery
————4
Hypoglossal trigone
y A
Glossopharyngeal nerve (IX)
AN
la \/
.
.
.
Posterior inferior
cerebellar artery
-
———}
:
{
AG
Vagal nerve (X)
“v
Accessory nerve (XI)
atte
Restiform body
Vagal trigone
9
Trigeminal tubercle (tuberculum cinereum)
Cuneate tubercle
Posterior spinal artery
Gracile tubercle
Gracile fasciculus
Cuneate fasciculus
cae
Superior (dorsal) view of the brainstem and caudal diencephalon showing the relationship of structures and some
of the cranial nerves to arteries. The vessels shown in this view have
originated ventrally and wrapped around the brainstem to gain their
dorsal positions. In this respect, these vessels, which all have specific
names that are widely recognized and used, can generally be referred to
as circumferential vessels. In addition to serving the medulla, branches
of the posterior inferior cerebellar artery also serve medial and pos-
terior cerebellar cortex and supply the choroid plexus of the fourth
ventricle. The tuberculum cinereum is also called the trigeminal tubercle. For an additional perspective on the blood supply to the choroid
plexus of the third and fourth ventricles see Figure 4-10. On the dorsal (superior) aspect of the medulla caudal to the obex, the gracile and
cuneate tubercles are the positions of their corresponding nuclei which
are the second-order cell bodies in the posterior column—medial lemniscus pathway.
Medial
geniculate body
Lateral geniculate
body
Crus cerebri
Superior colliculus
rve
Trochlear ne
Brachium of
inferior colliculus
ns
Basilar po
Optic tract
=
Optic nerve
=—
Inferior colliculus
a
Exit of trochlear nerve
Superior cerebellar
peduncle
Optic chiasm
Middle cerebellar
peduncle
Infundibulum
Motor root of
trigeminal nerve
Sensory root of
Restiform body
trigeminal nerve
g
Flocculus
Posterior inferior
cerebellar artery
Inferior olivary eminence
Pyramid
Tuberculum
cinereum
(trigeminal tubercle)
Lateral view of the left side of the brainstem emphasizing
structures that are located dorsally, laterally, and ventrally.
Note
the several
structures,
and
cranial
nerves,
seen
from
this
perspective in which the cerebellum and portions of the temporal
lobe have been removed. Compare with Figure 2-35 on the facing
page.
Medial eminence
of fourth ventricle
Superior cerebellar peduncle
7——Facial colliculus (abducens nucleus
and internal genu of VII)
Middle
cerebellar peduncle
i
Inferior cerebellar peduncle
Striae medullares
ts
See
oe:
Superior fovea
Vestibular area
(vestibular nuclei)
~S
\
Lateral recess
Foramen of Luschka
Hypoglossal trigone (hypoglossal nucleus)
Sulcus limitans
Vagal trigone (dorsal motor vagal nucleus)
Restiform body
Cuneate tubercle saeanaal\
Inferior fovea
Gracile tubercle
Tela choroidea
(cut edge)
The floor of the fourth ventricle (rhomboid fossa) and
immediately adjacent structures. The signs and symptoms
of lesions in this ventricle may present as deficits representing damage to the facial colliculus (6th nucleus, internal genu of VII), hypoglossal trigone (12th nucleus), or vestibular and possibly cochlear
nuclei, or may be more global, such as the area postrema syndrome,
reflecting injury to medullary and pontine centers and long ascending/descending tracts. An example of one global effect would be in
the area postrema syndrome as seen in neuromyelitis optica. The color coding for all structures, other than the cerebellar peduncles, is
consistent with that used for the brainstem nuclei in Chapter 6. See
Figures 2-31 and 2-32.
Choroid plexus, third ventricle
Fornix
Optic tract
Posterior choroidal arteries
Thalamogeniculate artery
Posterior cerebral artery
Lateral geniculate body
Mammillary body
Medial geniculate body
Quadrigeminal artery
Superior colliculus
Posterior communicating
artery
Crus cerebri
Internal carotid artery
Brachium of inferior colliculus
Oculomotor nerve
Superior cerebellar artery
Inferior colliculus
Trochlear nerve
Trigeminal nerve
Motor root
Sensory root
Superior cerebellar peduncle
Anterior medullary velum
Basilar artery
Middle cerebellar peduncle
Anterior inferior
Vestibulocochlear nerve
cerebellar artery
Labyrinthine artery
Abducens nerve
Glossopharyngeal nerve
Vagus nerve
Hypoglossal nerve
Accessory nerve
Posterior inferior cerebellar artery
Anterior spinal artery
Facial nerve
Posterior inferior
cerebellar artery
Choroid plexus,
fourth ventricle
Restiform body
Cuneate tubercle
Gracile tubercle
Posterior spinal artery
Vertebral artery
Lateral view of the brainstem and thalamus, which shows the
relationship of structures and cranial nerves to arteries. The
approximate positions of the labyrinthine and posterior spinal arteries,
when they originate from the basilar and vertebral arteries, respectively, are
shown as dashed lines. Arteries that distribute to posterior/dorsal structures
originate from the vertebral, basilar, and initial segments of the posterior
cerebral arteries and arch around the brainstem, or caudal thalamus, to
access their targets. From this view, notice the compact nature of the cranial
nerves at the pons—medulla junction and the lateral and ventral aspect of
the medulla (CNs VI-XII). Compare with Figure 2-33 on the facing page.
Anterior cerebral artery
Anterior
communicating
artery
Hypothalamus
Crus cerebri
Red nucleus
Middle cerebral artery (M1)
Posterior communicating
artery
Posterior cerebral artery
Cerebral aqueduct
Cortical branches of
posterior cerebral artery
(Pg, Pa)
An axial MRI through basal regions of the hemisphere
and through the midbrain showing several major vessels
that form part of the cerebral arterial circle (of Willis). Compare to
Figure 2-21. See Figures 10-9 and 10-10 for comparable MRAs of the
cerebral arterial circle.
A
Midbrain
Anterior
Anterior
quadrangular
lobe (AntLb)—
lobule
Posterior
quadrangular,
lobule
Posterior
fissure
superior
fissure
Superior semilunar
lobule
Hemisphere
Bpon
Vermis (Ver)
AntLb
SCP
Fourth ventricle
Basilar pons (Bpon)
Medulla (Med)
Tonsil (Ton)
Biventer
lobule
Gracile
lobule
Med
Ton
Inferior
semilunar
lobule
PostLb
Vermis (Ver)
Ver
C
Inferior colliculus
Cerebellar peduncles:
Superior (SCP)
Middle (MCP)
Inferior
Superior
Anterior
Inferior
G
lobe (AntLb)
|
Primary fissure
AntLb
Horizontal
fissure
MCP
Fl
Posterior
lobe (PostLb)
Nodulus
Rostral (A, superior surface), caudal (B, inferior surface),
s
and an inferior view (C, inferior aspect) of the cerebellum.
The view in C shows the aspect of the cerebellum that is continuous
into the brainstem via cerebellar peduncles. The views in C and G correlate with the superior surface of the brainstem (and middle and superior
cerebellar peduncles) as also shown in Figure 2-31.
Note that the superior view of the cerebellum (A) correlates
closely with cerebellar structures seen in axial MRIs at compara-
Med
PostLb
ble levels (D, E). Structures seen on the inferior surface of the cerebellum, such as the tonsil (F, B), an important structure in cases
of tonsillar herniations, correlate closely with an axial MRI at a
comparable level. In C and G, note the appearance of the mar-
gins of the cerebellum, the general appearance and position of
the anterior and posterior lobes, and the obvious nature of the middle cerebellar peduncle. All MRI images are T1 weighted in axial
view.
B
Hl, HI
Tentorium cerebelli (TenCbl)
V
PriFis
Wit
= IV
Primary
fissure (PriFis)
Midbrain (Mid)
ForVen
|
Vill
PostLatFis
IX
Basilar
pons (Bpon)
Fourth
ventricle
(ForVen)
s-
StSinus
X
PriFis
Medulla
(Med)
Posterolateral
ForVen
fissure (PostLatFis)
X
IX
VIII
Lobules I-V are the vermis parts of the anterior lobe; lobules VI-IX
are the vermis parts of the posterior lobe; and lobule X (the nodulus) is
the vermis part of the flocculonodular lobe. The hemispheres of the corresponding vermis lobules are preceded by an “H” (HII to HX; lobule I
does not have a hemisphere). Note the striking similarities between the
gross specimen (A) and a median sagittal view of the cerebellum in a
T1- (B) and T2-weighted MRI (C).
> 4%
A median sagittal view of the cerebellum (A) showing its
ee
relationships to the midbrain, pons, and medulla.
This sagittal view of the cerebellum (A-C) also illustrates the two
main fissures (posterolateral, first to appear; primary, second to appear),
the three main lobes (anterior, posterior, and flocculonodular), and the
vermis portions of lobules I-X. Designation of these lobules follows the
method developed by Larsell.
Vein of Galen
Superior colliculus
Brachium of inferior colliculus
Inferior colliculus
Exit of trochlear nerve
Medial geniculate body
Crus cerebri
Peduncles:
—S
Trochlear nerve
Superior cerebellar
Middle cerebellar
Trigeminal nerve:
Motor root
Sensory root
Basilar pons
Vestibulocochlear nerve
Flocculus
Lateral view of the brainstem showing the superior and inferior colliculi, exit of the trochlear nerve, and the lateral
aspect of the crus cerebri. The exit of the trigeminal nerve (motor and
sensory roots) differentiates the interface of the basilar pons (ventral/
inferior to the exit) with the middle cerebellar peduncle (dorsal/superior
to the exit).
External Morphology of the Central Nervous System—The Insula: Gross View, Vasculature, and MR ae
Precentral gyrus (PrCGy)
Superior frontal
gyrus
Central sulcus (CSul)
Postcentral gyrus
Middle frontal
(PoCGy)
gyrus (MFGy)
Gyri longi (GyLon: long
gyri of the insula)
Gyri breves
(GyBr-short gyri
of the insula)
Transverse temporal
Central sulcus
of the insula (CSulln)
gyrus (TrlemGy)
Limen insulae (LimIn)
PrCGy
PoCGy
CSul
MFGy
TrTlemGy
GyBr
GyLon
CSulln
LimIn
TLob
CSul
PrCGy
MFGy
GyBr
PoCGy
CSulln
GyLon
TLob
Lateral view of the left cerebral hemisphere with the frontal
and parietal opercula removed and the temporal operculum
retracted downward exposing the insular lobe. Structures characteristic of the insular cortex (including the long and short gyri, the central
sulcus of the insula, and the circular sulcus of the insula (not visible
here), and immediately adjacent areas, are clearly seen in the two MRI
in the sagittal plane through lateral portions of the hemisph
ane
sion recovery—upper; T1-weighted image—lower)
ae
Prerolandic branches of MCA (Mg)
Temporal and parietal
opercula removed
Rolandic branches of MCA (Ma)
Orbitofrontal branches
of MCA
Anterior and posterior parietal
branches of MCA (Ma)
TB)
Moa segments of MCA
on insula cortex
Angular branches
Deep middle cerebral vein
of MCA (Ma)
Bifurcation of M, into superior
Deep middle cerebral vein
and inferior trunks (M2—Mg)
Anterior tempoyal
branches of MCA (M,)
Posterior temporal
branches of MCA (M4)
Sevee (Come
Lateral view of the left cerebral hemisphere showing the
pattern of the middle cerebral artery (MCA) as it branches
from M, (sphenoidal) into M, (insular) segments that pass over the insular cortex (lobe). Also shown are the Mg (cortical) branches on the
operculum retracted
surface of the cortex (having exited from the lateral sulcus). The deep
middle cerebral vein is located on the surface of the insula. Compare this
view of the vasculature of the insula with the anatomy from the same
perspective in Figure 2-40 on the facing page.
M4 segment of MCA,
cortical part
Mg segment of MCA,
opercular part
Superior trunk of MCA
(segments Moa—Maz)
Ms segment of MCA,
insular part
—
Superficial middle
cerebral vein
Deep middle
cerebral vein
M4 segment of MCA,
Inferior trunk of MCA
(segments Moa—Maz)
cortical part
M3 segment of MCA,
opercular part
Ms segment of MCA,
insular part
Internal carotid
artery
Semi-diagrammatic cross-sectional representation of the
242
cerebral hemispheres showing the main arteries and veins
2-42
related to the insular cortex.
The internal carotid artery branches into the anterior and middle
cerebral (MCA) arteries. The first segment of the MCA (Mj, sphenoidal part) passes laterally and diverges into superior and inferior trunks
at the limen insulae (entrance to the insular cortex). In general, distal
branches of the superior trunk course upward and eventually serve the
cortex above the lateral sulcus (of Sylvius), and distal branches of the
Anterior cerebral
artery (Ay)
M, segment of MCA,
sphenoidal part
inferior trunk course downward to serve the cortex below the lateral
sulcus. En route, these respective branches form the M) (insular part
of MCA), M; (opercular part of MCA), and My, (cortical part of MCA)
segments, as shown here.
The deep middle cerebral vein receives small branches from the area of
the insula and joins with the anterior cerebral vein to form the basal vein
(see Figures 2-16 and 2-19). The superficial middle cerebral vein collects
blood from the lateral aspect of the hemisphere and drains into the cavernous sinus (see also Figures 2-13, 2-16, and 2-19).
Relevance
External Morphology of the Central Nervous System— Vascular Variations of Clinical
Internal carotid
(ICA)
PCAC
Basilar artery (BA)
Internal carotid artery
Anterior cerebral artery (ACA)
Middle cerebral
artery, M,
Early in development, the posterior cerebral artery (PCA)
originates from the internal carotid artery (A).
At this stage, the cerebral arterial circle (of Willis) is not complete.
Vascular sprouts from the basilar artery are growing to meet the PCAs
and from the anterior cerebral arteries (ACAs) to meet on the midline
where they will form the anterior communicating artery (ACom). The
initial connection between the basilar artery and the PCA is small (B);
this will become the adult P; segment. As development progresses, the
initially small P; segment enlarges in diameter (to form the major connection between the basilar and the distal PCA, the adult P,) and the initially large portion of the PCA between the internal carotid artery and
the PCA-P, junction becomes smaller in diameter (to form the posterior
communicating artery [PCom] of the adult, C).
In 22%-25% of adult individuals, the territory served by the PCA is
perfused mainly from the internal carotid artery. This is due to the fact
that the fetal pattern of the PCA arising from the internal carotid persists into the adult. This artery is called a fetal PCA, or a persistent fetal
PCA. Examples of a fetal PCA are shown here in a specimen (D, fetal
PCA is on the patient’s right, normal pattern on patient’s left) and in
MRI (E, arrows) and CT angiogram (F, arrows). Note that in the MRIT2 (E, axial), the PCA can be easily followed from the internal carotid
into the occipital lobe (arrows) with no evidence of any substantive
connection to a P).
A fetal PCA in the adult may coexist with other vascular patterns
that deviate from normal. In the axial images in F and G (CTA), a fetal
PCA is present on the patient’s left (F, arrows) and in the same patient,
a single trunk from the left internal carotid artery (G) gives origin to
both the right and left anterior cerebral arteries (ACA, becomes the
right ACA; ACA, becomes the left ACA). This is an azygos (single or
unpaired) ACA.
Vascular Variations of Clinical Relevance
PCom
;
A
a
,
Se
Two stem ThalPreArt
from P,
9
~~} )) ({Y}}/
fan.
SY
Sy
PN
Rsk
=
<=
Basilar a.
communicating
PCA-P,
>
Basilar a.
bifurcation
E (axial CT)
arteries
part of the PCA located between the bifurcation of the basilar artery and the junction of the
posterior communicating artery with the PCA.
This vessel serves primarily the rostral and
medial areas of the thalamus that are important
synaptic stations in the ascending reticular activating system that influences cortical arousal.
The most common pattern of origin for
the thalamoperforating vessels (about 42% of
cases) is a single stem artery on each side that
branches to serve the thalamus on that side
(A). One or two single stem vessels on one P;
with multiple branches from the opposite P,
(B) are seen in about 26% of cases, and small
multiple branches from each P, (C) are the
pattern present in about 20% of cases.
The least common, but perhaps most problematic, pattern of the thalamoperforating
artery is when a single stem vessel (sometimes
called the artery of Percheron) originates from
one P, and branches to serve both thalami
(D); this is seen in about 8% of cases. Damage to, or occlusion of, this single stem, or of
one stem when there is only one on each side,
may adversely affect cortical arousal, consciousness, and contribute to drowsiness, stu-
por, or coma (E-G) due to an interruption of
cortical arousal pathways. In patient E (white
arrows), a single stem (D) was inadvertently
trapped during aneurysm surgery, resulting in
bilateral lesions (hypodensities in the anterior
thalamus in CT). Patient F (white arrows)
had bilateral strokes in the thalamoperforator territory (hyperintensities in T2, etiology
unknown); both patients E and F were comatose post event. A predominately unilateral
stroke in this same arterial territory (G, hyperintensity in T2 at white arrow) resulted in a
patient who was lethargic, in and out of consciousness, and difficult to arouse, but was not
comatose. In H, the hemorrhagic event is in
the territory of the thalamogeniculate artery,
a branch of P;. This vessel serves the caudal
and lateral thalamus including portions of
the medial and lateral geniculate nuclei and
the ventral posterolateral and ventral posteromedial nuclei. Patient deficits reflect varying
degrees of damage to various combinations of
these thalamic nuclei.
,
Z
eee
Superior
Vv
4
thalamoperforating
Mii) if A
ot
A 1
Multiple + stem ThalPerArt
from Po
(ThalPerArt) arise from the P, segment of the posterior cerebral artery (PCA), the
Multiple ThalPerArt
from P;
Quadrigeminal a.
cerebellar a.
The
Ce
a. (PCom)———
P;
~
_—
{
Posterior
ms
he
Single ThalPerArt
ACA-Az2
MedStrArt from
ACA-ACom corner
B
MedsStrArt
from Ag
ICA
Ophthalmic a:
Anterior
choroidal a:
ACom
MedStrArt
from ACA-A,
D (axial T2 MRI)
Internal carotid a. (ICA)
Middle cerebral a. (Mj)
Posterior communicating a.
(ACA-A;)
E (Axial CT)
Blood in:
Frontal lobe
Third ventricle
from proximal A, (B), and less than 3% from the distal A, (C). Recog-
The medial striate artery (MedStrArt), also called the artery
of Heubner, arises from the anterior cerebral artery (ACA)
nizing that the origin of the medial striate artery from the ACA may be
in the vicinity of its junction with the anterior communicating artery
variable, it is convenient to remember this vessel as usually arising at, or
(ACom).
just distal, to the corner. Vascular patterns in this region are highly variable and include azygos (single) or three A, segments, both ACAs arising
from one side (Figure 2-43G), a duplicated or a fenestrated ACom, and
occasional asymmetrical origins of its branches.
Aneurysms in this area may arise from the medial aspect of the “corner” or from the branches of the ACom. When an aneurysm at this
location ruptures, the extravasated blood may be located in the subarachnoid cisterns in the immediate area, dissect into the frontal lobe, or
enter the third ventricle, and ventricular system, through damage to the
This intersection is frequently called the “ACA-ACom corner” (A,
D). Structures characteristically found in this area, in addition to the
vessels, are the optic nerve, chiasm, and tract, adjacent gyri of the frontal lobe, subarachnoid cisterns (chiasmatic, of the lamina terminalis,
interpeduncular), and the lamina terminalis (separating cisterns from
the third ventricle) (D).
The medial striate artery usually arises from the lateral aspect of the
ACA. A large sample of cadaver brains (200) and surgical procedures
(375) revealed that about 42% arose from the “corner” (A), about 26%
lamina terminalis (E).
Ex Coronal CT angiogram)
Internal carotid a. (ICA)
My;
a Single LatStrArt
from M,
B
Mi
Ophthalmic a:
M,
Posterior communicating a:
Pati stem brs.
from M,
C
Anterior cerebral a.
Anterior choroidal a.
oe
+ individual
brs. from My
neal and temporal brs.
Multiple LatStrArt from M,
The
lateral
(LatStrArt)
striate
are
arteries
commonly
called the lenticulostriate arteries; they
arise from the M, segment of the middle
cerebral artery in three general patterns.
About 40% originate as a single stem
and then branch into numerous vessels
that penetrate the hemisphere via the anterior perforated substance to serve much of
the lenticular nucleus and adjacent structures, such as the internal capsule (A, E). In
approximately 30% of cases, these vessels
arise as two stems that divide into numerous penetrating branches (B); a variation on
this theme is one stem with several direct M,
branches (C). In a similar number of cases
(about 30%), the lenticulostriate vessels
originate as a series of many small arteries
directly from the M, segment (D, E).
Hemorrhage of the lenticulostriate arteries within the hemisphere, assuming no
occlusion of the parent M, vessel but with
only damage to its branches, results in a
lesion within the hemisphere with sparing
of the blood supply (the M, is patent) to the
more distal cerebral cortex (F). In contrast,
occlusion of the parent vessel, for example
the M, segment, may result in infarction of
all territories served by this vessel distal to
the obstruction including the basal nuclei,
portions of the internal capsule, and all distal cortex. In the case of obstructions that
are more distal on the MCA, only cerebral
cortical regions reflecting the territories
on those specific vessels (G) are infarcted.
The deficits correlate with the vascular bed
deprived of arterial blood, in this example
predominately My.
‘LatStrArt
External Morphology of the Central Nervous System
A
Basilar artery (BA
PCA
LA from AICA
Superior
cerebellar a.
Choroid plexus in
foramen of Luschka
PSA from PICA
Posterior spinal a. (PSA)
AICA
Anterior spinal a.
C (Sagittal CT angiogram)
*
D (Sagittal CT angiogram)
i.
¢
Posterior
cerebral
a. (PCA)
BA
VA
7
vAl
PICA
The anterior (AICA) and posterior (PICA) inferior cerebellar arteries originate from the basilar (BA) and vertebral arteries (VA) respectively (A).
The AICA arises from approximately the lower third of the basilar
artery in about 75% of patients (A, B). In 50%-60% of individuals, it
is a single basilar branch on each side, two branches in 20%, and three
branches in 20%. The labyrinthine artery, an important blood supply to
PICA
the inner ear, arises from the AICA about 85% of the time and from the
basilar in 15% of individuals.
The PICA commonly arises as a single branch from each vertebral
artery (90% of cases) but is duplicated 6% of the time (A, C, D: C and
D are two different sagittal planes in the same patient to show the continuity of PICA). In 75% of cases, the posterior spinal artery is a branch
of PICA; it is a vertebral branch about 25% of the time.
B (Axial T2 MRI)
VA
Posterior inferior
cerebellar a. (PICA)
Anterior spinal a.
C (Coronal angiogram)
| tf
=
Internal carotid a. (
iy
2
The vertebral arteries (VAs) are generally equal in size in
about 25%-30% of cases, or one may be larger than the other (A, B). For example, the left vertebral may be slightly larger about 43%
of the time (C) and the right vertebral in about 33% of cases (D). Ina
¥
D (Coronal angiogram)
minority of individuals, either vertebral artery may be hypoplastic (about
4%—-6%; see also Figure 10-12). In less than 1% of cases, the vertebral artery may become the PICA on one side; the other vertebral becoming the
basilar. Occasionally one of these variations may coexist with a second.
Q&A for this chapter is available online on
TNC Point.
aa
Y
ed
©.
©
tee
Cranial Nerves
LJ
he adult central nervous system (CNS) consists of the forebrain
(telencephalon and diencephalon), the brainstem (mesencephawm
1On, metencephalon, and myelencephalon), the cerebellum, and
the spinal cord. The cerebellum is not part of the brainstem but is a
suprasegmental structure located within the posterior fossa but superior to the long axis of the brainstem. Generally speaking, lesions in a
specific CNS region may result in deficits that are unique to that region,
in deficits that may reflect damage to tracts or pathways traversing that
region, or to combinations of these. CNS divisions, representative structures located therein, and cranial nerves (CN) associated with each are
summarized below.
COMPARTMENTS
The cranial cavity is lined by the meninges; the inner portions (meningeal dura + arachnoid matter) of which form dural reflections. These
larger reflections, as the falx cerebri, separate the right cerebral hemisphere from the left, and as the tentorium cerebelli, separate the two
cerebral hemispheres (which are supratentorial) from the brainstem and
the cerebellum (which are infratentorial). The contents of the right and
left supratentorial compartments are continuous with the contents of
the single infratentorial compartment via the midbrain which occupies
the tentorial notch (incisura). Increases in intracranial pressure (ICP)
within one supratentorial compartment may result in herniation of CNS
structures across the midline and/or downward through the tentorial
notch. In a similar manner, increased ICP in the infratentorial compartment may result in upward herniation through the tentorial notch or
downward herniation through the foramen magnum (see Chapter 9).
MAIN BLOOD VESSELS
The blood supply to the spinal cord arises from the anterior spinal artery,
a branch of the vertebral artery, and from the posterior spinal arteries usually branches of the posterior inferior cerebellar arteries. This is supplemented by segmental arteries (cervical, posterior intercostal, and lumbar
arteries). Branches of segmental arteries are the anterior and posterior
radicular arteries, found at every spinal root level, and anterior and pos-
terior spinal medullary arteries, found at about 6—18+ spinal levels; their
numbers are variable. The radicular arteries serve each set of spinal roots
and the corresponding posterior root ganglion (there are radicular arteries
at each spinal level), while spinal medullary arteries are principally a supplemental supply to the anterior and posterior spinal arteries and to the
arterial vasocorona (spinal medullary arteries are not found at each spinal
level). The artery of Adamkiewicz, an especially large anterior spinal medullary artery, arises from lower thoracic or upper lumbar levels (usually
T8-L2, ~80%-85%) and is more commonly (75+%) seen on the left side.
The blood supply to the brain is from the two internal carotid arteries
and the two vertebral arteries; the latter join to form the basilar artery.
The former is commonly referred to as the internal carotid system, the
latter as the vertebrobasilar system. These two systems are connected
with each other by the posterior communicating arteries. Each internal
carotid artery divides into middle (segments M,—M,) cerebral and
anterior (segments A;-A;) cerebral arteries, which generally serve
superficial and deep structures in lateral and medial regions of the hemisphere, respectively. The two vertebral arteries join to form the basilar
artery; the basilar bifurcates to form the posterior cerebral (P;—P,)
arteries; proximal PCA branches primarily serve the thalamus and rostral
midbrain; its distal branches serve temporal and occipital cortices.
ee
Nerves (CNs)
Divisions of the CNS, Representative Structures, and Associated Cranial
EE
EE
RL
aC
pT Sa ee CR
ESSE
Forebrain
Telencephalon: cerebral cortex, lobes, gyri, sulci, subcortical white matter, internal capsule, basal nuclei, CN I
Diencephalon: various divisions of the dorsal thalamus, hypothalamus, subthalamus, epithalamus, metathalamus, CN II
Brainstem
Mesencephalon: midbrain, tectum, tegmentum, crus cerebri, substantia nigra, red nucleus, CNs III, IV
Metencephalon: pons, basilar and tegmental areas, cerebellar peduncles, CN V
as the nerves
Myelencephalon: medulla, pyramid, inferior olive, restiform body; CNs IX, X, XII; CNs VI, VII, and VIII, which are regarded
foramen
the
through
ascends
cord,
of the pons-medulla junction; CN XI arises from C1-C5/C6 cervical levels of the spinal
magnum, and joins with CNs IX and X to exit the cranial cavity via the jugular foramen
Cerebellum
Anterior, posterior, flocculonodular lobes; cerebellar peduncles, cortex, nuclei
Spinal Cord
spinal white and gray matter, spinal laminae
Anterior and posterior roots, posterior root ganglia, cervical and lum bosacral enlargements,
of Rexed, anterior and posterior horns
To
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SLIOWAC
VNINVUOA/NAWVUOT
CaALVIOOSSY
Optic nerve
Optic chiasm
Optic tract
Infundibulum
Mammillary
body
Crus cerebri
Interpeduncular
fossa
B
Optic nerve
Bulb of eye
Optic chiasm
Temporal lobe
Mammillary
body
Optic tract
Interpeduncular
fossa
Uncus
Midbrain
tegmentum
Crus cerebri
C
Dorsal thalamus
Frontal lobe
Optic nerve
Interpeduncular
fossa
Basilar pons
Bulb of eye
Infundibulum
Anterior communicating
artery
Optic chiasm
Optic tract
Infundibulum
Optic nerve
Anterior cerebral
artery, A; segment
Interpeduncular
fossa
Midbrain
Inferior view of the hemisphere showing the optic nerve (II),
3-1 chiasm, tract, and related structures (A).
The MRIs of cranial nerve (CN) II are shown in an axial
(B, T1-weighted; D, T2-weighted) and in a slightly oblique sagittal
(C, T1-weighted) plane. Note the similarity between the axial planes,
especially (B), and the gross anatomical specimen. In addition, note the
relationship between the anterior cerebral artery, anterior communicating artery, and the structures at the level of the optic chiasm (D).
The anterior communicating artery or its junction with the anterior
cerebral artery (D) is the most common site of supratentorial (internal carotid system) aneurysms. Rupture of aneurysms at this location
is one of the more common causes of spontaneous (also called nontraumatic) subarachnoid hemorrhage. The proximity of these vessels to
optic structures and the hypothalamus (D) explains the variety of visual
and hypothalamic disorders that may be experienced by these patients.
A lesion of the optic nerve results in blindness in that eye and loss of the
afferent limb of the pupillary light reflex. Lesions posterior to the optic
chiasm result in deficits in the visual fields of both eyes (contralateral
[right or left] homonymous hemianopia).
The anterior choroidal artery serves the optic tract and portions of
the internal capsule immediately internal to the optic tract and adjacent
crus cerebri. This explains the unusual combination of a homonymous
hemianopia coupled with a contralateral hemiplegia and hemianesthe-
sia (to all somatosensory modalities especially if the area of damage
extends into the posterior limb of the internal capsule) as in the anterior
choroidal artery syndrome.
A
Optic chiasm
Infundibulum
Internal carotid
artery
Middle cerebral
artery
Posterior communicating
Posterior cerebral
artery (P1)
artery
Oculomotor nerve
Basilar artery
Superior cerebellar
artery
Basilar pons
Optic tract
Bulb of the eye
Posterior cerebral
artery
Superior cerebellar
artery
Oculomotor nerve
Internal carotid
artery
Oculomotor
nerve
Basilar pons
(rostral portion)
Oculomotor
nerve
Temporal lobe
Uncus
Fourth ventricle
(rostral portion)
Corpus callosum
Dorsal thalamus
Frontal lobe
Interpeduncular
fossa
Optic chiasm
Oculomotor nerve
Inferior view of the hemisphere showing the exiting fibers of
the oculomotor nerve (III), and their relationship to the poste3-2
rior cerebral and superior cerebellar arteries (A).
The MRIs of the oculomotor nerve (CN III) are shown in sagittal
(B, T2-weighted; D, T1-weighted) and in axial (C, T1-weighted) planes.
Note the relationship of the exiting fibers of CN III to the posterior cerebral and superior cerebellar arteries (A, B) and the characteristic appearance of CN III as it passes through the subarachnoid space toward the
superior orbital fissure (C). The sagittal section (D) is just off the midline
and shows the position of the oculomotor nerve in the interpeduncular
fossa rostral to the basilar pons and caudal to the optic chiasm.
That portion of the posterior cerebral artery located between the
basilar artery and posterior communicating artery (A) is the P; segment.
Superior colliculus
Inferior colliculus
Cerebellum
Basilar pons
The most common site of aneurysms in the infratentorial area (vertebrobasilar system) is at the bifurcation of the basilar artery, also called
the basilar tip. Patients with aneurysms at this location may present
with eye movement disorders, pupillary dilation, and diplopia caused by
damage to the root of CN III. Based on the arrangement of fibers within
the oculomotor nerve, pupillary changes may precede eye movement
disorders in cases of gradual compression of the third nerve.
Rupture of a basilar tip aneurysm may result in the cardinal signs
(sudden severe headache, nausea, vomiting, and possibly syncope) that
signal a stroke as broadly defined. In addition, the extravasated blood
may dissect its way into the ventricular system through the floor of the
third ventricle, and/or spread through the cisterns located on the basilar
aspect of the brain.
Mammillary body
Lamina terminalis
Interpeduncular
fossa
Supraoptic recess
Cerebral aqueduct
Optic chiasm
Oculomotor nerve
Basilar pons
Infundibular recess
B
Optic tract
Posterior cerebral
artery
Superior cerebellar
artery
Optic nerve
Oculomotor nerve
Basilar pons
Oculomotor nerve
Posterior cerebral
artery
Interpeduncular
fossa
Posterior cerebral
artery
Superior cerebellar
artery
Crus cerebri
Midbrain
Anterior lobe
of cerebellum
Anterior cerebral artery
Middle cerebral artery
Hypothalamus
Interpeduncular fossa
Crus cerebri
Midbrain tegmentum
Fourth ventricle
(rostral portion)
“=
A median sagittal view of the brainstem and diencephalon (A)
Rar _ reveals the position of the oculomotor nerve (III) in relation to
adjacent structures as it passes through the interpeduncular fossa. The
MRI in B and C show the position of the oculomotor nerve in sagittal
(B, T1-weighted) and in axial (C, T2-weighted) planes. Note the relationship of the oculomotor nerve to the adjacent posterior cerebral and
superior cerebellar arteries (B, C). Also compare these images with that
of Figure 3-2B. In D (T2-weighted), the trochlear nerve is seen passing
through the ambient cistern around the lateral aspect of the midbrain
(compare with Figures 2-39 and 5-15).
The oculomotor (III) and trochlear (IV) nerves are the cranial
nerves of the midbrain. The oculomotor nerve exits via the interpeduncular fossa to innervate four major extraocular muscles, and
Optic tract
Mammillary body
Posterior cerebral artery
Trochlear nerve
(in ambient cistern)
through the ciliary ganglion, the postganglionic fibers innervate the
sphincter pupillae muscles. Damage to the oculomotor nerve may
result in paralysis of most eye movement, a dilated pupil, loss of the
efferent limb of the pupillary light reflex, and a slight drooping of
the upper eyelid (levator palpebrae superioris muscle), all in the ipsilateral eye. The trochlear nerve is unique in that it is the only cranial
nerve to decussate then exit the posterior (dorsal) aspect of the brainstem, and to innervate, exclusively, a muscle on the contralateral side
of the midline. In this respect, a lesion of the trochlear nucleus results
in muscle weakness on the contralateral side, while damage to the
trochlear nerve after its exit produces muscle weakness on the side of
the lesion. Consequently, damage to CN III and CN IV also results
in diplopia.
Basilar pons
Trigeminal nerve
Abducens nerve
Facial nerve
Vestibulocochlear
Flocculus
nerve
Pyramid
Internal carotid artery
Temporal lobe
Trigeminal nerve
Basilar artery
Middle cerebellar
peduncle
Trigeminal nerve
Basilar pons
Fourth ventricle
Pontine tegmentum
Cerebellum
C
Temporal lobe
Trigeminal
ganglion
Trigeminal
ganglion
Basilar artery
Superior cerebellar
Trigeminal nerve
artery
Tegmentum
of pons
Basilar pons
Fourth ventricle
Anterior lobe
of cerebellum
Third ventricle
Crus cerebri
Midbrain
tegmentum
Interpeduncular
fossa
Root of trigeminal
nerve
Sensory root of the
trigeminal nerve
Basilar pons
Basilar pons
Pyramid
The trigeminal nerve (V) is the largest of the cranial nerve
root of the brainstem (A). It exits at an intermediate posi24
tion on the lateral aspect of the pons, generally in line with the exits
of CNs VII, IX, and X. CN V, and the latter three, are mixed nerves
in that they all have motor and sensory components. The trigeminal
®
nerve is shown
in axial MRI
(B, T1-weighted; C, T2-weighted)
and
coronal planes (D, E, both T1-weighted images). Note the characteristic appearance of the root of the trigeminal nerve as it traverses the
subarachnoid space (B, C), origin of the trigeminal nerve, and position
of the sensory root of the nerve at the lateral aspect of the pons in the
coronal plane (D, E). In addition, the MRI in C clearly illustrates the
position of the trigeminal ganglion and the trigeminal cavity or cave
(the Meckel cavity or Meckel cave) in the middle cranial fossa; this
space contains the trigeminal root and ganglion. The exit of CN V
specifies the interface of the basilar pons with the middle cerebellar
peduncle (B).
Trigeminal neuralgia (TGN), also called tic douloureux, is a lancinating paroxysmal pain within the CN V, to CN V; territories frequently
triggered by stimuli around the corner of the mouth. The causes probably are multiple and may include neurovascular compression by aberrant branches of the superior cerebellar artery (in ~80% of cases; see the
apposition of this vessel to the nerve root in C), multiple sclerosis (rare
in unilateral TGN, more common in cases of bilateral TGN), tumors
(rare), and ephaptic transmission within the nerve or ganglion.
There are multiple medical treatments for trigeminal neuralgia; when
these options fail, surgical therapy may include peripheral nerve section
or neurectomy, microvascular decompression (of the SCA), or percutaneous trigeminal rhizotomy.
Facial nerve
Vestibulocochlear
nerve
Vestibulocochlear
Facial nerve
Glossopharyngeal
nerve
nerve
Pyramid
Vagus nerve
Olivary eminence
Hypoglossal nerve
Basilar artery
Cochlea
Abducens nerve
Semicircular canals
Pons-medulla junction
Vestibulocochlear
Lateral recess of
fourth ventricle
nerve
Facial nerve
Fourth ventricle
Tonsil of cerebellum
C
Abducens nerve
Cochlea
Cochlea
Cochlear portion of
eighth nerve (CPVIII)
Semicircular canals
VPVIII
Semicircular canals
CPVIII
Vestibular portion of
eighth nerve (VPVIII)
Fourth ventricle
Basilar pons
—garsu
%,
Pontine tegmentum
|
Cochlear portion of
eighth nerve
Cerebellum
Anterior inferior
1
cerebellar artery
—=
Cochlea
Cochlea
Semicircular canais
Semicircular canals
Cerebellar vermis
Cerebellar
hemisphere
The cranial nerves at the pons—medulla junction are the abducens (CN VI), the facial (CN VII), and the vestibulocochlear
(CN VIII) (A).
The facial and vestibulocochlear nerves both enter the internal
acoustic meatus, the facial nerve eventually distributing to the face
through the stylomastoid foramen, and the vestibulocochlear nerve
accessing structures of the inner ear. MRIs in the axial plane, B, C, D
(all T2-weighted images) show the relationships of the vestibulocochlear root and the facial nerve to the internal acoustic meatus. Also notice
the characteristic appearance of the cochlea and the semicircular canals
22
(B, C). In addition to these two cranial nerves, the labyrinthine branch
of the anterior inferior cerebellar artery also enters the internal acoustic
meatus and sends branches to serve the cochlea and semicircular canals
and their respective ganglia.
Vestibular portion of
eighth nerve
Cerebellar
tonsil
The tumor most commonly associated with CN VIII is correctly
called a vestibular schwannoma (VS) because it arises from the neurilemma sheath of the superior vestibular root. It is not correct to refer to
this as an acoustic neuroma; it is neither acoustic (does not arise from
the cochlear root) nor a neuroma (does not arise from nerve tissue), but
rather from Schwann cells.
Patients with this tumor commonly present with the clinical triad of
progressive hearing loss (~95% of cases), high-pitched tinnitus (70%),
and equilibrium problems or vertigo (~65%). Headache is seen in about
30% of cases. As the tumor enlarges (greater than about 2 cm) it may
cause facial weakness (seventh root), facial numbness (fifth root), or
abnormal corneal reflex (fifth or seventh root). Treatment is usually by
surgery, radiation therapy, or a combination thereof. The occurrence of
VS may be increased in patients with neurofibromatosis; bilateral VS is
pathognomonic for type 2 of this disease.
A
Facial nerve
Abducens nerve
Vestibulocochlear
nerve
Olivary eminence
Glossopharyngeal
Postolivary sulcus
nerve
Vagus nerve
Preolivary sulcus
Hypoglossal nerve
Preolivary sulcus
Pyramid
Retroolivary sulcus
(postolivary sulcus)
Olive (inferior)
Glossopharyngeal
nerve
Glossopharyngeal
nerve
Flocculus
Restiform body
Fourth ventricle
Tonsil of cerebellum
Cerebellum
Pyramid
Olive (inferior)
(\N
Retroolivary sulcus
Vagus nerve
Fourth ventricle
Tonsil of cerebellum
Cerebellum
Pyramid
Olivary eminence
Vagus nerve
Restiform body
Postolivary sulcus
Vagus nerve
Fourth ventricle
Tonsil of cerebellum
The glossopharyngeal (CN IX) and vagus (CN X) nerves
3-6
(A) exit the lateral aspect of the medulla via the postolivary sulcus; CN IX exits rostral to the row of rootlets comprising
CN X (A).
These nerves are generally in line with the exits of the facial and
trigeminal nerves; all of these CNs are mixed nerves. The exit of
the glossopharyngeal nerve (A, B) is close to the pons—medulla
junction and correlates with the corresponding shape (more rectangular) of the medulla and a larger fourth ventricle. The vagus
nerve exits at a slightly more caudal position (A, C, D); the shape of
the medulla is more square and the fourth ventricle is smaller. CNs
IX, X, and the accessory nerve (XI) exit the skull via the jugular
foramen.
Glossopharyngeal neuralgia is a lancinating pain originating from
the territories served by the CNs IX and X at the base of the tongue and
throat. Trigger events may include chewing and swallowing. Lesions
of nerves passing through the jugular foramen (IX, X, XI) may result
in loss of the gag reflex (motor limb via the ninth nerve), drooping of
the ipsilateral shoulder accompanied by an inability to turn the head
to the opposite side against resistance (eleventh nerve), and dysarthria
and dysphagia (tenth nerve). Syndromes of the jugular foramen may
result from lesions/tumors located inside the cranial cavity adjacent to
the foramen (as in the Vernet syndrome, roots of CNs IX, X, XI), within
the foramen itself, or external to the foramen at the skull base (ColletSicard syndrome, roots of CNs IX, X, XI, XII). In the latter case, the
lesion may also encompass only the roots of CNs X, XI, and XII.
A
Abducens nerve
Facial nerve
Vestibulocochlear
nerve
Glossopharyngeal
Olivary eminence
nerve
Postolivary sulcus
Vagus nerve
Preolivary sulcus
Hypoglossal nerve
Pyramid
Preolivary sulcus
Hypoglossal nerve
Olivary eminence
Postolivary sulcus
Restiform body
Vagus nerve
Tonsil of cerebellum
Hypoglossal nerve
Medulla
Tonsil of cerebellum
Cerebellum
coe
The hypoglossal
nerve
(CN XII) (A) exits the inferolateral
a7
aspect of the medulla via the preolivary sulcus and passes
through the hypoglossal canal.
This motor cranial nerve exits in line with the abducens nerve found
at the pons—medulla junction and in line with the exits of CNs nerves III
and IV of the midbrain. The exit of CN XII is characteristically located
laterally adjacent to the pyramid, which contains corticospinal fibers;
due to their close apposition, both may be damaged in the same neurologic event (medial medullary syndrome). In this syndrome, the damage
may reflect a vascular insult (anterior spinal artery) to the corticospinal
fibers of the pyramid, hypoglossal root, and the medial lemniscus.
In axial MRI (B, T2-weighted; C, T1-weighted), note the characteristic position of the hypoglossal nerve in the subarachnoid space and its
relation to the overall shape of the medulla. This shape is indicative of a
cranial nerve exiting at more mid-to-caudal medullary levels. In B, note its
relationship to the preolivary sulcus and olivary eminence. The hypoglossal nerve exits the base of the skull by traversing the hypoglossal canal.
A lesion of the CN XII root, or in its peripheral distribution, will result
in a deviation of the tongue to the ipsilateral side of the root damage on
attempted protrusion; the genioglossus muscle on that side is paralyzed.
A lesion in the medulla, such as a medial medullary syndrome (Déjérine
syndrome), can result in the same deviation of the tongue (to the ipsilateral side on protrusion) plus additional motor (corticospinal) and sensory
(medial lemniscus) deficits on the opposite side of the body.
The total picture of deficits seen in medullary lesions that involve the
hypoglossal nucleus, or nerve, or in posterior fossa lesions that involve
the hypoglossal root and other roots, will depend on what additional
structures are recruited into the lesion or are damaged. For example,
syndromes of the jugular foramen may involve roots of CNs IX, X, XI,
and XII either together or in various combinations.
Recall that the jugular foramen (CNs IX, X, XI) and the hypoglossal
canal (CN XII) are closely adjacent to each other, separated only by a
small bar of bone on the inner aspect of the skull (see Figure 2-23). This
separation may preclude an intracranial lesion from damaging all of
these roots simultaneously.
However, the roots of CNs [IX—XII come into close apposition imme-
diately upon their exit from the skull base and may be collectively
damaged by a lesion in this confined area. Deficits in the Collet-Sicard
syndrome (one of the jugular foramen syndromes) reflect damage to
CNs IX, X, XI, and XII.
These roots may be collectively damaged in a basal skull fracture involving both foramina or by a tumor involving these roots
in a confined area. A lesion of the internal capsule will result in
a deviation of the tongue to the contralateral side on attempted
protrusion, while a lesion of the hypoglossal root or nucleus results
in a deviation of the tongue to the ipsilateral side on protrusion,
an important difference to evaluate when diagnosing twelfth nerve
signs/symptoms.
Patient’s Right
Patient's Left
A.T2 Axial MRI (One and ah alf syndrome)
Medial rectus motor neuron
Medial rectus muscle
Medial rectus muscle
Oculomotor
nucleus
Medial longitudinal
fasciculus
Lateral rectus muscle
=—
Lateral rectus muscle
Corticospinal
fibers
B. Sagittal CT (One and a half syndrome)
Abducens nucleus
Abducens internuclear neuron
Lateral rectus motor
neuron
Lesions (shaded areas #1 to #5) of the abducens nerve (CN VI)
and/or nucleus and of the medial longitudinal fasciculus that
result in deficits of eye movements in the horizontal plane.
Lesion of the abducens nerve (#1): Motor neurons in the abducens
nucleus innervate the ipsilateral lateral rectus muscle. Consequently, a
*
patient with a lesion of the abducens root (CN VI) external to the pons
(see Figure 3-5 for the position of the sixth root) experiences a loss of
voluntary lateral gaze in the ipsilateral eye, indicating a paralysis of the
lateral rectus muscle. Other movements in the affected eye, and all movements in the contralateral eye, are normal. This patient will experience
diplopia, also called double vision. When looking straight ahead, the eye
on the lesioned side will deviate slightly toward the midline (medial strabismus), this being the unopposed action of the medial rectus muscle in
the same eye. To reduce this diplopia, the patient can rotate his/her head
toward the side of the lesion. With this movement the patient can see one
image because the medially deviated (affected) eye can line up with the
laterally deviated contralateral (nonaffected) eye.
Caudal basilar pontine lesion (#2): As axons arising from abducens
motor neurons pass through the basilar pons, they are located laterally
adjacent to corticospinal fibers (see Figure 6-19). A lesion in this portion
of the pons may simultaneously damage the exiting abducens fibers and
corticospinal axons. A patient with this lesion experiences an alternating (or crossed) hemiplegia, a paralysis of the lateral rectus muscle on
the side of the lesion (loss of voluntary lateral gaze to that side, and
diplopia), and a paralysis of the upper and lower extremities on the
opposite side of the body. Alternating, or crossed, deficits are character-
istic of these brainstem lesions.
Internuclear ophthalmoplegia (INO) (#3): In addition to abducens
motor neurons that innervate the ipsilateral lateral rectus muscle,
the abducens nucleus also contains interneurons. The axons of these
interneurons, called internuclear fibers, cross the midline, enter the
medial longitudinal fasciculus (MLF), and ascend to terminate on motor
neurons in the oculomotor nucleus that innervates the medial rectus
muscle on that (the contralateral) side. A lesion in the MLF interrupts
these axons and results in a loss of medial gaze (medial rectus paralysis)
in the ipsilateral eye during attempted conjugate eye movements. Other
movements in the affected eye and all movements in the contralateral
eye are normal. The laterality of the deficit reflects the side of the lesion
and of the deficit. For example, a right internuclear ophthalmoplegia
specifies a lesion in the right MLF and paralysis of the right medial
rectus muscle; a left internuclear ophthalmoplegia indicates a lesion in
the left MLF causing left medial rectus weakness. Internuclear ophthalmoplegia is seen in ~15%-35% of patients with multiple sclerosis, this
second only to vascular incidents.
Lesion
of the abducens
nucleus
(#4): A lesion of the abducens
nucleus damages alpha motor neurons innervating the ipsilateral lateral rectus muscle and the intranuclear fibers that terminate on medial
rectus alpha motor neurons residing in the contralateral oculomotor
nucleus. A patient with this lesion experiences a loss of horizontal gaze
in both eyes during attempted voluntary eye movement toward the side
of the lesion; horizontal gaze toward the contralateral side is normal.
This deficit is basically an abducens nerve lesion plus an INO. A lesion
of the abducens nucleus may also damage the facial motor fibers forming the internal genu of the facial nerve. In this case the patient may also
experience various degrees of weakness of the facial muscles on the side
of the lesion.
The one-and-a-half syndrome (#5 T2 weighted MRI, and CT): This
syndrome is so named because a unilateral pontine lesion may result
in a loss of medial and lateral voluntary horizontal eye movement on
the side of the lesion (the “one”) and a loss of medial horizontal eye
movement on the contralateral side (the “one-half”). The lesion resulting in this pattern of deficits involves the abducens nucleus on one side
(deficits = lateral rectus paralysis on the side of the lesion, medial rectus
paralysis on the contralateral side) and the immediately adjacent MLF
conveying the internuclear fibers of the contralateral abducens nucleus
(deficit = medial rectus paralysis on the side of the lesion). These lesions
are usually large and involve portions of the paramedian pontine reticular formation, commonly called the horizontal gaze center.
Cranial nerves (CNs) ILI, IV, VI, and XII share four things in
3-9 common: They arise from nuclei containing alpha motor neurons located close to the midline; they exit in a rostrocaudal axis adjacent to the midline; they innervate striated skeletal muscle; and these
muscles are paralyzed on the ipsilateral side if the root is damaged. The
same is true for CN XI except that this nerve arises from spinal levels
C1-C5/C6, enters the foramen magnum, joins with IX and X, and exits
via the jugular foramen.
CNs V, VII, LX, and X are mixed nerves; they selectively contain visceromotor, somatomotor, somatosensory, and/or special sense fibers,
and arise from motor or sensory nuclei located in an intermediate location in the brainstem. These roots enter or exit at a more lateral position
when compared to the motor roots.
CN VIII, the most lateral of the CNs, is regarded as purely sensory
even though it is well known that there is an olivocochlear (efferent
cochlear) bundle, the function of which is to decrease activity in the
auditory nerve. The overall function of CN VIII is auditory, balance,
and equilibrium.
Table 3-2 Brainstem Lesions Involve Cranial Nerve Nuclei and Roots and Correlated Deficits
| LEsION(S)/SYNDROME
Medulla
Medial medullary
(Déjérine) syndrome
STRUCTURES DAMAGED
DEFICITS
Hypoglossal nerve/nucleus
Corticospinal fibers
Medial lemniscus
Ipsilateral paralysis of tongue
Contralateral hemiplegia
Contralateral loss of discriminative touch, vibratory and
position sense on UE, trunk, and LE
Spinal trigeminal tract and nucleus
Nucleus ambiguus
Vestibular nuclei
Anterolateral system
|
=
Ipsilateral loss of pain and thermal sense on face
Dysphagia, hoarseness, deviation of uvula to contralateral side
Nystagmus, vertigo, nausea
Contralateral loss of pain and thermal sense on UE, trunk,
and LE
Lateral medullary (PICA or
Wallenberg) syndrome
Pons
Raymond syndrome *
(Foville syndrome)
Corticospinal fibers
Abducens fibers in pons
Corticospinal fibers
Facial nucleus or fibers
(Anterolateral system)
Contralateral hemiplegia
Ipsilateral abducens palsy, diplopia
Contralateral hemiplegia
Ipsilateral paralysis of facial muscles
(Contralateral loss of pain and thermal sensation on UE,
trunk, and LE)
(Ipsilateral paralysis of masticatory muscles, ipsilateral loss of
pain and thermal sensation on face)
(Trigeminal nerve)
Gubler syndrome
Corticospinal fibers
Midbrain
Oculomotor fibers
Weber (cerebral
peduncle) syndrome
et
Corticospinal fibers
Trigeminal nerve
Corticonuclear fibers
=
Oculomotor nerve
Cerebellothalamic fibers
—
Contralateral hemiplegia
Ipsilateral paralysis of masticatory muscles, ipsilateral loss of
pain and thermal sensation on face
Contralateral hemiplegia
Ipsilateral oculomotor paralysis, diplopia, dilated pupil, ptosis
Contralateral weakness of facial muscles on lower face;
deviation of tongue to contralateral side on protrusion;
ipsilateral trapezius + sternocleidomastoid weakness
Ipsilateral oculomotor palsy, diplopia, dilated pupil, ptosis
Contralateral ataxia, tremor, + red nucleus hyperkinesia
Claude (red nucleus)
syndrome
Benedikt syndrome = Deficits of Weber syndrome + Deficits of Claude syndrome.
* According to Wolf (1971)1), Fulgence Raymond described a patient with several complications and right hemiparesis
and left abducens palsy. Raymond localized the lesion
(he acknowledged potential causes) to the basilar pons involving corticospinal fibers and the abducens root. This
is called Foville s yndrome; Foville also recruits adjacent
structures with their corresponding def, icits. Both eponyms are acceptable.
LE, lower extremity; UE, upper extrem ity.
CRANIAL NERVES IN THEIR LARGER FUNCTIONAL/CLINICAL CONTEXT (FIGURES 3-10 TO 3-16)
a
aaa
rte
creel
Cranial nerves are usually an integral part of any neurologic examination; this is certainly the case in injuries, trauma, and/or diseases
that involve the head and neck. This chapter details their exit points
(or entrance points in the case of sensory nerves) their corresponding
appearance in MRI, examples of lesions causing deficits of eye movements, especially those in the horizontal plane, and of brainstem lesions
that include cranial nerve deficits.
Functional Components of Spinal and Cranial
Nerves (see also Figures 6-1 and 6-2)
The columns of cells within the spinal cord are continuous
rostrally with comparable cell columns in the brainstem
that have similar functions. For example, general (somatic) motor cell
columns of the spinal cord are continuous with the groups of motor
nuclei that innervate the tongue and the extraocular muscles; both cell
columns innervate skeletal muscles. The same is the case for general sensation. Nuclei conveying special senses are found only in the brainstem
and are associated with only certain cranial nerves.
Trigeminal Pathways and Deficits
(see also Figures 8-7 and 8-8A, B)
The trigeminal nerve conveys sensory input from the face
and oral cavity and provides motor innervation to the muscles of mastication. The spinal trigeminal tract and nucleus also receive
general sensation via CNs VII, IX, and X. In this respect, the spinal
trigeminal tract is the center for all general sensory sensations entering
the brainstem on all cranial nerves. In the same sense, the solitary tract
and nucleus (see Figure 8-9) is the brainstem center for all visceral sensations that enters the brainstem on CNs VII, IX, and X. Both of these
cranial nerve brainstem nuclei convey information to the thalamus and
eventually to the cerebral cortex.
Corticonuclear Pathways and Deficits
(see also Figures 8-13 and 8-14A, B)
The cerebral cortex influences cranial nerve nuclei via corticonuclear fibers. In the neurologic examination, this influence is most evident when testing motor functions of CNs VII, IX, X,
XI, and XII. In some situations, the deficit is seen by the inability of
the patient to perform a movement “against resistance.” Comparing the
deficit(s) of a lesion of these fibers to damage of cranial nerves within
the brainstem, or the periphery, is essential to localizing the lesion within
the central nervous system.
This chapter illustrates only part of a much larger picture that places
cranial nerves in a functional context and views their connections in the
periphery as well as within the central nervous system. Although these more
comprehensive cranial nerve connections, and their corresponding functions, are illustrated in Chapter 8 in their appropriate systems context, they
are briefly listed here to facilitate cross reference for those users wishing to
consider cranial nerves in a more integrated format at this point.
Cranial Nerve Efferents (III-VII and IX—XII) and
Deficits (see also Figures 8-19 to 8-22B)
Cranial nerve nuclei are either motor to skeletal muscle or
visceromotor to autonomic ganglia in the periphery. Lesions
involving the nuclei, or roots, of motor nuclei result in paralysis of the
muscles served, with the predictable deficits, such as weakness of the
facial muscles or deviation of the tongue on protrusion. Lesions that
damage the visceromotor fibers of a cranial nerve result in an expected
visceromotor response, such as dilation of the pupil, or a decrease in
secretory function or smooth muscle motility.
Cranial Nerve Reflex Pathways and Deficits
(see also Figures 8-23 to 8-32)
Testing cranial nerve reflexes is a routine part of any complete neurologic examination. This part of the neurologic
exam tests the integrity of the afferent and efferent limbs of the reflex.
Sometimes both components are on the same cranial nerve; sometimes
they are on different cranial nerves. In addition, deficits may be seen that
reflect damage affecting cranial nerve function, but this damage is not in
the afferent or efferent limbs of the reflex; this suggests a broader problem within the central nervous system, such as a lesion in the internal
capsule, particularly its genu.
Pupillary and Visual Pathways and Deficits
(see also Figures 8-44 to 8-47B)
_ The pupillary reflex (commonly called the pupillary light
reflex) has its afferent limb via the second cranial nerve and
its efferent limb via the third cranial nerve.
The reaction of the pupil when light is shined in one eye is a clear
hint as to the location of the lesion. The optic nerve, chiasm, tract,
and radiations and the visual cortex have a retinotopic representation
throughout. Lesions of any of these structures result in visual deficits,
such as a hemianopia or quadrantanopia, which reflect the particular
portion of the visual system that is damaged. Because visual pathways
are widespread within the brain, lesions at various different locations
may result in visual deficits, or various combinations of deficits.
Auditory and Vestibular Pathways and Deficits
(see also Figures 8-49 and 8-50)
The auditory portion of the eighth cranial nerve is concerned with the perception of sound. Damage to the cochlea
itself, or the cochlear root, may profoundly alter one’s perception of
sound or may result in deafness. The vestibular portion of the eighth
cranial nerve functions in the arena of balance, equilibrium, and maintenance of posture. Damage to the semicircular canals, to the vestibular
root, or to central structures that receive vestibular input, may result
in vertigo, ataxia, difficulty walking or maintaining balance, and/or a
variety of eye movement problems.
Q&A for this chapter is available online on (Ne Point.
Meninges, Cisterns, Ventricles,
and Related Hemorrhages
he meninges consist of dura mater (pachymeninx), arachnoid
mater, and pia mater; the latter two form the leptomeninx. The
muamans INeninges are composed of fibroblasts modified in different layers to serve specific functions. The outer layers, the periosteal dura and
meningeal dura, are composed of elongated fibroblasts, large amounts of
collagen, and have great strength. Vessels in the pachymeninx are located
at the dura-skull interface generally forming indentations/grooves in the
inner table of the skull. The periosteal dura forms the periosteum on the
inner table of the skull, is tightly adherent to the inner table particularly
at suture lines, and is located external to the dural sinuses. The meningeal
dura forms the dural reflections (falx cerebri, tentorium cerebelli, diaphragma sellae, falx cerebelli) that are located internal to specific venous
sinuses. Extradural (epidural) hemorrhages or hematoma are sequestered between the inner table of the skull and the periosteal dura. The
innermost part of the dura, the dural border cell layer, is attached to the
externally located meningeal dura and to the internally located arachnoid mater. It is made up of sinuous elongated fibroblasts separated by
extracellular spaces containing an amorphous material but no collagen;
this layer has markedly few cell junctions. The dural border cell layer
is a structurally weak plane at the dura—arachnoid interface; so-called
subdural hemorrhages or hematomas are sequestered within this layer.
There are no naturally occurring spaces between the inner table and
the periosteal dura or external to, within, or internal to, the dural border cell layer. Consequently, epidural hematoma and the so-called subdural hematoma, with their characteristic shapes, extents, and clinical
sequelae are usually the result of a traumatic or pathologic event. There
is a naturally occurring spinal epidural space between the spinal dural
sac and vertebral column; the vertebrae have their own periosteum.
=
Location of epidural hematoma oe
The arachnoid mater is composed of cells that are less elongate,
tightly packed with little/no extracellular space, and attached to each
other by desmosomes and tight junctions. The arachnoid membrane is
located internal to the dural border cell layer and, along with the meningeal dura, forms the various dural reflections. This layer is generally
two to four cells thick and forms a barrier against the movement of
cerebrospinal fluid (CSF), hence its designation as the arachnoid barrier cell layer. The naturally occurring subarachnoid (leptomeningeal)
space (SAS) is located between the arachnoid and pia and provides for
the egress of CSF from the ventricles, circulation around the brain and
spinal cord, and reabsorption into the venous system particularly at the
arachnoid villi. Arachnoid cap cells generally found in the vicinity of
these villi are a primary source of cells that develop into meningioma.
Blood within the SAS (subarachnoid hemorrhage) is most commonly
seen following trauma and secondarily after rupture of an intracranial
aneurysm. The causative agents for bacterial or viral meningitis may be
found in the leptomeningeal space. The arachnoid trabeculae are composed of numerous elongated sinuous fibroblasts that traverse the SAS.
These have cell junctions with the arachnoid layer and with the pia and
may contain collagen in folds of their cell membranes.
The fibroblasts forming the pia mater are adherent to the CNS surface and follow all of its various undulations, in some places forming
a single layer. Taken together the pia mater and the glial limiting membrane (protoplasmic astrocyte cell processes at the CNS surface) form
the pial-glial membrane. Occasional small subpial spaces containing
collagen fibers are found at the pia—brain interface. Large vessels located
in the SAS may be partially, or totally, enveloped by pial cell and/or
trabecular cell processes.
4 Skull
—
SQz
Periosteal dura
Dura mater
Meningeal dura
Dural border
cell layer
Location of subdural hematoma
Arachnoid barrier
cell layer
~ Basement
membrane
Position of subarachnoid hemorrhage
®
Arachnoid mater
Y Subarachnoid
space (SAS) :
Collagen
—/j
=
Sk
Pia—glia membrane (intima pia)
Brain surface
|Pia mater
wie
Occasional subpial space
=
membrane (intima pia
Basement membrane \ piaglia
(
pia)
of
Table 4-1 Comparison of Cerebral Versus Spinal Meninges
CEREBRAI
SPINAL
T
Dura
Dura
¢ Adherent to inner table of skull (no epidural space)
* Composed of two fused layers (periosteal, meningeal), which split
to form sinuses, and of the dural border cell layer (DBC)
° Composed of meningeal dura only (vertebrae have their own
periosteum), and of the DBC layer
Arachnoid (outer part of leptomeninges)
Arachnoid (outer part of leptomeninges)
¢ Attached to dura in living condition (no pre-existing subdural
¢ Attached to dura in living condition (no pre-existing subdural
space)
¢ Separated from vertebrae by epidural space
space)
e Arachnoid villi (in superior sagittal sinus)
¢ Arachnoid trabeculae in SAS
* Subarachnoid space with many cisterns
¢ No arachnoid villi
¢ Few or no arachnoid trabeculae but larger arachnoid septae
e Subarachnoid space with one main cistern
Pia (inner part of leptomeninges)
Pia (inner part of leptomeninges)
¢ Intimately adherent to surface of brain
¢ No pial specializations
¢ Follows vessels as they pierce the brain
e Intimately adherent to surface of cord
© Specializations in the form of denticulate ligaments, filum terminale,
and linea splendens
¢ Follows vessels as they pierce the cord
MENINGITIS, MENINGEAL HEMORRHAGES,
AND MENINGIOMA
A wide variety of disease processes and lesions may involve the meninges; only a few examples are mentioned here.
,, Infections of the meninges (bacterial meningitis) may be called
leptomeningitis because the causative organisms localize to the SAS and
involve the pia and arachnoid. Extension into the dura is called pachymeningitis. A variety of organisms cause bacterial meningitis; bacteria
most commonly associated with certain age groups or with trauma
are as follows: neonate = Streptococcus (S.) agalactiae, Escherichia
(E.) coli, Listeria (L.) monocytogenes; neonate to about 24 months =
S. agalactiae, E. coli, Haemophilus influenzae; about 2-50 years = S.
pneumoniae, Neisseria (N.) meningitidis; about 50 years + = S. pneumoniae, N. meningitidis, L. monocytogenes; basal skull fracture
S. pneumoniae, H. influenzae; head trauma = Staphylococcus. The
patient becomes acutely ill (i.e., headache, photophobia, confusion,
fever, stiff neck [nuchal rigidity], stupor), may have generalized or focal
signs/symptoms, and, if not rapidly treated (with appropriate antibiotics), will likely die. Patients with viral meningitis may become ill over a
period of several days, experience headache, confusion, and fever, but,
with supportive care, will usually recover after an acute phase of about
1-2 weeks with no permanent deficits.
The most common cause of an epidural (extradural) hematoma
(~85% of cases) is a skull fracture that results in a laceration of a
major dural vessel, such as the middle meningeal artery. In approximately 15% of cases, bleeding may come from a venous sinus. The
extravasated blood dissects the dura mater off the inner table of the
skull; there is no pre-existing cerebral extradural space for the blood to
enter. These lesions are frequently large, lens (lenticular) shaped, may
appear loculated, and are “short and thick” compared with subdural
hematomas (see Figure 4-4). The fact that epidural hematomas do not
cross suture lines correlates with their characteristic shape. The patient
may have headache, seizure, vomiting, hyperactive reflexes, or lapse into
a coma and, if the lesion is left untreated, death may result. In some
cases, the patient may be unconscious initially, followed by a lucid interval (the patient is wide awake), then subsequently deteriorate rapidly
and die; this sequelae is called “talk and die.” Treatment of choice for
large lesions is surgical removal of the clot and coagulation of the damaged vessel.
Tearing of bridging veins (veins passing from the brain outward
through the arachnoid and dura), usually the result of trauma, is a
common cause of subdural hematoma. This designation is somewhat
a misnomer because the extravasated blood actually dissects through
a specialized, yet structurally weak, cell layer at the dura—arachnoid
interface: the dural border cell layer. There is no pre-existing “subdural
space” in the normal brain. Acute subdural hematomas, more commonly seen in younger patients, usually are detected immediately or
within a few hours after the precipitating incident. Chronic subdural
hematomas, usually seen in the elderly, or in patients on anticoagulation therapy, are frequently of unknown origin. They may take days or
weeks to become symptomatic and, in the process, cause a progressive
change in the mental status of the patient. This lesion appears “long and
thin” compared with an epidural hematoma, follows the surface of the
brain, and may extend for considerable distances (see Figures 4-4 and
4-5). Treatment is surgical evacuation (for larger or acute lesions) or
close monitoring for small, asymptomatic, or chronic lesions.
The most common cause of subarachnoid hemorrhage is trauma.
In approximately 75% to 80% of patients with spontaneous (nontraumatic) subarachnoid hemorrhage, the precipitating event is rupture of
an intracranial aneurysm. Symptomatic bleeding from an arteriovenous
malformation occurs in ~5% of cases. Blood collects in and percolates
through the SAS and cisterns (see Figure 4-7). Sometimes, the deficits
seen (assuming the patient is not in a coma) may be a clue as to location,
especially if cranial nerves are nearby. Onset is sudden; the patient complains of a sudden and excruciatingly painful headache (“the worst of
my life,” or “thunderclap”), and may remain conscious, become lethargic and disoriented, or may be comatose. Treatment of an aneurysm is
to surgically separate the sac of the aneurysm from the parent vessel
(by clip or coil), if possible, and to protect against the development of
vasospasm.
Tumors of the meninges (meningiomas)
are classified in different
ways, but usually they arise from arachnoid cap/stem cells (a small
number are dural in origin) around the villi or at places where vessels or cranial nerves penetrate the dura—arachnoid. These tumors
may present with signs/symptoms based on their location and size.
They grow slowly (symptoms may develop almost imperceptibly over
years), are histologically benign, may result in hyperostosis of the
overlying skull, and frequently contain calcifications. In decreasing
order, meningiomas are found in the following locations: parasagittal
area + falx cerebri (together 29%), convexity 15%, sellar 13%, sphe-
noid ridge 12%, and olfactory groove 10%. Treatment is primarily by
surgical removal, although in some cases meningiomas are treated by
radiotherapy.
Superior sagittal sinus
Arachnoid villus
Lateral lacunae
Dura mater:
Periosteal dura
Meningeal dura
Arachnoid mater
Arachnoid trabeculae
Pia mater
:
'
\
=t
Cerebellum
7,
eer
WAMS
Transverse
sinus
[| ener
Hy]
AY
Falx cerebri
cerebelli
Cistern
ey
Skull
Dura mater:
Periosteal dura
Meningeal dura
Subarachnoid space
Arachnoid mater
Cerebral vessel
and branch
Pia mater
Arachnoid trabeculae
[
C=
1
Vertebrae
—s
MENGES;
Wa o>
Spinal nerves
Spinal vessel
ZLB)
Meningeal dura
Dura mater
Intervertebral
ligament
Epidural space
Conus medullaris
mi
ee
SL
|
4
We
: |
J
(
\\
5
‘
Dw
Vertebra
Cauda equina
@
Lumbar cistern
=
Arachnoid mater
Filum terminale (internum)
Denticulate ligament
A]
Pia mater
NY,
Coccygeal ligament (filum terminale externum)
Coccyx
Semi-diagrammatic representation of the central nervous
| system and its associated meninges. The details show the
2
relationships of the meninges in the area of the superior sagittal sinus, on the lateral aspect of the cerebral hemisphere, and around the
spinal cord. Cerebrospinal fluid is produced by the choroid plexuses
of the lateral, third, and fourth ventricles. It circulates through the
"
ventricular system (small arrows) and enters the subarachnoid space
via the medial foramen of Magendie and the two lateral foramina of
Luschka. In the normal healthy patient, the arachnoid is attached to
the inner surface of the dura. There is no actual or potential subdural space. This space is created resultant to a traumatic, infectious, or
pathologic process.
Meninges, Cisterns, Ventricles, and Related
|
Hemorrhages— Meningitis
%
Mastoiditis
Me4 }
:
Examples of meningitis (A—-D, all axial) in the adult. Meningitis is a disease that generally involves the subarachnoid
space (SAS) and the membranes bordering on this space, namely the
arachnoid mater and pia mater. Consequently, it is commonly called
leptomeningitis (arachnoiditis, or pia-arachnitis). Meningitis may
preferentially affect one side more than the other and, in some cases, present with unilateral deficits. Bacterial meningitis is a medical
emergency; it may present suddenly, progress rapidly, and must be
treated quickly or death may result. Patients with viral meningitis
may become ill over several days versus potentially hours, and after
a short acute period, and with supportive care, recover with no permanent deficits.
Sources of infections that may lead to meningitis are those involving
the paranasal sinuses or the mastoid air cells (mastoiditis,A).Mastoiditis
is almost always accompanied by other disease processes, most notably
acute or chronic otitis media. The close association of mastoid air cells
to the sigmoid sinus represents one comparatively direct route into the
central nervous system.
Once an infection of the mastoid accesses the central nervous system, it may involve the venous sinuses (A), which appear bright when
enhanced. The infection will layer out over the surface of brain within
the SAS, enter the sulci, and occupy the SAS immediately above and
below the tentorium cerebelli (see arrows in A, B, C). The SAS and the
sulci enhance when the patient is treated with IV gadolinium (C, D) and
appear bright in the image. In addition to these features, small enhance-
ments may appear within the SAS (D, arrows) that indicate the formation of small abscesses. This inflammation may also extend to involve
the dura mater in which case it is called pachymeningitis.
Meningitis
Wes,
Falx cerebri
4
Le
——Falx cerebri
sagittal
Superior
sagittal
sinus
—
sinus
Examples of meningitis (leptomeningitis) that extensively involves both sides of the central nervous system (A-D, all axial)
in the adult. In A and B, note the enhancement of the meninges over the
temporal lobe (arrows), at the location of the tentorium cerebelli, and of
the venous sinuses (SSS, superior sagittal; S, sigmoid; TS, transverse). At
different axial levels, enhancement is clearly visible on the brain surface
(B, C, arrows), along the dural reflections (tentorium cerebelli and falx
cerebri, B—D), and within the sulci (C). In addition, enhancements over
the curvature of the hemisphere (D) are suggestive of focal collections of
inflammation largely sequestered in the leptomeninges.
As seen in these samples, meningitis can be imaged using gadolinium
and to a reasonable level its degree and extent visualized. However, it
is also apparent that the meningeal inflammation and the inflammation within the SAS, are more subtle than lesions such as meningioma,
hemorrhage, or brain tumor. While these may enhance in similar ways,
such as a mild subarachnoid hemorrhage versus leptomeningitis, each
has its unique clinical features and presentation that leads to a correct diagnosis. Vessels located within the subarachnoid space may also
enhance as they most likely contain infectious material and the organisms may infiltrate the vessel walls. As noted in Figure 4-2, the inflammation may also extend to involve the dura mater (pachymeningitis).
The more common causative agents for meningitis, and the age groups
with which they are more frequently associated, are discussed earlier
in this chapter.
Meninges, Cisterns, Ventricles, and
Subdural Hemorrhage :
Related Hemorrhages—Epidural and
Hemorrhage in brain
Examples
of epidural
(extradural)
hemorrhage/hematoma
(A, B) and of acute (C, D) and subacute (E) subdural hematoma/
hemorrhage. Note the lenticular shape of the epidural lesions (they do
not cross suture lines—A, B), their loculated appearance, and their location external to the substance of the brain (see also Figure 4-5). In
contrast, the acute subdural lesions (C, D, arrows) are quite thin and
extend over a longer distance on the cortex; they are not constrained by
suture lines. Note the midline shift in patients (A, D).
In E, the subdural hematoma has both chronic and subacute
phases. The chronic phase is indicated by the upper two and lower
two arrows where the blood is replaced by fluid, and the subacute
phase by the middle arrow, where fresher blood has entered the
lesion. Note the extent of this lesion on the surface of the cortex and
its thinness compared with epidural lesions. The patient in E also has
small hemorrhages into the substance of the brain in the region of the
genu of the internal capsule. Images A-E are CT without contrast.
For additional comments on epidural and subdural hemorrhages,
see p. 58.
The treatment of choice for epidural hematoma, especially if the
patient is symptomatic, or if the patient is asymptomatic but the
acute lesion is greater than 1 cm thick at its widest point and has a
volume of greater than 30 cm’, is surgical removal and hemostasis of
bleeders. In subdural hematoma, surgical evacuation is the preferred
treatment in symptomatic patients with acute lesions that are 1 cm
thick (0.5 cm in pediatric patients) and where there is a midline shift
of greater than 5 mm. On the other hand, asymptomatic patients
with thin subdural lesions may be followed medically and may not
require surgery.
Epidural and Subdural Hemorrhage
Examples
of epidural
(extradural)
hemorrhage/hematoma
(A, B) and subdural hematoma/hemorrhage (C, D) resultant
to trauma to the head; all are CTs without contrast, and all are in the
axial plane. Epidural hematoma may occur in cases of skull fracture (A,
on the right side) in which the middle meningeal artery (or its larger
branches) is lacerated. The resulting hematoma is formed between the
inner table of the skull and the outer aspect of the dura (epidural, B, on
the right). In this significant trauma, there is a large epidural hematoma, a small iesion, probably also an epidural (small arrows), and small
amounts or air within the cranial cavity (B, black dots).
The mechanism of epidural hematoma formation is most likely twofold. First, the dura is stripped from the inner table of the skull during the traumatic event creating an artifactual space. Second, the sharp
edges of bone lacerate arteries, which bleed into this space, and, it is
believed, may further dissect the dura from the skull. Epidural hematomas, however, do not cross suture lines. Once the dissection reaches a
suture line it stops and the lesion becomes lenticular shaped.
Trauma to the head, without skull fracture, may also result in subdural hemorrhage/hematoma; in such cases, it is called acute subdural
hematoma (C, D). Subdural hematomas may also be subacute or chronic
and do occur in cases where trauma is not involved. In these examples,
trauma on the right side of the head (C, soft tissue damage at arrows)
resulted in a large acute subdural hematoma on the patient’s right side,
and trauma on the left side of the head (D, soft tissue damage at arrows)
resulted in a subdural lesion on the patient’s right. This latter lesion is
a type of contrecoup injury in which the lesion is on the side opposite
the initial impact. Note that the larger subdural lesion (C) has caused
considerable midline shift. Subdural hematomas are not restrained by
suture lines. Therefore, damage to the dural border cell layer may dissect
this friable cell layer over considerable distances and the resultant lesion
is thin and long.
As seen in B and C in this figure, and in Figure 4-4 A and D on the
facing page, epidural and subdural lesions may be sufficiently large to
result in effacement of the midline as indicated by a shift in the position
of the falx cerebri. This appearance, plus the frequent loss of sulci and
sometimes cisterns on the side of the lesion, foretells the very real possibility of brain herniation. This may present as a subfalcine herniation,
which may impinge on both hemispheres, or morph into a transtentorial
herniation; all result in characteristic deficits (see Chapter 9 for further
information of herniation syndromes).
Paracallosal cistern
Lamina terminalis
cistern
Quadrigeminal cistern
B
Chiasmatic cistern
Interpeduncular cistern
Fourth ventricle
C
Prepontine cistern
Premedullary cistern
D
Cisterna magna
Sylvian cistern
Crural cistern
Midbrain
Quadrigeminal cistern
Lamina terminalis cistern
Optic tract
Interpeduncular cistern
Ambient cistern
Inferior colliculus
Trigeminal nerve
Prepontine cistern
Basilar artery
Superior
cerebellopontine
cistern
Basilar pons
Fourth ventricle
Premedullary cistern
Medulla
Cisterna magna
Inferior
cerebellopontine
cistern
Tonsil of cerebellum
A median sagittal MRI (A, T2-weighted) of the brain showing the positions of the major cisterns associated with midline structures. Axial views of the midbrain (B, T1-weighted), pons (C,
T2-weighted), and medulla (D, T2-weighted) represent the corresponding planes indicated in the sagittal view (A).
Cisterns are the enlarged portions of the subarachnoid space that
contain arteries and veins, roots of cranial nerves, and, of course,
cerebrospinal fluid. Consequently, the subarachnoid space and cisterns are continuous one with the other. In addition, the subarachnoid space around the brain is continuous with that around
the spinal cord (Figure 4-1). Compare the locations and shapes
of these cisterns with the blood-filled parts of the subarachnoid
space and contiguous cisterns shown in Figure 4-7 on the facing
page.
_ Cisterns and Subarachnoid Hemorrhage
B
Subdural
hemorrhage
Lamina terminalis
cistern
Supraoptic recess
Sylvian
Interpeduncular
cistern
cistern
Crural
cistern
Temporal
horn
Blood on
insular cortex
Midbrain
Blood on tentorium
cerebelli
Ambient
cistern
Cerebellum
Quadrigeminal
cistern
'
Lamina terminalis
cistern
Third
ventricle
Sylvian
Blood on
cistern
insula
Interpeduncular
cistern
Crural
cistern
Cerebellopontine
cistern
Cerebellum
Blood on tentorium
cerebelli
| Blood in the subarachnoid space and cisterns (subarachnoid
- hemorrhage). In these CT examples, blood occupies the subarachnoid space and cisterns, outlining these areas in various shades of
white. Consequently, the shape of the cisterns is indicated by the configuration of the white area, the white area representing blood.
Around the base of the brain (A), it is easy to identify the cisterns
related to the midbrain, the supraoptic recess, which is devoid of blood,
and blood extending laterally into the Sylvian cistern. In some cases
(B), subdural hemorrhage may penetrate the arachnoid membrane and
result in blood infiltrating between gyri, such as this example with blood
on the cortex of the insula. In C, the blood is located around the midbrain (crural and ambient cisterns), extends into the Sylvian cistern, and
into the cistern of the lamina terminalis. The sharp interface between
the lamina terminalis cistern (containing blood) and the third ventricle
(devoid of blood) represents the position of the lamina terminalis. In D,
blood is located in cisterns around the pons, but avoids the rostral part
of the fourth ventricle. Also note the clearly enlarged temporal horn of
Ambient
cistern
Rostral part
of fourth
ventricle
the lateral ventricle in D; enlargement of this particular part of the ventricle is indicative of increased pressure within the ventricular system.
In fact, the presence of subarachnoid blood in the cisterns is in frank
contrast to the stark and total lack of blood in the ventricles (A-D)
Subarachnoid hemorrhage (SAH) is always a serious medical event.
In the case of SAH resulting from aneurysm rupture (about 75% to
80% of all spontaneous cases), 10% to 15% die prior to receiving
medical attention and about 20% after hospital admission; about 30%
have permanent disability; approximately 30% who survive may have
moderate to severe deficits, particularly depression and cognitive compromise. Other comparable statistics indicate that about 45% to 50%
die within the first 2-4 weeks, and about 30% have moderate to severe
deficits.
About 65% of patients who have the aneurysms successfully clipped
have a diminished quality of life. Compare these images with the locations of some of the comparable cisterns as seen in Figure 4-6. Images
A-D are CT.
a
Meninges, Cisterns, Ventricles, and Related Hemorrhages—Meningiom
Examples of a right-sided convexity meningioma (A, B), a
meningioma of the tentorium cerebelli (C, D), and a meningioma en plaque (E). Meningiomas are slow-growing, noninfiltrating,
usually benign, extra-axial tumors that are curable assuming they can
be completely removed (91+%, 5-year survival). They may present with
headache or seizure, but many are asymptomatic and some are discoyered as an incidental finding (~30+%). The convexity meningioma (A,
sagittal; B, coronal) is located in the medial aspect of the superior frontal gyrus rostral to the paracentral gyri. It is slightly off the midline;
meningiomas that are directly adjacent to the midline and involve the
superior sagittal sinus are called parasagittal meningiomas. Note its attachment to the dura (A, arrow); this attachment, seen in many meningiomas, is commonly called the dural tail. The slightly darker gray area
immediately adjacent to this tumor likely represents edema. Convexity
meningiomas are seen in about 15% of cases, and parasagittal meningiomas are found in about 21% of patients.
The tentorial meningioma (C, sagittal; D, coronal) is located on the
midline, close to the rostral edge of the tentorium, and on its inferior
surface. The tumor significantly impinges on the cerebellum (C, D), but
does not involve the occipital lobes. This patient has motor deficits of
the cerebellar type due to the involvement of the cerebellum. Due to
its location, this tumor presents a greater surgical challenge than does
the convexity meningioma and may contribute to eventual occlusion of
the cerebral aqueduct. Tentorial meningiomas are seen in 3% to 4% of
cases. The meningioma en plaque (E, arrows) can also be classified as a
convexity meningioma or sphenoidal meningioma, due to its location.
Based on its location, a meningioma in this configuration may go undetected for a considerable time, or be an incidental finding.
Meningioma
Examples of meningiomas that are located on the midline. The
sellar meningioma (A, sagittal; B, coronal, also called tuberculum sellae meningioma), arises from the sella turcica and, due to its position, may impinge on optic structures and/or cause deficits indicative
of involvement of the hypothalamus. Note that, although the tumor has
reached significant size, major structures in the central region of the hemisphere, such as large veins and the corpus callosum (G, genu; B, body; S,
splenium), are in their normal positions. Tumors are seen in this area in
about 12% to 13% of cases and may require special surgical approaches.
The large meningioma in C and D was diagnosed as a falcine meningioma, a tumor that arises from the falx cerebri. Such tumors may
arise at any point along the course of the falx cerebri, are frequently
bilateral, and may impinge on the medial aspects of both hemispheres.
In this location a falcine meningioma may result in unilateral or bilateral somatomotor and/or somatosensory deficits localized to the lower
extremities. Note that the central portions of the hemisphere have been
pushed caudally as seen by the foreshortened internal cerebral vein and
the change in shape and position of the corpus callosum (G, genu; S,
splenium). At the same time, olfactory groove meningiomas are also seen
in this location and have a similar appearance. These arise from the area
of the cribriform plate and enlarge upward to impinge on the frontal
lobes. Falcine meningiomas constitute about 8% and olfactory groove
meningiomas about 10% of all tumors of this type.
Meningiomas located in the immediate vicinity of the superior sagittal sinus (SSS) are called parasagittal; these may be attached to the lateral wall, invade the lateral recess or SSS in various patterns, or invade
and totally occlude the SSS.
The general appearance of these examples, and those in Figure 4-8
(facing page), illustrates that these lesions, in many cases, grow so slowly
that a significant portion of the brain can be displaced without untoward effects. The presenting deficits may be persistent headache and seizure. The sulci and midline may not be effaced and brain structures may
not be displaced from their normal position. However, meningiomas
that may block the egress of cerebrospinal fluid will likely result in signs
and/or symptoms characteristic of increased intracranial pressure (headache, vertigo, visual disturbances, seizure), or in deficits that reflect the
point of the blockage of CSF egress. Depending on their size and location meningiomas may also present with focal symptoms and/or signs.
Massa intermedia
Body of lateral
Pineal recess
ventricle
Suprapineal recess
Third ventricle
Anterior horn of
Posterior commissure
lateral ventricle
Atrium of lateral ventricle
Interventricular
foramen
(and glomus choroideum)
Posterior horn of
lateral ventricle
Anterior commissure
«
ri
Pr
Tectum
é
Lamina terminalis ———————+
|
Cerebral aqueduct
i]
Infundibular recess
Supraoptic recess
Fourth ventricle
Optic chiasm
Infundibulum
Lateral recess of fourth ventricle
Mammillary body
Amygdaloid nuclear complex
Foramen of
Luschka
Dorsal cerebellomedullary
cistern (cisterna magna)
Inferior horn of lateral ventricle
Bordering Structures
Ventricular Space
Genu of corpus callosum
Anterior horn of lateral ventricle
Head of caudate nucleus ———!—_..
Septum pellucidum
—
Body of caudate nucleus —_—=*
\
Fornix
Body of lateral ventricle
(ventral to body of corpus callosum)
Third ventricle
}
-_--
Suprapineal recess
oN
)
Amygdaloid nuclear complex ———j——__
{
{
Inferior horn of
lateral ventricle
~~
Tail of caudate nucleus
.
4
/
Hippocampal formation
Splenium of
corpus callosum
iu
/
1
]
/
/
Be"
Atrium of lateral ventricle
(contains glomus choroideum)
\
Optic radiations ———‘- \
\ \
Tapetum —_
Cerebral aqueduct
\ \
Lateral recess of
fourth ventricle
Fourth ventricle
Posterior horn of lateral ventricle
Lateral (above) and dorsal (below) views of the ventricles
and the choroid plexus. The dashed lines show the approximate positions of some of the important structures that border on the
ventricular space. These structures are easily identified in MRI and/or
CT in any plane. The choroid plexus is shown in red, and structures bordering on the various portions of the ventricular spaces are color coded;
these colors are continued in Figure 4-11 on the facing page. Note the
relationships between the choroid plexus and various parts of the ventricular system. The large expanded portion of the choroid plexus found
in the area of the atrium is the glomus (glomus choroideum). Note the
only naturally occurring constrictions to the flow of CSF through the
ventricular system are the interventricular foramina (of Monro), cerebral aqueduct, and foramina of Luschka and Magendie of the fourth
ventricle.
Corpus callosum
(body)
Caudate nucleus
orpus callosum
r
(body)
Anterior horn of
lateral ventricle
Septum
pellucidum
Septum
pellucidum
Caudate nucleus (body)
C
Stria terminalis
Corpus callosum (body)
Fornix (F)
Caudate nucleus
Body of lateral
ventricle
Body of lateral
(head)
ventricle
Interventricular
foramen
Corpus callosum
(rostrum)
Gyrus rectus
Choroid plexus (CP)
Fornix
Anterior
commissure
CP
Third ventricle
Third ventricle
Hypothalamus
Dorsal thalamus
Massa intermedia
Optic chiasm
Mammillary body
Hypothalamus
Caudate nucleus (body)
Fornix
Dorsal thalamus
Third ventricle
Amygdaloid nuclear
complex
Optic tract
Inferior horn of
lateral ventricle
Body of lateral
ventricle
Corpus callosum
Pulvinar
Optic radiations
Tapetum
Optic radiations
Tapetum
Pineal
Cerebral aqueduct
Inferior horn of
lateral ventricle
Hippocampal formation
Corpus callosum
(splenium)
Caudate nucleus (tail)
Atrium of lateral
ventricle
Calcarine
sulcus
Hippocampal formation
Calcar avis
Posterior horn of
lateral ventricle
Lateral view of the ventricular system and corresponding
4-11
semi-diagrammatic
cross-sectional
representations
from
rostral (A) to caudal (G) identifying specific structures that border on
the ventricular space. In the cross sections, the ventricle is outlined by
a heavy line, and the majority of structures labeled have some direct
relevance to the ventricular space at that particular level. In addition,
the configuration of structures lining the ventricular space, and the
shape of the space itself may provide important information during a
neurologic examination. The color coding corresponds to that shown in
Figure 4-10 on the facing page.
B
IDARD
Anterior horn of
lateral ventricle
Anterior horn
Third
ventricle
Atrium of
lateral ventricle
Posterior horn of
lateral ventricle
Temporal horn of
lateral ventricle
Basilar pons
Tegmentum of pons
Fourth ventricle
Cerebellum
Pons—medulla junction
Fourth ventricle
Lateral recess of
fourth ventricle
Cerebellum
ee
_ Examples of hemorrhage occupying portions of the ventricular system (intraventricular hemorrhage). In these CT
images, blood appears white within the ventricles. Consequently, the
shape of the ventricular system is outlined by the white area (these are
sometimes called casts), and the specific portion of the ventricular system is correspondingly identified.
Note blood in the anterior horn, atrium, and posterior horn of the
lateral ventricles (A, B), and blood clearly outlining the shape of the
third ventricle (B). Blood also clearly outlines central portions of the
fourth ventricle (C) and caudal portions of the fourth ventricle (D),
including an extension of blood into the left lateral recess of the fourth
ventricle (D). In addition to these images, Figure 4-13C on the facing
page shows blood in the most inferior portions of the third ventricle.
The presence of blood within the ventricular system occurs in about
25% of cases with ruptured aneurysm. The most common aneurysm
sites, and point at which blood may enter the ventricular system upon
rupture, are as follows: the distal posterior inferior cerebellar artery,
through the roof of the fourth ventricle or foramen of Luschka (fourth
ventricle); the basilar tip, through the floor of the third ventricle (third
ventricle); at the junction of the anterior communicating and anterior
cerebral arteries, through the lamina terminalis (third ventricle); or from
this same location into the anterior horn of the lateral ventricle. Blood
may also be found within the ventricles following traumatic brain injury,
bleeding from, or rupture of an arteriovenous malformation (AVM) in
certain locations, and bleeding from tumors, especially those located in
the brain parenchyma or in the ventricular system.
Ventricles and Hemorrhage into the Ventricles
B
Epidural
hematoma
Blood in
brain
Blood in lateral
ventricle
Blood in third
ventricle
Blood in third
ventricle
Blood in atrium of
lateral ventricle
Examples of blood in the ventricles resulting from head
trauma and/or traumatic brain injuries (TBI). Note the soft
tissue damage and skull fractures (especially in patients A and B). In patient A, there is blood in the right anterior horn of the lateral ventricle.
Patient B has blood in the right anterior horn, in the third ventricle, in the
substance of the brain in the right frontal lobe, as well as a small epidural
at the right frontal pole. Patient C has blood in the third ventricle and in
the atrium of the lateral ventricle on the right side. In addition to trauma,
as illustrated here, intraventricular hemorrhage (also called intraventricular blood) may occur in a variety of situations. Intracerebral hemorrhage
is a bleed into the substance of the brain (also called parenchymal hemorrhage). This blood extends into a ventricular space, arises from a brain
tumor or from an arteriovenous malformation, or a tumor of the choroid
Subarachnoid blood on
tentorium cerebelli
plexus. In addition, blood from a ruptured aneurysm may preferentially
dissect into adjacent ventricular spaces as described in Figure 4-12. Intraventricular blood may also occur in newborns who have bleeding internal
to the ependymal lining of the ventricle (subependymal hemorrhage) that
extends into the ventricle, in a patient of any age who may bleed from an
arteriovenous malformation, or from a highly vascular tumor of the choroid plexus within the ventricular space. As a general principle, the larger
the ventricles become, in cases of intraventricular blood, the more serious
the prognosis for the patient.
These axial CT images (A-C) illustrate the important fact that, especially in patients with head trauma, blood may be found at different
locations (meningeal, intraventricular, within the substance of the brain
[parenchymatous]) sometimes all in the same patient.
Choroid plexus (CP) in
body of lateral ventricle
CP in atrium of lateral ventricle
CP in temporal horn
CP in roof of third ventricle
of lateral ventricle
CP in fourth ventricle
Anterior choroidal artery
PICA
Posterior cornmunicating artery
Lateral posterior choroidal artery
Medial posterior choroidal artery
Medial striate artery
Internal carotid artery
Middle cerebral artery (Mj)
Anterior choroidal artery
Anterior choroidal artery
Posterior communicating artery
Posterior cerebral artery (P2)
Lateral posterior choroidal artery
Superior cerebellar artery
Medial posterior choroidal artery
Basilar artery (BA)
Anterior inferior cerebellar artery (AICA)
AICA branch to choroid plexus
at the foramen of Luschka
Vertebral artery (VA)
Posterior inferior cerebellar artery (PICA)
Li
Blood supply to the choroid plexus of the lateral, third, and
4-14
fourth ventricles. Branches of the vertebrobasilar system and
of the internal carotid artery and P, segment of the posterior cerebral artery
that supply the choroid plexus are accentuated by appearing in a darker red
shade. In A, a representation of these vessels (origin, course, termination) is
shown from the lateral aspect. Anterior, medial posterior, and lateral poste-
PICA branch to choroid plexus
in the fourth ventricle
rior choroidal arteries serve the plexuses of the lateral and third ventricles.
The choroid plexus in the fourth ventricle and the clump of choroid plexus
protruding out of the foramen of Luschka are served by posterior inferior
and anterior inferior cerebellar arteries, respectively. In B, the origins of these
branches from their main arterial trunks are shown. See also Figures 2-24,
2-32, and 2-35.
aS The Choroid Plexus: Locations, Blood Supply, Tumors
Tumor in third ventricle
Tumors of the choroid plexus (CP) constitute about 1%
“=
of all intracranial tumors and are generally classified as
“aie 22
CP tumors) or
choroid plexus papilloma (benign, most common of
are most
tumors
These
rare).
choroid plexus carcinoma (malignant,
nsuprate
located
years,
2
commonly seen in children younger than
ined
increas
of
s/signs
torially, and may present with symptom
d
enlarge
e,
headach
,
tracranial pressure (nausea/vomiting, lethargy
tumors
these
adults
In
ventricles, craniomegaly or macrocephaly).
vascularized;
are more common infratentorially. The CP is highly
ventricular
the
into
consequently, tumors of this structure may bleed
g its
outlinin
cast
a
space (intraventricular hemorrhage) and create
(A-D),
axial
in
shape. Examples of tumors of the choroid plexus
Tumor in atrium
coronal (E), and sagittal (F) planes. The tumor in A-C is from the
same patient and shows the lesion in the area of the atrium of the
lateral ventricle on the left (A) with bleeding from the tumor into
the posterior and temporal horns of the lateral ventricle on the same
side (B, C). Note the enlarged ventricles (A-C). The image in D shows
of the
a large tumor originating from the choroid plexus in the roof
icuinterventr
the
d
obstructe
partially
has
tumor
third ventricle. This
.
ventricles
lateral
the
of
nt
enlargeme
t
lar foramina, with consequen
choroideglomus
the
in
tumors
with
patients
of
Images E and F are
plexus
um (choroid glomus or choroid enlargement) of the choroid
with
MRI
are
D-F
and
CT,
are
A-C
Images
of the lateral ventricle.
enhancement of the tumor.
Blood in frontal lobe
Blood in third
ventricle
Blood in cerebral
aqueduct
The presence of blood within the substance of the brain
may be called parenchymatous hemorrhage (a more general me global term), or cerebral hemorrhage (blood into the cerebral
hemisphere), brainstem hemorrhage (blood into the brainstem), pontine
hemorrhage (blood into the pons), or by any of a number of other terms
that indicate a more specific location and size (Duret hemorrhage), shape
(splinter hemorrhage), or extent of the extravasated blood. The large
hemorrhages into the hemisphere (A, B) have resulted in enlargement of
the ventricles, a midline shift (with the real possibility of brain herniation), and, in the case of A, a small amount of blood in the right posterior
horn of the lateral ventricle. In these examples, the lesion is most likely a
result of hemorrhage from lenticulostriate branches of the M; segment.
Blood in the substance of the brain and in the ventricular system may
also result from trauma (C). In this example (C), blood is located in the
frontal lobe, the third ventricle, and cerebral aqueduct. The enlarged
temporal horns (C) of the lateral ventricles are consistent with the interruption of CSF flow through the cerebral aqueduct (noncommunicating
hydrocephalus). Images A-C are CT.
Other causes of blood within the brain include bleeding from a variety of tumors, more commonly from malignant tumors and metastatic
tumors and less so from benign tumors. Traumatic iinjury, commonly
referred to as traumatic brain injury (TBI), may be a source of blood
within the brain as well as the transformation of an ischemic stroke into
a hemorrhagic stroke.
|
Q&A for this chapter is available online on TU!|r 1e Point.
Internal Morphology of the Brain
in Unstained Slices and in MRI
Part |
Brain Slices in the Coronal Plane
Correlated with MRI
rientation to Coronal MRIs: When a physician is viewing a
coronal MRI or CT, he/she is viewing the image as if looking
at the patient’s face. Consequently, the observer’s right is the
left side of the brain in the MRI and the left side of the patient’s brain.
Conversely, the observer's left is the right side of the brain in the MRI
and the right side of the patient’s brain. Obviously, the concept of what
is the left side versus what is the right side of the patient’s brain is enormously important when using MRI (or CT) to diagnose a neurologically
impaired individual.
To reinforce this concept, the rostral surface of each coronal brain
slice appears in each photograph. So, when looking at the slice, the
observer’s right field of view is the left side of the brain slice, and
the observer’s left field of view is the right side of the brain slice. This
view of the slice correlates exactly with the orientation of the brain as
seen in the accompanying coronal MRIs.
Coronal view
Orientation to Axial MRIs: When a physician is looking at an
axial MRI, he/she is viewing the image as if standing at the patient’s
feet and looking toward his or her head while the patient is lying on
his or her back. Consequently, and as is the case in coronal images,
the observer’s right is the left side of the brain in the MRI and the left
side of the patient’s brain. The observer's left is the right side of the
brain in MRI and the right side of the patient’s brain. It is absolutely
essential to have a clear understanding of this right-versus-left concept when using MRI (or CT) in the diagnosis of the neurologically
impaired patient.
To reinforce this concept, the ventral surface of each axial slice was
photographed. So, when looking at the slice, the observer’s right is the
left side of the brain slice, and the observer’s left is the right side of the
brain slice. This view of the slice correlates exactly with the orientation
of the brain as seen in the accompanying axial MRIs.
Axial view
19
internal Morphology of the Brain in Unstained Slices and in MRI—Part |:Brai 1
Position of
falx cerebri
Cingulate gyrus (CinGy)
Cingulum (Cin)
Body of corpus
callosum (BCorCl)
Head of caudate nucieus
(HCaNu)
Anterior horn of lateral
ventricle (AHLVen)
- Anterior limb of
internal capsule
(ALIntCap)
Septum pellucidum
Claustrum (Cl)
Rostrum of corpus
callosum (RCorCl)
Putamen (Put)
Insula (In)
Extreme capsule
(ExtrmCap)
Subcallosal gyrus
External capsule
(ExtCap)
Middle cerebral
artery
Nucleus accumbens
Temporal lobe
(TemLb)
(NuAcc)
Temporal lobe
Orbital
eae gyri
(TemLb)
Olfactory sulcus
Olfactory
tract (OlfTr
Ee
)
Gyrus rectus
Anterior cerebral artery (A,)
CinGy
BCorCl
Cin
AH
HCaNu
LVen
ExtrmCap
NuAcc
\
MS
‘
7“
BCorCl
AH
LVen
ALIntCap
:
7
:
:
Put
3
=,
4
Ff
fe
RCorCl
c
ExtrmCap
TemLb
Optic Nerve
OlfTr
The rostral surface of a coronal brain section through the anlobes appear detached from the cerebral hemisphere and the anterior
terior limb of the internal capsule and the head of the caudate _ limb of the internal capsule is beginning to appear between the head of
nucleus. The head of the caudate nucleus is especially prominent at this _the caudate and putamen. The body of the corpus callosum is charactercoronal plane. In patients with Huntington disease (an inherited neuro- _ istically dorsal extending from rostral (genu) to caudal (splenium). The
degenerative disease), the head of the caudate has largely, or completely, disappeared, and the anterior horn of the lateral ventricle would be
noticeably large at this level. At this more rostral plane, the temporal
four portions of the corpus callosum are rostrum genu, body iene
The MRIs (both are inversion recovery) Pret aiate the same (ane
and show many of the structures identified in the brain slice.
i
: Brain Slices in the Coronal Plane Correlated with MRI
Body of corpus
callosum (BCorCl)
Head of caudate nucleus
(HCaNu)
Anterior limb of
internal capsule (ALIntCap)
Putamen (Put)
Septum pellucidum (Sep)
Corona radiata (CorRad)
Extreme capsule (ExtCap)
Anterior horn of lateral
ventricle (AHLVen)
Claustrum (Cl)
Globus pallidus (GP)
External Capsule
(ExtCap)
Insula (In)
Middle cerebral
Globus pallidus (GP)
artery
Anterior
commissure (AC)
Anterior
commissure (AC)
Ventral pallidum
Ventral striatum
Ventral pallidum
Temporal lobe
Supraoptic recess
Optic chiasm (OpCh)
Optic tract
Uncus
Infundibulum (Inf)
Sep
CorRad
Column
of Fornix
BCorCl
HCaNu
Sep
AblnicaP
In
CorRad
Put
GP
GP
AC
AC
Optic
tract
rac
Third
a
ventricle
AC
OpCh
Inf
ExtrmCap
The rostral surface of a coronal brain section through the level
of the anterior commissure and just rostral to the level of the
column of the fornix and genu of the internal capsule. This level begins
the transition from the head of the caudate nucleus into the body of the
caudate nucleus. The caudate nucleus is somewhat smaller in size (when
compared to the more rostral plane in Figure 5-1), the globus pallidus
is obvious in its position medially adjacent to the putamen, and both of
these parts of the lenticular nucleus are lateral to the anterior limb of
the internal capsule. At this location, the temporal lobe is continuous
with the hemisphere. The MRIs (both are inversion recovery) approximate the same plane and show many of the structures identified in the
brain slice.
Internal Morphology of the Brain in Unstained Slices and in MRI
Body of corpus callosum (BCorCl)
Position of falx cerebri
Anterior tubercle of
thalamus (AntTub)
Septum pellucidum
Head of caudate nucleus
{
Body of lateral
(HCaNu)
ventricle (BLatVen)
_ internal capsule (IntCap,
“. level of Genu)
Terminal vein
Corona radiata (CorRad)
Putamen (Put)
Column of fornix (ColFor)
External capsule
(ExtCap)
Interventricular foramen
Globus pallidus (GP):
Lateral segment
Medial segment
Claustrum (Cl)
Extreme capsule
(ExtrmCap)
Insula (In)
Third ventricle (ThrVen)
Column of fornix (ColFor)
in hypothalamus (Hyth)
Anterior commissure
Optic Tract (OpTr)
Column of fornix (ColFor)
in hypothalamus (Hyth)
Amygdaloid nuclear
complex (AmyNu)
Amygdaloid nuclear
complex (AmyNu)
i
Posterior cerebral artery (P,)
Basilar artery
Mammillary body
‘Superior cerebellar artery(ies)
——
BLatVen
BCorCl
HCaNu
CorRad
ColFor
IntCap
AntTub
Anterior
nucleus
Ventral
anterior
nucleus
|
ExtCap
Put —
In
GP
bryen
OpTr
OpTr
;
Hippotans
Hyth
AmyNu
ThrVen
a
The rostral surface of a coronal brain section through the
level of the anterior tubercle of the thalamus and the column
of the fornix just caudal to the anterior commissure. At this general
level the interventricular foramina, the continuation of the two lateral
ventricles into the single midline third ventricle, can be located between
the anterior tubercle of the thalamus, and the column of the fornix
(see Figure 7-1).
A level that includes these structures also passes through the genu
of the internal capsule. This section also includes the two portions
of the globus pallidus: a medial or internal segment and a lateral or
external segment. The terminal vein is also called the superior thalamostriate vein. The MRIs (both are inversion recovery) approximate
i
F“a
fs
the same plane and show many of the structures identified in the
brain slice.
The hippocampus is located in the ventromedial aspect of the temporal horn of the lateral ventricle and sometimes appears to have texture
in MRI representing its alternating layers of cell bodies and fibers
(see Figure 5-4). On the other hand, the amygdaloid nucleus (also called
the amygdaloid complex) is located in the rostral end of the temporal
horn and appears very homogeneous in MRI (see above). An easy way
to recall these relationships is: ventricular space + texture = hippocampus,
whereas no ventricular space + homogeneous appearance = amygdala.
Based on the coronal plane, the transition from one to the other may
take place quickly.
| ‘| Plane Correlated with MRI
Septum pellucidum
Body of corpus callosum (BCorCl)
Body of fornix (BFor)
Body of lateral ventricle (BLatVen)
Stria terminalis and
terminal vein
Body of caudate nucleus
(BCaNu)
Ventral anterior nucleus
of thalamus (VA)
Corona radiata (CorRad)
Posterior limb of
Anterior nucleus
of thalamus (AntNu)
internal capsule (PLIntCap)
Ventral anterior nucleus
Putamen (Put)
of thalamus (VA)
Mammillothalamic
tract
Insula (In)
External capsule
(ExtCap)
Globus pallidus (GP):
Lateral segment
Medial segment
Extreme capsule
(ExtrmCap)
Third ventricle (ThrVen)
Claustrum
Optic Tract
Dorsomedial nucleus
of thalamus
Tail of caudate nucleus
Hypothalamus (Hyth
»
we
Hippocampal formation
Inferior horn of lateral
ventricle (IHLatVen)
Mammillary body (MB)
Hippocampal formation (Hip)
Basilar pons (BP)
Interpeduncular fossa
Posterior cerebral artery
Crus cerebri
BLatVen
BCaNu
BCorCl
BCorCl
BLatVen
tN
BFor
pattie
VA
AntNu
VA
BFor
PLIntCap
Thalamus
Put
Put
2
GP
Hip
|
:
IHLatVen
IHLatVen
BP
—ge
ae
-
ee
-
-
,
>
*
SFE
ii
i
The rostral surface of a coronal brain section through the
anterior nucleus of the thalamus, ventral anterior thalamic
nucleus, mammillothalamic tract, and caudal mammillary bodies.
This plane also includes the basilar pons (seen in the slice and MRI)
and structures associated with the interpeduncular fossa (seen in the
slice). The two MRIs (both are inversion recovery) are at the same
plane and show many of the structures identified in the brain slice.
PLIntCap
Hip
Hyth and
MB
The globus pallidus is clearly divided into its lateral and medial seg-
ments in the brain slice and the location of the hippocampus in the
medial aspect of the temporal horn, and its textured appearance, is
obvious (compare with Figure 5-3). The globus pallidus has the same
color/texture as the body of the caudate nucleus; they both arise
from the same anlage. In addition, the terminal vein is also called
the superior thalamostriate vein.
Internal Morphology of the Brain in Unstained
Slices and in MRI
Position of falx cerebri
Body of corpus callosum (BCorCl)
Body of fornix (BFor)
Body of caudate
nucleus (BCaNu)
Body of lateral ventricle (BLatVen)
Lateral dorsal nucleus
of thalamus
Stria terminalis and
superior thalamostriate vein
Dorsomedial nucleus
of thalamus (DMNu)
Corona radiata
External capsule
Ventral lateral nucleus,
caudal part __ @
Posterior limb of internal
capsule (PLIntCap)
Putamen (Put)
Claustrum
Internal medullary
Ventral posterolateral
nucleus (VPL)
lamina (IML)
Centromedian nucleus
Red nucleus (RNu)
Ventral posteromedial
nucleus
Tail caudate nucleus
Inferior horn of lateral
ventricle (IHLatVen)
Hippocampal formation
(Hip)
Posterior cerebral artery
Crus cerebri (CC)
Trigeminal nerve (TriNr)
Substantia nigra
Facial nerve
;
Interpeduncular fossa (IPF)
Facial nerve
Vestibulocochlear nerve
Corticospinal fibers in basilar pons (BP)
Abducens nerve
Hypoglossal nerve
Inferior olivary eminence
Pyramid (Py)
et
Fr,
BFor
BCorCl
BFor
BLatVen ——
IML
BCaNu
PLIntCap
DMNu
NG
Put
IHLatVen
IML
VPL
Put
PLintCap
bie
ce
aN
TriNr
IHLatVen
IPF
BP
é
Hip
Py
The rostral surface of a coronal brain section through caudal
parts of the ventral lateral nucleus, massa intermedia, ventral
posterolateral nucleus, red nucleus, substantia nigra, and basilar pons.
This slice clearly illustrates that fibers within the internal capsule (posterior limb in this slice) traverse the crus cerebri and enter the basilar
pons (MRI and brain slice); these fibers within the crus are the corti-
cospinal, corticopontine (parieto-, occipito-, temporo-, and frontopontine), and the corticonuclear fibers. At this more caudal coronal level
the globus pallidus is essentially absent and the putamen is diminished
in size as reflected in the left MRI. Also, note the continuity of fibers
of the internal capsule into the basilar pons. The exits of the trigeminal nerve and the nerves characteristic of the pons—medulla junction
(CNs VI, VII, VIII) and the hypoglossal nerve (CN XII) are seen in
this brain slice. The MRIs (both are inversion recovery) approximate
the same plane and show many of the structures identified in the
brain slice.
Part I: Brain Slices in the Coronal Plane Correlated
Position of falx cerebri
:
with MRI
Body of corpus callosum (BCorCl)
Quadrigeminal cistern (QuadCis)
Body of lateral ventricle (BLatVen)
Body of caudate nucleus
Fimbria of fornix (FFor)
(BCaNu)
Pulvinar (Pul)
Pulvinar (Pul) —
Pretectal area (PrTecAr)
Retrolenticular limb of
internal capsule
Lateral geniculate
nucleus (LGNu)
eis
Tail of caudate
‘
:
Posterior commissure
a
nucleus
i
Sc
.
\
ite
Medial geniculate
nucleus (MGNu)
Lateral geniculate
hee (LGNu)
Inferior horn of lateral
ventricle (IHLatVen)
Hippocampal
formation (Hip)
Periaqueductal gray and >
cerebral aqueduct (CA)
Brachium conjunctivum
Medial geniculate
nucleus (MGNu)
Middle cerebellar peduncle (MCP)
“4
Flocculus
Vestibulocochlear nerve
Glosopharyngeal nerve
Vagus nerve
Corticospinal fibers
Inferior olivary nuclei
BCorCl
BLatVen
BFor
BCaNu
FFor
QuadCis
Pul
Pul
Pul
MGNu
PrTecAr
LGNu
LGNu
IHLatVen
Hip
MGNu
Basilar
Basilar
pons
pons
CA
MCP
quadrigeminal cistern are both midline spaces, the former is a VED:
The rostral surface of this coronal section of brain is through
tricular space and the latter isa subarachnoid space (SAS). The genicthe pulvinar nucleus, medial and lateral geniculate nuclei,
ulate bodies are characteristically located inferior to the overlying
the tegmentum of the midbrain and pons, the middle cerebellar pepulvinar in both the brain slice and MRI. The position of the putamen
duncle, and the inferior olivary complex of the ventral medulla. The
is replaced by the retrolenticular limb of the internal ea dae
corticospinal fibers that had traversed the posterior limb, crus cerebri,
contains the optic radiations. In the wall of lateral tine eee
and basilar pons are now located in the pyramid of the medulla as
continuation of the caudate eae The :
corticospinal fibers. Note the position and relations of the quadri- _ side) is the body-tail
(T1) approximate the same plane and show many of the structures
geminal cistern and that it is clearly different from the position, size,
in the brain slice.
and shape of the third ventricle. Although the third ventricle and the _ identified
Internal Morphology of the Brain in Unstained
Slices and in MRI
Corpus callosum, body (BCorCl) to splenium (SpCorCl)
Pineal
Crus of fornix (CrF)
Fimbria of fornix (FFor)
Body of lateral ventricle (BLatVen)
Body of caudate nucleus
(BCaNu)
Pulvinar (Pul)
Body of lateral ventricle
(BLatVen)
Retrolenticular limb
of internal capsule
Caudate, body to tail
Optic —-
ae
‘iii Nie
Atrium of lateral ventricle
Fimbria of hippocampus
-Tapetum
range ~
Inferior horn of lateral
Fimbria of hippocampus
ventricle (IHLatVen)
Inferior horn of lateral
ventricle (IHLatVen)
Hippocampal
formation (Hip)
Cerebral aqueduct (CA)
Parahippocampal gyrus
Medial longitudinal fasciculus
Superior colliculus (SC)
Periaqueductal
Middle cerebellar peduncle (MCP)
Restiform body
Restiform body
gray (Pa
Srayetag)
Spinal trigeminal tract
Medulla
BCorCl
FFor
SpCorCl
BLatVen
Pul
BLatVen
SC
IHLatVen
Hip
Hip
cA
Pag
MCP
Med
‘.
The rostral surface of this coronal brain section through
.
the pineal, caudal aspects of the pulvinar, superior colliculi,
brainstem tegmentum, and the middle cerebellar peduncle. Note the
characteristics and relationships of the middle cerebellar peduncle
(brachium pontis). The plane of this section is a coronal of the hem-
Pag
MCP
Pyramid
isphere and a section that is roughly perpendicular to the long axis
of the brainstem (see also Figure 5-6). The MRIs (both are inversion
recovery) approximate the same plane and show many of the structures identified in the brain slice. For details of the cerebellum
Figures 2-37 and 2-38.
thie
Position of falx cerebri
Splenium of corpus
callosum (SpCorCl)
Hippocampal
commissure
(HipCom)
Quadrigeminal cistern (QuadCis)
Tapetum (Tap)
Tapetum (Tap)
Atrium of lateral —
to posterior (PHLatVen) and
inferior (IHLatVen) horns
Optic radiations
(OpRad)
Optic radiations
(OpRad)
eee
Crus of fornix
(CrFor)
Hippocampal
formation
Inferior colliculus (IC)
Inferior colliculus (IC)
Trochlear nerve
Position of tentorium cerebelli
Superior cerebellar
peduncle (SCP)
Middle cerebellar peduncle
MCP)
Middle cerebellar peduncle (MCP)
CrFor
SpCorCl
ae
QuadCis
alleles
IHLatVen
;
SCP
~
MCP
}=
ae
iC
Medulla
ForVen
=
==
?
es
vets “AG
"= The rostral surface of a coronal brain section through the
2) splenium of the corpus callosum, caudal portions on the
quadrigeminal cistern, atrium of the lateral ventricle, the superior and
middle cerebellar peduncles (brachium conjunctivum and brachium
pontis, respectively), and the medially adjacent fourth ventricle. Note
that the hippocampal commissure is located on the inferior aspect of
the splenium of the corpus callosum, and the tapetum and the optic
radiations in the lateral wall of the lateral ventricle. The atrium of the
lateral ventricle is the junction of the posterior horn, the temporal horn,
and the body of the lateral ventricle. Note the relationship of the inferior
colliculi to the space of the quadrigeminal cistern. The MRIs (T1) are
at the approximate plane and show many of the structures identified in the brain slice. For details of the cerebellum, see Figures 2-37
and 2-38.
Internal Morphology of the Brain in Unstained Slices and in el
Splenium of corpus callosum
(SpCorCl)
*
Quadrigeminal cistern
Posterior horn of
lateral ventricle
Optic radiations (OpRad)
(PHLatVen)
Tapetum (Tap)
Tapetum (Tap)
Optic
radiations
(OpRad)
Posterior horn of lateral
ventricle (PHLatVen)
Position of tentorium
cerebelli
Lateral cerebellar (dentate) nucleus (DNu)
OpRad
PHLatVen
OpRad
PHLatVen
Tap
Superior (anterior) aspects of the cerebellum
DNu
Inferior (posterior) aspects of the cerebellum
The rostral surface of a coronal brain section through the splenium of the corpus callosum, posterior horn of the lateral ventricle, and the cerebellum including a portion of the dentate nucleus.
Prominent structures in the lateral wall of the posterior horn of the
lateral ventricle at this level include the tapetum and the optic radiations. The former are commissural fibers crossing in the splenium of the
corpus callosum and taking a position on the ventricular surface, and
the latter arise from the lateral geniculate nucleus and course caudally as
optic radiations, immediately lateral to the tapetum, to end in the visual
cortex. The MRI (T1) is at the same approximate plane show many of
the structures identified in the brain slice. For details of the cerebellum,
see Figures 2-37 and 2-38.
Internal Morphology of the Brain
in Unstained Slices and in MRI
Part Il
Brain Slices in the Axial Plane
Correlated with MRI
rientation to Axial MRIs: When looking at an axial MRI, the
physician is viewing the image as if standing at the patient’s
uum feet and looking toward his or her head while the patient is
lying on his or her back. Consequently, and as is the case in coronal
images, the observer's right is the left side of the brain in the MRI and
the left side of the patient’s brain, and the observer’s left is the right side
of the brain in MRI and the right side of the patient’s brain. It is absolutely essential to have a clear understanding of this right-versus-left
concept when using MRI or CT in the diagnosis of the neurologically
impaired patient.
To reinforce this concept, the ventral surface of each axial slice was
photographed. So, when looking at the slice, the observer’s right is the
left side of the brain slice, and the observer’s left is the right side of the
brain slice. The observer is viewing the inferior surface of the slice. This
view of the slice correlates exactly with the orientation of the brain as
seen in the accompanying axial MRIs.
>
Axial view
85
Internal Morphology of the Brain in Unstained Slices and in MRI—Part Il: Brain Slices in“e =
cel
Anterior cerebral artery,
A, segment
Anterior horn of lateral ventricle
Body of corpus callosum
(AHLatVen)
(CorCl), toward the genu
Head of caudate nucleus
(HCaNu)
Septum pellucidum (Sep)
Corona radiata (CorRad)
Internal surface,
body of corpus callosum
Body of caudate nucleus
(BCaNu)
Body of lateral
ventricle (BLatVen)
Body of corpus callosum
(CorCl) toward the splenium
Anterior
forceps
AHLatVen
CorCl
BCaNu
HCaNu
as
CorRad
BLatVen
BCaNu
Sep
Posterior
forceps
i)
The ventral surface of an axial brain section through portions of the corpus callosum, the rostrocaudal extent of
more superior parts of the lateral ventricle, and the head and body of
the caudate nucleus. At this level, the large bundle of white matter within the hemisphere, the corona radiata, is obvious; at more ventral levels
portions of this white matter will participate in the formation of
the
internal capsule. Note the position of the septum pellucidum and the
internal surface of the corpus callosum, the roof of the lateral ventricles
.
The MRIs (both are inversion recovery) are at the approximate
plane
and show some of the structures identified in the brain slice.
Part Il: Brain Slices in the Axial Plane Correlated with MRI
Anterior cerebral artery,
A,, segment
Anterior horn of lateral ventricle (AHLatVen)
Genu of corpus
callosum
Stria terminalis and superior
thalamostriate vein
Septum pellucidum
(Sep)
Anterior limb of internal capsule
(ALIntCap)
Head of caudate
nucleus (HCaNu)
Putamen (Put)
Genu of internal capsule
(GIntCap)
Corona radiata
Claustrum
Anterior nucleus of
thalamus (AntNu)
Anterior nucleus
of thalamus
Ventral anterior
nucleus of thalamus
Lateral thalamic nuclei
(Nv) —
+
——
F ig {;
Body of fornix
ars
Vin
Zz
=
*
Be
—
*
Tail of caudate nucleus —
2
**
Posterior limb of internal
capsule (PLIntCap)
Ventral lateral nucleus
of thalamus
Ventral posterolateral
nucleus of thalamus
Centromedian nucleus
of thalamus
Velum interpositum
Pulvinar (Pul)
Tapetum
Atrium of lateral ventricle
Posterior horn of lateral ventricle
(ALatVen)
(PHLatVen)
Optic radiations (OpRad)
Crus of fornix
Splenium of corpus callosum
Dorsomedial nucleus of thalamus (DMNu)
GlntCap
Put
AHLatVen
HCaNu
AntNu
ALIntCap
re
U
PLintCap
Pul
DMNu
OpRad
PHLatVen
ALatVen
™ The ventral surface of an axial brain section through the
splenium and genu of the corpus callosum, and the head
of the caudate nucleus. The septum pellucidum forms the medial wall
of the lateral ventricles and may be subject to a variety of congenital variations, such as cavum septum pellucidum and agenesis of the
corpus callosum. This plane is slightly tilted (sometimes also seen in
MRI), showing the superior most part of the thalamus on the patient’s
right and a slightly lower axial plane on the patient’s left. The MRIs,
both are T2-weighted, are at a comparable plane and show some of the
structures identified in the brain slice.
:
internal Morphology of the Brain in Unstained Slices and in MRI
A
Anterior cerebral artery, Mae
of lateral
Anterior
(AHLatVen)
ventriclehorn
Column of
Genu of corpus callosum
4
fornix (ColFor)
Septum pellucidum
Genu of internal
capsule (GIntCap)
Head of caudate nucleus (HCaNu)
Ventral anterior
nucleus of thalamus
Anterior limb of
internal capsule (ALIntCap)
External capsule
Putamen (Put)
Extreme capsule
Choroid plexus in
interventricular foramen
Claustrum
Globus pallidus (GP):
Lateral (external) segment
Medial (internal) segment
Internal medullary lamina
Posterior limb of internal
Ventral lateral nucleus
of thalamus
capsule (PLIntCap)
Ventral posterolateral
of thalamus (DMNu)
Dorsomedial nucleus
nucleus of thalamus
Third ventricle (ThrVen)
Centromedian nucleus
Bistros
of thalamus (CMNu)
|
~~,
—
Be — Retrolenticutar limb of
Bie capsule (RLIntCap)
Tail of caudate nucleus
Pulvinar (Pul)
Fimbria of hippocampus
Habenular nucleus
(Hab)
Hippocampal formation (Hip)
Tapetum
Atrium of lateral
ventricle (ALatVen)
:
eee
Optic radiations
Splenium of corpus callosum
(SpCorCl)
Posterior horn of lateral ventricle (PHLatVen)
ALIntCap
AHLatVen
Ginter
HCaNu
ALIntCap
Put
PLintCap
GIntCap
ColFor
ThrVen
PLintCap
GP
Lateral
Lateral
thalamic
thalamic
nuclei
nuclei
DMNu
RLintCap
CMNu
RLIntCap
ALatVen
Pul
Hab
PHLatVen
Hip
The
ThrVen
ventral surface
the
the lenticular
of an
axial
nucleus, » fourfou limbs
brain
section
through
of the internal
cap-
SpCorCl
pallidus (the paleostriatum)
axial
brain
slice. The
are clearly visible on the left side of the
arrowheads
are pointing
to the mammillo-
sule (anterior limb, genu, posterior limb, retrolenticular limb), the
thalamic tract in both MRIs. The MRIs (T1, left; T2 right) are at a
main thalamic nuclei, third ventricle, caudate + putamen = neostricomparable plane and show many of the structures
a: identified i
atum, and the pineal. The medial and lateral segments of the globus _ brain slice.
teattie
Part ll: Brain Slices in the Axial Plane Correlated
with MRI
Anterior commissure (AC)
Anterior limb of internal
Anterior horn of lateral ventricle
capsule (ALIntCap)
|
oe
ey Head of caudate nucleus (HCaNu)
Massa intermedia (MI)
, Putamen (Put)
Globus pallidus (GP):
Lateral segment
Medial segment
Column of fornix (ColFor)
Subthalamic nucleus
Insula (In)
Claustrum
Posterior limb of internal capsule
toward crus (PLIntCap)
Third ventricle
Ventral posteromedial nucleus
Mammillothalamic tract (MtTr)
Centromedian nucleus (CMNu)
Lateral geniculate
nucleus (LGNu)
Ventral posterolateral nucleus
Medial geniculate
nucleus (MGNu)
Pulvinar (Pul)
Pulvinar (Pul)
Tapetum (Tap)
Fimbria of hippocampus (FHip)
Atrium of lateral ventricle
(ALatVen)
Optic radiation (OpRad)
Posterior horn of lateral ventricle
Hippocampal formation (Hip)
(PHLatVen)
Brachium of superior
colliculus
Brachium of superior
colliculus
Superior colliculus (SC)
Habenular commissure
AC
HCaNu
ColFor
ALIntCap
Put
GP
ColF
al
MtT r
pe
MI
=a
MtTr
PLintCap
Lateral
thalamic
nuclei
CMNu
:
Tap
Pul
Dorsomedial
nucleus
S
ALatVen
FHip
e
PHLatVen
OpRad
Vein of Galen
The ventral surface of an axial section of the brain through
the anterior commissure, column of the fornix, portions of
the medial and lateral geniculate nuclei, and superior colliculus. In this
axial plane, the anterior limb is diminished in size and the head of the
caudate and putamen will soon join. The medial and lateral segments of
the globus pallidus are visible on the right side of the axial brain slice.
Note the location of the subthalamic nucleus and its position adjacent
to the posterior limb as it condenses to form the crus cerebri. The MRIs
(both T2-weighted) are at approximately the same plane and show
many of the structures identified in the brain slice.
—
Internal Morphology of the Brain in Unstained Slices and in MRI
Anterior cerebral arteries (ACA),
Head of
caudate nucleus
Cistern of the lamina terminalis
Lamina terminalis (LT)
Third ventricle (ThrVen)
Hypothalamus (HyTh)
Hypothalamus (HyTh)
Optic tract (OpTr)
Anterior commissure (AC)
Optic tract (OpTr)
Substantia
Mamumillary body (MB)
Interpeduncular
fossa (IPF)
%
Medial geniculate nena
<a ©
2
—
Lateral geniculate nucleus
(LGNu)
Pulvinar
‘
2a
oe
_—
Ss
os
:
5
ee
ee
ee
i ii
:
ee
Red nucleus (RNu)
:
e
cerebri (CC)
ff
s
5
Choroid plexus in
inferior horn
Hippocampal formation (Hip)
Fimbria of hippocampus
.
Periaqueductal gray
Hippocampal formation (Hip)
Cerebral aqueduct (CA)
Choroid plexus in atrium
of lateral ventricle
Optic radiations pee
Superior colliculus (SC)
Posterior horn of
lateral ventricle
Quadrigeminal cistern (QuadCis)
ACA
ay
ThrVen
AC
-— [hrVen
OpTi
OpTr
el
(ele
LGNu
CA
QuadCi
re
Cerebellum
OpRad
that the anterior commissure
and the optic tract (brain slice, MRI)
artery
OpRad
CA
The ventral surface of an axial brain section through the
optic tract, hypothalamus, mammillary body, red nucleus,
superior colliculi, and the medial and lateral geniculate nuclei. Note
Posterior
cerebral
by brain parenchyma (see Figure 5-13) while the optic tract is always
on the brain surface (of the crus cerebri). Note the structures surrounding the lower portions of the third ventricle (lamina terminalis
hypothalamus, mammillary body). The MRIs
1
(11, left; T2
right) are
may appear similar but have important spatial relationships that difat approximate planes and show many of the structures identified in
ferentiate one from the other. The anterior commissure is surrounded _ the brain
slice
Brain Slices in the Axial Plane Correlated with MRI
Gyrus rectus (GyRec)
Optic nerve
Anterior cerebral artery, A, segment
Internal carotid artery
Optic nerve
Middle cerebral artery (MCA),
M, segment
Middle cerebral artery
Posterior cerebral artery (PCA),
P,, segment
Uncus (Un)
Amygdaloid nuclear complex
(AmyNu)
Amygdaloid nuclear complex
(AmyNu)
Hippocampal formation (Hip)
Inferior horn of lateral
ventricle (IHLatVen)
Hippocampal formation (Hip)
Mammillary body
Interpeduncular cistern (IPCis)
Crus cerebri (CC)
Decussation of superior
cerebellar peduncle
Substantia nigra (SN)
Inferior colliculus (IC)
Cerebral aqueduct (CA)
Ambient cistern (AmbCis)
Trochlear nerve
Cerebellum (Cbl)
Inferior colliculus (IC)
Periaqueductal gray
MCA
GyRec
PCA
IPCis
Un
IHLatVen
AmyNu
,
Hip
CC
ic
SN
AmbCis
IHLatVen
CG
AmbCis
CA
Cbl
The ventral surface of an axial brain section through the
amygdaloid nucleus, hippocampus, and mid to caudal levels of the midbrain. The hippocampus occupies the medial wall of the
temporal horn while the amygdala is found in its rostral wall. These
relationships are helpful when looking at coronal sections through
the hemisphere. At this midbrain level, note the decussation of the
superior cerebellar peduncle, inferior colliculus, the trochlear nerve in
the ambient cistern, and the shape and relationships of the midbrain
to adjacent structures and cisterns. Mammillary bodies are also seen in
relation to the interpeduncular cistern. The MRIs (T1, left; T2, right)
are at approximately the same plane and show many of the structures
identified in the brain slice. The portion of the cerebellum seen at this
level is the anterior lobe. For details of the cerebellum, see Figures 2-37
and 2-38.
Internal Morphology of the Brain, in U
W2Corticospinal fibers
Basilar pons (BP)
Middle cerebellar peduncle (MCP),
rostral edge
Nucleus (locus) caeruleus
Cerebral aqueduct
Medial lemniscus (ML)
Pontine tegmentum (TegP)
Subarachnoid space (SAS) adjacent to SCPed
Superior cerebellar peduncle (SCPed)
Fourth ventricle (ForVen)
Lateral (dentate)
Lateral (dentate) cerebellar nucleus
cerebellar nucleus
Vermis of cerebellum
(VerCbl)
Hemisphere of cerebellum (HCbl)
The ventral surface of an axial section of the brain through
‘
~ the rostral portions of the basilar pons, rostral parts of the
fourth ventricle, the adjacent superior cerebellar peduncle (brachium
conjunctivum), and the dentate nucleus in the white matter core of the
cerebellar hemisphere. Note the very characteristic appearance of the
small part of the subarachnoid space laterally adjacent to the superior cerebellar peduncle; this is a foramen cecum (blind or false foramen). It is not an actual foramen, but rather a sharp indentation of the
subarachnoid space on the brain surface that creates the impression of
a foramen commonly seen in MRI/CT. The pons, the midbrain, and the
medulla, collectively constitute the brainstem. Although the cerebellum
arises from the rhombic lip of the rhombencephalon, it is not considered
a part of the brainstem but rather a suprasegmental structure within the
posterior fossa. The MRIs (both T1-weighted) are at approximately the
same plane and show many of the structures identified in the brain slice.
For details of the cerebellum, see Figures 2-37 and 2-38.
PartIl:Brain Slices in the Axial Plane Correlated with MRI
ican
rigeminal nerve (TriNr)
Basilar pons (BP)
Medial lemniscus (ML)
Tegmentum of pons (TegP)
Middl
iddle cerebell
bellar
peduncle (MCP)
Fourth ventricle (ForVen)
Choroid plexus (CP) in ForVen
Dentate nucleus (DNu)
Vermis of posterior lobe
Hemisphere of posterior lobe
Bo ee
CU)
of cerebellum (HCbI)
Prepontine
cistern
BP
Temporal
lobe
:
TriNr
Trigeminal
ganglion
MCP
TriNr
Basilar artery (BA)
TriNr
Superior cerebellar
artery
BP
ForVen
HCbl
TegP
Superior cerebellar
peduncle
BA
BP
TegP
MCP
ForVen
DNu
CP) in
ForVen
VCbl
The ventral surface of an axial brain section through
the basilar pons at the level of the trigeminal nerve, and
Aioueh the large part of the middle cerebellar peduncle. This also
correlates with the widest parts of the basilar pons and with the pontine tegmentum. The exit of the trigeminal nerve is an important landmark in the posterior fossa; ventral (inferior) to the exit is the basilar
pons, dorsal (superior) to the exit is the middle cerebellar peduncle.
That part of the pons immediately rostral (anterior) to the root of V
may be called the pretrigeminal pons, that part caudal (posterior) to
the root is the posttrigeminal pons. The four MRIs (inverted inversion
recovery, upper left; T2, upper right; T1, both lower) are at approximately the same general plane and show many of the structures identified in the brain slice. For details of the cerebellum, see Figures 2-37
and 2-38.
Basilar pons
Abducens nerve
Pyramid (Py)
Anterior median fissure (AMF)
Preolivary sulcus (PreOlS)
Olivary eminence (OIEm)
Facial nerve
Vestibulocochlear nerve
Vestibulocochlear nerve
Flocculus
Retroolivary sulcus
(Postolivary sulcus) (PoOIS)
Lateral recess of fourth ventricle
Restiform body (RB)
Restiform body (RB)
Tonsil of cerebellum (TonCbl)
Hemisphere of posterior lobe
of cerebellum (HCbl)
Medial lemniscus (ML)
Fourth ventricle (ForVen)
AMF
ML
PreOlS
PoOlS
TonCbl
HCbl
VCbl
OlEm
Be
Lesion: posterior inferior
cerebellar artery (PICA)
syndrome; lateral medullary
syndrome; Wallenberg
syndrome
4
RB
ForVen
The ventral surface of an axial brain section through the medullary surface at the general level of the pons—medulla junction.
This level is characterized by the restiform body (which when joined by the
juxtarestiform body will form the inferior cerebellar peduncle), pyramid,
olivary eminence and related sulci, and the fourth ventricle and the lateral
recess of the fourth ventricle. Note the close apposition of the cerebellar
tonsil to the medulla; this is an important relationship in cases of increased
intracranial pressure in the posterior fossa and the probability of tonsillar
herniation through the foramen magnum. Note the position of the lateral
recess of the fourth ventricle and its appearance when containing blood
(CT). The four images (T1 MRI, both upper; T2 MRI, lower left; CT, lower
right) are at approximately the same general plane and show many of the
structures identified in the brain slice. Note that the blood in the fourth
ventricle extends into the lateral recess but not into the subarachnoid space
immediately external to the foramen of Luschka (compare brain slice with
the CT). For details of the cerebellum, see Figures 2-37 and 2-38.
Q&A for this chapter is available online on (Ne Point.
Internal Morphology of the
Spinal Cord and Brain: Functional
Components, MRI, Stained Sections
asic concepts that are essential when one is initially learning
how to diagnose the neurologically impaired patient include:
wxmmes (1) an understanding of cranial nerve nuclei, their exiting and
entering roots and, (2) how these structures relate to long tracts. The
importance of these relationships is clearly seen in the combinations
of deficits that characterize lesions at different levels of the neuraxis.
First, deficits of the body only, excluding the head, that may present
as motor or sensory losses (long tracts) on the same side, or opposite
sides, are indicative of spinal cord lesions (e.g., Brown-Séquard syndrome). Spinal cord injuries characteristically have motor and sensory
levels which are the lowest functional levels remaining in the compromised patient. Second, ipsilateral cranial nerve deficits in combination
with contralateral long tract signs characterize lesions in the brainstem
(e.g., lateral medullary and Weber syndromes). These patterns of loss
are frequently called alternating or crossed deficits. In these examples,
cranial nerve signs are better localizing signs than are long tract signs.
A localizing sign can be defined as an objective neurologic abnormality that correlates with a lesion (or lesions) at a specific neuroanatomical location (or locations). Third, motor and sensory deficits on the
same side of the head and body are usually indicative of a lesion in
the forebrain.
COLOR-CODED SPINAL AND CRANIAL
NERVE NUCLEI AND LONG TRACTS
Spinal and cranial nerve motor nuclei are coded by their function; nuclei
innervating skeletal muscle (somatic efferent) are salmon/dark pink,
and preganglionic visceral efferent nuclei are rust. Similarly, the primary
sensory nuclei of the spinal cord and brainstem that receive somatic
afferent sensation are light pink, and nuclei receiving visceral afferents
information are purple. For example, one can easily correlate damage
to the hypoglossal nerve root and the corticospinal fibers on one side,
while comparing this pattern to a lateral medullary syndrome on the
other side.
Long tracts are color coded beginning at the most caudal spinal cord
levels (e.g., see Figures 6-3 and 6-4), with these colors extending into the
dorsal thalamus (see Figure 6-33) and the posterior limb of the internal capsule (see Figures 6-34 and 6-35). The colorized spinal tracts are
the fasciculus gracilis (dark blue), the fasciculus cuneatus (light blue),!
the anterolateral system (dark green), and the lateral corticospinal tract
(gray). In the brainstem, these spinal tracts are joined by the spinal
trigeminal tract and ventral trigeminothalamic fibers (both are light
green). The long tracts are color coded on one side only, to emphasize:
‘The dark and light blue colors represent information originating from lower
and upper portions of the body, respectively.
(1) laterality of function and dysfunction; (2) points at which fibers in
these tracts may decussate; and (3) the relationship of these tracts to
other pathways and cranial nerves.
Each set of facing pages (line drawing/stained section) through spinal
and brainstem parts of this chapter features a version of the overview
of motor and sensory nuclei (or cell columns) next to the stained section. The line on this view, and the few labels, specifically identify the
sensory and motor nuclei at that particular level, and the color code
matches that on the line drawing. This organization allows the user to
easily identify the relationships and continuity of functionally related
cell columns at any level.
A color key appears on each page. This key identifies the various
tracts and nuclei by their color and specifies the function of each structure on each page.
CORRELATION OF MRI AND CT WITH
INTERNAL SPINAL CORD AND BRAINSTEM
ANATOMY
As one is mastering basic anatomical concepts, it is essential to
understand how this information is used in the clinical environment.
To show the relationship between basic anatomy and how MRI (T1and T2-weighted) and CT (myelogram/cisternogram) are viewed, a
series of illustrations and MRI/CT of the spinal cord and brainstem
are shown on the right-hand page above the stained sections. This
continuum of images consists of: (1) a small version of the colorized
line drawing in an Anatomical Orientation; (2) a top-to-bottom flip
that brings the same image into a Clinical Orientation; and (3) a
CT (spinal cord) or MRI and CT (brainstem) that follows this clinically oriented image. To further enhance the seamless application of
basic neuroscience to clinical images (and to do so in their proper
context), especially important anatomical structures are outlined,
in white, on CT (spinal cord) and on the T1-weighted MRI (brainstem) images. This setup allows the user to understand where these
anatomical structures are located in clinical images as viewed in the
Clinical Orientation. One essential aspect of diagnosis is developing the ability to visualize what structures are involved in brainstem lesions and how the patient’s deficits correlate with the location
and extent of the lesion. In addition, the “flip symbol” at the lower
left of each page indicates which anatomical images may be flipped
to a clinical orientation using online resources available with the
Atlas.
Every effort is made to identify and use MRI and CT that correlate with their corresponding line drawing and stained section.
This approach recognizes and retains the strength of the anatomical
approach and introduces essential clinical concepts while at the same
time allowing the user to customize the material to suit a range of educational applications.
95
FUNCTION COMPONENTS
IN THE NEURAL TUBE, SPINAL CORD, AND BRAINSTEM
(FIGURES 6-1 AND 6-2)
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E
Neural tube
posterior
v ae . | [reat version
v
E E/AAA
VE
\V
SE
VA
|
|Contemporary version
SA
medial
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A
lateral
Spinal cord
SE
VE
S
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Vv
EC
Mf pepe
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ee
S
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’ The concept of functional components (of both spinal and craie
nial nerves) recognizes that primary afferent fibers entering,
and the efferent fibers leaving, the spinal cord or brainstem convey specific types of information.
There are two versions of functional components: (1) a traditional
version that originated early in the 20th century and was the standard
for many decades; and (2) a contemporary version that reflects recent
discoveries in head, neck, and brain development. Either of these plans
can be used as they are complementary, one to the other.
Traditional version: In this version (Figures 6-1 and 6-2), the components seen in the developing neural tube (left), that are associated with the
alar plate (GSA, GVA), are located posterior to the sulcus limitans (SL);
those components associated with the basal plate (GVE, GSE) are located
anterior to the SL (Figure 6-1, left). These general features are also seen in
the contemporary version. In the adult spinal cord, this general posterior—
anterior relationship is maintained (Figure 6-1, lower center).
At the spinal cord—brainstem transition, two important changes occur.
First, as the central canal enlarges into the fourth ventricle, and the cerebellum develops, the alar portion of the neural tube is rotated laterally.
The SL is present in the adult brainstem and separates the medially located
basal plate derivatives (motor nuclei) from the laterally located alar plate
derivatives (sensory nuclei). Second, in the brainstem, special functional
components, as traditionally identified (SVE to muscles of the pharyngeal
arches; SVA to taste; SSA to vestibular and auditory), form cell columns
that are restricted to the brainstem and not represented in the spinal cord.
Within the brainstem, there are transpositions of the SVE and GSA components. Early in development, cells associated with the SVE component
(nucleus ambiguus, facial and trigeminal motor nuclei) appear in the floor
of the ventricle, but then migrate ventrolaterally to their adult locations. In
a similar manner, cells with the GSA component (spinal trigeminal, principal sensory) that appear in the ventricular floor in the alar area also migrate
ventrolaterally to their adult locations. Cells of the mesencephalic nucleus
arise from the neural crest and migrate into the brainstem to become part
of the GSA cell column. The border between motor and sensory areas of the
brainstem is represented by an oblique line beginning at the SL. The relative
positions, and color coding, of the various components shown in the above
image (right) are directly translatable to Figure 6-2 on the facing page.
Contemporary version: This version (Figure 6-1, right), as was the traditional version, is based on development, but incorporates more detailed
data concerning neurons, muscle origins, and their respective migration patterns. For example, striated muscles innervated by cranial nerves (CNs) III,
IV, V, VI, VII, EX, X, and XII all arise from the epimere (paraxial mesoderm),
which segments into somitomeres. Consequently, the cells of all of these
motor nuclei are designated as an somatic efferent (SE) functional component. The neurons of CN III that influence orbital smooth muscles, the cells
of CNs VII and IX which influence vascular smooth muscle and glandular
epithelium in the head, and the cells of CN X that influence the same tissues
in the thorax and abdomen, are all designated as visceral efferent (VE). All
visceral afferent information (traditionally divided into general and special)
is associated with the solitary tract and nuclei and is designated visceral
afferent (VA). The components traditionally associated with the vestibulocochlear nuclei (SSA) and with the trigeminal sensory nuclei (GSA) are
consolidated into a somatic afferent (SA) category. The correlation between
the traditional and contemporary versions is shown in Figure 6-1, far right.
ABBREVIATIONS
GSA/SA — General Somatic Afferent/Somatic Afferent
GSE/SE
General Somatic Efferent/Somatic Efferent
GVA/VA — General Visceral Afferent/Visceral Afferent
GVE/VE
General Visceral Efferent/Visceral Efferent
SSA/SA
Special Somatic Afferent/Somatic Afferent
SVA/VA
Special Visceral Afferent/Visceral Afferent
SVE/VE — Special Visceral Efferent/Visceral Efferent
SL
SA
SE
VA
VE
Sulcus Limitans
Somatic Afferent
Somatic Efferent
Visceral Afferent
Visceral Efferent
Functional components of cranial nerve nuclei
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Midbrain
Midbrain
1. Oculomotor nuc. (GSE/SE)
2. Edinger—Westphal preganglionic nuc. (GVE/VE)
3. Trochlear nuc. (GSE/SE)
4. Mesencephalic nuc. & tr.
of V (GSA/SA)
Pons
Pons
5. Abducens nuc. (GSE/SE)
6. Sup. salivatory nuc. (GVE/VE)
7. Motor trigeminal nuc. (SVE/SE)
8. Motor facial nuc. (SVE/SE)
9. Principal sensory nuc of V (GSA/SA)
10. Spinal trigeminal nuc. (GSA/SA)
(pars oralis)
Medulla oblongata
11. Hypoglossal nuc. (GSE/SE)
12. Dorsal motor nuc. of vagus (GVE/VE)
13. Inf. salivatory nuc. (GVE/VE)
14. Nuc. ambiguus (SVE/SE)
15. Solitary nuc. and tr.
15a: gustatory nuc. (SVA/VA)
15b: cardiorespiratory nuc (GVA/VA)
16. Vestibular nuclei (SSA/SA)
S = Sup; L = Lat; M = Med; Sp. = Spinal
Medulla
oblongata
17. Cochlear nuc. (SSA/SA)
18. Spinal trigeminal nuc. (GSA/SA)
(pars interpolaris, pars caudalis)
Spinal cord
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19. Medial motor cell column (GSE/SE)
20. Accessory nuc. (GSE/SE)
21. Lateral motor cell columns (GSE/SE)
22. Intermediolateral cell column (GVE/VE)
23. Visceral afferent (sympathetic) receptive
areas (GVA/VA)
24. Substantia gelatinosa, nucleus proprius
and associated GSA/SA receptive areas
25. Sacral parasympathetics (GVE/VE)
26. Visceral afferent (parasympathetic) receptive
areas (GVA/VA), also called the sacral
parasympathetic nuclei
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Functional components of spinal nerve nuclei
The medial-to-lateral positions of brainstem cranial nerve and
spinal cord nuclei in this figure are the same as in Figure 6-1. This
6-2
diagrammatic posterior (dorsal) view shows: (1) the relative positions and
names of specific cell groups and their associated functional components;
(2) the approximate location of particular nuclei in their specific division
of brainstem and/or spinal cord; and (3) the rostrocaudal continuity of cell
columns (either as continuous or discontinuous cell groups) from one division of the brainstem to the next or from brainstem to spinal cord. The
nucleus ambiguus is a column of cells composed of distinct cell clusters
interspersed with more diffusely arranged cells, much like a string of beads.
Nuclei associated with CNs I and II are not shown. The color coding used
in this figure correlates with that on Figure 6-1 (facing page).
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176
Internal Morphology of the Brain
in Stained Sections: Axial-Sagittal
Correlations with MRI
Ithough the general organization of Chapter 7 has been
described in Chapter 1 (the reader may wish to refer back to
smmmaaes this section), it is appropriate to reiterate its unique features at
this point. Each set of facing pages has photographs of an axial-stained
section (left-hand page) and a sagittal-stained section (right-hand page).
On each right-hand and left-hand page are corresponding MRIs in the
same orientation and the same plane. In addition to individually labeled
structures, a heavy red line appears on each photograph. This prominent
red line on the axial section represents the approximate plane of the sagittal section located on the facing page. On the sagittal section, this red
line signifies the approximate plane of the corresponding axial section
on the facing page. The reader can identify features in each photograph
and then, using this line as a reference point, visualize structures that are
located either above or below that plane (axial-to-sagittal comparison)
or medial or lateral to that plane (sagittal-to-axial comparison). This
method of presentation provides a useful format that will form the basis
for a three-dimensional understanding of structures and relationships
within the central nervous system.
chapter
The magnetic resonance image (MRI) placed on every page in this
chapter gives the reader an opportunity to compare internal brain anatomy, as seen in stained sections, with those structures as visualized in
clinical images generated in the same plane. Even a general comparison
reveals that many features, as seen in the stained section, can be readily
identified in the adjacent MRI.
This chapter is also organized so that one can view structures in
either the axial or the sagittal plane only. Axial images appear on lefthand pages and are sequenced from dorsal to ventral (odd-numbered
Figures 7-1 to 7-9), whereas sagittal images are on the right-hand pages
and progress from medial to lateral (even-numbered Figures 7-2 to
7-10). Consequently, the user can identify and follow structures through
an axial series by simply flipping through the left-hand pages or through
a sagittal series by flipping through the right-hand pages. The inherent flexibility in this chapter should prove useful in a wide variety of
instructional/learning situations. The drawings shown in the images
below illustrate the axial and sagittal planes of the photographs and
MRI in this chapter.
Axial Planes
Sagittal
Planes
AAT
Internal Morphology of the Brain in Stained Sections: :
Corpus
callosum
Anterior horn of
lateral ventricle
Septum
pellucidum
Caudate
iy
nucleus,
head j
a6
6 “A
ig
a
Internal capsule, anterior limb
¥
fy
P
Internal capsule, genu
F Putamen
Interventricular
foramen
Claustrum
Fornix,
column
Globus pallidus
Anterior
nucleus
of thalamus
Ventral anterior nucleus of thalamus
Internal capsule, posterior limb
Dorsomedial nucleus
of thalamus
Ventral lateral nucleus of thalamus
Internal medullary lamina
External medullary lamina and
thalamic reticular nucleus
Habenular
Ventral posterolateral nucleus
Centromedian nucleus of thalamus
Pineal
—
yw
Caudate nucleus, tail
Stria terminalis
Hippocampal
Choroid plexus
commissure
Atrium of
lateral ventricle
Hippocampus, fimbria
Optic radiations
_ Axial section through the head of the caudate nucleus and
several key thalamic nuclei (anterior, centromedian, pulvinar,
and habenular). In this plane of section, the internal medullary lamina
separates the dorsomedial nucleus of the thalamus from a lateral row
of thalamic nuclei comprising the ventral anterior, ventral lateral, and
ventral posterolateral nuclei. Rostrally, the internal medullary lamina
encompasses the anterior nucleus of the thalamus, and the pulvinar is
located caudal to the centromedian and ventral posterolateral nuclei.
Collectively the anterior nucleus and the pulvinar form the rostral and
caudal extents of the thalamus (this portion of the diencephalon is
commonly called the dorsal thalamus to differentiate it more specifically
from the hypothalamus and subthalamus), respectively, of the dorsal
thalamus in this axial section. The centromedian nucleus is located
within the internal medullary lamina and is the largest of the intralaminar nuclei. In this axial plane, the four (of five) limbs of the internal
capsule (anterior, genu, posterior, retrolenticular) are seen in relation to
their adjacent, and important, structures. The heavy red line represents
the approximate plane of the sagittal section shown in Figure 7-2 (facing page). Many of the structures labeled in this photograph can be
clearly identified in the adjacent T1-weighted MRI.
Fornix, body
Lateral dorsal
nucleus
Dorsomedial nucleus
of thalamus
Corpus
callosum,
genu
Pretectal
nuclei
Stria
medullaris
thalami
Anterior
commissure
Habenular
nuclei
Fornix,
column
Superior
colliculus
Mammillo-
Posterior
commissure
thalamic
tract
Inferior
colliculus
Mammillary Wh
body
Hypothalamus
Optic nerve
Trochlear
nerve
Oculomotor
nerve
Medial
longitudinal
fasciculus
Superior cerebellar peduncle, decussation
Fastigial
Basilar pons
aa8/013
nucleus
(medial
Medial
lemniscus
Abducens nerve
Pyramid
Principal olivary nucleus
cerebellar
nucleus)
Abducens
nucleus
Nucleus
gracilis
Hypoglossal nucleus
Lateral corticospinal tract
Sagittal section through the column of the fornix, anterior thalamic nucleus, red nucleus, and medial portions of the pontine
tegmentum (abducens nucleus), cerebellum (fastigial nucleus), basilar
pons, and medulla (nucleus gracilis). Note that the fibers of the basilar
pons (corticospinal) condense at the pons—medulla junction to form the
pyramid of the medulla.
As the fernix (body to column) arches around the anterior thalamic
nucleus, the space formed between the column of the fornix and the
anterior thalamic nucleus is the interventricular foramen (see Figure 7-1
on the facing page). The column of the fornix continues immediately
caudal to the anterior commissure, as the postcommissural fornix, to
end mainly in the mammillary body. The smaller population of fibers
that diverge rostral to the anterior commissure form the precommissural fornix: these fibers are not easily identified as fascicles but rather
are diffusely organized fibers. Note the relative positions of the red
nucleus and decussation of the superior cerebellar peduncle within the
midbrain tegmentum.
In this sagittal plane, the general structures seen at the level of the
superior and inferior colliculi can be fully appreciated. A cross section
through the midbrain at the level of the superior colliculus contains the
oculomotor nucleus and roots, red nucleus, substantia nigra, and crus
cerebri. A cross section of the midbrain at the level of the inferior colliculus is characterized by the trochlear nucleus, decussation of the superior cerebellar peduncle, substantia nigra, and crus cerebri. The heavy
red line represents the approximate plane of the axial section shown in
Figure 7-1 (facing page). Many of the structures labeled in this photograph can be clearly identified in the adjacent T1-weighted MRI (RNu,
red nucleus; CNIII, oculomotor nucleus; CNIV, trochlear nucleus).
Internal capsule, anterior limb
Globus pallidus:
MedSeg
LatSeg
External capsule
Claustrum
Genu, corpus callosum
Anterior horn of
lateral ventricle
Caudate »
nucleus, »//
Septum pellucidum
head
|
; iy)A
“Sram
ante
Fornix, column
Interventricular foramen
Ventral anterior nucleus
of thalamus
Dorsomedial nucleus
of thalamus
Internal capsule, posterior limb
Ventral lateral nucleus
of thalamus
Ventral posteromedial nucleus
of thalamus
Centromedian nucleus
of thalamus
Habenula
Ventral posterolateral nucleus
of thalamus
Habenular
commissure
Stria terminalis
Caudate nucleus, tail
Superior colliculus
Optic radiations
Tapetum
Superior
colliculus,
brachium
Pulvinar nuclear complex
Hippocampal formation
Medial geniculate nucleus
Axial section through the head of the caudate nucleus, centromedian nucleus, medial geniculate body, and superior colGens. In this more inferior plane of section, the anterior—posterior
medial geniculate nucleus to the auditory cortex and temporal lobe.
The main fiber bundles in the other limbs of the internal capsule are
as follows: anterior limb (anterior thalamic radiations, frontopon-
relationship of the ventral anterior, ventral lateral, and ventral pos-
tine), genu (corticonuclear fibers), posterior limb (superior thalamic
radiations, corticospinal, pallidothalamic, parietopontine), and retrolenticular limb (optic radiations, occipitopontine). Other smaller fiber
pathways also traverse these limbs. The heavy red line represents the
approximate plane of the sagittal section shown in Figure 7-4 (facing
Y
teromedial nuclei is evident as is the relative position of the centromedian nucleus to the ventral posterolateral, medial geniculate, and
the pulvinar nuclei. As seen here, and in Figures 7-1 and 7-5, the four
major portions of the internal capsule are obvious in the axial plane,
these being the anterior limb, genu, posterior limb, and the retrolenticular limb. The sublenticular limb (not labeled) contains auditory radiations, and diffusely arranged occipitotemporal fibers extend from the
page). Many of the structures labeled in this photograph can be clearly
identified in the adjacent T2-weighted MRI (MedSeg, medial segment
of globus pallidus; LatSeg, lateral segment of globus pallidus).
Anterior nucleus of thalamus
Ventral lateral nucleus of thalamus
'
Mammillothalamic tract
Ventral anterior nucleus of thalamus
Corpus
Lateral
callosum,
body
dorsal
nucleus
Dorsomedial nucleus of thalamus
Fornix, body
:
Centromedian nucleus
Corpus
callosum,
splenium
Lateral
ventricle,
anterior
horn
Pulvinar
nuclear
Anterior.
commissure
complex
Superior
colliculus
Thalamic
fasciculus
Lenticular
fasciculus
lenticularis
Optic tract
oy
e
Hypothalamus
Olfactory tract
Inferior
colliculus
\
Ansa
Crus
cerebri .
Superior
cerebellar
peduncle
(brachium
conjunctivum)
Substantia nigra
Medial
lemniscus
Fourth
ventricle
Basilar pons
Nucleus
:
gracilis
Facial nucleus
Principal olivary nucleus
Solitary nuclei and tract
Nucleus cuneatus
Lateral corticospinal tract
Sagittal section through anterior and ventral anterior thalamic nuclei, ventral lateral thalamic nucleus, red nucleus,
crus cerebri, substantia nigra, central areas of the pons, cerebellum
(and superior peduncle), and medulla (solitary nuclei and tract,
principal olivary nucleus). Note the position of the facial motor
nucleus at the pons—medulla junction. In this sagittal plane, several
of the thalamic nuclei are clearly demarcated, and the important
relationships between the red nucleus, substantia nigra, and crus
cerebri are seen. Note that the fibers of the crus cerebri traverse the
basilar pons (as corticospinal fibers) and that the medial lemniscus is located at the interface of the basilar pons and the pontine
tegmentum and contains the fibers of the posterior column mediallemniscus system.
The teardrop shape of the anterior thalamic nucleus, which is clearly
seen in this image, illustrates how the anterior nucleus may be seen in
some coronal sections that also include the ventral lateral thalamic
nucleus (see Figure 6-35A, B). Many additional clinically significant
structures in the brainstem also stand out. The heavy red line represents
the approximate plane of the axial section shown in Figure 7-3 (facing
page). Many of the structures labeled in this photograph can be clearly
identified in the adjacent T1-weighted MRI (H, Forel field H [prerubral
area]; RNu, red nucleus).
Internal Morphology of the Brain in Stained Sections: Axial-Sagitt
eagh
%y
,
Caudate / ; yr?A i
nucleus, # //
Anterior
commissure
head '
»
{%
:
Lamina
terminalis
Insula
Internal capsule, anterior limb
Globus
LatSeg
pallidus:
MedSeg
Fornix, column
Claustrum
Hypothalamus
Mammillothalamic
—=
bo
Internal capsule, posterior limb
tract—e
Ventral lateral nucleus of thalamus
Ventral posteromedial nucleus of thalamus
Red nucleus
Centromedian nucleus of thalamus
Habenulopeduncular
tract
Central gray
(periaqueductal
Ventral posterolateral nucleus of thalamus
b..
f
Internal capsule, retrolenticular limb
gray) =
Pulvinar nuclear complex
oe
are
Hippocampus, fimbria
formation~
Superior colliculus
Atrium of
lateral
ventricle
Optic radiations
Choroid plexus
Medial geniculate nucleus
Superior colliculus, brachium
Axial section through the head of the caudate nucleus, ventral
posteromedial nucleus, medial geniculate body, ventral parts
of the pulvinar, and the four clearly visible limbs of the internal capsule
(anterior, genu, posterior, retrolenticular).
This axial section is through the upper portions of the hypothalamus
and the lower, and widest, portions of the lenticular nucleus. The anterior
limb of the internal capsule is beginning to disappear (the caudate head
and putamen will join), and inferior portions of the ventral lateral, ventral
posterolateral, and pulvinar nuclei of the thalamus are still present.
The column of the fornix, which lies immediately caudal to the ante-
rior commissure, arches caudally to enter in the mammillary nuclei, and
the mammillothalamic tract arises from the mammillary nuclei and
ascends to enter the anterior thalamic nucleus. These particular nuclei
are part of a circuit of emotion, the Papez circuit, that goes from the
hippocampus to the hypothalamus, to the anterior thalamic nucleus, to
the cingulate cortex, to the hippocampus. Note the relative rostrocaudal
position of these tracts within the stained section and within the MRI.
The heavy red line represents the approximate plane of the sagittal section shown in Figure 7-6 (facing page). Many of the structures labeled
in this photograph can be clearly identified in the adjacent T1-weighted
MRI (MedSeg, medial segment of globus pallidus; LatSeg, lateral segment of globus pallidus).
Axial-Sagittal Correlations with MRI
Ventral lateral nucleus of thalamus
Dorsomedial nucleus of thalamus
Ventral anterior nucleus
Corpus
of thalamus
Ventral posteromedial nucleus of thalamus
Lateral dorsal
callosum
nucleus of thalamus
genu
Centromedian nucleus
of thalamus
Corpus callosum
i
splenium
4
Pulvinar nuclear
complex
Superior colliculus
_(Caudate
—
» nucleus,
head
|
\
Inferior colliculus
Lateral lemniscus
a
Optic
A nsa
tract
lenticularis
Anterior
commissure
Superior cerebellar
peduncle (brachium
conjunctivum)
Supraoptic nucleus
Emboliform nucleus
(anterior interposed
cerebellar nucleus)
Crus
cerebri
lenticular fasciculus
Substantia nigra
Principal sensory
nucleus
Medial lemniscus
Facial nerve
Trigeminal motor
nucleus
Olivocerebellar fibers
Nucleus cuneatus
Sagittal section through central regions of the diencephalon
(centromedian nucleus) and midbrain (red nucleus), and
through lateral areas of the pons (trigeminal motor nucleus) and
medulla (nucleus cuneatus). A clear separation of the thalamic nuclei is
seen in this sagittal plane along with the characteristics of the interface
of midbrain structures with the diencephalon. The substantia nigra is
located internally, and immediately adjacent, to the crus cerebri. Note
how the fibers of the crus cerebri splay out into the basilar pons (see
also Figure 7-4), the characteristic position of the medial lemniscus, and
the clarity of the crus cerebri and substantia nigra in the MRI. Some of
the fibers entering the basilar pons from the crus cerebri will end in the
pons (corticopontine), end in cranial nerve motor nuclei of the brainstem ‘corticonuclear), or coalesce as the pyramid of the medulla (corticospinal). The superior cerebellar peduncle (brachium conjunctivum)
is prominent and is a major path of cerebellar efferent fibers to the
brainstem and thalamus. The heavy red line represents the approximate
plane of the axial section shown in Figure 7-5 (facing page). Many of
the structures labeled in this photograph can be clearly identified in the
adjacent T1-weighted MRI (H, Forel field H [prerubral area]; RNu, red
nucleus).
Internal Morphology of the Brain in Stained Sections : xi
Anterior commissure
Lamina terminalis
Insula
Optic tract
Fornix (For)
Globus pallidus:
LatSeg
MedSeg
Amygdaloid nucleus
Mammillothalamic
tracts
Substantia nigra
Lateral geniculate nucleus
Caudate nucleus, tail
Crus cerebri
Lateral ventricle, inferior
(temporal) horn
Optic radiation
Hippocampal formation
(Hip)
Trochlear nuclei
Inferior colliculus
Inferior colliculus,
brachium
Axial section through the hypothalamus, third ventricle, lamina
terminalis, red nucleus, inferior colliculus, and the medial and
lateral geniculate nuclei.
This axial section is slightly tilted; the sides (right/left) of the stained
section are considered the same as the sides (right/left) in the adjacent
MRI. The right side is more ventral and shows the optic tract in close
proximity to the crus cerebri, the junction of the fornix and mammillothalamic tract immediately dorsal to the mammillary body, and the amygdaloid nucleus and hippocampus in the medial temporal horn. The left
side is more dorsal and contains the fornix and mammillothalamic tract
separate within the hypothalamus (see also Figure 7-5), the subthalamic
nucleus adjacent to the crus cerebri, the red nucleus, and junction of the
caudate and putamen. The geniculate nuclei of the thalamus are also seen
on the patient’s left; the trochlear nuclei are present on both sides.
The optic tract is always located on the surface of the crus cerebri (see also Figure 7-8 on the facing page) no matter what the plane
Medial geniculate nucleus
of section. In contrast, the fornix is always surrounded by brain tissue. Also note the thin membranous nature of the lamina terminalis
(see also Figures 7-5 and 7-9) separating the cistern of the lamina terminalis (rostral to it) from the space of the third ventricle (caudal to
it). This structure frequently separates blood within the cistern from
a lack of blood within the third ventricle (see Figure 4-7), or blood
within the third ventricle from a lack of blood within the cistern
(see Figure 4-13).
The heavy red line represents the approximate plane of the sagittal
section shown in Figure 7-8 (facing page). The axial plane through the
hemisphere, when continued into the midbrain, represents an almost
cross section through the long axis of the mesencephalon. Compare the
appearance of the midbrain in this axial section with Figures 6-24 to
6-29. Many of the structures labeled in this photograph can be clearly
identified in the adjacent T1-weighted MRI (MedSeg, medial segment of
globus pallidus; LatSeg, lateral segment of globus pallidus)
Axial-Sagittal Correlations with MRI
Ventral lateral nucleus of thalamus
Zona incerta
Globus pallidus, medial segment
Globus pallidus, lateral segment
Putamen
Anterior
commissure
Lenticular fasciculus
Thalamic
fasciculus
Ventral posteromedial
nucleus of thalamus
gfe
Cie
ne
Pulvinar nuclear complex
2%
Brachium of
superior
colliculus
Subthalamic
nucleus
Medial
geniculate
nucleus
Crus
cerebri
Optic tract
4
‘
;
Hippocampal
formation
Amygdaloid nucleus (complex)
Dentate
nucleus
(lateral
cerebellar
nucleus)
Middle cerebellar peduncle
(brachium pontis)
Posterior cochlear nucleus
Sagittal section through the caudate nucleus, central to more
medial parts of the diencephalon (ventral posteromedial
nucleus, ventral posteromedial nucleus, pulvinar), lateral portions of the
middle cerebellar peduncle, cochlear nuclei, and the cerebellum (dentate
nucleus). In this sagittal plane, several important relationships are seen.
First, the head of the caudate and putamen coalesce in the rostral and
ventral area of the hemisphere. Second, the important structures in the
immediate vicinity of the zona incerta and subthalamic nucleus are obvious. Third, the medial geniculate nucleus is characteristically located
just inferior to the pulvinar and separated from it by the brachium of
the superior colliculus. This bundle of fibers conveys an important connection in the pupillary light pathway. As noted in other figures in this
chapter, the optic tract has an intimate apposition to the crus cerebri
regardless of the plane of section. Note the relationships of the amygdaloid complex and the hippocampus in the rostral temporal lobe. The
heavy red line represents the approximate plane of the axial section
shown in Figure 7-7 (facing page). Many of the structures labeled in this
photograph can be clearly identified in the adjacent T1-weighted MRI.
Internal Morphology of the Brain in Stained Sections:
Supraoptic recess
of third ventricle
Lamina terminalis
}
"Right
Optic tract (OpTr)
Hypothalamus
Amygdaloid
nucleus
Anterior commissure
Uncus
Mammillary
body
Lateral geniculate nucleus
Fimbria of hippocampus
Crus cerebri
o%
-
mf
=
z
Caudate nucleus, tail
FtDentate gyrus
Lateral ventricle, inferior
(temporal) horn
Substantia
nigra (SN)
Hippocampal formation (Hip)
Superior
Optic radiations
cerebellar
peduncle,
decussation
Lateral
lemniscus
Superior
cerebellar
peduncle
Medial
longitudinal
fasciculus
»
Axial section through ventral portions of the hypothalaSS
mus (supraoptic recess and mammillary body) and forebrain
(amygdaloid nucleus, hippocampal formation), through the decussation of the superior cerebellar peduncle in the midbrain, and through
the anterior lobe of the cerebellum. This axial section is slightly tilted
through the lowest portions of the hypothalamus as evidenced by the
presence of the supraoptic recess, a relatively small portion of the
hypothalamus, lower parts of the mammillary bodies, and part of the
supraoptic nucleus.
Note the close relationship of the uncus to the crus cerebri (also in
the MRI), particularly on the right side, and the fact that the amygdaloid nucleus is internal to the uncus in the rostral and medial wall of
the temporal horn of the lateral ventricle (also on the right). This close
apposition of the uncus to the crus is the anatomical basis for damage to
Trochlear nerve, exit
midbrain structures in cases of uncal herniation when there is impingement on, or shifting of, the midbrain structures resultant to enlarging
temporal lobe lesions that force the uncus over the edge of the tentorium cerebelli and into the midbrain (see also Chapter 9). Also note, on
the left, that the optic tract is located directly adjacent to the crus and
ends in the lateral geniculate nucleus. The tail of the caudate is in the
lateral wall of the temporal horn of the ventricle, and the hippocampus
is located medially.
The heavy red line represents the approximate plane of the sagittal
section shown in Figure 7-10 (facing page). The axial plane through
the hemisphere, when continued into the midbrain, represents a slightly
oblique section through the mesencephalon. Many of the structures
labeled in this photograph can be clearly identified in the adjacent
T1-weighted MRI.
era
: ‘Axial-Sag ital Correlations with MRI
External medullary lamina
Globus pallidus, medial segment
Globus pallidus, lateral segment
and thalamic reticular
nuclei
Ventral lateral nucleus of thalamus and
ventral posterolateral nucleus of thalamus
Optic
Caudate nucleus,
tract
Atrium of lateral ventricle
Pulvinar nuclear complex
Calcarine sulcus
Hippocampal
formation
Optic radiations
Lateral geniculate
nucleus
Fimbria of
hippocampus
Dentate gyrus
Dentate nucleus
Hippocampal
formation
Amygdaloid nucleus
(complex)
Lateral ventricle,
;
~
tw
inferior (temporal) horn
X
Sagittal section through the putamen, amygdaloid nucleus,
and hippocampus, and through the most lateral portions of
the diencephalon (external medullary lamina, pulvinar, lateral geniculate,
and ventral posterolateral nucleus). The relationship of the amygdaloid
nucleus, anterior to the space of the temporal horn within the rostromedial portion of the temporal lobe, is clearly seen. This section emphasizes
the fact that the hippocampus, located in the medial wall of the temporal
horn, is separated by a ventricular space, from the amygdaloid nucleus,
which is located in the rostral wall of that same ventricle space. This close
apposition of the hippocampus, parahippocampal gyrus, amygdala, and
uncus in the medial temporal lobe correlates with the fact that, in extreme
cases, uncal herniation may not only include the uncus but also the parahippocampal gyrus and even portions of the hippocampus. In this sagittal section, the optic tract is seen entering the lateral geniculate nucleus
which, as was the case for its medial counterpart (see Figure 7-8), is also
located immediately inferior to the pulvinar. This sagittal plane also passes
through the long axis of the hippocampal formation. The heavy red line
represents the approximate plane of the axial section shown in Figure 7-9
(facing page). Many of the structures labeled in this photograph can be
clearly identified in the adjacent T1-weighted MRI.
Q&A for this chapter is available online on TC Point.
188
Tracts, Pathways, and Systems in
Anatomical and Clinical Orientation
he study of regional neurobiology (brain structures in gross
specimens, brain slices, stained sections, and MRI and CT) is
the basis for the study of systems neurobiology (tracts, path-
mannan
ways, and cranial nerves and their functions, clinical applications,
etc.), which in turn is the basis for understanding and diagnosing the
neurologically impaired patient. Building on the concepts learned in
earlier chapters, this chapter explores systems neurobiology, with a
particular emphasis on clinical relevance, applications, and correlations.
The modifications made in this chapter recognize an essential reality
for users of this book who are preparing for a career in medicine, as
broadly defined. Although it is common to teach the anatomy of the
central nervous system (CNS) in an Anatomical Orientation (e.g., in the
medulla, the pyramid is “down” in the image and the fourth ventricle is
“up”), this information will be viewed and used, in the clinical years and
beyond, in a Clinical Orientation (pyramid “up” in the image, fourth
ventricle “down”). Therefore, it is essential to present systems information in a format that resembles, as closely as reasonably possible,
how these systems (and dysfunctions thereof) are viewed in the clinical
setting. To this end, selected systems are illustrated in the Clinical Orientation on MRI.
ANATOMICAL
ORIENTATION
Major pathways, especially those essential to diagnosis of the neurologically compromised patient, are illustrated in line drawings in an
Anatomical Orientation. The format of each set of these facing pages is
designed to summarize, accurately, and concisely, the relationships of a
given tract or pathway. This includes, but is not limited to: (1) the location of its cells of origin; (2) its entire course throughout the neuraxis
and cerebrum; (3) the location of the decussation of these fibers, if applicable; (4) the neurotransmitters associated with the neurons comprising
the tract or pathway; (5) a brief review of its blood supply; and (6) a
summary of a number of deficits seen as a result of lesions at various
points in the tract or pathway.
CLINICAL ORIENTATION
Twelve of the systems pathways, with particular emphasis on those
essential to understanding the patient with neurologic deficits, are
also illustrated in Clinical Orientation. These pathway illustrations
do not replace their counterparts shown in Anatomical Orientation,
but are designed to complement these existing drawings. These sets
of facing pages are formatted to show the pathway superimposed on
MRI at representative levels of the (CNS) (left page) and summarize
the deficits seen following lesions at various CNS levels that involve
the pathway (right page). These illustrations show: (1) the position of
the tract/fibers in MRI at representative levels; (2) the somatotopy (if
applicable) of the tract as it appears in MRI/clinical orientation; (3)
the trajectory of the tract/fibers through the CNS; (4) deficits correlated with the location of lesions at various locations and levels; and
(5S) the laterality (R/L) of the deficit as dictated by the position of the
lesion in the MRI.
Intra-axial brainstem lesions frequently result in both sensory and
motor deficits. Recognizing this fact, both types of deficits are listed for
those lesions illustrated on the MRI pathways. However, for sensory
pathways, sensory deficits are listed first and motor deficits are listed
last. For motor pathways, the reverse is used: motor deficits are listed
first, and sensory deficits listed last. This approach emphasizes the particular pathway being described but, at the same time, acknowledges
the multiplicity of deficits resulting from CNS lesions.
ADDITIONAL
POINTS
The structure of an Atlas does not allow a detailed definition of each
clinical term on the printed page. However, as in other chapters, the
full definition of each clinical term or phrase, when used, is available
from the online resources (on the Point) that come with this Atlas;
here these definitions follow the current edition of Stedman’s Medical
Dictionary, but they are also available from any standard medical
dictionary, neurology text, or from clinical colleagues. Researching the
full definition of a clinical term or phrase is a powerful and effective
learning tool.
The layout of all illustrations in this chapter clearly shows the laterality of the tract or pathway. That is, the relationship between the
location of the cell of origin and the termination of the fibers making up a tract or pathway or the projections of cranial nerve nuclei.
Although this is clear in the anatomical drawings, it is particularly
relevant to the clinical setting, as shown in the MRI pathway illustrations. This information is absolutely essential to understand the
position of a lesion and correlate this fact with the deficits seen in the
neurologically compromised patient. For example, is the deficit on the
same side as the lesion (ipsilateral), the opposite side (contralateral), or
both sides (bilateral)? The concept of laterality is expressed as “right”
or commonly as R ina
circle, “left” or as L ina circle, or “bilateral”
in reference to the side of the deficit(s) when written on the patient’s
chart.
This chapter is designed to maximize the correlation between structure and function, provide a range of clinical examples for each tract or
pathway, and help the user develop a knowledge base that can be easily
integrated into the clinical setting.
189
er Siege
ee
an
O
Tracts, Pathways, and Systems in Anatomical Paice
eA
ORIENTATION
DRAWING
=
FOR PATHWAYS
Orientation drawing for pathways. The trajectories of pathways in the Anatomical Orientation are illustrated in Chapter 8
on individualized versions of a representation of the central nervous
system (CNS). Although slight changes are made in each drawing, so
as to more clearly diagram a specific pathway, the basic configuration
of the CNS is as represented here. This allows the user to move from
pathway to pathway without being required to learn a different representation or drawing for each pathway; also, laterality of the pathway,
a feature essential to diagnosis, is inherently evident in each illustration.
In addition, pathways that are particularly essential to diagnosis, are
also shown on MRI and are, therefore, in a Clinical Orientation.
The forebrain (telencephalon and diencephalon) is shown in the
coronal plane, and the midbrain, pons, medulla, and spinal cord are
represented through their longitudinal axes. The internal capsule is rep-
resented here in the axial plane in an effort to show the limbs of the internal capsule and the rostrocaudal distribution of fibers located therein.
The reader can become familiar with the structures and regions as
shown here because their locations and relationships are easily transferable to subsequent illustrations. It may be helpful to refer back to this
illustration when using subsequent sections of this chapter.
Neurotransmitters
Three important facts are self-evident in the descriptions of neurotransmitters that accompany each pathway drawing. These are illustrated by
noting, as an example, that glutamate is found in corticospinal fibers
(see Figure 8-11). First, the location of neuronal cell bodies containing a specific transmitter is indicated (glutamate-containing cell bodies
are found in cortical areas projecting to the spinal cord). Second, the
trajectory of fibers containing a particular neurotransmitter is obvious
from the route taken by the tract (glutaminergic corticospinal fibers are
found in the internal capsule, crus cerebri, basilar pons, pyramid, and
lateral corticospinal tract). Third, the location of terminals containing
ntatior =o
me
IN ANATOMICAL
ORIENTATION
specific neurotransmitters is indicated by the site(s) of termination of
each tract (glutaminergic terminals of corticospinal fibers are located in
the spinal cord gray matter). In addition, the action of most neuroactive
substances is indicated as excitatory (+) or inhibitory (-). This level of
neurotransmitter information, as explained here for glutaminergic corticospinal fibers, is repeated for each pathway drawing.
Clinical Correlations
Spumante rematna am een
a eee
ee
The clinical correlations are designed to give the user an overview
of specific deficits (i.e., hemiplegia, resting tremor) seen in lesions of
each pathway and to provide examples of some syndromes or diseases
(e.g., Brown-Séquard syndrome, Parkinson disease [PD]) in which these
same deficits are seen. Although purposefully brief, these correlations
highlight examples of deficits for each pathway and provide a built-in
mechanism for expanded study. For example, the words in bold in each
correlation are clinical terms and phrases that specify a particular clinical condition; these are available in the current edition of Stedman’s
Medical Dictionary, but they are also available from any standard medical dictionary, neurology text, or clinical colleague.
An especially useful feature of this Atlas is the fact that the full definition of all clinical terms that are indicated in bold (PICA syndrome,
hemiplegia, resting tremor, etc.) is easily available when using the online
resources through thePoint; instructions to access thePoint
are in the inside of the front cover. Consulting these sources, especially the
online resources, will significantly enhance understanding of the deficits
seen in the neurologically compromised patient. Expanded information,
based on the deficits mentioned in this chapter, is integrated into some
of the questions for Chapter 8. Referring to such sources allows the user
to glean important clinical points that correlate with the pathway under
consideration, and enlarge his or her knowledge and understanding by
researching the italicized words and phrases.
ABBREVIATIONS
CE
Cer
CinSul
Cervical enlargement of spinal cord
Cervical levels of spinal cord
Cingulate sulcus
CaNu
CM
Caudate nucleus (+ Put = neostriatum)
Centromedian (and intralaminar) nuclei
CorCl
Dien
DMNu
Corpus callosum
Diencephalon
Dorsomedial nucleus of thalamus
For
Fornix
GP
GPl
GPm
HyTh
IC
IntCap, AL
IntCap, G
IntCap, PL
Globus pallidus (paleostriatum)
Globus pallidus, lateral segment
Globus pallidus, medial segment
Hypothalamic area
Internal capsule
Internal capsule, anterior limb
Internal capsule, genu
Internal capsule, posterior limb
IntCap, RL
Internal capsule, retrolenticular limb
LatSul
LatVen
LSE
LumSac
Lateral sulcus (Sylvian sulcus)
Lateral ventricle
Lumbosacral enlargement of spinal cord
Lumbosacral level of spinal cord
L-VTh
Mes
Met
Myelen
Lateral‘and ventral thalamic nuclei
excluding VPM and VPL
Mesencephalon
Metencephalon
Myelencephalon
Put
Putamen (+ CaNu = neostriatum)
SThNu
Telen
Thor
VPL
Subthalamic nucleus
Telencephalon
Thoracic levels of spinal cord
Ventral posterolateral nucleus of thalamus
Ventral posteromedial nucleus of
thalamus
|
VPM
Orientation
8-1 ORIENTATION
DRAWING
FOR PATHWAYS
IN ANATOMICAL
ORIENTATION
1
Midline —>'
Cerebral cortex
CinSul
LatVen
Basal ganglia
Telen
and
Dien
LatSul
IntCap, Bhat
HyTh
VPM
Internal Capsule in
Axial Orientation
Rostral
ae
SThNu
Midbrain
Mes
Pons & Cerebellum
Met
Medulla
— Myelen
IntCap,G
aa RE
niga
We
Dien
Caudal
AxialT1 MRI
;
——
5
nee
CEs!
t— Spinal Cord
ESE
t- LumSac
|
Midline —>
i)
|
|
and Clinical Orient
Tracts, Pathways, and Systems inAnatomical
S SYSTEM IN ANATOMICAL ORIENTATION
COLUMN-MEDIAL LEMNISCU
POSTERIOR (DORSAL)
near Ei ee
thea tena serena
phat
stereoagnosis, or tactile agnosia are sometimes
The origin, course, and distribution of fibers comprising the pos-
used to describe PC
Clinical Correlations
damage, they are more commonly used to specify parietal lobe lesions.
The term stereoanesthesia is also frequently used to specify a lesion
of peripheral nerves that results in an inability to perceive proprioceptive and tactile sensations. Bilateral damage (e.g., tabes dorsalis [tabetic
neurosyphilis] or subacute combined degeneration of the spinal cord)
produces bilateral losses. Although ataxia is the most common feature
in patients with tabes dorsalis, they also have a loss of muscle stretch
reflexes, severe lancinating pain over the body below the head (more
common in the lower extremity), and bladder dysfunction. The ataxia
that may be seen in patients with posterior column lesions (sensory
ataxia) is due to a lack of proprioceptive input and position sense. These
individuals tend to forcibly place their feet to the floor in an attempt to
stimulate the missing sensory input. A patient with mild ataxia due to
posterior column disease may compensate for the motor deficit by using
visual cues. Patients with subacute combined degeneration of the spinal
cord first have signs and symptoms of posterior column involvement,
followed later by signs of corticospinal tract damage (spastic weakness
of legs, increased muscle stretch reflexes [hyperreflexia], Babinski sign).
Rostral to the sensory decussation, medial lemniscus lesions result
in contralateral losses that include the entire body, excluding the head.
Brainstem lesions involving medial lemniscus fibers usually include
An ipsilateral loss of vibratory sensation, position sense, and discriminative touch (stereoanesthesia, impaired graphesthesia, and tactile
localization) on one side of the body below the level of the lesion correlates with damage to the posterior column (PC) on the same side of
the spinal cord (e.g., Brown-Séquard syndrome). While astereognosis,
adjacent structures, result in motor and additional sensory losses, and
may reflect the distribution patterns of vessels (e.g., medial medullary
or medial pontine syndromes). Large lesions in the forebrain may result
in a complete contralateral loss of modalities carried in the posterior
columns and anterolateral systems, or may produce pain or paresthesia
(e.g., the thalamic syndrome).
terior (dorsal) column—medial lemniscus (PC-ML) system. This
illustration shows the longitudinal extent, positions in representative cross
sections of brainstem and spinal cord, and somatotopy of fibers in both
the posterior column (PC) and medial lemniscus (ML) portions of this
system at all levels. The ML undergoes positional changes as it courses
from the myelencephalon (medulla) rostrally toward the mesencephalic—
diencephalic junction. In the medulla, ML and anterolateral system (ALS)
fibers are widely separated from each other and receive different blood
supplies, whereas in the midbrain they are served by a common arterial source. As the ML makes positional changes, the somatotopy therein
follows accordingly. Fibers of the postsynaptic—posterior column system
(shown in green) are considered in detail in Figure 8-6.
Neurotransmitters
Acetylcholine and the excitatory amino acids, glutamate and aspartate,
are associated with some of the large-diameter, heavily myelinated fibers
of the posterior horn and in the posterior columns.
ABBREVIATIONS
ALS
BP
GG
Cli
FCu
FGr
IAF
IC
Anterolateral system
Basilar pons
Crus cerebri
Central tegmental tract
Cuneate fasciculus
Gracile fasciculus
Internal arcuate fibers
Internal capsule
ML
MLF
NuCu
NuGr
PC
PO
PoCGy
PPGy
Medial lemniscus
Medial longitudinal fasciculus
Cuneate nucleus
Gracile nucleus
Posterior column
Principal olivary nucleus
__ Postcentral gyrus
Posterior paracentral gyrus
SOMATOTOPY
LE
N
aT;
| UE
OF
Fibers conveying input from lower extremity
Fibers conveying input from neck
Fibers conveying input from trunk
Fibers conveying input from upper extremity
BODY
G2
$5
TS
PRG
Py
RB
RNu
SenDec
SN
VPL
Posterior (dorsal) root gangliai
Pyramid
Restiform body
Red nucleus
—_ Sensory decussation
Substantia nigra
Ventral posterolateral
nucleus of thalamus
AREAS
Fibers from approximately the second cervical level
Fibers from approximately the fifth sacral level
Fibers from approximately the fifth thoracic level
Review of Blood Supply to PC-ML System
Structures
Arteries
PC in Spinal Cord
Penetrating branches of arterial vasocorona (see Figure 6-8)
ML in Medulla
ML in Pons
ML in Midbrain
VPL
Posterior Limb of IC
Anterior spinal (see Figure 6-16)
Overlap of paramedian and long circumferential branches of basilar (see Figure 6-23)
Short circumferential branches of posterior cerebral, quadrigeminal, choroidal arteries
(see Figure 6- 30)
Thalamogeniculate branches of posterior cerebral (see Figure 6-41)
Lateral striate branches of middle cerebral (see Figure 6-41)
a
8-2 POSTERIOR (DORSAL) COLUMN-MEDIAL LEMNISCUS
IN ANATOMICAL ORIENTATION
SYSTEM
Somatosensory cortex
Somatotopy in PC and ML
Posterior limb, IC
UE
T
EE
Position of oe
E
AL Ss}
ML
ec
S) N
A LS
MLF
CTT
Se
o
ML =
ey,
oa
ML
SenDec
IAF
N uGr
EGh
®S
PRG, {16
S
Laminae III-V
-
Pend and
.
| Tracts, Pathways,
Syst
eR Su
UN
OC
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;
oh
Cie
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aton
Systemsn ii eeeconieclere
POSTERIOR COLUMN-MEDIAL
LEMNISCUS
Postcentral gyrus (middle
third is upper extremity area
of somatosensory cortex)
SYSTEM
IN CLINICAL ORIENTATION
Posterior paracentral gyrus
(lower extremity area of
somatosensory cortex)
Head of caudate nucleus
Anterior limb, internal capsule
W_
Putamen
Genu, internal capsule
Ventral anterior thalamic nucleus
Thalamocortical fibers
in posterior limb of
internal capsule
Posterior limb, internal capsule
Ventral lateral thalamic nucleus
Ventral posterolateral
thalamic nucleus
Ventral posterolateral
nucleus
Crus cerebri
ML in midbrain
Substantia nigra
ALS in midbrain
Midbrain tegmentum
Red nucleus
:
;
Inferior colliculus
Cerebral aqueduct
Basilar pons
ML in pons
ALS in pons
;
Pontine tegmentum
Fourth ventricle
Superior cerebellar peduncle
ML in medulla
Pyramid
Anterolateral system a”
(ALS) in medulla
a
Inferior olive
Retro-olivary sulcus
Spinal trigeminal
tract and nucleus
FESHMCUNL TE er
Fourth ventricle
Medial lemniscus (ML)
Sensory decussation
Cuneate nucleus
Internal arcuate fibers
Gracile nucleus ON
Sak
a
eo
Gracile fasciculus hy
Posterior columns lanes
Pai
LK
Posterior root
ganglia above T6
Posterior root
ganglia below T6
The posterior column-medial lemniscus (PC-ML) system
topography, and trajectory of this pathway in a clinical orientation. The
.
superimposed on CT (spinal cord, myelogram) and MRI _ tract shifts from left to right sides
at the sensory decussation. The red
(brainstem and forebrain, T2-weighted MRI) showing the location,
and blue fibers correlate with those of the same color in Figure 8-2
Sensory Pathways
POSTERIOR COLUMN-MEDIAL LEMNISCUS SYSTEM IN CLINICAL ORIENTATION:
REPRESENTATIVE LESIONS AND DEFICITS
Postcentral gyrus (middle
third is upper extremity area
of somatosensory cortex)
Posterior paracentral gyrus
(lower extremity area of
somatosensory cortex)
Thalamocortical fibers
in posterior limb of
internal capsule
¢ Diminution/loss proprioception, dis-
Ventral posterolateral
nucleus
criminative touch, vibratory sense, pain,
and thermal sense on right UE and LE
plus face and oral cavity if VPM involved
e Paresthesias
¢ Transient right hemiplegia
ML in midbrain
¢ Loss of proprioception, discriminative
touch, and vibratory sense on right LE
(plus UE if medial part of ML involved)
¢ Loss of pain and thermal sensation
on right UE and LE
ALS in midbrain
Red nucleus
Mid-to-rostral pons
¢ Loss of proprioception; discriminative
touch; and vibratory, pain, and thermal
senses on right UE and LE
¢ Loss of discriminative touch, pain, and
thermal sense on left side of face;
paralysis of masticatory muscles
(trigeminal nuclei involved)
Caudal pons
¢ Proprioception and pain/thermal loss
as in mid-to-rostral pons
¢ Left-sided facial and lateral rectus
paralysis (facial/abducens nucleus/nerve)
¢ Loss pain/thermal sense on left face
¢ Left ptosis, miosis, and anhidrosis
(Horner)
ML in pons
ALS in pons
ML in medulla
¢ Loss of proprioception, discriminative
touch, and vibratory sense of right UE/LE
¢ Tongue weakness: Deviates to left on
attempted protrusion
¢ Hemiplegia of right UE and LE
Anterolateral system
(ALS) in medulla
Spinal trigeminal
tract and nucleus
Medial lemniscus (ML)
Sensory decussation —————
Cuneate nucleus
qe
Internal arcuate fibers
Gracile nucleus —————
Spinal cord hemisection
¢ Right-sided loss of proprioception,
discriminative touch, and vibratory sense
below lesion
¢ Left-sided loss of pain/thermal sensation
beginning about two levels below lesion
« Right-sided paralysis below lesion
Right Horner, if lesion at cervical levels
\se
RY Sy
Posterior column lesion
¢ Right-sided loss of proprioception,
discriminative touch, and vibratory sense
below lesion
Gracile fasciculus oe
Posterior columns ic uneate fasciculus
Representative
PC-ML
system
lesions within
and
the
the CNS
deficits
that involve
the
boxes)
that
(in pink
correlate with the level and laterality of each lesion. Note that the
Posterior root
ganglia above T6
Posterior root
Ce ganglia below T6
laterality (R/L) of the deficits is determined by whether the lesion
is on the left or right side of the MRI/CT; this reinforces important
clinical concepts.
v
ee
Anatomical andClinica Ori
Tracts, Pathways, and systems in
Be
Ne
Be
Ba
ne
ANTEROLATERAL
SYSTEM
IN ANATOMICAL
The longitudinal extent and somatotopy of fibers comprising
the anterolateral system (ALS). The ALS is a composite bundle containing ascending fibers that terminate in the reticular formation
(spinoreticular fibers), mesencephalon (spinotectal fibers to deep layers
of the superior colliculus, spinoperiaqueductal fibers to the periaqueductal gray), hypothalamus (spinohypothalamic fibers), and sensory
relay nuclei of the dorsal thalamus (spinothalamic fibers). Other fibers
in the ALS include spino-olivary projections to the accessory olivary
nuclei. Spinothalamic fibers terminate primarily in the VPL and reticulothalamic fibers terminate in some intralaminar nuclei and medial areas
of the posterior thalamic complex.
Descending fibers from the PAG and nucleus raphe dorsalis enter
the nucleus raphe magnus and adjacent reticular area. These latter sites,
in turn, project to laminae I, II, and V of the spinal cord via raphespinal and reticulospinal fibers that participate in the modulation of pain
transmission in the spinal cord.
Neurotransmitters
Glutamate (+), calcitonin gene-related peptide, and substance P (+)-containing posterior (dorsal) root ganglion cells project into laminae I, II (heavy),
V (moderate), and III, IV (sparse). Some spinoreticular and spinothalamic
fibers contain enkephalin (—), somatostatin (—), and cholecystokinin (+). In
addition to enkephalin and somatostatin, some spinomesencephalic fibers contain vasoactive intestinal polypeptide (+). Neurons in the PAG and
nucleus raphe dorsalis containing serotonin and neurotensin project into
the nuclei raphe magnus and adjacent reticular formation. Cells in these
latter centers that contain serotonin and enkephalin send processes to spinal cord laminae I, II, and V. Serotonergic raphespinal or enkephalinergic
reticulospinal fibers may inhibit primary sensory fibers or projection neurons, conveying nociceptive (pain) information.
ORIENTATION
Clinical Correlations
A loss of pain and temperature sensations on one side of the body signifies a lesion involving the ALS; the deficit begins about two levels
caudal to the lesion but on the contralateral side (e.g., Brown-Séquard
syndrome). A bilateral loss of the same modalities, but in a dermatomal distribution, is characteristic of syringomyelia; the anterior white
commissure is damaged by a cavitation (not ependymal lined) in the
central cord area. A central cord cavitation lined by ependymal cells
is a hydromyelia. Vascular lesions in the spinal cord (e.g., acute central
cervical cord syndrome) may result in a bilateral and splotchy loss of
pain and thermal sense below the lesion because the ALS has a dual
vascular supply.
Vascular lesions in the lateral medulla (posterior inferior cerebellar
artery [PICA] syndrome) or lateral pons (anterior inferior cerebellar
artery occlusion) result in a loss of pain and thermal sensations over
the entire contralateral side of the body (ALS) as well as on the ipsilateral face (spinal trigeminal tract and nucleus), coupled with other
motor and/or sensory deficits based on the damage to structures these
vessels serve. Note that the ALS and PC-ML systems are separated
in the medulla (in different vascular territories) but are adjacent to
each other in the midbrain (the same vascular territory). Consequently,
medullary lesions will not result in deficits related to both pathways,
whereas a lesion in the midbrain may result in a contralateral loss of
pain, thermal, vibratory, and discriminative touch sensations on the
body, excluding the head.
Profound loss of posterior column and anterolateral system
modalities,or intractable pain and/or paresthesias (e.g., the thalamic
syndrome), may result from vascular lesions in the posterolateral thalamus. So-called thalamic pain also may be experienced by patients
who have brainstem lesions that damage fibers in the ALS and PC-ML
system.
ABBREVIATIONS
ALS
AWCom
Anterolateral system
Anterior (ventral) white
commissure
Crus cerebri
Internal capsule
Input from lower extremity
regions
Middle cerebellar peduncle
Medial lemniscus
Medial longitudinal
fasciculus
CG
NG
LE
MCP
ML
MLF
Nu
NuDark
NuRa,d
NuRa,m
PAG
PoCGy
PPGy
PRG
Py
RaSp
RB
RetF
Nuclei
Nucleus raphe, dorsalis
Nucleus raphe, magnus
Periaqueductal gray
Postcentral gyrus
Posterior paracentral gyrus
Posterior (dorsal) root
ganglion
Pyramid
Raphespinal fibers
Restiform body
Reticular formation
RNu
S
SC
SpRet
SpTec
SpTh
VPL
Red nucleus
Input from sacral regions
Superior colliculus
Spinoreticular fibers
Spinotectal fibers
Spinothalamic fibers (rostral
midbrain and above)
Input from thoracic regions
Input from upper extremity
regions
Ventral posterolateral
I-VI
Laminae I-VIII of Rexed
li
UE
(of midbrain)
— Nucleus of Darkschewitsch
RetTh
Reticulothalamic fibers
nucleus of thalamus
Review of Blood Supply to ALS
ee
Structures
Arteries
ALS in Spinal Cord
ALS in Medulla
ALS in Pons
ALS in Midbrain
Penetrating branches of arterial vasocorona and branches of anterior spinal (see Figures 6-8 and 6-16)
Caudal third, vertebral; rostral two-thirds, posterior inferior cerebellar (see Figure 6-16)
VPL
Posterior Limb of IC
Long circumferential branches of basilar (see Figure 6-23)
Short circumferential branches of posterior cerebral, superior cerebellar (see Figure 6-30)
Thalamogeniculate branches of posterior cerebral (see Figure 6-41)
Lateral striate branches of middle cerebral (see Figure 6-41)
SSS
oy
OS
8-4 ANTEROLATERAL
SYSTEM
Ne
IN ANATOMICAL
eee
pammaes
ORIENTATION
Somatosensory cortex
Posterior limb, IC
Somatotopy of ALS fibers
FaCe
(f
a
Intralaminar Nu
Position of ALS fibers
SC, RetF, PAG
N\ NG
NuDark
PAG, NuRa,d
RetTh
q
ALS
AWCom
|
°
RaSp
PRG
~
Laminae I-VIII
:
RaSp to
AWCom
laminae
1, ll, V
ALS
0”
Sensory Pathways . i. t
:
ANTEROLATERAL
SYSTEM
Postcentral gyrus (middle
third is upper extremity area
of somatosensory cortex)
IN CLINICAL ORIENTATION
Posterior paracentral gyrus
(lower extremity area of
somatosensory cortex)
Anterior limb, internal capsule
Genu, internal capsule
Ventral anterior thalamic nucleus
Thalamocortical fibers
in posterior limb of
internal capsule
Ventral lateral thalamic nucleus
Posterior limb, internal capsule
Ventral posterolateral
thalamic nucleus
Ventral posterolateral
nucleus
Crus cerebri
ALS in midbrain
Substantia nigra
ML in midbrain
Midbrain tegmentum
Red nucleus
Cerebral aqueduct
Basilar pons
ALS in pons
Pontine tegmentum
ML. in pons
Superior cerebellar peduncle
Fourth ventricle
Pyramid
Inferior olive
ALS in medulla
Spinal trigeminal
Restiform body
tract and nucleus
ML in medulla
Anterolateral system (ALS)
Input from upper extremity
Anterior white
commissure (AWC)
ALS in spinal cord
Posterior root
ganglia
Posterior horn
Input from lower extremity
ae
The anterolateral system (ALS) superimposed on CT (spinal cord, myelogram) and MRI (brainstem and forebrain ,
T2-weighted MRI) showing the location, topography, and trajectory of this pathway in a clinical orientation. Axons of second-order
eee,
neurons in the ALS arise in the posterior horn, cross in the anterior
white commissure, and are somatotopically organized in the tract.
The blue and green fibers correlate with those of the same color in
Figure 8-4.
Sensory Pathways
ANTEROLATERAL
SYSTEM IN CLINICAL ORIENTATION:
LESIONS AND DEFICITS
REPRESENTATIVE
Postcentral gyrus (middle
third is upper extremity area
of somatosensory cortex)
Posterior paracentral gyrus
(lower extremity area of
somatosensory cortex)
yw
° Diminution/loss pain, thermal, and
vibratory senses; discriminative touch;
and proprioception on right face and oral
caniy i VPM included), and on right UE
Thalamocortical fibers
in posterior limb of
internal capsule
¢ Paresthesias on right face, trunk, UE/LE
¢ Transient right hemiplegia
Ventral posterolateral
nucleus
¢ Loss of pain and thermal sensation on
right UE and LE
¢ Loss of proprioception, discriminative
touch, and vibratory sense on right LE
(plus UE if medial part of ML involved)
Mid-to-rostral pons
ALS in midbrain
¢ Loss of pain, thermal, and vibratory
sense; discriminative touch; and
proprioception on right UE/LE
¢ Loss of pain/thermal sense and discriminative touch on left side of face;
paralysis of masticatory muscles
ML in midbrain
Red nucleus
(trigeminal nuclei involved)
Caudal pons
¢ Pain/thermal sense and proprioception
loss as in mid-to-rostral pons
¢ Left-sided facial and lateral rectus
paralysis (facial/abducens nucleus/nerve)
¢ Left-sided loss pain/thermal sense of face
¢ Left ptosis/miosis/anhidrosis (Horner)
ALS in pons
¢ Loss of pain/thermal sense on right VE,
LE, and on left side of face (alternating
hemianesthesia)
¢ Dysarthria and dysphagia (nu. ambiguus)
¢ Vertigo, ataxia, and nystagmus
(vestibular nucleus; restiform body)
¢ Nausea, vomiting, and singultus (area
postrema, reticular formation)
¢ Left ptosis/miosis/anhidrosis (Horner)
ML in pons
&
ALS in medulla
Anterolateral quadrant lesion
¢ Loss of pain/thermal sensation beginning
about two levels below lesion on right
side of body
Spinal trigeminal
tract and nucleus
ML in medulla
&
Spinal cord hemisection
¢ Right-sided loss of pain/thermal sensation
beginning about two levels below lesion
¢ Left-sided loss of proprioception, discriminative touch, and vibratory sense
Anterolateral system (ALS)
below lesion
¢ Left-sided paralysis below lesion
* Left Horner if lesion at cervical levels
Z
|
Input from upper extremity
Anterior white
commissure (AWC)
ALS in spinal cord
Posterior root
anglia
ey
Posterior horn
Input from lower extremity
ae
lesions within the CNS
_ =p | Representative
oa) ~ the ALS and the deficits (in pink boxes)
that involve
that correlate
with the level and laterality of each lesion. Note that the laterality
ee
&
(R/L) of the deficits is determined by whether the lesion is on the
left or right side of the MRI/CT; this reinforces important clinical
concepts.
*
es
POSTSYNAPTIC-POSTERIOR (DORSAL) COLUMN SYSTEM AND
THE SPINOCERVICOTHALAMIC PATHWAY IN ANATOMICAL ORIENTATION
The origin, course, and distribution of fibers comprising the
postsynaptic—posterior column system (upper) and the spinocervicothalamic pathway (lower).
Postsynaptic—posterior column fibers originate primarily from cells
>)
in lamina IV (some cells in laminae III and V-VII also contribute),
ascend in the ipsilateral dorsal fasciculi, and end in their respective
nuclei in the caudal medulla. Moderate-to-sparse collaterals project to a
few other medullary targets.
Fibers of the spinocervical part of the spinocervicothalamic pathway
also originate from cells in lamina IV (less so from III and V). The axons
of these cells ascend in the posterior part of the lateral funiculus (this is
sometimes called the dorsolateral funiculus) and end in a topographic
fashion in the lateral cervical nucleus: lumbosacral projections terminate posterolaterally and cervical projections anteromedially. Axons
arising from cells of the lateral cervical nucleus decussate in the anterior
white commissure, and ascend to targets in the midbrain and thalamus.
Cells of the posterior column nuclei also convey information to the contralateral thalamus via the medial lemniscus.
Neurotransmitters
Glutamate (+) and possibly substance P (+) are present in some spinocervical projections. Because some cells in laminae III-V have axons
that collateralize to both the lateral cervical nucleus and the dorsal column nuclei, glutamate (and substance P) also may be present in some
postsynaptic—dorsal column fibers.
Clinical Correlations
The postsynaptic—posterior column and spinocervicothalamic pathways are not known to be major circuits in the human nervous system. However, the occurrence of these fibers may explain a well-known
clinical observation. Patients who have received an anterolateral cordotomy (this lesion is placed just ventral to the denticulate ligament)
for intractable pain may experience complete or partial relief, or there
may be a recurrence of pain perception within days, weeks, or months.
Although the cordotomy transects fibers of the anterolateral system (the
main pain pathway), this lesion largely spares the posterior horn, posterior columns, and spinocervical fibers. Consequently, the recurrence of
pain perception (or even the partial relief of pain) in these patients may
be explained by these postsynaptic—dorsal column and spinocervicothalamic projections. Through these connections, some nociceptive (pain)
information may be transmitted to the ventral posterolateral nucleus
and on to the sensory cortex, via circuits that bypass the anterolateral
system and are spared in a cordotomy.
ABBREVIATIONS
ALS
AWCom
FCu
FGr
IAF
LCerNu
Anterolateral system
Anterior (ventral) white commissure
Cuneate fasciculus
Gracile fasciculus
Internal arcuate fibers
Lateral cervical nucleus
ML
NuCu
NuGr
PRG
SenDec
:
Medial lemniscus
Cuneate nucleus
Gracile nucleus
Posterior (dorsal) root ganglion
Sensory decussation
Review of Blood Supply to Posterior Horn, FGr, Fcu, and LcerNu
Structures
Arteries
FGr, FCu in Spinal Cord
Penetrating branches of arterial vasocorona and some branches from central (sulcal) (see Figure 6-8)
Penetrating branches of arterial vasocorona and branches from central (see Figure 6-8)
LCerNu
NuGr NuCu
EE
EEE nnn
Posterior spinal (see Figure 6-16)
nnn
nnn,
SSS
8-6 POSTSYNAPTIC-POSTERIOR (DORSAL) COLUMN SYSTEM AND
THE SPINOCERVICOTHALAMIC PATHWAY IN ANATOMICAL ORIENTATION
Other
brainstem
targets
Laminae IV
(II-VI)
Laminae IV
(II-VII)
FCu
Laminae IV (III-VII)
Dorsolateral region
of lateral funiculus
ALS
TRIGEMINAL PATHWAYS
oF
-__
IN ANATOMICAL
The distribution of general sensory GSA or SA information
originating on CNs V (trigeminal), VII (facial), IX (glossopha-
ORIENTATION
Clinical Correlations
A loss of: (1) pain, temperature, and tactile sensation from the ipsilateral
ryngeal), and X (vagus); these are mixed nerves.
Some of these primary sensory fibers end in the principal sensory
nucleus, but many form the spinal trigeminal tract and end in the spinal
trigeminal nucleus.
Neurons in the spinal trigeminal nucleus and in ventrolateral parts
of the principal sensory nucleus give rise to crossed ventral trigeminothalamic fibers. Collaterals of these fibers influence the hypoglossal, facial (corneal reflex, supraorbital, or trigeminofacial reflex), and
trigeminal motor nuclei; mesencephalic collaterals are involved in
the jaw reflex, or the jaw-jerk reflex. Collaterals also enter the dorsal
motor vagal nucleus (vomiting reflex), the superior salivatory nucleus
(tearing/lacrimal reflex), and the nucleus ambiguus and adjacent
reticular formation (sneezing reflex). Uncrossed dorsal trigeminothalamic fibers arise from dorsomedial regions of the principal sensory
nucleus.
Neurotransmitters
Substance P (+)-containing and cholecystokinin (+)-containing
trigeminal ganglion cells project to the spinal trigeminal nucleus,
especially its caudal part (pars caudalis). Glutamate (+) is found in
many trigeminothalamic fibers arising from the principal sensory
nucleus and the pars interpolaris of the spinal nucleus. It is present in fewer trigeminothalamic fibers from the pars caudalis and in
almost none from the pars oralis. The locus ceruleus (noradrenergic
fibers) and the raphe nuclei (serotonergic fibers) also project to the
spinal nucleus. Enkephalin (—)-containing cells are present in caudal
regions of the spinal nucleus, and enkephalinergic fibers are found in
the nucleus ambiguus and in the hypoglossal, facial, and trigeminal
motor nuclei.
face, oral cavity, and teeth; (2) ipsilateral paralysis of masticatory mus-
cles; and (3) ipsilateral loss of the corneal reflex may indicate a lesion of
the trigeminal ganglion or nerve proximal to the ganglion. Damage to
peripheral portions of the trigeminal nerve may be traumatic (skull fracture, especially of supraorbital and infraorbital branches), inflammatory (e.g., herpes zoster), or result from tumor growth (large vestibular
schwannoma or meningioma). The deficit would reflect the peripheral
portion of the trigeminal nerve damaged.
Trigeminal neuralgia (tic douloureux) is a severe burning pain
restricted to the peripheral distribution of the trigeminal nerve, usually
its V> (maxillary) division. This pain may be initiated by any contact to
areas of the face, such as the corner of the mouth, nose, lips, or cheek
(e.g., shaving, putting on makeup, chewing, or even smiling). The attacks
frequently occur without warning, may happen only a few times a month
to many times in a single day, and are usually seen in patients 40 years of
age or older. One probable cause of trigeminal neuralgia is compression
of the trigeminal root, or its entry zone, by aberrant vessels, most commonly a loop of the superior cerebellar artery. Other causes may include
tumor, multiple sclerosis (MS), and ephaptic transmission (ephapse) in
the trigeminal ganglion. About 2% of patients that present with MS may
have TGN, while ~18% to 20% of patients with bilateral TGN are likely
candidates for MS. This is the most common type of neuralgia.
In the medulla, fibers of the spinal trigeminal tract and ALS are
served by the PICA. Consequently, an alternating (alternate or crossed)
hemianesthesia is one characteristic feature of the PICA syndrome. This
is a loss of pain and thermal sensations on one side of the body and the
opposite side of the face. Pontine gliomas may produce a paralysis of
masticatory muscles (motor trigeminal damage) and some loss of tactile
input (principal sensory nucleus damage), as well as other deficits based
on the adjacent structures involved.
ABBREVIATIONS
ALS
CC
| DTTr
Anterolateral system
Crus cerebri
Dorsal (posterior)
trigeminothalamic tract
FacNu
Facial nucleus
GSA
HyNu
1@
ManV
General somatic afferent
Hypoglossal nucleus
Internal capsule
Mandibular division of
trigeminal nerve
Maxillary division of
trigeminal nerve
Mesencephalic nucleus
MaxV
MesNu
ML
OpthV
PSNu
Medial lemniscus
Ophthalmic division of
trigeminal nerve
Principal (chief) sensory
nucleus
RB
RetF
RNu
SpTNu
SpTTr
TriMoNu
TMJ
Restiform body
Reticular formation
Red nucleus
Spinal trigeminal nucleus
Spinal trigeminal tract
Trigeminal motor nucleus
Temporomandibular joint
VPL
Ventral posterolateral
nucleus of thalamus
Ventral posteromedial
nucleus of thalamus
VPM
VTTr
.
Ventral (anterior)
trigeminothalamic tract
Ganglia
AR Triseminaioen
al
- a ae a ares
3 S os ee
met
ra ee Be ee
Bae! EI
Review of Blood Supply to SpTT, SpTNu, and Trigeminothalamic Tracts
Structures
SpTTr and SpTNu in Medulla
SpTTr and SpTNu in Pons
Trigeminothalamic Fibers in Midbrain
VPM
Posterior Limb of IC
Arteries
Caudal third, vertebral; rostral two-thirds, posterior inferior cerebellar (see Figure 6-16)
Long circumferential branches of basilar (see Figure 6-23)
Short circumferential branches of posterior cerebral and superior cerebellar (see Figure 6-30)
Thalamogeniculate branches of posterior cerebral (see Figure 6-41)
Lateral striate branches of middle cerebral (see Figure 6-41)
$e
by aa ee
Se
8-7 TRIGEMINAL PATHWAYS
ae
& scapearyeanbaye
NG
IN ANATOMICAL
a
ri
ORIENTATION
Trunk
Thigh
Somatosensory
SAS
Leg
Ww?
S
Foot
cortex
TON
®
Ww&
Posterior
LL
Origin of SA data
Position of trigeminal tracts
GSA/SA, skin of face; forehead
and part of scalp; membranes of nose and of
nasal, maxillary, and frontal
sinuses;
ALS
g ps
DTTr
VTTr
TriMoNu
SpTTr
RNu
ML
=
oral cavity; teeth;
anterior two-thirds of tongue;
muscles of mastication; TMJ;
cornea and conjunctiva; and
dura of middle and anterior
cranial fossae
SpTNu
:
GSA/SA, external auditory meatus
'
and medial and lateral
surfaces of ear (conchae)
‘
'
1
!
'
:
3
Somatotopy in SpTTr and SpTNu
Input from VII, IX, X
GSA/SA, small area on ear
GSA/SA, medial and lateral surfaces
\a
SpTTr
SpTNu
of ear (conchae); posterior
wall ! and floor of external
auditory meatus; tympanic
membrane; and dura of posterior cranial fossa
HE
RNRene
Ea
aa
l Orientation
Tracts, Pathways, and Systems in Anatomical and Clinica
TRIGEMINAL PATHWAYS
Bre
eae
IN CLINICAL ORIENTATION
Postcentral gyrus (lateral
third is face area of somatosensory cortex)
Putamen
,
Genu, internal
capsule
Thalamocortical fibers
in posterior limb of
internal capsule
Posterior limb, internal capsule
Dorsal thalamus
Ventral posteromedial
nucleus
Crus cerebri
bstantia nigra
eal
g
Red nucleus
ML in midbrain
ALS in midbrain
TriThalFib in midbrain
Trigeminal ganglion —___
Trigeminal nerve root
Trigeminal nerve root
Basilar pons
Medial lemniscus (ML)
in pons
Spinal trigeminal tract
Middle cerebellar peduncle
TriThalFib in pons
Pontine tegmentum
Corticospinal fibers/pyramid
TriThalFib in medulla
Inferior olivary eminence
Anterolateral system
(ALS) in medulla
Restiform body
Spinal trigeminal tract
Medial
lemniscus (ML)
!
Spinal trigeminal nucleus, pars interpolaris
:
g
P
in medulla
Ganglia of cranial nerves VII, IX, X
;
%
;
Trigeminothalamic fibers
Spinal trigeminal tract
Spinal trigeminal fibers to dorsolateral
tract in upper cervical spinal cord
(TriThalFib) in medulla
———
Spinal trigeminal nucleus, pars caudalis
Spinal trigeminal and trigeminothalamic fibers superimsecond-order cells are in the spinal trigeminal nucleus, pars caudalis.
posed on MRI (brainstem and forebrain, T2-weighted MRI)
These second-order neurons project to the ventral posteromedial thashowing the location, topography, and trajectory of these fibers in a
_lamic nucleus (VPM), and from the VPM to the face area of the somatoclinical orientation. The cells of origin of the first-order neurons in the _ sensory cortex. The red and blue fibers correlate with those of the same
trigeminal sensory pathways are located in the trigeminal ganglion; the
color in Figure 8-7.
ee
Se
ai
TRIGEMINAL PATHWAYS IN CLINICAL ORIENTATION:
REPRESENTATIVE LESIONS AND DEFICITS
Postcentral gyrus (lateral
third is face area of somatosensory cortex)
Putamen
Genu, internal capsule
Posterior limb, internal capsule
Thalamocortical fibers
in posterior limb of
internal capsule
* Diminution/loss pain, thermal sense, and
discriminative touch on left side of face
plus UE/LE if VPL involved
¢ Paresthesias; dysesthesias
Ventral posteromedial
nucleus
Crus cerebri
¢ Possible transient left hemiplegia
Substantia nigra
Red nucleus
ML in midbrain
ALS in midbrain
TriThalFib in midbrain
Damage to trigeminal root
_
e Left-sided loss pain, thermal sense, and
discriminative touch on face and in oral
cavity (including teeth)
:
¢ Loss of corneal reflex on left: Damage to
afferent limb
¢ Paralysis of masticatory muscles on left
and slight deviation of jaw to righton
closure
:
Trigeminal nerve root
Middle cerebellar peduncle
Pontine tegmentum
Irritation of trigeminal root
¢ Trigeminal neuralgia (tic douloureux) on
left side of face
Inferior olivary eminence
Restiform body
Medial lemniscus (ML)
in medulla
=]
Ganglia of cranial nerves VII, IX, X
Spinal trigeminal tract ——
—
<
Spinal trigeminal fibers to dorsolateral
tract in upper cervical spinal cord——————_——
¢ Loss of pain/thermal sense on left side of
face and on right UE and LE
(alternating hemianesthesia)
e Dysarthria, dysphagia, and hoarseness
(nucleus ambiguus)
¢ Vertigo, ataxia, and nystagmus (vestibula
~ nucleus; restiform body)
e Nausea, vomiting, and singultus (area
postrema; reticular formation)
e Left ptosis/miosis/anhidrosis (Horner)
Spinal trigeminal nucleus, pars caudalis
Trigeminothalamic fibers
(TriThalFib) in medulla
Berar
on Representative lesions of the brainstem and thalamus that
involve elements of the trigeminal system and the deficits (in
8pink boxes) that correlate with the level and laterality of each lesion.
Damage to the trigeminal nerve (a mixed nerve) is usually perceived
as pain from the forehead, face, and/or oral cavity. This may present
as sharp, lancinating pains that can be triggered by stimuli in V2 or
V; territories of the trigeminal nerve around the mouth on the face. It
may be commonly (~80% of cases) attributed to compression of the
trigeminal root entry zone by an aberrant branch of the superior cerebellar artery. Proprioception is conveyed through the principal sensory
nucleus, and is perceived as, for example, pressure or displacement but
not frank pain. Note that the laterality (R/L) of the deficits is determined
by whether the lesion is on the left or right side of the MRI; this reinforces important clinical concepts.
al andand
Tracts, Pathways, and Systemssi in Anatomic
mical
SOLITARY PATHWAYS
iB
Cli ical
= :
n
Orientatio
al |rier
Clinic
IN ANATOMICAL
Visceral afferent input (SVA/VA, taste; GVA/VA, general visceral
sensation) on CNs VII (facial), IX (glossopharyngeal), and X
the solitary nuclei via the solitary tract and terminate on
enters
(vagus)
the cells of the surrounding nucleus. All of these are mixed nerves.
Recall that the SVA and GVA functional components may be collectively grouped as VA; Visceral Afferent. What is commonly called the
solitary “nucleus” is a series of small nuclei that collectively form this
rostrocaudal-oriented cell column.
Solitary cells project to the salivatory, hypoglossal, and dorsal motor
vagal nuclei and the nucleus ambiguus. Solitary projections to the
nucleus ambiguus are the intermediate neurons in the pathway for the
gag reflex. The afferent limb of the gag reflex is carried on the glossopharyngeal nerve, and the efferent limb originates from the nucleus
ambiguus; the efferent Jimb travels on both CNs IX and X. Although
not routinely tested, the gag reflex should be evaluated in patients with
dysarthria, dysphagia, or hoarseness. Solitariospinal fibers are bilateral
with a contralateral preponderance and project to the phrenic nucleus,
intermediolateral cell column, and ventral horn. The VPM is the thalamic center through which visceral afferent information is relayed onto
the cerebral cortex. See Figures 8-27 to 8-31, and Table 8-1 for brainstem reflexes.
Neurotransmitters
Substance P (+)-containing and cholecystokinin (+)-containing cells in
the geniculate ganglion (facial nerve) and the inferior ganglia of the glossopharyngeal and vagus nerves project to the solitary nucleus. Enkephalin
ORIENTATION
(-), neurotensin (+, —), and GABA (-) are present in some solitary neu-
rons that project into the adjacent dorsal motor vagal nucleus. Cholecystokinin (+), somatostatin (-), and enkephalin (—) are present in solitary
neurons, cells of the parabrachial nuclei, and some thalamic neurons that
project to taste and other visceral areas of the cortex.
Clinical Correlations
~a
Vice Ere aes
n
ee
An ipsilateral loss of taste (ageusia) from the anterior two-thirds of the
tongue and an ipsilateral facial (Bell) palsy may indicate damage to the
geniculate ganglion or facial nerve proximal to the ganglion. Although
a glossopharyngeal nerve lesion will result in ageusia from the posterior
third of the tongue on the ipsilateral side, this loss is difficult to test, or
rarely ever tested. On the other hand, glossopharyngeal neuralgia (this
may also be called glossopharyngeal tic) is an idiopathic pain localized
to the peripheral sensory branches of the ninth nerve in the posterior
pharynx, posterior tongue, and tonsillar area. Although comparatively
rare, glossopharyngeal neuralgia may be aggravated by talking or even
swallowing. Occlusion of the PICA results in a PICA or lateral medullary syndrome, in addition to producing an alternate hemianesthesia,
also results in ageusia from the ipsilateral side of the tongue because the
PICA serves the solitary tract and nuclei in the medulla. The ageusia is
rarely if ever tested in a PICA syndrome.
Interestingly, lesions of the olfactory nerves or tract (anosmia, loss of
olfactory sensation; dysosmia, distorted olfactory sense) may affect how
the patient perceives taste. Witness the fact that the nasal congestion
accompanying a severe cold markedly affects the sense of taste.
ABBREVIATIONS
AmyNu
CardResp
GustNu
Amygdaloid nucleus (complex)
Cardiorespiratory portion (caudal) of solitary
nucleus
Gustatory nucleus (rostral portion of solitary
nucleus)
GVA
HyNu
HyTh
InfVNu
MVNu
NuAm
PBNu
RB
General visceral afferent
Hypoglossal nucleus
Hypothalamus
SalNu
SolTr and Nu
SVA
Tr
VA
VPM
Salivatory nuclei
Solitary tract and nuclei
Special visceral afferent
ulract
Visceral afferent
Ventral posteromedial nucleus of thalamus
Number Key
Inferior (or spinal) vestibular nucleus
Medial vestibular nucleus
Nucleus ambiguus
Parabrachial nuclei
Restiform body
1. Geniculate ganglion of facial
2. Inferior ganglion of glossopharyngeal
3. Inferior ganglion of vagus
4. Dorsal motor vagal nucleus
eee
—_——
Review of Blood Supply to SolNu and SolTr
Structures
Arteries
SolNu and Tr in Medulla
Ascending Fibers in Pons
VPM
Posterior Limb of IC
Caudal medulla, anterior spinal; rostral medulla, posterior inferior cerebellar (see Figure 6-16)
Long circumferential branches of basilar and branches of superior cerebellar (see Figure 6-23)
Thalamogeniculate branches of posterior cerebral (see Figure 6-41)
Lateral striate branches of middle cerebral (see Figure 6-41)
eS
ee
eee cee
ee
8-9 SOLITARY PATHWAYS
Bee
WM ee
tasteee
IN ANATOMICAL
Thigh
Fe
Se ye ces 2 GUS Ni
ORIENTATION
Trunk
&y
Foot
We
va
Origin of VA data
to HyNu,
SalNu
SVA/VA, taste, anterior two-thirds of tongue
1
es
GVA/VA, submandibular, sublingual, and
lacrimal glands
\
SVA/VA
(GustNu)
LE
4 WY
SolTr and Nu
NOS
SIF
GVA/VA
SVA/VA, taste, posterior third of tongue
5
GVA/VA, parotid gland; mucosa of
pharynx; tonsillar sinus;
posterior third of tongue;
carotid body
(CardResp)
if
ee
SVA/VA, taste buds at root of
NuAm
tongue and on epiglottis
- GVA/VA, pharynx; larynx; aortic
bodies; and thoracic and
abdominal viscera
Solitariospinal tract
Position of SolTr and Nu
y-
BLANK MASTER DRAWING
8-10
FOR SENSORY PATHWAYS
standing, for the instructor to expand on sensory pathways not covered
Blank master drawing for sensory pathways. This illustration
is provided for self-evaluation of sensory pathway under- _ in the Atlas, or both.
OlinicalOrientation.
2
anc
Tracts, Pathways, and Systems in Anatomical and
CORTICOSPINAL TRACTS IN ANATOMICAL
The longitudinal extent of corticospinal fibers and their
position and somatotopy at representative levels within the
neuraxis. The somatotopy of corticospinal fibers in the basilar pons are
less compactly organized than are these fibers in the internal capsule,
crus cerebri, pyramid, or spinal cord. In the motor decussation (pyramidal decussation), fibers originating from upper extremity areas of
the motor cortex cross rostral to those that arise from lower extremity
areas. In addition to fibers arising from the precentral gyrus (somatomotor area, area 4), a significant contingent also originates from the post-
central gyrus (areas 3, 1, 2); the former terminate primarily in laminae
VI-IX, whereas the latter end mainly in laminae IV and V. Frontal area
6, and parietal areas 5 and 7 also contribute to the corticospinal tract.
Neurotransmitters
Acetylcholine, y-aminobutyric acid (—), and substance P (+, plus other peptides) are found in small cortical neurons presumed to function as local
circuit cells or in cortico-cortical connections. Glutamate (+) is present in
cortical efferent fibers that project to the spinal cord. Glutaminergic corticospinal fibers and terminals are found in all spinal levels, but are especially
concentrated in cervical and lumbosacral enlargements. This correlates
with the fact that approximately 55% of all corticospinal fibers terminate in cervical levels of the spinal cord, approximately 20% in thoracic
levels, and approximately 25% in lumbosacral levels. Some corticospinal
fibers may branch and terminate at multiple spinal levels. Lower motor
neurons are influenced by corticospinal fibers, either directly or indirectly,
via interneurons. Acetylcholine and calcitonin gene-related peptides are
present in these large motor cells and in their endings in skeletal muscle.
Clinical Correlations
Myasthenia gravis (MG), a disease characterized by moderate to profound
weakness of skeletal muscles, is caused by circulating antibodies that
react with postsynaptic nicotinic acetylcholine receptors. Characteristic
ORIENTATION
symptoms are: (1) progressive muscle fatigability and fluctuating muscle
weakness; (2) ocular muscles (diplopia, ptosis) are usually affected first
(~45%, eventually in ~85% of cases); and (3) muscle reaction to cholinergic drugs. In over 50% of patients, facial and oropharyngeal muscles
are commonly affected (facial weakness, dysphagia, dysarthria). Weakness also may be seen in limb muscles, but almost always in combination
with facial/oral weaknesses.
Injury to corticospinal fibers on one side of the cervical spinal cord
(e.g., the Brown-Séquard syndrome) results in paralysis (hemiplegia) of the
ipsilateral upper and lower extremities. With time, these patients may also
exhibit features of an upper motor neuron lesion (hyperreflexia, spasticity,
loss of superficial abdominal reflexes, and the Babinski sign). Bilateral cord
damage above C4—C5 may result in quadriplegia; at C1—C2, respiratory and
cardiac arrest are additional complications. Unilateral cord lesions in thoracic levels may result in paralysis of the ipsilateral lower extremity (monoplegia). If the thoracic spinal cord damage is bilateral both lower extremities
may be paralyzed (paraplegia). Small lesions within the decussation of the
pyramids may result in a bilateral paresis of the upper extremities (lesion in
rostral portions) or a bilateral paresis of the lower extremities (lesion in caudal portions) based on the crossing patterns of fibers within the decussation.
Recall that -plegia, as in hemiplegia, refers to a paralysis whereas -paresis, as
in hemiparesis, refers to a weakness or incomplete paralysis.
Rostral to the motor (pyramidal) decussation, vascular lesions in the
medulla (the medial medullary syndrome or Déjérine syndrome), pons
(the Millard—Gubler or Foville syndromes), or midbrain (the Weber syndrome) all produce crossed (alternate or alternating) hemiplegias. These
present as a contralateral hemiplegia of the upper and lower extremities,
coupled with an ipsilateral paralysis of the tongue (medulla), facial muscles or lateral rectus muscle (pons), and most eye movements (midbrain).
Sensory deficits are frequently seen as part of these syndromes. Lesions in
the internal capsule (lacunar strokes) produce contralateral hemiparesis
sometimes coupled with various cranial nerve signs due to corticonuclear
fiber involvement. Bilateral weakness, indicative of corticospinal involvement, is also present in amyotrophic lateral sclerosis.
ABBREVIATIONS
:
ACSp
ALS
APGy
BP
Anterior corticospinal tract
Anterolateral system
Anterior paracentral gyrus
Basilar pons
CSp
IC
LCSp
ML
Corticospinal fibers
Internal capsule
Lateral corticospinal tract
Medial lemniscus
CG
PrCGy
Py
RB
RNu
Crus cerebri
Precentral gyrus
Pyramid
Restiform body
Red nucleus
MLF
Medial longitudinal fasciculus
SN
Substantia nigra
CNu
Corticonuclear (corticobulbar) fibers
PO
Principal olivary nucleus
SOMATOTOPY
OF CSP FIBERS
7
|
Position
of fibers
coursing to lower extremity
regions of spinal cord
Position of fibers coursing to thoracic regions of
spinal cord
Position of fibers coursing to upper extremity
regions of spinal cord
Review of Blood Supply to Corticospinal Fibers
Structures
Arteries
Posterior Limb of IC
Lateral striate branches of middle cerebral (see Figure 6-41)
Paramedian and short circumferential branches of basilar and posterior communicating
Crus Cerebri in Midbrain
CSp in BP
Py in Medulla
LCSp in Spinal Cord
Paramedian branches of basilar (see Figure 6-23)
Anterior spinal (see Figure 6-16)
Penetrating branches of arterial vasocorona (LE fibers), branches
(see Figure 6-30)
of central artery (UE fibers) (see Figure 6-8)
eee
Eee
oe
8-11 CORTICOSPINAL TRACTS IN ANATOMICAL
ee = . MotorPathways:
P
5 4 1 |a
ORIENTATION
Somatomotor cortex
Somatotopy of CSp
Posterior limb, IC
CSp fibers in CC
Face
(CNu Fibers)
CSp fibers in BP
CSp fibers in \-j
CORTICOSPINAL TRACTS IN CLINICAL ORIENTATION
aie
Precentral gyrus (middle
Anterior paracentral gyrus
(lower extremity area of
third is upper extremity are
of somatomotor cortex)
somatomotor cortex)
Head of caudate nucleus
Anterior limb, internal capsule
Putamen
Corticospinal (CSp) fibers
in posterior limb of the
internal capsule
Thalamus
Frontopontine fibers
CSp fibers in crus cerebri
Parieto-, occipito-, and
temporopontine fibers
Midbrain tegmentum
Cerebral aqueduct
Basilar pons
CSp fibers in basilar pons
Pontine tegmentum
Superior cerebellar peduncle
Fourth ventricle
CSp fibers in pyramid of medulla
Inferior olive
Medial lemniscus
Restiform body
Fourth ventricle
ste
CSp fibers e
Motor (pyramidal) decussation
Lateral CSp tract (LCSp)
LCSp
fears
Cervical spinal cord
at C7-C8
LCSp fiber termination in anterior
horn at cervical levels
LCSp fiber termination in anterior
horn at lumbosacral levels
The corticospinal system superimposed on CT (spinal cord, myelogram) and MRI (brainstem and foreT2-weighted
showing
the location, topography,
MRI)
8-12A
i
brain,
and trajectory of this pathway
in a clinical orientation. With the
eee
exception of the posterior limb and basilar pons, corticospinal fibers are generally compactly arranged at all levels of the CNS. The
blue and green fibers correlate with those of the same color in
Figure 8-11.
csae
ee
CORTICOSPINAL TRACTS IN CLINICAL ORIENTATION:
AND DEFICITS
Precentral gyrus (middle
third is upper extremity area
of somatomotor cortex)
532
a
as-
Motor Pathways —
REPRESENTATIVE
Oe
.>
LESIONS
Anterior paracentral gyrus
(lower extremity area of
somatomotor cortex)
Corticospinal (CSp) fibers
in posterior limb of the
internal capsule
¢ Hemiplegia of right UE and LE
¢ Reduced sensation (pain, thermal sense,
proprioception, discriminative touch, and
vibratory sense on right side of face and
on right UE and LE)
¢ Hemiplegia of right UE and LE
¢ Paralysis of most eye movement on left;
CSp fibers in crus cerebri
eye oriented down and out: Superior
oblique and lateral rectus preserved
¢ Dilated left pupil
¢ Paralysis of lower face on right
¢ Tongue weakness: Deviates to the right
on attempted protrusion
Mid-to-rostral pons
¢ Hemiplegia of right UE and LE
¢ Loss of all sensation on left side of
face/oral cavity, paralysis of left
masticatory muscles (if trigeminal
nerve involved)
¢ Loss of proprioception, discriminative
touch, and vibratory sense if ML involved
CSp fibers in basilar pons
Caudal pons
¢ Hemiplegia of right UE and LE
e Abducens (lateral rectus) paralysis on left
¢ Paralysis of upper/lower facial muscles
on left (if facial nerve involved)
¢ Loss of proprioception, discriminative
touch, and vibratory sense if ML involved
CSp fibers in pyramid of medulla
¢ Hemiplegia of right UE and LE
¢ Loss of proprioception, discriminative
touch, and vibratory sense on right UE/LE
¢ Tongue weakness: Deviates to left on
attempted protrusion
Medial lemniscus
CSp fibers
* Bilateral paralysis of UE and/or LE
depending on position and extent
of midline lesion
Cervical spinal cord
at C7-C8
Lateral CSp tract (LCSp)
LCSp
fibers
Spinal cord hemisection
¢ Right-sided paralysis below lesion
¢ Right-sided loss of proprioception,
discriminative touch, and vibratory
sense below lesion
Left-sided loss of pain/thermal
sensation beginning about two
levels below lesion
¢ Right ptosis/miosis/anhidrosis
(Horner) if lesion at cervical levels
LCSp fiber termination in anterior
horn at cervical levels
LCSp fiber termination in ee
ees
horn at lumbosacral levels
Representative lesions within the CNS that involve the
corticospinal system and the deficits (in pink boxes) that
correlate with the level and laterality of each lesion. At all brainstem
levels the vascular territory of corticospinal fibers is also the territory
ya
of a cranial nerve nucleus or root; the cranial nerve deficit is the best
localizing symptom. Note that the laterality (R/L) of the deficits is determined by whether the lesion is on the left or right side of the MRI/CT;
this reinforces important clinical concepts.
oy: el
Tracts, Pathways, and Systems in Anatomical andClinical Orientation
CORTICONUCLEAR
FIBERS IN ANATOMICAL
The origin, course, and distribution of corticonuclear fibers
to brainstem motor nuclei. These fibers influence—either
directly or through interneurons in the immediately adjacent reticular formation—the motor nuclei of oculomotor, trochlear, trigeminal, abducens, facial, glossopharyngeal and vagus (both via nucleus
ambiguus), accessory (nucleus at C1-C5/C6), and hypoglossal nerves.
Corticonuclear fibers arise in the frontal eye fields (areas 6 and 8
in caudal portions of the middie frontal gyrus), the precentral gyrus
(somatomotor cortex, area 4, many), and some originate from the postcentral gyrus (areas 3, 1, and 2). Fibers from area 4 occupy the genu of
the internal capsule, but those from the frontal eye fields (areas 8 and
6) may traverse caudal portions of the anterior limb, and some (from
areas 3, 1, and 2) may occupy the most rostral portions of the posterior
limb. Fibers that arise in areas 8 and 6 terminate in the rostral interstitial
nucleus of the medial longitudinal fasciculus (vertical gaze center) and
the paramedian pontine reticular formation (horizontal gaze center);
these areas, in turn, project respectively to the third, fourth, and sixth
nuclei. Fibers from area 4 terminate in, or adjacent to, cranial nerve
motor nuclei excluding those of III, IV, and VI.
Although not illustrated here, the superior colliculus receives cortical
input from area 8 and from the parietal eye field (area 7) and also pro-
jects to the riMLF and PPRF. In addition, note that descending cortical
fibers (many arising in areas 3, 1, and 2) project to sensory relay nuclei
of some cranial nerves and to other sensory relay nuclei in the brainstem.
Neurotransmitters
Glutamate (+) is found in many corticofugal axons that directly innervate cranial nerve motor nuclei and in those fibers that terminate near,
but not in, the various motor nuclei (indirect).
Clinical Correlations
Lesions involving the motor cortex (e.g., cerebral artery occlusion) or the
posterior limb of the internal capsule (e.g., lacunar strokes or occlusion
of lenticulostriate branches of M,;) give rise to a contralateral hemiplegia
ie
ORIENTATION
of the upper and lower extremities (corticospinal fiber involvement)
coupled with certain possible cranial nerve signs. Strictly cortical lesions
may produce a transient gaze palsy in which the eyes deviate toward the
lesioned side and away from the side of the hemiplegia. In addition to
a contralateral hemiplegia, common cranial nerve findings if the genu
of the internal capsule is also involved may include: (1) deviation of
the tongue toward the side of the weakness and away from the side of
the lesion when protruded; and (2) paralysis of facial muscles on the
contralateral lower half of the face (central facial palsy). This reflects
the fact that corticonuclear fibers to genioglossus motor neurons and
to facial motor neurons serving the lower face are primarily crossed.
Interruption of corticonuclear fibers to the nucleus ambiguus may result
in weakness of palatal muscles contralateral to the lesion; the uvula will
deviate toward the ipsilateral (lesioned) side on attempted phonation.
In addition, a lesion involving corticonuclear fibers to the accessory
nucleus may result in drooping of the ipsilateral shoulder (or an inability to elevate the shoulder against resistance) due to trapezius weakness,
and difficulty in turning the head (against resistance) to the contralateral side due to weakness of the sternocleidomastoid muscle. In contrast to the crossed (alternating) hemiplegia characteristic of brainstem
lesions, hemisphere lesions result in spinal and cranial nerve deficits that
are generally, but not exclusively, contralateral to the cerebral injury.
Brainstem lesions, especially in the midbrain or pons, may result in
the following: (1) vertical gaze palsies (midbrain); (2) the Parinaud syndrome—paralysis of upward gaze (tumors in area of pineal); (3) internuclear ophthalmoplegia (lesion in the MLF between motor nuclei of III
and VI); (4) horizontal gaze palsies (lesion in abducens nucleus + PPRF);
or (5) the one-and-a-half syndrome (see also Figure 3-8 and Tables 3-1
and 3-2). In the latter case, the lesion is adjacent to the midline and
involves mainly the abducens nucleus, internuclear fibers from the ipsilateral abducens that are crossing to enter the contralateral MLE, and
internuclear fibers from the contralateral abducens nucleus that cross to
enter the MLF on the ipsilateral (lesioned) side. The result is a loss of
ipsilateral abduction (lateral rectus) and adduction (medial rectus, the
“one”) and a contralateral loss of adduction (medial rectus, the “half”);
the only remaining horizontal movement is contralateral abduction via
the intact abducens motor neurons.
ABBREVIATIONS
AbdNu
AccNu
EWpgNu
FacNu
HyNu
IC
NuAm
Abducens nucleus
Accessory nucleus
Edinger—Westphal nucleus
Facial nucleus
Hypoglossal nucleus
Internal capsule
Nucleus ambiguus
OcNu
PPRF
riMLF
Oculomotor nucleus
Paramedian pontine reticular formation
Rostral interstitial nucleus of the medial
longitudinal fasciculus
TriMoNu
Trigeminal motor nucleus
TroNu
Trochlear nucleus
Review of Blood Supply to Cranial Nerve Motor Nuclei
—_————“
——
~
—eee
eSEEE
Structures
Arteries
OcNu and EWpgNu
Paramedian branches of basilar bifurcation and medial branches of posterior cerebral and
TriMoNu
Long circumferential branches of basilar (see Figure 6-23)
Long circumferential branches of basilar (see Figure 6-23)
Posterior inferior cerebellar (see Figure 6-16)
Anterior spinal (see Figure 6-16)
posterior communicating (see Figure 6-30)
AbdNu and FacNu
NuAm
HyNu
eee
ee
Pe
8-13 CORTICONUCLEAR
ees
FIBERS IN ANATOMICAL
errs oe
ORIENTATION
Motor cortex,
precentral gyrus
Frontal eye fields
Genu of IC
TroNu
TriMoNu
Bilateral for upper face
PPRF
AbdNu
FacNu
Crossed for lower face
NuAm
oe
= Direct to motor
neurons of nucleus
Crossed for uvula
x
ee
(soft palate)
= Indirect to motor
neurons via adjacent
Crossed for
genioglossus muscle
reticular formation
HyNu
= Bilateral projections
KZ
os
= Primarily crossed
projections
AccNu
~
;
8 a
eats fa, ane
Anatomical a
Tracts, Pathways, and Systems in
FIBERS IN CLINICAL ORIENTATION
CORTICONUCLEAR
Head of caudate nucleus
Precentral gyrus (lateral third is
face area of somatomotor cortex) —
Anterior limb, internal capsule
Genu, internal capsule
Putamen
Posterior limb, ‘ internal capsule
Tibers (Conran)
Corticonuciear
in genu of internal capsule
Dorsal thalamus
CortNuFib in crus
Frontopontine fibers
cerebri
Corticospinal fibers
in crus cerebri
Parieto-, occipito-, and
temporopontine fibers
Substantia nigra
Interpeduncular fossa
Midbrain tegmentum
Cerebral aqueduct
Basilar pons
Portion of faciat nucleus
innervating lower face
Portion of facial nucleus
Facial (motor) nucleus
innervating upper face
CortNuFib in pons
Facial colliculus
Nucleus ambiguus ARES
+
aS
CortNuFib in medulla
am
:
z
IS
e
\y
Inferior olive
Z
Restiform body
Hypoglossal nucleus
Fourth ventricle
Corticospinal fibers/pyramid
Preolivary sulcus
Nucleus ambiguus
Retro-olivary sulcus
Hypoglossal nucleus
Fourth ventricle
;
CortNuFib to accessory nucleus
Accessory nucleus (C1—
C5 cord levels)
Fibers
comprising
posed on MRI
the corticonuclear
system
superim-
(brainstem and forebrain, T2-weighted
MRI) showing their location, topography, and trajectory in a clinical
orientation. The main projection
is indicated
by the larger diame-
ter branches. The red fibers correlate with those of the same color in
Figure 8-13.
te
CORTICONUCLEAR
FIBERS IN CLINICAL ORIENTATION:
AND DEFICITS
Precentral gyrus (lateral third is
face area of somatomotor cortex) —
REPRESENTATIVE
LESIONS
Head of caudate nucleus
Anterior limb, internal capsule
Genu, internal capsule
Putamen
* Lesion in genu of internal capsule
on right: deficits predominantly on
left; see below
Posterior limb, internal capsule
Dorsal thalamus
ancien
CortNuFib in crus
cerebri
Frontopontine fibers
Corticospinal fibers
in crus cerebri
Parieto-, occipito-, and
temporopontine fibers
Substantia nigra
Interpeduncular fossa
Midbrain tegmentum
Cerebral aqueduct
* No effect on masticatory muscles;
corticonuclear input to motor V is bilateral
Portion of facial nucleus
innervating lower face
¢ Paralysis of lower facial muscles on left;
Portion of facial nucleus
predominant input from right motor cortex
¢ Upper facial muscles normal; bilateral
input from motor cortex
innervating upper face —
CortNuFib in pons
Facial colliculus
Nucleus ambiguus
¢ Dysphagia, dysarthria, and deviation of
uvula to right on phonation; hoarseness
CortNuFib in medulla
¢ Deviation of tongue to left on protrusion;
predominant input from right motor cortex
Hypoglossal nucleus
Corticospinal fibers/Pyramid
* Dysphagia, dysarthria, and deviation of
uvula to right on phonation; hoarseness
Nucleus ambiguus
Hypoglossal nucleus
* Deviation of tongue to left on protrusion;
predominant input from right motor cortex
CortNuFib to accessory nucleus
Accessory nucleus (C1—
C5 cord levels)
Representative lesion of corticonuclear fibers in the
re ~~
ke Ei ouedl genu of the internal capsule that results in deficits (in
pink boxes) related to the motor function of certain cranial nerves.
Lesion in the genu of the internal capsule may result in particular combinations
of motor
deficits of cranial nerves
without motor
¢ Unable to rotate head to left against
resistance
e Unable to elevate right shoulder against
resistance
deficits of the extremities; there are no corticonuclear fibers in the
posterior limb and no corticospinal fibers in the genu. Note that
the laterality (R/L) of the deficits is determined by the location of
the lesion in the genu on the right; this reinforces important clinical
concepts.
Rea
~
.
218
rs
eS
a
3 / Tracts, Pathways, and System
at it
se od
uy Apel
nd
TECTOSPINAL AND RETICULOSPINAL TRACTS IN ANATOMICAL
The origin, course, and position in representative cross
sections of brainstem and spinal cord, and the general distribution of tectospinal and reticulospinal tracts. Tectospinal fibers
originate from deeper layers of the superior colliculus, cross in the
posterior (dorsal) tegmental decussation, and distribute to cervical
cord levels. Several regions of cerebral cortex (e.g., frontal, parietal,
temporal) project to the tectum, but the most highly organized corticotectal projections arise from the visual cortex. Pontoreticulospinal
fibers (medial reticulospinal) tend to be uncrossed, whereas those from
the medulla (bulboreticulospinal or lateral reticulospinal) are bilateral, but with a pronounced ipsilateral preponderance. Corticoreticular fibers are bilateral with a slight contralateral preponderance and
originate from several cortical areas.
Neurotransmitters
Corticotectal projections, especially those from the visual cortex, use
glutamate (+). This substance is also present in most corticoreticular fibers. Some neurons of the gigantocellular reticular nucleus that send their
axons to the spinal cord, as reticulospinal projections, contain enkephalin (—) and substance P (+). Enkephalinergic reticulospinal fibers may be
part of the descending system that modulates pain transmission at the
spinal level. Many reticulospinal fibers influence the activity of lower
motor neurons.
ORIENTATION
Clinical Correlations
Isolated lesions of only tectospinal and reticulospinal fibers are essentially never seen in isolation but are part of a variety of somatomotor
syndromes. Tectospinal fibers project to upper cervical levels where they
influence reflex movements of the head and neck. Such movements may
be diminished or slowed in patients with damage to these fibers. Pontoreticulospinal (medial reticulospinal) fibers are excitatory to extensor
motor neurons and to neurons innervating axial musculature; some of
these fibers also may inhibit flexor motor neurons. In contrast, some bulboreticulospinal (lateral reticulospinal) fibers are primarily inhibitory to
extensor motor neurons and neurons innervating muscles of the neck and
back; these fibers also may excite flexor motor neurons via interneurons.
Reticulospinal (and vestibulospinal) fibers contribute to the spasticity
that develops in patients having lesions of corticospinal fibers. These fibers, particularly reticulospinal fibers, also contribute to the tonic extension
of the arms and legs seen in decerebrate rigidity when spinal motor neurons are released from descending cortical control. The sudden increase in
extensor rigidity, seen in decerebrate patients when a noxious stimulus is
applied to, for example, the skin between the toes, is mediated via spinoreticular fibers ascending in the ALS that, in turn, branch into and excite the
reticular nuclei whose axons, as reticulospinal fibers, descend to increase
the level of excitation to extensor motor neurons. When the noxious stimulus is removed, the momentarily increased level of rigidity decreases to
the level that was present before the stimulus was applied. This ascending
part of the pain pathway contains spinoreticular fibers that traverse the
ALS to terminate in the medullary reticular formation, where they activate
descending reticulospinal fibers that increase the activity of spinal motor
neurons during the period of increased drive on the motor neurons.
ABBREVIATIONS
ALS
ATegDec
Anterolateral system
Anterior tegmental decussation
(rubrospinal fibers)
Basilar pons
Crus cerebri
Corticoreticular fibers
Corticotectal fibers
Gigantocellular reticular nucleus
Lateral corticospinal tract
Medial lemniscus
Medial longitudinal fasciculus
Medial vestibular nucleus
Oculomotor nucleus
BP
CC
CRet
CTec
GigRetNu
LCSp
ML
MLF
MVNu
OcNu
PO
PTegDec
Py
RB
RetNu
RetSp
RNu
RuSp
SC
SN
SpVNu
TecSp
Principal olivary nucleus
Posterior tegmental decussation
(tectospinal fibers)
Pyramid
Restiform body
Reticular nuclei
Reticulospinal tract(s)
Red nucleus
Rubrospinal tract
Superior colliculus
Substantia nigra
Spinal (or inferior) vestibular nucleus
Tectospinal tract
Review of Blood Supply to SC, Reticular Formation of Pons and Medulla, and TecSp and RetSp Tracts
Structures
Arteries
XC
Long circumferential branches (quadrigeminal branch) of posterior cerebral plus some from superior
cerebellar and posterior choroidal (see Figure 6-30)
Pontine Reticular Formation
Long circumferential branches of basilar plus branches of superior cerebellar in rostral pons
Medullary Reticular Formation
Branches of vertebral plus paramedian branches of basilar at medulla—pons junction (see Figure 6-16)
Branches of central artery (TecSp and Medullary RetSp); tracts penetrating branches of arterial
(see Figure 6-23)
TecSp and RetSp
vasocorona (Pontine RetSp) (see Figures 6-16 and 6-8)
eee
————
e Pathways Ce: y
eks
e
e
nN a
8-15 TECTOSPINAL AND RETICULOSPINAL TRACTS IN ANATOMICAL
ORIENTATION
CRet
CTec
VY
Position of TecSp and RetSp
PTegDec
ML
RNu
CRet
PTegDec (TecSp)
ATegDec (RuSp)
MLF
Pontine RetNu
oralis -
TecSp
RetNu of Pons
caudalis
InfVNu
ALS
t
|
|
Sh
“i
LCSp
Medullary RetSp
to laminae VII
(VI, VIII, 1X)
F
oe
5
et
(VII, IX)
to laminae VI, VII (VIII)
of cervical levels
Tracts, Pathways, and Systems in Anatomical and Clinical Orient t
RUBROSPINAL AND VESTIBULOSPINAL TRACTS IN ANATOMICAL
The origin, course, and position in representative cross sections of brainstem and spinal cord, and the general distribution of rubrospinal and vestibulospinal tracts.
Rubrospinal fibers cross in the anterior (ventral) tegmental decussation
and distribute to all spinal levels, although projections to cervical levels clearly
predominate. There is a topographic map in the corticorubral-rubrospinal
pathway. Cells in dorsomedial regions of the red nucleus receive input from
upper extremity areas of the motor cortex and project to cervical levels, while
those in ventrolateral areas of the nucleus receive some fibers from lower
extremity areas of the motor cortex and may project in sparse numbers to
lumbosacral levels. The red nucleus also projects, via the central tegmental
tract, to the ipsilateral inferior olivary complex (rubro-olivary fibers).
Medial and lateral vestibular nuclei give rise to the medial and lateral
vestibulospinal tracts, respectively. The former tract is primarily ipsilateral, projects to upper spinal levels, and is considered a component
of the medial longitudinal fasciculus in the spinal cord. The latter tract
is ipsilateral and somatotopically organized; fibers to lumbosacral levels
originate from dorsal and caudal regions of the lateral nucleus, whereas
those to cervical levels arise from its rostral and more ventral areas.
Neurotransmitters
Glutamate (+) is present in corticorubral fibers. Some lateral vestibulospinal fibers contain aspartate (+), whereas glycine (—) is present in
a portion of the medial vestibulospinal projection. There are numerous y-aminobutyric acid (—)-containing fibers in the vestibular complex;
these represent the endings of cerebellar corticovestibular fibers.
Clinical Correlations
Isolated injury to rubrospinal and vestibulospinal fibers is really not
seen in isolation in humans but damage to these tracts are important
ORIENTATION
elements in a variety of motor system lesions. Deficits in fine distal limb
movements seen in monkeys following experimental rubrospinal lesions
may be present in humans. However, these deficits are overshadowed by
the hemiplegia associated with injury to the adjacent corticospinal fibers. The rubral tremor (Holmes tremor) and the cerebellar ataxia/tremor
(all predominately contralateral), as seen in patients with the Claude
syndrome (a lesion of the medial midbrain), is related to damage to
the red nucleus and the adjacent cerebellothalamic fibers, respectively.
These patients may also have a paucity of most eye movement on the
ipsilateral side and a dilated pupil (oculomotor palsy and mydriasis) due
to concurrent damage to exiting rootlets of the oculomotor nerve. The
sudden increase in extensor rigidity, seen in decerebrate patients when a
noxious stimulus is applied to, for example, the skin between the toes,
is mediated via spinoreticular fibers (traveling in the ALS) that end on
reticulospinal neurons whose axons descend to further excite extensor
motor neurons.
Medial vestibulospinal fibers primarily inhibit motor neurons
innervating extensors and neurons serving muscles of the back and
neck. Lateral vestibulospinal fibers may inhibit some flexor motor
neurons, but they mainly facilitate spinal reflexes via their excitatory influence on spinal motor neurons innervating extensors. Vestibulospinal and reticulospinal (see Figure 8-17) fibers contribute to
the spasticity seen in patients with damage to corticospinal fibers
or to the tonic extension of the extremities in patients with decerebrate rigidity. In the case of decerebrate rigidity, the descending
influences on spinal flexor motor neurons (corticospinal, rubrospinal) are removed; the descending brainstem influence on spinal
extensor motor neurons predominates; this is augmented by excitatory spinoreticular input (via ALS) to some of the centers giving rise
to reticulospinal fibers (see also Figure 8-15). See Figure 8-17 for
lesions that influence the activity of rubrospinal and reticulospinal
fibers.
ABBREVIATIONS
ATegDec
Ge
CorRu
FacNu
InfVNu
LCSp
LRNu
LVNu
LVesSp
ML
Anterior tegmental decussation
(rubrospinal fibers)
Crus cerebri
Corticorubral fibers
Facial nucleus
Inferior (or spinal) vestibular nucleus
Lateral corticospinal tract
Lateral reticular nucleus
Lateral vestibular nucleus
Lateral vestibulospinal tract
Medial lemniscus
MLF
Medial longitudinal fasciculus
MVesSp
MVNu
OcNu
PTegDec
Py
RNu
RuSp
SC
SVNu
TecSp
VesSp
Medial vestibulospinal tract
Medial vestibular nucleus
Oculomotor nucleus
Posterior tegmental decussation
(tectospinal fibers)
Pyramid
Red nucleus
Rubrospinal tract
Superior colliculus
Superior vestibular nucleus
Tectospinal tract
Vestibulospinal tracts
Review of Blood Supply to RNu, Vestibular Nuclei, MFL and RuSp, and Vestibulospinal Tracts
Structures
Arteries
RNu
Medial branches of posterior cerebral and posterior communicating plus some from short
circumferential branches
of posterior cerebral (see Figure 6-30)
Posterior inferior cerebellar in medulla (see Figure 6-16) and long circumferential branches
in pons (see Figure 6-23)
Long circumferential branches of basilar in pons (see Figure 6-23) and anterior spinal
in medulla (see Figure 6-16)
Branches of central artery (see Figures 6-8 and 6-16)
Penetrating branches of arterial vasocorona plus terminal branches of central artery
(see Figure 6-8)
Vestibular Nuclei
MLF
MVesSp
LVesSp and RuSp
a
aae a eee
SAANTAS
mn
Motor
RR
Pathway:
a
NY
\
:
ik
‘\
8-16 RUBROSP
INAL AND VESTIBU
LOSPINAL
TRACTS IN AAR
ANATOMI
CAL ORIENTAT
e
a
eee
s
ee
e
s
VNIENTALION
IVN
Thigh
Foot
Face
Position of RuSp
and VesS
OCNu
RNu
PTegDec
(TecSp)
ATegDec (RuSp)
LVNu
MVesSp
in MLF
LCSp
LE
RuSp
RuSp
to laminae
V-VIII
MVesSp
to laminae
Vil and VIII
a
ae
oe
2 ee
ae
a1ane lice
Tracts, Pathways,
andSystems My natomical
ae
FIBERS:
RETICULOSPINAL, AND VESTIBULOSPINAL
CLINICAL ORIENTATION
RUBROSPINAL,
Corticorubral fibers
Corticoreticular
fibers
Posterior limb of internal capsule
Anterior (ventral) tegmental
decussation (RuSp fibers)
Red nucleus
Corticoreticular fibers
>
—_
Pontine (medial) RetSp fibers
Pontine reticular (caudalis
and some oralis) nuclei
Rubrospinal (RuSp)
fibers
Basilar pons
at
é
: pons—
medulla junction
Medulla at pons—medulla
junction Medial (+ some spinal)
vestibular nucleus
=
;
Gigantocellular reticular
nucieus of medulla
Lateral vestibular nucleus
Lateral vestibulospinal
(LVesSp) fibers
RuSp fibers
Medullary (lateral) reticulospinal (RetSp) fibers
Pontine (medial) reticulospinal (RetSp) fibers
Medial vestibulospinal (MVesSp) 7
fibers in the MLF
—F—
LVesSp fibers
MVesSp fibers in the MLF
——————.
————
BSN
7a
(BS.
wat
Pontine (medial) RetSp fibers
SY
Medullary (lateral) RetSp fibers
RuSp fibers
RuSp fibers to lower
cervical levels
LVesSp fibers to lower
spinal cord levels =|
Medullary RetSp fibers to
lower spinal cord levels
|—_—_—_ Pontine RetSp fibers to
lower spinal cord levels
Rubrospinal, reticulospinal, and vestibulospinal fibers
(brainstem and forebrain, T2-weighted MRI) showing their origin, locasuperimposed on CT (spinal cord, myelogram) and MRI _ tion, and trajectory in clinical orientation.
Se erie
RUBROSPINAL, RETICULOSPINAL, AND VESTIBULOSPINAL FIBERS: CLINICAL
ORIENTATION—LESIONS AFFECTING THEIR INFLUENCE ON SPINAL MOTOR NEURONS
Lesion for decorticate rigidity
¢ Flexion (Sometimes slow) of UE at
elbow and wrist
¢ Extension and internal rotation of LE
¢ Plantar flexion of feet and toes
Corticorubral fibers
Corticoreticular
fibers
Posterior limb of internal capsule
Red nucleus
Extension of lesion through
tentorial notch for decerebrate
rigidity
¢ Extension and internal rotation
of UE; wrist and fingers flexed
¢ Rigidity/extension of neck, back,
and LE (with internal rotation)
¢ Plantar flexion of feet and toes
¢ Opisthotonos
Pontine reticular (caudalis
and some oralis) nuclei
Pontine (medial) RetSp fibers
Rubrospinal (RuSp)
fibers
Basilar pons
at
:
: pons—
medulla junction
Medulla at pons—medulla
junction
Medial (+ some spinal)
vestibular nucleus
;
;
Gigantocellular reticular
nucleus of medulla
Lateral vestibular nucleus
RuSp fibers
Lateral vestibulospinal
(LVesSp) fibers
Medial vestibulospinal (MVesSp)
fibers in the MLF
eer ace reticulo-
spinal (RetSp) fibers
Ls
Pontine (medial) reticulospinal (RetSp) fibers
Pontine (medial) RetSp fibers
LVesSp fibers
MVesSp fibers in the MLF
7
WEE: Ged
LVesSp fibers to lower
Spinalicord levels
Representative lesions in the forebrain that are supratenge
torial (located above the tentorial notch) and then extend
her sith
downward through the notch and become infratentorial. These lesions
alter the activity of rubrospinal, vestibulospinal, and reticulospinal
fibers that results in the characteristic deficit (in pink boxes) seen in
these patients. In a large supratentorial lesion (decorticate rigidity),
all brainstem nuclei (including the red nucleus) are intact. When the
™
i
Czas)
Medullary (lateral) RetSp fibers
:
a
“
SY
RuSp fibers
RuSp fibers to lower
cervical levels
Medullary RetSp fibers to
lower spinal cord levels
|
Pontine RetSp fibers to
lower spinal cord levels
lesion becomes infratentorial, the red nucleus influence is removed, the
extensor rigidity predominates and the patient becomes decerebrate.
This extensor (decerebrate) posturing is exacerbated by incoming signals from the anterolateral system (such as noxious stimulus to the skin
between the toes); the decerebrate posturing is increased during stimulation and decreases when it is removed. See Chapter 9 for additional
information on herniation syndromes.
BLANK MASTER DRAWING
8-18
Blank master drawing for motor pathways. This illustration is provided for self-evaluation of motor pathways
FOR MOTOR PATHWAYS
understanding, for the instructor to expand on motor pathways not
covered in this Atlas, or both.
IV, VI, XI-ACCNU, XII) IN ANATOMICAL ORIENTATION
CRANIAL NERVE EFFERENTS (Ill, see
eee
8-19. The origin and peripheral distribution of GSE or SE fibers from
oculomotor, trochlear, abducens, accessory, and hypoglosthe
sal nuclei; these somatomotor cell groups innervate skeletal muscles.
Edinger-Westphal cells (visceromotor preganglionic) adjacent to the
oculomotor nucleus are organized into the Edinger—Westphal centrally
projecting nucleus (EWcpNu) and the Edinger-Westphal preganglionic
nucleus (EWpgNu). Neurons of the EWcpNu project to the spinal cord and
a variety of brainstem nuclei (such as parabrachial, inferior olivary, dorsal
raphe) that are involved in stress and food/drink intake behaviors. Neurons
of the EWpgNu are the origin of the VE preganglionic parasympathetic
input to the ciliary ganglion traveling on the third nerve; this is part of
the pupillary light reflex pathway. Internuclear abducens neurons (in green)
project, via the MLE to contralateral oculomotor neurons that innervate
the medial rectus muscle (internuclear ophthalmoplegia pathway).
The trapezius and sternocleidomastoid muscles originate from cervical somites located caudal to the last pharyngeal arch; they are designated here as SE. In addition, the motor neurons innervating these same
muscles are found in cervical cord levels C1 to about CS/C6.
Neurotransmitters
Acetylcholine (and probably calcitonin gene-related peptide, CGRP)
is found in the motor neurons of cranial nerve nuclei and in their
peripheral endings. This substance is also found in cells of the EdingerWestphal preganglionic nucleus and the ciliary ganglion.
Clinical Correlations
MG is a disease caused by autoantibodies that may directly block nicotinic acetylcholine receptors or damage the postsynaptic membrane
(via complement-mediated lysis) thereby reducing the number of viable
receptor sites. Ocular movement disorders (diplopia, ptosis) are the initial deficits observed in approximately 45% of patients and is eventually
present in approximately 85% of all MG patients. Movements of the
neck and tongue also may be impaired, with the latter contributing to
dysphagia and dysarthria.
The patient who presents with: (1) ptosis; (2) lateral and downward
deviation of the eye; and 3) diplopia (except on ipsilateral lateral gaze)
may have a lesion of third nerve (e.g., as in the Weber syndrome or ina
carotid cavernous aneurysm). In addition, the pupil may be unaffected
(pupillary sparing) or dilated and fixed. Lesions in the midbrain that
involve the root of the third nerve and the crus cerebri give rise to a
superior crossed (alternating) hemiplegia. This is an ipsilateral paralysis
of most eye movement and a dilated pupil on the ipsilateral side anda
contralateral hemiplegia of the extremities.
Damage to the MLF (e.g., MS or small vessel occlusion) between
the sixth and third nuclei results in internuclear ophthalmoplegia;
on attempted lateral gaze, the opposite medial rectus muscle will not
adduct. A lesion of the fourth nerve (frequently caused by trauma) produces diplopia on downward and inward gaze (tilting the head may
give some relief), and the eye is slightly elevated when the patient looks
straight ahead. Recall, the trochlear nucleus innervates the superior
oblique muscle on the side opposite (contralateral to) the nucleus.
Diabetes mellitus, trauma, or pontine gliomas are some causes of sixth
nerve dysfunction. In these patients, the affected eye is slightly adducted,
and diplopia is pronounced on attempted gaze to the lesioned side. Damage
in the caudal and medial pons may involve the fibers of the sixth nerve and
the adjacent corticospinal fibers in the basilar pons, giving rise to a middle
crossed (alternating) hemiplegia. The deficits are an ipsilateral paralysis of
the lateral rectus muscle and a contralateral hemiplegia of the extremities.
The eleventh nerve may be damaged centrally (e.g., syringobulbia or amyotrophic lateral sclerosis) or at the jugular foramen with resultant paralysis of
the ipsilateral sternocleidomastoid and upper parts of the trapezius muscle.
Central injury to the twelfth nucleus or fibers (e.g., the medial medullary syndrome or in syringobulbia) or to its peripheral parts (e.g.,
polyneuropathy, trauma, or tumor) results in deviation of the tongue
toward the lesioned side on attempted protrusion. A lesion in the medial
aspects of the medulla will give rise to an inferior crossed (alternating)
hemiplegia. This is characterized by a paralysis of the ipsilateral side of
the tongue (twelfth root damage) and contralateral hemiplegia of the
extremities (damage to corticospinal fibers in the pyramid); a medial
medullary syndrome (Déjérine syndrome).
ABBREVIATIONS
AbdNr
AbdNu
AccNr
AccNu
BP
CG
EWpgNu
FacCol
HyNr
Abducens nerve
Abducens nucleus
Accessory nerve
Accessory nucleus
Basilar pons
Crus cerebri
Edinger—Westphal
preganglionic nucleus
Facial colliculus
Hypoglossal nerve
HyNu
ML
MLF
OcNr
OcNu
PO
Py
RNu
SC
Hypoglossal nucleus
Medial lemniscus
Medial longitudinal
fasciculus
Oculomotor nerve
Oculomotor nucleus
Principal olivary nucleus
Pyramid
Red nucleus
Superior colliculus
SGP. Dec
TroDec
TroNr
TroNu
Superior cerebellar
peduncle, decussation
Trochlear decussation
Trochlear nerve
Trochlear nucleus
Ganglion
legentee
ae sci
Review of Blood Supply to OcNu, TroNu, AbdNu, and HyNu and the Internal Course of Their Fibers
Structures
OcNu and Fibers
TroNu
AbdNu
Abducens Fibers in BP
HyNu and Fibers
Arteries
Medial branches of posterior cerebral and posterior communicating (see Figure 6-30)
Paramedian branches of basilar bifurcation (see Figure 6-30)
Long circumferential branches of basilar (see Figure 6-23)
Paramedian branches of basilar (see Figure 6-23)
Anterior spinal (see Figure 6-16)
Se
ne eae
+...2
Ge. lalNowvess % 2 Ee
8-19 CRANIAL NERVE EFFERENTS (Ill, IV, VI, XI—ACCNU, AND XII)
IN ANATOMICAL ORIENTATION
Position of nucleus
and internal
route of fibers
SC
SN
OcNu and
EWpgNu
OcNu
OcNr
¢
RNu
Bs
:
ON (6)
s
Medial rectus
eanee
;
Non
NI
Muscles innervated
Ciliary; sphincter of iris
Inferior oblique; inferior and
TroDec
medial recti
TroNu
Superior rectus
MLF
Levator palpebrae
Superior oblique
Lateral rectus
\
\
HyNr
Intrinsic tongue muscles,
and styloglossus,
hyoglossus,
genioglossus
me
ee
ees
Sternocleidomastoid
Trapezius
Tracts, Pathways, and Systems a Anatomical andCini
Cl
sous
CRANIAL NERVE EFFERENTS (Ill, 1V, VI, AND XII) IN CLINICAL ORIENTATION
Mammillary body/nuclei
Frontopontine fibers
Interpeduncular fossa
Red nucleus
Oculomotor nerve
Corticospinal and
corticonuclear fibers
z %
Red nucleus
Substantia nigra
Oculomotor nucleus
(GSE and GVE cells)
Midbrain tegmentum
Cerebral aqueduct and
periaqueductal gray
Superior colliculus
Medial longitudinal fasciculus
rs
Substantia nigra
Decussation of superior
cerebellar peduncle
Parieto-, occipito-, and
temporopontine fibers
Trochlear nucleus
Cerebral aqueduct
Inferior colliculus
Trochlear nerve exit
Superior oblique muscle—
Medial longitudinal fasciculus
Lateral rectus muscle —
Abducens nerve
Corticospinal fibers
in basilar pons
Basilar pons
ML in pons
Pontine tegmentum
Abducens nucleus
Facial colliculus
Sulcus limitans
Pyramid
Intrinsic tongue muscles andj
stylo-, hyo-, and genio-—>—
Inferior olive
glossus muscles
Hypoglossal nerve
Medial lemniscus (ML)
in medulla
Anterolateral system
Spinal trigeminal
tract and nucleus
Fourth ventricle
Hypoglossal nucleus
The nuclei and efferent fibers of CNs III, IV, VI, and XII
superimposed on MRI (brainstem, T2-weighted MRI)
shown in a clinical orientation. As they traverse the brainstem toward
their exit, the roots of these cranial nerves may share various vascular territories with corticospinal fibers. Brainstem vascular lesions
may result in weakness of upper and lower extremities on one side
and motor weakness of a cranial nerve on the contralateral side. For
example, weakness of upper and lower extremities on the right and
deviation of the tongue to the left on protrusion localizes the lesion to
the medulla on the left; the cranial nerve deficit is the best localizing
sign/symptom. In some examples the long-track signs/symptoms (anterolateral system, corticospinal, posterior column—medial lemniscus) may
be diminished or missing. Also shown is the internuclear pathway from
the sixth nucleus on one side to the third nucleus on the contralateral
side. The red and green fibers correlate with those of the same color in
Figure 8-19.
SURED go SS
ake
ee
SESS
SA ORE
Sa eae
ns Lae .
Ca
5
Re
ke oa
© Cranial tates .
<
CRANIAL NERVE EFFERENTS (Ill, IV, VI, AND XII) IN CLINICAL ORIENTATION:
REPRESENTATIVE LESIONS AND DEFICITS
Mammillary body/nuclei
Interpeduncular fossa
Oculomotor nerve
Corticospinal and
corticonuclear fibers
Damage to oculomotor root
¢ Paralysis of most eye movement
on left; eye oriented down and out:
Superior oblique and lateral rectus
preserved
¢ Ptosis of left upper eyelid
¢ Left pupil dilated; diplopia
Red nucleus
Oculomotor nucleus
(GSE and GVE cells)
Cerebral
aqueduct and
:
periaqueductal grey
Oculomotor deficits from other causes
¢ Cerebral peduncle/Weber syndrome on
left = left-sided oculomotor paralysis:
Right-sided hemiplegia of UE/LE:
Paralysis of lower face on right: deviation
of tongue to right on protrusion
¢ Red nucleus/Claude syndrome on left =
left-sided oculomotor paralysis: Rightsided loss of proprioception, discriminativ
touch, and vibratory sense on UE: Right. |
sided hyperkinesia (red nucleus): Rightsided akinesia (substantia nigra)
¢ Benedikt syndrome = Weber + Claude
Medial longitudinal fasciculus
Substantia nigra
Decussation of superior
My
cerebellar peduncle
Damage to trochlear root
¢ Paralysis of left superior oblique muscle
¢ Diplopia; head-tilt to healthy right side
Lesion in medial longitudinal fasciculus
¢ Lesion on left = left internuclear
ophthalmoplegia (INO)
|
Superior oblique muscle —
Lateral rectus muscle—
Abducens nerve
Damage to abducens root
¢ Paralysis of left lateral rectus muscle
¢ Diplopia on left lateral gaze
Abducens deficits from other causes
¢ Caudal pontine base/Foville syndrome on
left = paralysis of left lateral rectus:
Right-sided hemiplegia UE/LE: Diplopia
ML in pons
¢ Lesion of facial colliculus on left =
paralysis of facial muscle on left and left
gaze palsy consisting of paralysis of left
Abducens nucleus
Facial colliculus :
Pyramid
Intrinsic tongue muscles andg
stylo-, hyo-, and genio-—>—=
glossus muscles
Hypoglossal nerve
>
ff
lateral rectus muscles and right internuclear ophthalmoplegia
¢ Lesion of abducens nucleus and adjacent MLF = one-and-a-half syndrome
Damage to hypoglossal root
* Deviation of the tongue to the left on
protrusion
A paid ota
Spinal trigeminal
tract and nucleus
Hypoglossal nucleus
—
Hypoglossal deficits from other causes
¢ Medial medullary/Déjérine syndrome on
left = deviation of the tongue to the left
on protrusion: Right-sided hemiplegia:
Right-sided loss of proprioception,
discriminative touch, and vibratory sense
on UE and LE
¢ Lesion of genu of internal capsule on
right = deviation of the tongue to left
on protrusion
longitudinal fasciculus. Additional examples of the causes of deficits related
Representative lesions of the roots of CNs III, IV, VI, and
e27INn1
of
and the deficits (in pink boxes) that correlate with each _ to these particular cranial nerves are also indicated. Note that lesions
XI
lesion.
the
of
side
the
on
deficits
motor
in
result
these cranial nerve roots
lesion. These are motor cranial nerves. Also shown is a lesion of the medial
‘i
a
‘
ee
a
e
Orientation
Tracts, Pathways, and Systems in Anatomical andClinical
— fe
CRANIAL NERVE EFFERENTS (V, VII, 1X, AND X) IN ANATOMICAL
The origin and peripheral distribution of fibers arising from
the motor nuclei of the trigeminal, facial, and glossopharyngeal and vagus (via the nucleus ambiguus) nerves; these are mixed
cranial nerves, having both motor and sensory functional components.
Also shown is the origin of GVE or VE preganglionic parasympathetic
fibers from the superior (to facial nerve) and inferior (to glossopharyngeal nerve) salivatory nuclei and from the dorsal motor vagal nucleus.
The functional component for cranial nerve motor nuclei innervating
muscles arising from pharyngeal arches may be classified as SE neurons
(see Figures 6-1 and 6-2). Muscles innervated by the trigeminal nerve
(V) come from the first arch, those served by the facial nerve (VII) from
the second arch; the stylopharyngeal muscle originates from the third
arch and is innervated by the glossopharyngeal nerve (IX), and the muscles derived from the fourth arch are served by the vagus nerve (X).
Neurotransmitters
The transmitter found in the cells of cranial nerve motor nuclei, and in
their peripheral endings, is acetylcholine; calcitonin gene-related peptide
(CGRP) is also colocalized in these motor neurons. This substance is also
present in preganglionic and postganglionic parasympathetic neurons.
Clinical Correlations
Patients with MG frequently have oropharyngeal symptoms and complications that result in dysarthria and dysphagia. These individuals
have difficulty chewing and swallowing, their jaw may hang open, and
the mobility of facial muscles is decreased. Impaired hearing (weakness
of tensor tympani) and hyperacusis (increased hearing sensitivity caused
by weakness of the stapedius muscle) also may be present.
Symptoms are: (1) a loss of pain, temperature, and touch on the ipsilateral face and in the oral and nasal cavities; (2) paralysis of ipsilateral
masticatory muscles (jaw deviates to the lesioned side when closed); and
(3) loss of the afferent limb of the corneal reflex may specify damage to
the fifth nerve (e.g., meningioma, trauma). If especially large (>2.0 to 2.5
cm), a vestibular schwannoma may compress the trigeminal nerve root
and result in a hemifacial sensory loss that may include the oral cavity.
Trigeminal neuralgia (tic douloureux) is an intense, sudden, intermittent
pain in the area of the cheek, oral cavity, or adjacent parts of the nose
(distribution of V2 or V3, see also Figure 8-7). One cause is an aberrant
loop of the superior cerebellar artery impinging on the trigeminal root
(see Figure 3-4).
Tumors (e.g., chordoma or vestibular schwannoma), trauma, or men-
ingitis may damage the seventh nerve, resulting in: (1) an ipsilateral facial
palsy (or Bell palsy); (2) loss of taste from the ipsilateral two-thirds of the
tongue; and (3) decreased secretion from the ipsilateral lacrimal, nasal, and
sublingual and submandibular glands. Injury distal to the chorda tympani
produces only an ipsilateral facial palsy. A paralysis of the muscles on one
side of the face with no paralysis of the extremities is a facial hemiplegia,
whereas intermittent and involuntary contraction of the facial muscles is
called hemifacial spasm. One cause of hemifacial spasm is compression of
the facial root by an aberrant loop from the anterior inferior cerebellar
artery. These patients also may have vertigo, tinnitus, or hearing loss suggesting involvement of the adjacent vestibulocochlear nerve.
Because of their common origin from NuAm, adjacent exit from the
medulla, and passage through the jugular foramen, the ninth and tenth
nerves may be damaged together (e.g., amyotrophic lateral sclerosis or
in syringobulbia). The results are dysarthria, dysphagia, dyspnea, loss of
taste from the ipsilateral caudal tongue, and loss of gag reflex. Damage
to structures at, or traversing, the jugular foramen results in combinations of deficits called jugular foramen syndromes. Internal to the foramen, the deficits may reflect injury to CNs IX, X (described above), and
XI (ipsilateral trapezius and sternocleidomastoid weakness), the Vernet
syndrome, while a lesion immediately external to the foramen may compromise CNs IX to XI plus XII (Collet-Sicard syndrome). In this latter
case, along with the other deficits, the tongue will deviate to the side
of the lesion on protrusion. Bilateral lesions of the tenth nerve may be
life-threatening because of the resultant total paralysis (and closure) of
the muscles in the vocal folds (vocalis muscle).
ABBREVIATIONS
AbdNu
ALS
BP
DVagNu
FacNr
FacNu
GINr
HyNu
ISNu
MesNu
ML
MLF
NuAm
PSNu
Abducens nucleus
Anterolateral system
Basilar pons
Dorsal motor nucleus of vagus
Facial nerve
Facial nucleus
Glossopharyngeal nerve
Hypoglossal nucleus
Inferior salivatory nucleus
Mesencephalic nucleus
Medial lemniscus
Medial longitudinal fasciculus
Nucleus ambiguus
Principal (chief) sensory nucleus
ORIENTATION
:
SpTNu
SpTTr
SSNu
TecSp
Spinal trigeminal nucleus
Spinal trigeminal tract
Superior salivatory nucleus
Tectospinal tract
TriMoNu
Trigeminal motor nucleus
TriNr
VagNr
Trigeminal nerve
Vagus nerve
Ganglia
1. Pterygopalatine
2. Submandibular
SOLE
4. Terminal and/or intramural
Review of Blood Supply to TriMoNu, FacNu, DMNu, and NuAm and the Internal Course of Their Fibers
Structures
Arteries
TriMoNu and Trigeminal Root
Long circumferential branches of basilar (see Figure 6-23)
FacNu and Internal Genu
Long circumferential branches of basilar (see Figure 6-23)
Branches of vertebral and posterior inferior cerebellar (see Figure 6-16)
DMNu
and NuAm
$$
ees
aes
Oe
8-21 CRANIAL NERVE EFFERENTS (V, VII, IX, AND X) IN ANATOMICAL
Position of nucleus
and internal
)
route of fibers
iN
eee
ae ew
ORIENTATION
TriMotNu
MLF
TecSp
Motor root
ALS
Structures
innervated
SEE
— EES
of TriNr
/
ML
Motor root
of TriNr
Masticatory muscles and
tensor tympani, tensor
veli palatini, mylohyoid,
and digastric (anterior
belly)
TriMotNu
ey,
AbdNu
Muscles of facial expression
and stapedius, buccinator,
stylohyoid, platysma, and
digastric (posterior belly)
ee
Lacrimal gland; mucous
o
membranes of nose
and mouth
Submandibular and
pvt
r)
sublingual glands
TS
Parotid gland
Stylopharyngeus
Striated muscle of pharynx,
larynx, and esophagus
~SpTTr and
SpTNu
fitt
Vay
:< be Thoracic and abdominal
viscera; smooth and
cardiac muscle; and
glandular epithelium
ine
=
v
ue
7
-
Seah, Fase
eget
phe
oe
r
d stem |
Masta; Pathways, anSy
CLINICAL ORIENTATION
CRANIAL NERVE EFFERENTS (V, VII, IX, AND X) IN
Trigeminal nerve
Masticatory muscles (including
medial and lateral pterygoids),
tensor tympani, tensor veli palatini,
mylohyoid, digastric (anterior belly)
Corticospinal (CSp)
fibers
Middle cerebellar
peduncle
Principal sensory trigeminal
nucleus
Basilar pons
Medial lemniscus (ML)
Anterolateral
|
system (ALS)
Trigeminal motor nucleus
Fourth ventricle
Superior cerebellar peduncle
ML at pons—medulla junction
CSp fibers
Facial nucleus
Muscles of facial expression,
stapedius, buccinator, stylohyoid, platysma, digastric
(posterior belly)
Facial nerve
ALS in medulla
Spinal trigeminal tract
(SpTTr) and nucleus (SpTNu)
Abducens nucleus
CSp fibers in pyramid
ML in medulla
Inferior olive
ALS in medulla
Stylopharyngeus muscle
Restiform body
Nucleus ambiguus
SpTTr + SpTNu
ALS in medulla
Striated muscles of pharynx,
larynx, including vocalis muscle
‘
and of upper esophagus
eer
PESTA
Nucleus ambiguus
Vagus nerve
SpTTr+ SpTNu
Nucleus ambiguus
Fourth ventricle
_ The nuclei and efferent fibers of CNs V, VII, IX, and X
superimposed on MRI (brainstem, T2-weighted MRI)
shown in clinical orientation. These are mixed (cranial) nerves and may
i
ML in medulla
contain somatomotor or visceromotor (preganglionic) fibers as well as
general sense or special sense fibers. The red fibers correlate with those
of the same color in Figure 8-21.
. : . . © ?’ eae
*
eres 23
:
CRANIAL NERVE EFFERENTS (V, VII, IX, AND X) IN CLINI
CAL ORIENTATION:
REPRESENTATIVE LESIONS AND DEFICITS
Masticatory muscles (including
medial and lateral pterygoids),
tensor tympani, tensor veli palatini,
mylohyoid, and digastric
(anterior belly)
Basilar pons
Damage to trigeminal root
* Paralysis of masticatory muscles
on left and slight deviation of jaw to right —
on closure
* Left-sided loss of pain, thermal sense,
and discriminative touch on face and in
oral cavity (including teeth)
° oe
of afferent limb of corneal reflex on
z
Middle cerebellar
peduncle
Principal sensory trigeminal
nucleus
[@
Trigeminal motor nucleus
Irritation of trigeminal root
* Trigeminal neuralgia (tic douloureux) on
left side of face
Superior cerebellar peduncle
ML at pons—medulla junction
edulla junction
Facial nucleus
Muscles of facial expression,
stapedius, buccinator, stylohyoid, platysma, and digastric
(posterior belly)
Facial nerve
Damage to facial root
* Paralysis of upper and lower facial
muscles on left
* Left-sided loss of pain/thermal sensation
on posterior surface of ear and part of
auditory canal
* Loss of taste on anterior two-thirds of
tongue on left
¢ Decreased secretions of lacrimal,
sublingual, and submaxillary glands and
mucous membranes of mouth
Facial deficits from other causes
Abducens nucleus
CSP fibers in pyramid
Lesion of genu of internal capsule
on right = left lower facial paralysis
Lesion of right internal facial genu =
paralysisof upper and lower facial
muscles on right
* Irritation of facial root = facial tic
on that side
ML in medulla
Stylopharyngeus muscle
Glossopharyngeal nerve
Nucleus ambiguus
SpTTr and SpTNu
ALS in medulla
Striated muscles of pharynx,
larynx, including vocalis ms.,
and of the upper esophagus
Vagus nerve
Nucleus ambiguus
Representative lesions of the roots of CNs V, VII, IX,
|O- 2 and X and the deficits (in pink boxes) that correlate with
each lesion. Also indicated are deficits related to the fifth and seventh
Damage to roots of IX and X
* Left-sided loss of pain/thermal sense
on tympanic membrane, external
auditory meatus, and posterior ear (small)
¢ Loss of taste (not testable)
¢ Loss of sensation on tonsils, hard/soft
palate, posterior pharyngeal wall,
posterior/root of tongue, fauces, and
eustachian tube opening
¢ Dysphagia, dysarthria, and hoarseness
¢ Glossopharyngeal neuralgia
¢ Loss of gag, palatal/uvular reflexes
¢ Lowering of left palatal arch, deviation
of uvula to right on phonation
cranial nerves that may originate from other causes. Note that lesions
of these cranial nerve roots result in motor deficits on the side of the
lesion.
.
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Tracts, Pathways, elses
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SPINAL AND CRANIAL NERVE REFLEXES
Examining reflexes is an essential part of any neurologic examination
because it provides information critical to the diagnosis of the neurologically compromised patient. All reflexes have an afferent limb (usually
a primary sensory fiber with a cell body in a ganglion) and an efferent limb (usually a fiber innervating skeletal muscle) originating from
a motor nucleus. The afferent fiber may synapse directly on the efferent neuron, in which case it is a monosynaptic reflex, or there may be
one, or more, interneurons insinuated between the afferent and efferent
limbs; these are polysynaptic reflexes. In many reflexes, the influence
on the motor neuron may be both monosynaptic and polysynaptic. In
the case of cranial nerves, polysynaptic reflexes may also be mediated
through the immediately adjacent reticular formation of the brainstem.
The primary sensory fiber may also be regarded as the first-order
neuron in a pathway. Although the first-order neuron may participate
in a reflex, via a collateral branch to motor neurons, it also contributes
information to ascending pathways. The primary sensory fiber may synapse directly on a tract cell, or may communicate through interneurons.
In either case, this tract cell is regarded as the second-order neuron in
the pathway.
__—
Spinal reflexes may rely on sensory/afferent information that arises
from the body, enters the spinal cord, influences lower motor neurons,
and results in an appropriate response. The same principle applies to
cranial nerve reflexes. The afferent input enters the brainstem on a
cranial nerve and may influence motor neurons, or join a sensory tract,
and the efferent outflow exits the brainstem on the same, or another, cranial nerve. Because of these structural/functional similarities, the reflex
circuits are placed at this location in Chapter 8, following “Sensory
and Motor Pathways and Cranial Nerves.” The circuits for the more
routinely tested reflexes are described; this is not intended as an allinclusive list.
Particularly brisk or hyperactive reflexes, commonly demonstrated
in muscle stretch reflexes, are specified as hyperreflexia. Decreased or
hypoactive reflexes are described as hyporeflexia. A complete absence of
reflex activity in response to a proper stimulus is areflexia. These deviations from normal may be seen in spinal reflexes as well as in cranial
nerve reflexes. The aberrations from normal reflex activity may indicate
peripheral nerve disease or injury/disease of the brainstem, spinal cord,
or forebrain.
Ascending fibers conveying proprioception from lower extremity
Posterior root
_— Posterior root ganglion
|
——Muscle spindles in
quadriceps muscles
"~Extensor muscles of lower
a
= Inhibitory interneurons
extremity containing
Anterior root
activated spindles
Flexor muscles of
lower extremity
The muscle stretch reflex (also called a stretch or myotatic
reflex) is sometimes incorrectly called a tendon reflex or deep
tendon reflex (these are clear misnomers); the receptor for this reflex is
the muscle spindle (within the muscle itself, hence muscle stretch reflex
is the correct designation).
The afferent limb is activated by tapping the tendon of a muscle
and momentarily stretching muscle spindles (primary or secondary)
within the muscle. These action potentials are propagated on A-alpha
(13 to 20 mm in diameter, 80 to 120 m/s conduction velocity) or A-beta
(6 to 12 mm, 35 to 75 m/s) fibers. Their cell bodies are in posterior root
ganglia; these fibers monosynaptically excite motor neurons innervating
the muscle from which the afferent volley arose, and the muscle contracts, precipitating the reflex. Collaterals of the afferent axons synapse
on interneurons that, in turn, inhibit motor neurons innervating antagonistic muscles.
Muscle stretch reflexes test the functional integrity of different spinal
levels. Examples of these reflexes, and their corresponding levels are: triceps
(C7—-C8), biceps (C5-C6), brachioradialis (C5—C6), Achilles/ankle jerk
(S1), patellar/knee jerk (L2-L4), and the finger flexor (C7-C8). Concurrent
with the reflex, the central processes send ascending collaterals that relay
information to the nuclei gracilis or cuneatus, depending on the level of
the input, and the sensation is perceived. The patellar reflex is shown here.
ee
Wey
Bielerracer eweriioes"
5
Posterior root
Ascending fibers
conveying pain to VPL
__
Posterior root ganglion
Anterolateral system
Receptors for
pain and
thermal
sensations
.
e—"TL_—S
T=
Inhibitory interneuron
OS Extensor muscles
of lower extremity
Anterior root
e—"-—T—Sr"= Excitatory interneuron
Flexor muscles of
lower extremity
---—-‘ The nociceptive reflex (also called a withdrawal reflex or
flexor reflex) is activated by tissue damage; action potentials
are propagated on A-delta (1 to 5 mm in diameter, 5 to 30 m/s conduction velocity) and C (0.2 to 5.0 mm, 0.5 to 2 m/s) fibers. These
afferent fibers have cell bodies in the posterior root ganglion and they
terminate on inhibitory and/or excitatory spinal interneurons. When a
patient steps on a nail, extensor motor neurons of the stimulated LE are
inhibited and flexor motor neurons of the stimulated lower extremity
are excited, and the extremity is pulled away from the noxious stimulus.
The same principle and arrangement of circuits applies when the hand
encounters a noxious stimulus and the upper extremity is withdrawn.
Concurrent with this reflex, the recognition of pain is achieved via second-order neurons that ascend in the ALS on the contralateral side of
the spinal cord.
_/
ev
= !nhibitory interneuron
Posterolateral tract
Posterior root
e—-——
‘= Excitatory interneuron
_—
Posterior root ganglion
/ Receptors for
pain and
thermal
sensations
oe:
Extensor muscles
muscles
of lower extremity
Anterior root
of lower extremity
Flexor muscles of lower extremity
~~ we The crossed extension reflex affects extremities on both sides
of the body. The afferent fibers, their input to spinal interneurons, and their respective action (excitatory/inhibitory) on flexor and
extensor spinal motor neurons on the side of the noxious stimulus is the
same as in the nociceptive reflex (see Figure 8-24). The stimulus occurs
and the extremity on that side is withdrawn. In an effort to maintain
Flexor muscles of
lower extremity
stability, when an injured foot is withdrawn on the side of the stimulus,
the opposite LE is extended to maintain posture and balance. Consequently, on the side opposite the stimulus, flexor motor neurons are
inhibited and extensor motor neurons are excited and the relative posture of the patient is maintained. This reflex also gives rise to ascending
information that reaches a conscious level of perception.
|
ee
de
Tracts, Pathways, and Syst ms inAnat2micaland¢
3
Posterior root
__—
Posterior root ganglion
__— Cutaneous
= Excitatory interneuron
le
Deep back muscles—
_
arises from receptors on A-delta and C fibers. It is mediated
through lower thoracic spinal levels (T8-T11) and is activated by lightly
stroking the abdomen about 4 to 5 cm lateral to, and parallel with,
the midline. The afferent fibers enter the posterior root and synapse on
interneurons. Some of these are excitatory interneurons that, in turn,
excite lower motor neurons that innervate the abdominal musculature; the muscles of the abdomen contract and the trunk flexes slightly.
Ascending fibers conveying pain to VPM
Other interneurons inhibit the alpha motor neurons that are innervating deep back muscles; inactivation of these motor neurons decreases
the tension in the deep back muscles and increases the efficacy of the
abdominal reflex. These deep back muscles extend the trunk. A normal response is occurring when the abdominal muscles contract and the
umbilicus rotates slightly to the stimulated side. The sensations created
by stroking the abdominal wall will also enter ascending spinal cord
pathways and are consciously perceived by the patient.
Pain receptors in cornea
\
Trigeminal ganglion
O
Ss
—
ae
~Trigeminal sensory root
Anterior trigeminothalamic ee
Spinal trigeminal tract
Facial nucleus
e
\
Facial nucleus
Ne
=~
Facial muscles
<S
a
beta
The
limb
_-— Abdominal muscles
ete SesInhibitory interneuron
R 2 4, - The abdominal reflex is a cutaneous reflex; the afferent limb
TAY
receptors
corneal reflex (also called the lid reflex) has its afferent
in the trigeminal nerve (CN V) and its efferent limb
in the facial nerve (CN VII). An irritating stimulus to the cornea activates C fibers, the cell bodies of which are in the trigeminal ganglion.
These axons enter the brainstem on the trigeminal nerve, descend in the
spinal trigeminal tract, and terminate in the spinal trigeminal nucleus,
pars caudalis. Pars caudalis neurons project to the contralateral ventral
posteromedial thalamic nucleus and, en route, send collaterals to the
Facial muscles
Facial nerve
—
Spinal trigeminal tract
a
trigeminal nucleus, pars caudalis
facial motor nucleus bilaterally; the facial response is generally more
active on the side of the stimulation. Axons of the motor neurons in
the facial nucleus exit in the facial nerve to eventually exit the skull via
the stylomastoid foramen. Axons in the zygomatic branch of the facial
nerve innervate the orbicularis oculi muscle and the eyelids close in
response to a noxious stimulus of the cornea. The noxious information
being relayed via ascending fibers eventually reaches conscious perception via anterior trigeminothalamic fibers.
ies
[EE
peels nucleus
es
tract
Masseter and temporalis Swan
(Kee
f
Trigeminal motor root
Trigeminal motor root
Muscle spindles in masseter
and temporalis muscles
OHS)
Trigeminal motor nucleus
e*
Trigeminal motor nucleus
S
De. WE
(™
‘ 8-28
The jaw jerk reflex (also called the jaw-jerk or mandibular
a:
reflex) is a cranial nerve version of a spinal muscle stretch
reflex; this reflex is mediated through the trigeminal nerve (CN V). The
axons of the afferent limb synapse on the motor neurons that innervate
skeletal muscles (it is a monosynaptic reflex). A gentle tap on the chin
stretches muscle spindles in the temporalis and masseter muscles, initiating
action potentials on A-alpha (primary muscle spindles) and A-beta (secondary muscle spindles) fibers. These fibers enter the brain on the sensory
root of the trigeminal nerve, and have their primary afferent cell bodies
in the mesencephalic nucleus. Collaterals of these afferent fibers project
directly, and bilaterally, to the trigeminal motor nucleus; axons of these
motor cells exit via the motor root of the trigeminal nerve to innervate
the temporalis and masseter muscles, resulting in jaw closure in response
to the tap on the chin. This information also reaches a conscious level: the
patient perceives the tap on the chin. The jaw-jerk reflex is often increased/
brisk (hyperreflexia) in patients with amyotrophic lateral sclerosis.
Pain receptors
Ascending fibers conveying pain to <a SE
—S
eS
+
Trigeminal ganglion
Trigeminal sensory root
Anterior trigeminothalamic fibers
Superior salivatory nucleus
Superior salivatory nucleus
Facial nerve
Lacrimal gland, nasal sae
Pterygopalatine ganglion
eee
gland, nasal glands
Pterygopalatine ganglion
Spinal trigeminal tract
Spinal trigeminal nucleus, pars caudalis
There are a variety of reflexes in which sensory input results
in a visceral motor response. Examples are the lacrimal (tearsalivatory reflexes. The lacrimal reflex is used here as an
the
and
ing)
somatovisceral reflex. The afferent limb is activated by
a
of
example
C fibers and A-delta receptors/fibers in the cornea and
of
stimulation
sclera. This afferent message enters the brainstem on the trigeminal
nerve (cell bodies in the trigeminal ganglion), descends within the spinal
trigeminal tract, and synapses in the spinal trigeminal nucleus, pars caudalis. Collaterals of ascending trigeminothalamic fibers (en route to the
ventral posteromedial thalamic nucleus) send collaterals into the superior salivatory nucleus (SSN) either directly (shown here), or through
interneurons, where they synapse. Parasympathetic preganglionic fibers
from the SSN exit on the facial nerve, travel to the pterygopalatine
ganglion, where they synapse, and the postganglionic fibers course to
the lacrimal gland and to mucous membranes of the nose. A nocuous
stimulus to the cornea results in tearing and increased nasal secretions
and the discomfort is perceived through ascending fibers that eventually
influence the sensory cortex.
Nucleus ambiguus
Glossopharyngeal nerve
Superior ganglion of IX
Receptors in caudal mouth
Stylopharyngeus muscle
Stylopharyngeus muscle
Constrictor and palatal muscles
Constrictor and palatal muscles
Vagus nerve
a
= Excitatory interneuron
The gag reflex (also called the faucial reflex) is mediated
through the glossopharyngeal (CN IX) and the vagus (CN X)
nerves. The afferent limb is activated by cutaneous stimulation of A-delta
and probably C fibers on the caudal base of the tongue and/or caudal
roof of the mouth (soft palate). This space between the mouth and pharynx is the fauces, hence the term faucial reflex. The afferent limb is via
CN IX with its cell bodies in the superior ganglion of CN IX; the central
terminations are in the nucleus ambiguus, either directly or through interneurons (both shown here). The efferent limb from the nucleus ambiguus
travels on CNs IX and X to the stylopharyngeus muscle (via IX), to the
pharyngeal constricter muscles, and to muscles that move the palate
(via X). In response to irritation in the caudal oral cavity, the pharynx
constricts and elevates in an attempt to extrude the offending object, and
the discomfort is perceived through pathways to the cerebral cortex.
Trigeminal ganglion
Ascending fibers conveying sensation to VPM
Pee
hehe
cutaneous
receptors
Principal sensory
nucleus —____ >,
Anterior trigeminothalamic ta]
Spinal trigeminal tract
Facial nucleus
me
Facial muscles
Nucleus ambiguus
Glossopharyngeal nerve
Stylopharyngeus muscle
Vagus nerve
Pharyngeal, laryngeal, palatal muscles—.
Trapezius, sternocleidomastoid muscles—
Intrinsic/extrinsic tongue eae
Accessory nucleus
Aq
There are a variety of reflexes seen in infants mediated by CNs
~—
V, VII, IX, or XI and XII. Examples of these are the snout,
sucking, and rooting reflexes; they usually disappear by about 1 year of
age. These are commonly referred to as “primitive reflexes.” However,
these reflexes may reappear in patients with dementia, or in individuals
with degenerative diseases, or dysfunction, of the frontal lobe.
The afferent limb for these reflexes is via CN V and is activated by
touching around (snout, rooting), or in (sucking), the mouth opening.
These afferent fibers enter the brainstem via CN V and have cell bodies in
the trigeminal ganglion. They terminate in the spinal trigeminal nucleus
(information relayed on A-delta fibers from free nerve endings) and in
the principal sensory nucleus (information relayed on A-beta fibers from
endings such as Meissner corpuscles and Merkel cell complexes).
ei
Accessory nerve
Hypoglossal nerve
Spinal trigeminal nucleus
Hypoglossal nucleus
Secondary trigeminal fibers, en route to the ventral posteromedial
nucleus of the thalamus from both the spinal trigeminal and principal sensory nuclei, send collaterals to the facial nucleus, the nucleus
ambiguus, the accessory nucleus, and the hypoglossal nucleus, either
directly, or via interneurons located in the reticular formation (only
the direct are shown here). In response to stimulation around, or in,
the mouth opening, the infant’s facial muscles respond (via the facial
nucleus), the head orients toward or away from the source of the stimulus (accessory nucleus), the laryngeal and pharyngeal muscles contract
during sucking (nucleus ambiguus), and the tongue moves in and out
of the mouth or protrudes toward the stimulus (hypoglossal nucleus).
These reflexes are absolutely essential to survival (orienting toward
nutrition, sucking, tongue, and facial muscle responses).
SaandSra NeveRtas a
Sphincter pupillae
ve and
ciliary muscles
=—Sphincter pupillae and ciliary muscles
Short ciliary nerves—
Ciliary ganglion—r
— Short ciliary nerves
(parasympathetic postganglionic)
cy, va
\
ganglion
Optic chiasm
—Parasympathetic preganglionic fibers in CN Ill
Oculomotor nerve
Oculomotor nerve
Optic tract
Crus cerebri
Edinger—Westphal
preganglionic nucleus
Lateral geniculate nucleus
Brachium of superior colliculus
Pulvinar
nucleus
Pretectal nucleus
Posterior commissure
‘The
pupillary light reflex (also called the pupillary reflex or
light
reflex) has its afferent limb in the optic nerve (CN II)
and its efferent limb in the oculomotor nerve (CN III).
Light shined in the eye results in the neural activity conveyed on fibers of the optic nerve, optic chiasm (where some cross), optic tract, and
the brachium of the superior colliculus, which synapse bilaterally in the
pretectal area/nucleus.
The Edinger-Westphal complex consists of two portions both of
which are immediately adjacent to the oculomotor nucleus (see Figure
6-28). The Edinger—Westphal centrally projecting nucleus (EWcpNu)
projects to a number of central targets such as the spinal cord, posterior
column, parabrachial, trigeminal, and facial nuclei, but not to the ciliary
ganglion. The Edinger—-Westphal preganglionic nucleus (EWpgNu) preferentially projects to only the ciliary ganglion; these EWpgNu cells are
the parasympathetic preganglionic neurons of the third cranial nerve.
After receipt of retinal input via the above pathway, both pretectal areas
project bilaterally to the EWpgNu. In turn, the EWpgNu sends parasympathetic preganglionic fibers on the ipsilateral oculomoter nerve to
the ciliary ganglion, which in turn sends postganglionic fibers, as short
ciliary nerves, to the sphincter pupillae muscle of the iris. In the normal
patient, light shined in one eye will result in a pupillary reflex in that eye
(direct response) and in the opposite eye (consensual response).
Example One; In the case of a patient with previously diagnosed ret-
initis pigmentosa and absolutely no perception of light in that eye, when
a light is shined in the blind eye, the patient has a direct and consensual pupillary light reflex. The explanation of this response is that there
is a small population (<1%) of melanopsin-containing ganglion cells
in the retina that are characterized by large cell bodies and expansive
dentritic fields. These cells are intrinsically sensitive to light, do not rely
on input from rods or cones, and project to central targets such as the
suprachiasmatic nucleus and the EWpgNu. Melanopsin ganglion cells
do not appear to participate in form recognition (vision, actually seeing/
recognizing things in visual space). Their presence not only explains the
pupillary reflex in a blind eye, but is the likely explanation of the fact
that some patients who are blind in both eyes may have reasonably
normal circadian rhythms.
Example Two: In the case of a patient with a lesion of the optic nerve
and a light is shined in the eye on the lesioned side, this patient perceives
no light in that eye, both the direct and consensual pupillary responses
are absent, and the afferent limb of the reflex is interrupted. In this
example, there is no input to either of the pretectal areas from the eye
on the side with the optic nerve lesion.
Example Three: In the case of a patient with a lesion of one optic
nerve and a light is shined in the eye opposite the side of the lesion (the
good eye), this patient perceives the light in this eye, and there is both
a direct and consensual response. In this example, the afferent limb to
both pretectal nuclei is intact, and there is a response in the blind eye
because its efferent limb is intact.
Example Four: In the case of a patient with a lesion of the oculomotor nerve on one side and a light is shined in the eye on the side of
the lesion, the patient perceives the light (the afferent limb is intact) but
there is no direct response in that eye; the efferent limb is interrupted
by the lesion. There is a consensual response in the opposite eye in this
situation. If the light is shined in the eye on the side opposite the oculomotor root lesion, the light is perceived, and there is a direct response
but no consensual response.
>
Tracts, Pathways, and systems inAnatomical « nd Clinigat Or ent:
Table 8-1 Flow Diagrams of Additional Common Reflexes*
Receptors in -——————--_-_-_-——>_
eecienihenee
to nucleus ambiguus
jection
i
i
projection
i
al
> Trigeminal
jecti
to spin
Projection
(NuAmb) and reticular formation (RetFor)
trigeminal nucleus
i
ies
in
Cell bodies
trigeminal ganglion
'
~<———.
Phrenic nucleus to diaphragm
and anterior horn cells
Patient sneezes >
NuAmb and RetFor to phrenic
nucleus and anterior horn cells
to intercostal muscles
Vomiting
Cell bodies in inferior vagal, ——and posterior root ganglia
Receptors in the pharynx and gut
travel via the vagus and splanchnic
Reticulospinal fibers to intermediolateral
cell column (IMLCC), to phrenic nucleus,
and anterior horn cells
IMLCC projects to sympathetic preganglionic <——
cells, DVagNu to preganglionic parasympathetic
cells, phrenic nucleus to diaphragm, anterior
horn cells to intercostal muscles
Smooth muscles of gut activated, intercostal >
muscles and diaphragm activated
<———
Projection to solitary nucleus (SolNu),
dorsal motor vagal nucleus (DVagNu)
SolNu and DVagNu project to RetFor
and to intramural ganglia via DVagNu
Patient vomits (Note that a gag reflex
may proceed on to a vomiting reflex)
Swallowing
i
Receptors in larynx ——_—__—_—>
and pharynx
Patient swallows
Cell bodies in inferior———
ganglia of CNs 9 and 10
~—————
Contraction along length
of esophagus
<—_——.
Project to DVagNu and SolNu;
SolNu projects to DVagNu
DVagNu projects to intramural
ganglia in esophagus
Baroreceptor
Receptors in carotid ———_
body and aortic arch
>
Peripheral vascular tone and ~~
cardiac rate and output increased
|
Cell bodies in inferior ——————-_
ganglia of CNs 9 and 10
Projects to SolNu; SolNu projects to DVagNu and
to vasopressor neurons in medulla (VaPress)
IMLCC projects to postganglionic cells ~————
serving heart and peripheral vessels
VaPrress projects to IMLCC via reticulospinal fibers
(DVagNu activity is decreased while sympathetic
activity is increased)
Patient’s blood pressure and cardiac output
maintained upon rising from a recumbent
position
Vagovagal
Sh
ee
nen
Vagal receptors may be in airway, thorax, ———_>
abdomen (may be mechanical stimulation)
Me RO
Pere
Cell bodies in inferior——__________
ganglia of CN 10
Postganglionic parasympathetic fiber activation <-—DVVagNu projects to intramural ganglion ~-results in (vagal cardioinhibition)
in thoracic and abdominal nieeers
SolNu
Projects to SolNu
projects t
scr
ay cae
Patient experiences bradycardia, hypotension,
palor, and light-headedness
eee
EEE
thes reflexes are mediated through the brainstem. As is the case with brainstem reflexes, the
* All off these
nuclei, within the brainstem, only the basic pathways are diagrammed here.
iia
IU
eN
BLANK DRAWING
8.33
FOR THE SPINAL CORD AND BRAINSTEM
Blank master drawings for spinal cord and cranial nerve/
brainstem reflexes. These illustrations are provided for
self-evaluation of the understanding of circuits related to reflexes, for
the instructor to expand on reflexes not covered in this Atlas, or for both
activities. For a wider variety of review possibilities, a cervical spinal
cord level and brainstem diagram is given here.
ae A
ie
oe.
Saree
ie
Pattaya SystemsinAnatomica!andCh
Tats
-<
eae
ian eee
25
SPINOCEREBELLAR TRACTS IN ANATOMICAL
~The origin, course, and distribution pattern of fibers to the
cerebellar cortex and nuclei from the spinal cord (posterior
{dorsal] and anterior [ventral] spinocerebellar tracts, rostral spinocerebellar fibers) and from the accessory (latera!) cuneate nucleus (cuneocerebellar fibers). Also illustrated is the somatotopy of those fibers that enter
the cerebellum via the restiform body, the larger portion of the inferior
cerebellar peduncle, or in relationship to the superior cerebellar peduncle. Recall that restiform body+juxtarestiform body equals the inferior
cerebellar peduncle. After these fibers enter the cerebellum, collaterals
are given off to the cerebellar nuclei while the parent axons of spinocerebellar and cuneocerebellar fibers pass on to the cortex, where they end as
mossy fibers in the granule cell layer. Although not shown here, there are
ascending spinal projections to the medial and dorsal accessory nuclei of
the inferior olivary complex (spino-olivary fibers). The accessory olivary
nuclei (as well as the principal olivary nucleus) project to the cerebellar
cortex and send collaterals into the nuclei (see Figure 8-35).
Ks
>
PTh
ORIENTATION
Clinical Correlations
Ly
Neurotransmitters
Glutamate (+) is found in some spinocerebellar fibers, in their mossy
fiber terminals in the cerebellar cortex, and in their collateral branches
that innervate the cerebellar nuclei.
Lesions, or tumors, that selectively damage only spinocerebellar fibers
are rarely, if ever, seen in humans. The ataxia one might expect to see in
patients with a spinal cord hemisection (e.g., the Brown-Séquard syndrome) is masked by the hemiplegia of the ipsilateral UE and LE resulting from the concomitant damage to lateral corticospinal (and other)
fibers. On the other hand, there are numerous spinocerebellar ataxias
that are genetically based and may damage the cerebellum or its afferent
fiber bundles.
Friedreich ataxia (hereditary spinal ataxia) is an autosomal recessive
disorder, the symptoms of which usually appear between 8 and 15 years
of age. There is degeneration of anterior and posterior spinocerebellar
tracts plus the posterior columns and corticospinal tracts. Degenerative changes are also seen in cerebellar Purkinje cells, in posterior root
ganglion cells, in neurons of the Clarke column, and in some nuclei of
the pons and medulla. These patients have ataxia (early onset), dysarthria, muscle weakness/paralysis (particularly in the LEs), and skeletal
defects. The axial and appendicular ataxia seen in these patients correlates partially with the spinocerebellar degeneration and also partially
with proprioceptive losses via the degeneration of posterior column
fibers.
ABBREVIATIONS
ACNu
ALS
AMV
ASCT
Cbl
CbINu
CCbIF
DNuC
FNL
IZ
Ls
MesNu
ML
PRG
Accessory (lateral) cuneate nucleus
Anterolateral system
Anterior medullary velum
Anterior (ventral) spinocerebellar tract
Cerebellum
Cerebellar nuclei
Cuneocerebellar fibers
Dorsal nucleus of Clarke
Flocculonodular lobe
Intermediate zone
Lumbar representation
Mesencephalic nucleus
Medial lemniscus
Posterior (dorsal) root ganglion
PSCT
PSNu
Py
RB
RSCF
RuSp
S
SBC
SCP
SpTNu
SpTTr
iD
TriMoNu
VesNu
Posterior (dorsal) spinocerebellar tract
Principal (chief) sensory nucleus of trigeminal nerve
Pyramid
Restiform body
Rostral spinocerebellar fibers
Rubrospinal tract
Sacral representation
Spinal border cells
Superior cerebellar peduncle
Spinal trigeminal nucleus
Spinal trigeminal tract
Thoracic representation
Trigeminal motor nucleus
Vestibular nuclei
Review of Blood Supply to Spinal Cord Gray Matter, Spinocerebellar Tracts, RB, and SCP
Structures
Arteries
Spinal Cord Gray
Branches of central artery (see Figure 6-8)
PSCT and ASCT in Cord
Penetrating branches of arterial vasocorona (see Figure 6-8)
RB
Posterior inferior cerebellar (see Figure 6-16)
SCP
Long circumferential branches of basilar and superior cerebellar (see Figure 6-23)
Posterior and anterior inferior cerebellar and superior cerebellar
Cerebellum
eee
=
ts
vi
S AN
ih
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oo
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Soy
aN =
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i
ty
:
mee:
ao aN ot
i
7
J
ae i
Cerebellum and Basal Nuclei
8-34 SPINOCEREBELLAR TRACTS IN ANATOMICAL
ORIENTATION
Position of SCP
Lobules II-lV
Anterior
Lobule
\\
V
lobe
Recrossing ASCT
fibers in Cbl
Posterior lobe
Paes
i]
Lobule VIII
Lobule VIII
Somatotopy position
Lamina VII
at C4—C8
Cerebellar atrophy — Familial, Sporadic, and
Inherited types
ASCT
Intermediate
zone (IZ) and
"spinal border"
cells (SBC)
AR,
PONTOCEREBELLAR, RETICULOCEREBELLAR, OLIVOCEREBELLAR, CERULEOCEREBELL
HYPOTHALAMOCEREBELLAR, AND RAPHECEREBELLAR FIBERS IN
ANATOMICAL ORIENTATION
Afferent fibers to the cerebellum from selected brainstem areas
4
and the organization of corticopontine fibers in the internal
~~
capsule and crus cerebri are shown here. Pontocerebellar axons are mainly
crossed, reticulocerebellar fibers may be bilateral (from RetTegNu) or
mainly uncrossed (from LRNu and PRNu), and olivocerebellar fibers
(OCDbIF) are exclusively crossed. Raphecerebellar, hypothalamocerebellar, and ceruleocerebellar fibers are, to varying degrees, bilateral projections. Although all afferent fibers to the cerebellum give rise to collaterals
to the cerebellar nuclei, those from pontocerebellar axons are relatively
small, having comparatively small diameters. Olivocerebellar axons end
as climbing fibers, reticulocerebellar and pontocerebellar fibers as mossy
fibers, and hypothalamocerebellar and ceruleocerebellar axons end in all
cortical layers. These latter fibers have been called multilayered fibers in
the literature because they branch in all layers of the cerebellar cortex.
Neurotransmitters
Glutamate (+) is found in corticopontine projections and in most pontocerebellar fibers. Aspartate (+) and corticotropin (+)-releasing factor are
present in many olivocerebellar fibers. Ceruleocerebellar fibers contain
noradrenalin, histamine is found in hypothalamocerebellar fibers, and
some reticulocerebellar fibers contain enkephalin. Serotonergic fibers to
the cerebellum arise from neurons found in medial areas of the reticular
formation (open gray cell in Figure 8-35 on the facing page) and, most
likely, from some cells in the adjacent raphe nuclei.
Clinical Correlations
ge
ne
eee
Te
Common symptoms seen in patients with lesions involving nuclei and
tracts that project to the cerebellum are ataxia (of trunk or limbs), an
ataxic gait, dysarthria, dysphagia, and disorders of eye movement such
as nystagmus. These deficits are seen in some hereditary diseases (e.g.,
olivopontocerebellar degeneration, ataxia telangiectasia, or hereditary
cerebellar ataxia), in tumors (brainstem gliomas), in vascular diseases
(lateral pontine syndrome), or in other conditions, such as alcoholic
cerebellar degeneration or pontine hemorrhages.
Examples of other lesions that result in cerebellar signs and symptoms are cerebellopontine angle lesions (CPA), cerebellar infarction, and
cerebellar liponeurocytoma. About 80% to 90% of CPA tumors are
vestibular schwannoma, the remaining comprise meningioma (at 5% to
10%). Cerebellar stroke is relatively rare, seen in <1% of all CT. Early
signs/symptoms are characteristic of cerebellar damage; nausea/vomiting,
vertigo/dizziness, nystagmus, truncal ataxia, and others. Cerebellar
liponeurocytoma are found only in the cerebellum in patients of ~50 years
of age. (See Figures 8-36 and 8-38A, B for more information on cerebellar
lesions.)
ABBREVIATIONS
AntLb
CbINu
CerCblF
CPonF
CSp
DAO
FPon
Hyth
HythCblIF
IC
IO
LoCer
LRNu
MAO
MCP
ML
NuRa
OCDbIF
OPon
PCbIF
Anterior limb of internal capsule
Cerebellar nuclei
Ceruleocerebellar fibers
Cerebropontine fibers
Corticospinal fibers
Dorsal accessory olivary nucleus
Frontopontine fibers
Hypothalamus
—= Hypothalamocerebellar fibers
Internal capsule
Inferior olive
Nucleus (locus) ceruleus
Lateral reticular nucleus
Medial accessory olivary nucleus
Middle cerebellar peduncle
Medial lemniscus
Raphe nuclei
Olivocerebellar fibers
Occipitopontine fibers
Pontocerebellar fibers
PostLb
Posterior limb of internal capsule
PonNu
Pontine nuclei
PO
Principal olivary nucleus
PPon
Parietopontine fibers
PRNu
Paramedian reticular nuclei
Py
Pyramid
RB
Restiform body
RCDbIF
Reticulocerebellar fibers
RetLenLb __ Retrolenticular limb of internal capsule
RNu
Red nucleus
RetTegNu —_ Reticulotegmental nucleus
SEP.
Superior cerebellar peduncle
SubLenLb — Sublenticular limb of internal capsule
SN
Substantia nigra
TPon
Temporopontine fibers
Number Key
1. Nucleus raphe, pontis
2. Nucleus raphe, magnus
3. Raphecerebellar fibers
Review of Blood Supply to Precerebellar Relay Nuclei in Pons and Medulla, MCP, and RB
Structures
Arteries
Pontine Tegmentum
Long circumferential branches of basilar plus some from superior cerebellar (see Figure 6-23)
Paramedian and short circumferential branches of basilar (see Figure 6-23)
Basilar Pons
Medulla RetF and IO
MCP
RB
Branches of vertebral and posterior inferior cerebellar (see Figure 6-16)
Long circumferential branches of basilar and branches of anterior inferior and superior cerebellar
(see Figure 6-23)
Posterior inferior cerebellar (see Figure 6-16)
eee
—
um i
llNucle
beBasal
Gereand
8-35 PONTOCEREBELLAR, RETICULOCEREBELLAR, OLIVOCEREBELLAR,
CERULEOCEREBELLAR, HYPOTHALAMOCEREBELLAR, AND RAPHECEREBELLAR FIBERS IN
ANATOMICAL ORIENTATION
Position of associated
tracts and nuclei
__
AntLb
(FPon)
PostLb
(PPon)
SubLenLb
(TPon)
RetLenLb
(OPon)
\
\
\PonNu
1
th
/
/ PCbIF
\
|S-
cos
SR Rent
Se n
Marrs
AN 2
Tracts, Pathways, and Systems in Anatomical and linical Orient
CEREBELLAR CORTICONUCLEAR, NUCLEOCORTICAL, AND CORTICOVESTIBULAR
FIBERS IN ANATOMICAL ORIENTATION
Cerebellar corticonuclear fibers arise from all regions of the
cortex and terminate in an orderly (mediolateral and rostrocaudal) sequence in the ipsilateral cerebellar nuclei.
Corticonuclear fibers from the vermal cortex terminate in the fastigial
nucleus, those from the intermediate cortex in the emboliform and globose
nuclei, and those from the lateral cortex in the dentate nucleus (DNu). Also,
cerebellar corticonuclear fibers from the anterior lobe typically terminate
more rostrally in these respective nuclei whereas those from the posterior
lobe terminate more caudally. Cerebellar corticovestibular fibers originate
primarily from the vermis and flocculonodular lobe, exit the cerebellum via
the juxtarestiform body, and end in the ipsilateral vestibular nuclei. Corticonuclear and corticovestibular fibers arise from Purkinje cells.
Nucleocortical processes originate from cerebellar nuclear neurons and
pass to the overlying cortex in a zone pattern that reciprocates the corticonuclear projection; they end as mossy fibers. Some nucleocortical fibers are
collaterals of cerebellar efferent axons. The cerebellar cortex may influence
the activity of lower motor neurons through many combinations of circuits, for example, the cerebellovestibular—vestibulospinal route.
Neurotransmitters
y-Aminobutyric acid (GABA) (-) is found in Purkinje cells and is the
principal transmitter substance present in cerebellar corticonuclear and
corticovestibular projections. However, taurine (—) and motilin (—) are
also found in some Purkinje cells. GABA-ergic terminals are numerous
in the cerebellar nuclei and vestibular complex. Some of the glutamatecontaining mossy fibers in the cerebellar cortex represent the endings
of nucleocortical fibers that originate from cells in the cerebellar nuclei.
Clinical Correlations
Numerous disease entities can result in cerebellar dysfunction, including
viral infections (echovirus), hereditary diseases (see Figure 8-35), trauma,
tumors (glioma, medulloblastoma), occlusion of cerebellar arteries (cerebellar stroke), arteriovenous malformations, developmental errors (e.g.,
the Dandy-Walker syndrome or the Arnold—Chiari deformity), or the
intake of excessive alcohol or of toxins. Damage to only the cortex results
in transient deficits unless the lesion is quite large or causes an increase
in intracranial pressure. However, lesions involving both the cortex and
nuclei, or only the nuclei, may result in long-term deficits.
Lesions involving midline structures (vermal cortex, fastigial nuclei)
and/or the flocculonodular lobe result in truncal ataxia (titubation or
tremor), nystagmus, and head tilting. These patients may also have a
wide-based (cerebellar) gait, are unable to walk in tandem (heel to toe),
and may be unable to walk on their heels or on their toes. Generally,
midline lesions result in bilateral motor deficits affecting axial and prox-
imal limb musculature.
Damage to the intermediate and lateral cortices and the globose,
emboliform, and dentate nuclei results in various combinations of the following: dysarthria, dysmetria (hypometria, hypermetria), dysdiadochokinesia, tremor (static, kinetic, intention), rebound phenomenon, unsteady
and wide-based (cerebellar) gait, and nystagmus. A commonly observed
deficit in patients with cerebellar lesions is an intention tremor, which
is best seen in the finger-nose test; as the finger approaches the nose the
tremor intensifies. The finger-to-finger test is also used to assess cerebellar
function. The heel-to-shin test (sliding one heel down the opposite shin)
will show dysmetria in that lower extremity. If the heel-to-shin test is normal in a patient with his or her eyes open, the cerebellum is intact. If this
test is repeated in the same patient with eyes closed and is abnormal, this
would suggest a lesion in the posterior column—medial lemniscus system.
Cerebellar damage in intermediate and lateral areas (nuclei or cortex
plus nuclei) causes movement disorders on the same side of the body as
the lesion; the patient may tend to fall toward the side of the lesion. This
is explained by the fact that the cerebellar nuclei project to contralateral
VL of thalamus, VL projects to ipsilateral motor cortex, motor cortex
projects (via corticospinal fibers) to the contralateral spinal cord. Other
circuits (cerebellorubral-rubrospinal) and feedback loops (cerebelloolivary—olivocerebellar) follow similar routes. The motor expression of
unilateral cerebellar damage is toward the lesioned side because of these
doubly crossed pathways.
Lesions of cerebellar efferent fibers, after they cross the midline in the
decussation of the superior cerebellar peduncle, will give rise to motor
deficits on the contralateral side of the body (excluding the head). This
is seen in midbrain lesions such as the Claude syndrome.
ABBREVIATIONS
CorNu
CorVes
Flo
Corticonuclear fibers
Corticovestibular fibers
Flocculus
MLF
MVesSp
MVNu
Medial longitudinal fasciculus
Medial vestibulospinal tract
Medial vestibular nucleus
IC
InfVesNu
JRB
rc
LVesSp
LVNu
Intermediate cortex
Inferior (spinal) vestibular nucleus
Juxtarestiform body
Lateral cortex
Lateral vestibulospinal tract
Lateral vestibular nucleus
NL, par
Lateral cerebellar nucleus, parvocellular
region
Medial cerebellar nucleus, parvocellular region
Nucleocortical fibers
Superior vestibular nucleus
Vermal cortex
NM, par
NuCor
SVNu
VC
Review of Blood Supply to Cerebellum and Vestibular Nuclei
Structures
Arteries
Cerebellar Cortex
Branches of posterior and anterior inferior cerebellar and superior cerebellar
Cerebellar Nuclei
Anterior inferior cerebellar and superior cerebellar
Vestibular Nuclei
Posterior inferior cerebellar in medulla, long circumferential branches of basilar in pons
esa
|
4,
: Sete
AN
=
Nes
&
wes
: “ . = aes
Ss
ye
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igeye ARS
Cerebellum and Basal Nucletnn
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‘
8-36 CEREBELLAR CORTICONUCLEAR, NUCLEOCORTICAL, AND CORTICOVESTIBULAR
FIBERS IN ANATOMICAL ORIENTATION
CorNu
VC
IC
\
—
|
CorVes
4
em
NuCor
=
G x
24
Nee)
Ny
(~
(D
\
|Nous
\
|
||
~JIX
ie
SVNu
Flo
Distal PICA lesion; Mainly cortex
|
JRB
aa
NM, par
peat
aa
NL,
ce
|
=
MLF
“
InfVNu
i
\
LVesSp
MVesSp
1= Medial (Fastigial)
2= Posterior Interposed (Globose)
3= Anterior Interposed (Emboliform)
4= Lateral (Dentate) _
ahe
|
|
\\y
ae
1 |a
:
\
\
:
\
Cerebellar Nuclei:
|]
i
\
MVNu
‘dle
—<p>|
t
q\ |
Nil
ee
|
<
SCA lesion; Cortex plus nuclei
;
.
ro.
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;
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a
fe
a
i
CEREBELLAR
ORIENTATION
EFFERENT FIBERS IN ANATOMICAL
The origin, course, topography, and general distribution of
fibers arising in the cerebellar nuclei.
Cerebellofugal fibers (cerebellar efferent fibers commonly called cer-
>)
.
hy
:
\ Dow t Seeticess
ebellothalamic fibers) project to several thalamic areas (VL and VA), to
intralaminar relay nuclei in addition to the centromedian, and a number of
midbrain, pontine, and medullary targets. Most of the latter nuclei project
back to the cerebellum (e.g., reticulocerebellar, pontocerebellar), some in
a highly organized manner. For example, cerebello-olivary fibers from the
DNu project to the principal olivary nucleus (PO), and neurons of the PO
send their axons back to the lateral cerebellar cortex, with collaterals
going to the DNu.
The cerebellar nuclei can influence motor activity through, as
examples, the following routes: (1) cerebellorubral-rubrospinal; (2)
cerebelloreticular—reticulospinal; (3) cerebellothalamic-thalamocorticalcorticospinal; and (4) others. In addition, some sparse direct cerebellospinal projections arise in the fastigial nucleus as well as in the interposed
nuclei. These minor projections are of little clinical significance.
Neurotransmitters
Many cells in the cerebellar nuclei contain glutamate (+), aspartate
(+), or y-aminobutyric acid (-). Glutamate and aspartate are found
some
cerebellothalamic fibers, whereas
and
in cerebellorubral
GABA-containing cells give rise to cerebellopontine and cerebelloolivary fibers. Some cerebelloreticular projections also may contain
GABA.
Clinical Correlations
ee
ee
Lesions of the cerebellar nuclei result in a range of motor deficits depending on the location, size, and type of the injury/lesion.
Lesions of only the cerebellar cortex usually results in deficits that
may resolve within a very few weeks especially with smaller lesions.
Damage to the cerebellar cortex + nuclei, or to only the nuclei, may
result in long-term deficits (months or years), this may especially be
the case in the elderly patient. Lesions that are more medially located,
in the vermis, may present as a wide-based stance, truncal ataxia,
and inability to walk in tandem. Lesions in the lateral regions of the
hemispheres result more in dyssynergia, intention tremor, dysdiadochokinesia, and dysmetria. Many of these are described in Figures 8-36
and 8-38B.
ABBREVIATIONS
ALS
AMV
Anterolateral system
Anterior medullary velum
BP
CbIOI
CbITh
CbIRu
Ce
CeGy
Basilar pons
Cerebello-olivary fibers
Cerebellothalamic fibers
Cerebellorubral fibers
Crus cerebri
Central gray
(periaqueductal gray)
Centromedian nucleus of
thalamus
Corticospinal fibers
Dorsal accessory olivary
nucleus
CM
CSp
DAO
(€
InfVNu
INu
LRNu
LVNu
MAO
ML
MLE
MVNu
NuDark
Inferior colliculus
Inferior (spinal) vestibular
SVNu
Superior vestibular
nucleus
nucleus
Interstitial nucleus
Lateral reticular nucleus
Lateral vestibular nucleus
Medial accessory olivary
nucleus
Medial lemniscus
Medial longitudinal
fasciculus
Medial vestibular nucleus
Nucleus of
Darkschewitsch
ThCor
ThFas
TriMoNu
VL
Thalamocortical fibers
Thalamic fasciculus
Trigeminal motor nucleus
Ventral lateral nucleus of
thalamus
Ventral posterolateral
nucleus of thalamus
Ventral spinocerebellar
tract
Zona incerta
VEL
VsGr
Zi
DNu
Dentate nucleus (lateral
OcNu
Oculomotor nucleus
ENu
cerebellar nucleus)
Emboliform nucleus
PO
PonNu
Principal olivary nucleus
Pontine nuclei
‘ gues: are rt supeney
colliculus, and possibly ventral lateral
(anterior interposed
cerebellar nucleus)
Edinger—Westphal
preganglionic nucleus
RetForm
RNu
RuSp
SC
Reticular formation
Red nucleus
Rubrospinal tract
Superior colliculus
ane bigest 2) Eine MOS
2: Pde tele crossed fibers from
SUP cerebellar peduncle
paca desaculus (of Russell)
Fastigial nucleus (medial
SCP
Superior cerebellar
piJuxtaiestiony pasey AS ESED OL
EWpgNu
FNu
cerebellar nucleus)
GNu
peduncle
Globose nucleus (posterior
SCP, Dec
interposed cerebellar
Superior cerebellar
eae
as
wee!
a Rete
mane
peduncle, decussation
nucleus)
SN
Substantia nigra
Review of Blood Supply to Cerebellar Nuclei and Their Principal Efferent Pathways
Structures
Cerebellar Nuclei
a
Midbrain Tegmentum (RNu :
CbITh, CbIRu, OcNu)
VPL, CM, PA VL, les VA
Ke
Arteries
Anterior inferior cerebellar and superior cerebellar
Long circumferential branches of basilar and superior cerebellar (see Figure 6-23)
Paramedian branches of basilar bifurcation, , sh short circumferential b
1
branches of superior cerebellar (see Figure 6-30)
nme
OS:
Thalamogenicul
é
ate branches of posterior
i cerebral, thalamoperforating
branch
R
group of posterior cerebral (see Figure 6-41)
:
meee
ee)
Lateral striate branches of middle cerebral (see Figure 6-41)
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MSGS
RENAN
_. . . |
8-37 CEREBELLAR
EAs
eyes
Nes
. Cerebellum‘and Basal Nucl! oe
EFFERENT FIBERS IN ANATOMICAL
ORIENTATION
Motor cortex
Position of SCP,
NuDark, INu,
CbITh, and CbiRu
OcNu, EWNu
RNu
SC
CeGy
CeGy
}
C)
\ CAP
—
RNu
ENu
GNu
LVNu
InfVNu
CT of lesion involving CDS
nuclei
Cerebellospinal
fibers
aay
CbhITh &
CbliRu
-
ses)
;
Tracts, Pathways, and Systems in nal
é
:
-
CEREBELLAR
SS.
ae
;
EFFERENT FIBERS IN CLINICAL ORIENTATION
Cerebral cortex
(motor area)
Corticospinal fiber
Thalamocortical fiber
Body of caudate nucleus
al
-
Ventral lateral
nucleus (pars caudalis)
Posterior limb of
internal capsule
Red nucleus
Thalamic fasciculus
Decussation of the
Red nucleus
superior cerebellar
peduncle
Corticospinal fiber
in crus cerebri
Superior cerebellar
| ~~
Cerebellothalamic fibers
peduncle
(also cerebellorubral fibers)
Crossed descending cerebellar
Reticular formation
projections to pons and medulla
Cerebellar efferent fibers
forming the superior
cerebellar peduncle
Juxtarestiform body (JRB)
Dentate nucleus
Dentate nucleus
Emboliform nucleus
Emboliform nucleus
Globose nucleus
Globose nucleus
Fastigial nucleus
Fastigial nucleus
aT
|—
+
~~
Principal olivary nucleus
Dorsal accessory
olivary nucleus
Medial accessory
olivary nucleus
ry 3 | Efferent fibers of the cerebellar nuclei superimposed on MRI __ decussating, they either descend or ascend to various brainstem and tha~~
(brainstem and forebrain, T2-weighted images) showing — lamic targets (see Figure 8-37). The red fibers originating in the fastigial
their origin, location, and trajectory in a clinical orientation. The blue, _nucleus project bilaterally to various nuclei of the brainstem and. in much
gray, and green fibers are shown arising in the right cerebellar nuclei,
lesser numbers, to select thalamic nuclei. The blue, gray. Breen, and red
crossing in the decussation of the superior cerebellar peduncle, and after __fibers correlate with those of the same color in Figure 9-37.
,
;
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— . a
i
: "Cerebellum and Basal Nuclei
va
CEREBELLAR EFFERENT FIBERS IN CLINICAL ORIENTATION:
REPRESENTATIVE LESIONS AND DEFICITS
Cerebral cortex
(motor area)
Corticospinal fiber
Thalamocortical fiber
Body of caudate nucleus
Ventral lateral
Midbrain lesion
nucleus (pars caudalis)
-Involves red nucleus, root of third nerve,
cerebellothalamic fibers (Claude
syndrome)
-Right-sided ocuiomotor paralysis
-Hyperkinesia/tremor (red nucleus) and
akinesia (substantia nigra) on left
-Left-sided cerebellar tremor
-Possible left-sided proprioceptive loss
Thalamic fasciculus
Red nucleus
Corticospinal fiber
i—
in crus cerebri
Superior cerebellar
peduncle
Cerebellothalamic fibers
(also cerebellorubral fibers)
Reticular formation
Crossed descending cerebellar
projections to pons and medulla)
ss,
Cerebellar efferent fibers
forming the superior
cerebellar peduncle
_
.
.
;
Cortex + nuclei lesion
d
..
=
-Left-sided intention tremor
‘
(finger—nose test) |
:
-Dyssynergia, ataxia, hypotonia,
unsteady gait
-Dysdiadochokinesia
Dentate nucleus
-Rebound phenomenon
Emboliform nucleus
-Dysmetria (heel-to-shin test)
(also hypermetria/hypometria)
-Dysarthria, nystagmus, static
Globose nucleus
-Lesion on left = deficits on left
tremor
Cortex lesion only
-Ataxia, tremor (static/kinetic),
unsteady gait, dysmetria
-Lesion on left = deficits on left
-Deficits usually transient, full
recovery commonly seen
Midline lesion
-Lesion usually bilateral
-Truncal ataxia, wide-based stance
-Unable to walk-in-tandem or on heels
or on toes
-Titubation, nystagmus
——
Principal olivary nucleus
"——~ Dorsal accessory
olivary nucleus
Medial accessory
olivary nucleus
Representative lesions of the cerebellum and of cerebel-
distal to the decussation, the deficits are on the contralateral side. As one
cerebellar lesions are expressed through the corticospinal tract. Consequently, if a lesion is proximal to the decussation of the superior cerebellar peduncle, the deficits are ipsilateral to the lesion; if a lesion is
left or right side of the MRI; this reinforces important clinical concepts.
For additional information on deficits related to cerebellar lesions,
see Figure 8-36.
example, right cerebellar nuclei to left thalamus to left cerebral cortex
lothalamic fibers in the midbrain (and the adjacent red
spinal cord via corticospinal fibers. Note that the laternucleus) and the deficits (in pink boxes) that correlate with each lesion. _ to right side of
deficits is determined by whether the lesion is on the
the
of
ality (R/L)
It is important to remember that the motor deficits seen in patients with
BLANK MASTER DRAWING
FOR EFFERENT CEREBELLAR CONNECTIONS
pathways to the cerebellar cortex and from the cerebellar nuclei, for
8-39 Blank master drawing for pathways projecting to the cerethe instructor to expand on cerebellar afferent/efferent pathways not
bellar cortex, and for efferent projections of cerebellar nuclei.
~_
This illustration is provided for self-evaluation of understanding of — covered in the Atlas, or both.
%
8-39 BLANK MASTER
in
DRAWING
x
.
:
FOR EFFERENT CEREBELLAR CONNECTIONS
AN
’
é
cree
ee
ee
2'xere7
ukey
Tracts, Pathways, and Systems in Anatomical and Clinical Orient
STRIATAL CONNECTIONS
IN ANATOMICAL
The origin, course, and distribution of afferent fibers to, and
efferent projections from, the neostriatum. These projections
are extensive, complex, and, in large part, topographically organized; only
their general patterns are summarized here. Afferents to the caudate and
putamen originate from the cerebral cortex (corticostriate fibers), from the
intralaminar thalamic nuclei (thalamostriate), from the substantia nigra—
pars compacta (nigrostriate), and from the raphe nuclei. Neostriatal cells
send axons into the globus pallidus (paleostriatum) as striopallidal fibers
and into the substantia nigra—pars reticulata as a strionigral projection.
Neurotransmitters
CUR
ee | ee 2
ee
Glutamate (+) is found in corticostriate fibers, and serotonin is found
in raphe striatal fibers from the nucleus raphe dorsalis. Four neuroactive substances are associated with striatal efferent fibers, these being
y-aminobutyric acid (GABA) (-), dynorphin, enkephalin (—), and substance P (+). Enkephalinergic and GABA-ergic striopallidal projections
are numerous to the lateral pallidum (origin of pallidosubthalamic fibers), whereas GABA-ergic and dynorphin-containing terminals are more
concentrated in its medial segment (source of pallidothalamic fibers).
Enkephalin and GABA are also present in strionigral projections to the
pars reticulata. Substance P and GABA are found in striopallidal and
strionigral fibers. Dopamine is present in nigrostriatal projection neurons and in their terminals in the neostriatum.
Clinical Correlations
Degenerative changes, inherited disorders, neuron loss, or loss of afferent fibers in the caudate nucleus, putamen, or substantia nigra result in
movement disorders related to the basal nuclei. Examples are Sydenham
chorea (rheumatic chorea); Huntington disease (a dominantly inherited
disease); Wilson disease (a genetic error in copper metabolism); PD,
dopaminergic cell loss in the substantia nigra and pars compacta; and
pantothenate kinase—associated neurodegeneration (PKAN), an inherited disorder causing iron accumulation in the basal nuclei.
Sydenham chorea is seen in children between 5 and 15 years of age,
resulting from infection with hemolytic streptococcus. The choreiform
movements are brisk and flowing, irregular, and may involve muscles of
the limbs, face, oral cavity, and trunk. Dystonia may be seen; muscle weakness is common. The disease may resolve after treatment of the infection.
Huntington disease is an inherited disorder; the symptoms appear
at 35 to 45 years of age and are progressive. A feature of this disease is
ORIENTATION
excessive CAG repeats on chromosome 4 (4p 16.3); the greater the number of repeats, the earlier the onset, and more severe the disease. There
is loss of GABA-ergic and enkephalinergic cells in the neostriatum (primarily the caudate) and in the cerebral cortex. Loss of neostriatal cell
terminals in the lateral and medial segments of the globus pallidus correlates with the development of choreiform movements and later with
rigidity and dystonia. Loss of cortical neurons correlates with personality changes and eventual dementia. Huntington chorea is rapid, unpredictable, and may affect muscles of the extremities, face, and trunk.
Patients commonly attempt to inask the abnormal movement by trying
to make it appear to be part of an intended movement (parakinesia).
Symptoms in Wilson disease (hepatolenticular degeneration) appear
between 10 and 25 years of age. Copper accumulates in the basal
nuclei and the frontal cortex, with resultant spongy degeneration in the
putamen. These patients may show athetoid movements, rigidity and
spasticity, dysarthria, dysphagia, contractures, and tremor. A unique
movement of the hand and/or upper extremity in these patients is called
a flapping tremor (asterixis) or a wing-beating tremor. Copper also can
be seen in the cornea (Kayser—Fleischer ring) in these patients.
Adult PD (onset at 45 to 65 years of age) is a progressive loss of
dopaminergic cells in the substantia nigra—pars compacta, their terminals in
the caudate and putamen, and their dendrites that extend into the substantia nigra—pars reticulata. Patients with PD characteristically show a resting
tremor (pill rolling), rigidity (cogwheel or lead pipe), and bradykinesia or
hypokinesia. The slowness of movement also may be expressed in speech
(dysarthria, hypophonia, trachyphonia) and writing (micrographia). These
patients have a distinct stooped flexed posture and a festinating gait. Although
rare, PD may appear as juvenile PD (onset >20 years of age), young-onset PD
(onset 20 to 40 years of age), and pugilistic PD (traumatic onset).
PKAN is an inherited disorder appearing in childhood that presents as
a variety of motor deficits. These appear slowly and include basal nuclei
signs (rigidity, choreoathetosis, dystonia) and corticospinal signs (Babinski signs, spasticity, hyperreflexia) and may involve upper and lower
extremities, deep back muscles, and musculature of the face (risus sardonicus) and oral cavity (swallowing, speech). As the disease progresses the
deposition of iron in the pallidum may present as the eye-of-the-tiger sign.
Dystonia, as seen in some patients with basal nuclei disease, is characterized by increased/sustained muscle contractions, twisting of the
trunk or extremities, and abnormal postures. These patients may have
repetitive movements of the extremities or neck (cervical dystonia or
spasmodic torticollis), Dystonia may be an inherited progressive disease
or have other causes. The symptoms may initially appear during movements or when talking, but in later stages may be present at rest.
ABBREVIATIONS
CaNu
CorSt
GPL
GPM
Ic
\
Caudate nucleus
Corticostriate fibers
Globus pallidus, lateral
segment
Globus pallidus, medial
segment
Internal capsule
NigSt
Put
RaNu
RaSt
SNpc
Nigrostriatal fibers
Putamen
Raphe nuclei
Raphestriatal fibers
Substantia nigra, pars
compacta
SNpr
StNig
StPal
SThNu
ThSt
ZI
Substantia nigra, pars
reticulata
Striatonigral fibers
Striatopallidal fibers
Subthalamic nucleus
Thalamostriatal fibers
Zona incerta
S|
=e
SSS
Review of Blood Supply to Caudate, Putamen, SN, CC, and IC
2)
EE
E
Structures
Arteries
Caudate, Putamen, and IC
Medial striate artery for head of caud ate and lateral striate branches of middle cerebral for Put and IC
(see Figure 6-41)
SN and CC
Paramedian branches of basilar bifurcation, short circumferential branches of posterior cerebral and some
from superior cerebellar (see Figure 6-30)
ees
Cerebellum
8-40 STRIATAL CONNECTIONS
IN ANATOMICAL
and Basal
ORIENTATION
Cerebral cortex
Normal axial T1 MRI
ThSt
Intralaminar
nuclei
NigSt
RaNu
Pantothenate kinase-associated
Huntington disease
Wilson disease
Neurodegeneration
(PKAN)
Nuclei
PALLIDAL EFFERENTS AND NIGRAL CONNECTIONS
The origin, course, and distribution of efferent projections of
biel the globus pallidus (upper illustration), and connections of the
substantia nigra (lower drawing) that were not shown in relation to the
7
7
We
rat
cea
er
pallidum or in Figure 8-40 (see also Figure 8-42A). The ansa lenticularis (dashed line) arches around the internal capsule and passes caudally
to join in the formation of the thalamic fasciculus. Pallidosubthalamic
fibers originate primarily from the lateral pallidal segment, but pallidothalamic projections, via the ansa lenticularis and lenticular fasciculus,
arise mainly from its medial segment. The substantia nigra has extensive connections, the clinically most important being the dopaminergic
nigrostriatal fibers; these fibers may excite or inhibit striatial neurons
depending on which striatial pathway (direct, indirect) they activate (see
Figure 8-42A). The globus pallidus influences motor activity by way
of pallidothalamic-thalamocortical—corticospinal (and corticonuclear)
pathways.
Neurotransmitters
y-Aminobutyric acid (—)-containing cells in the globus pallidus give rise
to pallidonigral projections, which end primarily in the substantia nigra—
pars reticulata. Although GABA is also found in some subthalamopallidal axons, this latter projection contains many glutaminergic (+) fibers.
Dopamine-, GABA (-)-, and glycine (—)-containing cells are present
in the substantia nigra. Of these, dopamine is found in pars compacta
neurons, which give rise to nigrostriatal. nigroamygdaloid, and several other projections; GABA in pars reticulata cells, which give rise
to nigrocollicular and nigrothalamic fibers; and glycine in some local
|
AmyNig
AmyNu
AnLent
CaNu
CM
CorNig
CSp
GPL
GPM
IN ANATOMICAL
ORIENTATION
circuit nigral neurons. Glutamate (+) is found in corticonigral fibers,
and serotonin (-) is associated with raphenigral fibers; these latter fibers
originate primarily from the nucleus raphe dorsalis.
The dopaminergic projections to the frontal cortex, shown here
as arising only from SNpe, originate from this cell group as well as
from the immediately adjacent ventral tegmental area. Excessive activity in neurons comprising this projection may play a partial role in
schizophrenia.
Clinical Correlations
ee
a
ee
re
Movement disorders associated with lesions in the neostriatum and
substantia nigra are reviewed in Figures 8-40 and 8-42B. Hemorrhage
into, the occlusion of vessels serving, or a tumor within, the subthalamic nucleus will result in violent flailing movements of the extremities, particularly the upper extremity, a condition called hemiballismus.
The subthalamic nucleus may also play a role in inhibiting movement.
Through subthalamopallidal fibers to the medial segment of the globus
pallidus and pallidothalamic fibers to the ipsilateral VL of the thalamus,
the subthalamic nucleus influences the motor cortex on the same side,
which, in turn, influences spinal motor neurons on the side opposite the
primary lesion.
Hemiballistic movements are seen contralateral to the lesion because
the motor expression of this lesion is through the corticospinal tract.
Lesions confined to the globus pallidus, as in hemorrhage of the lenticulostriate arteries, branches of M, may result in hypokinesia and rigidity
without tremor.
ABBREVIATIONS
Amygdalonigral fibers
Amygdaloid nucleus (complex)
Ansa lenticularis
Caudate nucleus
Centromedian nucleus of thalamus
Corticonigral fibers
Corticospinal fibers
Globus pallidus, lateral segment
Globus pallidus, medial segment
PedPonNu
Put
RaNu
SC
SNpc
SNpr
SThFas
SThNig
SThNu
Pedunculopontine nucleus
Putamen
Raphe nuclei
Superior colliculus
Substantia nigra, pars compacta
Substantia nigra, pars reticulata
Subthalamic fasciculus
Subthalamonigral fibers
Subthalamic nucleus
LenFas
Lenticular fasciculus (H,)
ThCor
Thalamocortical fibers
NigAmy
NigCol
NigTec
NigSTh
NigTh
PalNig
Nigroamygdaloid fibers
Nigrocollicular fibers
Nigrotectal fibers
Nigrosubthalamic fibers
Nigrothalamic fibers
Pallidonigral fibers
ThFas
VA
VL
VM
ZI
Thalamic fasciculus (H;)
Ventral anterior nucleus of thalamus
Ventral lateral nucleus of thalamus
Ventromedial nucleus of thalamus
Zona incerta
Review of Blood Supply to Pallidum, Subthalamic Area, and SN
Structures
Arteries
GPM/GPL
Lateral striate branches of middle cerebral and branches of anterior choroidal (see Figure 6-41)
Posteromedial branches of posterior cerebral and posterior communicating (see Figure 6-41)
Branches of basilar bifurcation, medial branches of posterior cerebral and posterior communicat
ing, short circumferential
branches of posterior cerebral (see Figure 6-30)
SThNu
SN
eee
Motor cortex
Intralaminar
nuclei
ThFas
LenFas
Zl
Forel field H
.
SThNu
‘
SThNig and
NigSTh
:
1
SNpc
4s
/
SThFas
4,
x ie
‘
A
AnLent
PalNi
SNpr
:
PedPonNu
Nigral efferents
to frontal cortex
GPL
NigTh
Z|
GPM
SThNu
Nigral efferents to
olfactory tubercle
SC
and bed nucleus of
the stria terminalis
AmyNu
SNp
NigAmy and AmyNig
oat
or
- a!
aah
Lak
Tracts, Pathways, and Systems in Anatomical a
ndClinicalOrientath
ee
es =
PALLIDAL EFFERENTS, SUBTHALAMIC, AND NIGRAL
CONNECTIONS IN CLINICAL ORIENTATION
Cerebral cortex
Corticospinal
fibers
White matter
Thalamocortical
fibers
Corpus callosum
Corticostriate
fibers
Ventral lateral nucleus
Bhi
:
Body of fornix
ao
Body of caudate nucleus
Dorsal thalamus
Posterior limb, internal capsule
=
Putamen
Insular cortex
Internal and external —
segments, globus pallidus
Subthalamic nucleus
Nigrostriatal
fibers
Substantia nigra
Corticospinal fibers
in crus cerebri
Crus cerebri
Corticospinal fibers
in basilar pons
Basilar pons
Corticospinal fibers
in pyramid
Pyramid of medulla
Corticospinal fiber
Corticostriate fiber (+)
Striatopallidal cell/fiber (—)
Lenticular fasciculus
Pallidosubthalamic cell/fiber (—)
Striatopallidal cell/fiber (—)
Pallidothalamic fiber (—)
Subthalamopallidal
)
Corticospinal fiber
Direct pathway = Gray Red > Blue> Gray
Indirect pathway = Gray > Green > Blue> Gray
The direct and indirect pathways through the basal nuclei,
subthalamic nucleus, and substantia nigra superimposed
on MRI
(forebrain, T2-weighted MRI) shown in clinical orientation.
The exploded view below the MRI illustrates the specific fiber types,
by name, that comprise these two pathways and specifies whether the
synaptic influences are excitatory (+) or inhibitory (-).
The direct pathway essentially functions as follows. The corticostriatal (+) fiber excites the striatopallidal (—) fiber, which inhibits the
pallidothalamic (—) fiber. In this situation, the thalamus is disinhibited
(removed from the inhibition of the pallidothalamic fiber), and the
activity of the thalamus and motor cortex is upregulated.
ie
cell/fiber (+)
Nigrostriatal cell/fiber
(+ through direct pathway;
— through indirect pathway)
The indirect pathway functions in the following way. The corticostriatal (+) fiber excites the striatopallidal (—) fiber, which inhibits the
pallidosubthalamic (—) fiber. In this situation, the subthalamic nucleus
is disinhibited (removed from the inhibition of the pallidosubthalamic
fiber), and the subthalamopallidal (+) fiber excites the pallidothalamic
(—) fiber, which inhibits the thalamus; the activity of the thalamus and
the motor cortex is downregulated.
These two pathways work together. However, their influence takes
into account the different number of synapses in each pathway; the
respective messages are temporally separated with regard to the time of
arrival at the target neurons.
CerebellumandBasal Nuclei
PALLIDAL EFFERENTS, SUBTHALAMIC, AND NIGRAL CONNECTIONS IN
a
Sa Nes
CLINICAL ORIENTATION:
REPRESENTATIVE
LESIONS AND DEFICITS
Huntington disease
Corticospinal
fibers
Thalamocortical
fibers
Corticostriate
fibers
Ventral lateral nu.
Insular cortex
Nigrostriatal
fibers
Corticospinal fibers
in crus cerebri
Corticospinal fibers
in basilar pons
Corticospinal fibers
in pyramid
Representative lesions of the basal nuclei, subthalamic
nucleus, and substantia nigra and the deficits (in pink boxes)
with
that correlate with lesions at each of these locations. As was the case
nuclei
the cerebellum, motor deficits resulting from lesions of the basal
tract.
and related structures are expressed through the corticospinal
either
is
Through these circuits, the activity of thalamocortical neurons
of activity
maintained, increased, or decreased with a corresponding level
¥
-Inherited disorder (excessive CAG
nucleotide repeats)
-Loss of medium-sized spiny neostriatial
neurons
-Choreiform movements (fingers, wrist,
extremities, face, tongue)
-Dysarthria, dysphagia
-Dystonia and/or myoclonus
-Forgetfulness, diminished attention,
irritability, depression, memory loss
-Dementia
-Lesion/deficits usually bilateral
Wilson disease
-Inherited error of copper metabolism:
copper accumulates in liver and lenticular
nucleus
-Kayser-Fleischer ring
-Aminoaciduria
-Asterixis (flapping tremor)
-Tremor, rigidity, dysarthria, dysphagia
-Cognitive decline, personality change
-Lesion/deficits usually bilateral
-Treatable
Subthalamic lesion
-Usually vascular in origin
-Hemiballism/hemiballismus (one side of
body involved: deficits contralateral to
lesion)
-Ballism/ballismus (both sides of body
involved)
-Rapid jerky, flinging movements: more
common in UE
Parkinson disease
-Neurodegenerative disease of unknown
etiology: progressive
-Loss of dopamine-containing cells in
substantia nigra, pars compacta
-Resting/pill-rolling tremor
-Akinesia, bradykinesia, hypokinesia
-Rigidity (lead-pipe/cog-wheel)
-Flexed posture, shuffling/festinating gait;
unsteady posture
-Expressionless face
-Dysarthria, hypophonia, micrographia,
dystonia
-Dementia in late stages
in corticospinal tract. In addition, there is a temporal/timing element in
this pathway. Transmission through the direct pathway 1s quicker (fewer
synaptic delays, faster thalamocortical/corticospinal responses), while
that through the indirect pathway is slower (more synaptic delays, slower
thalamocortical/corticospinal responses). Note that the laterality (R/L)
of the deficits is determined by whether the lesion is on the left or right
side of the MRI; this reinforces important clinical concepts.
BLANK MASTER
DRAWING
FOR CONNECTIONS
8.43
Blank master drawing for connections of the basal nuclei.
s
This illustration is provided for self-evaluation of under-
OF THE BASAL NUCLEI
standing of basal nuclei connections, for the instructor to expand on
basal nuclei pathways not covered in this Atlas, or both.
See
=
=
ae
8-43 BLANK MASTER
DRAWING
FOR CONNECTIONS
OF THE BASAL NUCLEI
Tracts, Pathways, and Systems in Anatomical and Clinical Orientation—Optic, Auditory, and Vestibular S perc eatin
PUPILLARY PATHWAYS
The origin, course, and distribution of fibers involved in the
pathway for the pupillary light reflex. In addition, the pathway for sympathetic innervation of the dilator pupillae muscle of the
iris is also depicted. The intermediolateral cell column of the spinal
cord receives input predominately from the paraventricular nucleus
and also from cells in the lateral hypothalamic zone and posterior
hypothalamus. This projection may be supplemented, in a minor way,
by descending fibers through the reticular formation of the brainstem.
Postganglionic sympathetic fibers to the head originate from the superior cervical ganglion. Although not shown, descending projections to
the intermediolateral cell column also originate from various hypothalamic areas and nuclei (hypothalamospinal fibers), some of which
receive retinal input.
Neurotransmitters
Acetylcholine is the transmitter found in the preganglionic and postganglionic autonomic fibers shown in this illustration. In addition,
N-acetylaspartylglutamate is present in some retinal ganglion cells
(retinogeniculate projections).
Clinical Correlations
Total or partial blindness in one or both eyes may result from a variety
of causes (e.g., gliomas, meningiomas, strokes, aneurysms, infections,
and demyelinating diseases); lesions may occur at any locus along the
visual pathway. A complete lesion (i.e., a transection) of the optic nerve
will result in blindness and loss of the pupillary light reflex (direct
response) in the eye on the injured side and a loss of the pupillary light
reflex (consensual response) in the opposite eye when shining a light
in the blind eye. On the other hand, shining a light in the normal eye
will result in a pupillary light reflex (direct response) in that eye anda
consensual response in the blind eye. See also Figure 8-32. A pituitary
adenoma may damage the crossing fibers in the optic chiasm (producing
a bitemporal hemianopia) or damage the uncrossed fibers in the right
(or left) side of the optic chiasm. These lateral lesions produce a right
(or left) nasal hemianopia.
Optic (geniculocalcarine) radiations (see Figures 8-45 and 8-47) may
pass directly caudal to the upper lip (cuneus) of the calcarine sulcus
or follow an arching route (the Meyer, or Meyer—Archambault loop)
through the temporal lobe to the lower bank (lingual gyrus) of the
calcarine sulcus. Temporal lobe lesions involving the Meyer-Archambault loop, or involving fibers entering the lingual gyrus, can produce a
homonymous superior quadrantanopia. A homonymous inferior quadrantanopia is seen in patients with damage to upper (parietal) parts
of the geniculocalcarine radiations or to these fibers as they enter the
cuneus. See Figure 8-47B for additional lesions of the visual pathways
and the corresponding visual field deficits.
Damage to the visual cortex adjacent to the calcarine sulcus (distal
posterior cerebral artery occlusion) results in a right (or left) homonymous hemianopia. With the exception of macular sparing, this deficit is
the same as that seen in optic tract lesions. See Figure 8-47B on p. 267
for additional lesions of the optic radiations and visual cortex and the
corresponding visual field deficits.
Vascular lesions (e.g., the lateral medullary syndrome), tumors (e.g.,
brainstem gliomas), or syringobulbia may interrupt the descending projections from hypothalamus (hypothalamospinal fibers) and midbrain
to the intermediolateral cell column at upper thoracic levels. This may
result in a Horner syndrome (ptosis, miosis, and anhidrosis) on the ipsilateral side. The enophthalmos (a slight sinking of the eyeball into the
orbit) frequently mentioned in relation to Horner syndrome is not really
very apparent in afflicted patients.
ABBREVIATIONS
AmbCis
CC
CilGang
EWpgNu
IRGC
IFP
LGNu
Ambient cistern
Crus cerebri
Ciliary ganglion
Edinger—Westphal preganglionic nucleus
Intermediolateral cell column
Interpeduncular fossa
Lateral geniculate nucleus
OpTr
QuadCis
PoCom
PrTecNu
PulNu
RetF
RNu
MGNu
ML
OcNr
OpCh
Optic tract
Quadrigeminal cistern
Posterior commissure
Pretectal nucleus
Pulvinar nuclear complex
Reticular formation
Red nucleus
Medial geniculate nucleus
Medial lemniscus
Oculomotor nerve
Optic chiasm
SC
SC, Br
SCerGang
SN
OpNr
Superior colliculus
Superior colliculus, brachium
Superior cervical ganglion
Substantia nigra
Optic nerve
WRCom
White ramus communicans
Review of Blood Supply to OpTr, MGNu, LGNu, SC, and Midbrain Tegmentum, Including PrTecNu
Structures
Arteries
OpIr
Anterior choroidal (see Figure 6-41)
MGNu, LGNu
Thalamogeniculate branches of posterior cerebral (see Figure 6-41)
Long circumferential branches (quadrigeminal) of posterior cerebral, posterior choroidal,
SC and PrTecNu
superior cerebellar (to SC) (see Figures 6-30 and 6-41)
Midbrain Tegmentum
and some from
Paramedian branches of basilar bifurcation, medial branches of posterior cerebral
and posterior communicating,
short circumferential branches of posterior
cerebral (see Figure 6-30)
sg
SSSSSSSeeSSS
SSFSsesF
8-44 PUPILLARY PATHWAYS
Dilator muscles of iris
Sphincter muscle of iris
Sphincter muscle of ciliary body
Ganglion cells
of retina
/ \.
\
\
CilGang es
% ‘
\
/
OpNr
>
OcNr
OpCh
-OpTr
Via blood
vessels
ML
LGNu
PulNu
SCerGang
EWpgNu
Spinal nerve
WRCom
Anterior root
Thoracic cord
T1-1T3
VISUAL PATHWAYS
CoS
ec
ee
Ganglion cells
of retina
<«——_—__——— Retinae —————_—_>-
LGNu laminae
Optic nerve
bos
Optic chiasm
Optic tract
Red nucleus
Substantia nigra
Crus cerebri
Ge
?
> Ss
CX =
‘
ae
‘ti
By
SSS
;
SC,Br
PulNu
S
:
llicul
Oculomotor nucleus
peace nce
— Edinger—Westphal centrally
Pretectal nucleus
Edinger--Westphal
preganglionic nucleus
projecting nucleus
Guneus
:
Optic radiations
(in retrolenticular
limb of internal
capsule)
Lingual gyrus
CalSul
_____- The origin, course, and distribution of the visual pathway
Clinical Correlations
a5
,
are
shown. Uncrossed retinogeniculate fibers terminate in
laminae 2, 3, and S (red fibers), whereas crossed fibers end in laminae
Deficits seen following lesions of various parts of visual pathways are
1, 4, and 6 (blue fibers). Geniculocalcarine fibers arise from laminae — described in Figures 8-44 and 8-47B.
3 through 6. Retinogeniculate and geniculocalcarine pathways are
ABBREVIATIONS
retinotopically organized (see facing page).
a
Neurotransmitters
Cholecystokinin (+) is present in some geniculocalcarine fibers.
N-acetylaspartylglutamate is found in some retinogeniculate fibers, and
in some lateral geniculate and visual cortex neurons.
CalSul
LGNu
Mc
Pc
Calcarine sulcus
Lateral geniculate nucleus
Magnocellular
Parvocellular
MGNu
PulNu
SC, Br
Medial geniculate nucleus
Pulvinar nuclear complex
Superior colliculus, brachium
VISUAL PATHWAYS
EEE
A
B'
RIGHT
Visual fields
overlapped for ——>
both eyes
Orientation to all levels
except visual cortex
Dor
A
Dor
A
taie( > Med «(ota
v
v
Ven
Ven
ee
Visual fields for
|
individual eyes ———>} —
Retinae ———>~
Optic nerves ———>
Lateral
OIE
re
nuclei
Optic radiations
Primary visual cortex
Cuneus
Calcarine sulcus
Lingual gyrus
raphic
Semi-diagrammatic representation of the retinog
ent
subsequ
the
and
fields,
arrangement of visual and retinal
Upper
system.
visual
the
topography of these projections throughout
B, C, D), the macula
case letters identify the binocular visual fields (A,
D’).
C’,
B’,
(M), and the monocular visual fields (A’,
Clinical Correlations
Deficits seen following lesions of various parts of the visual pathway are
described in Figures 8-44, 8-47A, and 8-47B.
Lh
Tracts, Pathways, and Systems in Anatomicé
VISUAL PATHWAYS
and Clini al
Orientation
IN CLINICAL ORIENTATION
Ganglion cell
yo* # .
of retina
Optic nerve
Optic nerve
Optic nerve
Optic chiasm
Optic chiasm
Optic tract
Crus cerebri
Lateral geniculate nucleus
Lateral geniculate nucleus
Meyer loop
Medial geniculate nucleus
Medial geniculate nucleus
Pulvinar
Brachium of
superior colliculus
Pulvinar
Optic radiations
Pretectal nucleus
Optic radiations
Cuneus
Lingual gyrus
Cuneus
Calcarine sulcus
Cuneus
Optic radiations
Calcarine sulcus
Lingual gyrus
Lingual gyrus
The visual pathway from retina to primary visual
cortex superimposed on MRI in clinical orientation.
The upper T1-weighted image is in the axial plane and the lower
Tl-weighted image is in the coronal plane. The red, blue, and gray
fibers in the upper image correlate with those of the same color in
Representative lesions at 13 different locations in the
visual pathway and the patterns of visual field deficits (in
pink boxes) that correlate with each lesion. As indicated by the letters
(A-I), some lesions, especially those caudal to the optic chiasm, may
result in comparable visual field deficits even though the lesions may be
at different locations within the pathway.
International clinical convention dictates that visual field deficits
are illustrated as the patient sees the environment. In this respect, the
patient’s right eye and visual field are on the right and the patient’s
left eye and visual field are on the left. Axial and coronal MRI and
CT images are viewed as if the observer is standing at the patient’s
feet looking toward the head (axial) or looking at the patient’s face
Figure 8-45.
a
ie
itr
Optic, Auditory, and Vestibular Systems
VISUAL PATHWAYS
IN CLINICAL ORIENTATION:
REPRESENTATIVE
Ganglion cell
LESIONS AND DEFICITS
Retinal disorders/trauma
¢ Visual field defects of various patterns
¢ Scotoma
of retina
Optic nerve
Optic nerve lesion
¢ Blind in left eye
¢ Loss of pupillary light reflex in both eyes
when light shined in left eye
B
é
Midline optic chiasm lesion
¢ Bitemporal hemianopia
¢ May have relative afferent pupillary defect
(RAPD)
Optic nerve
Lateral optic chiasm lesion
¢ Binasal hemianopia
¢ May have RAPD
D
Optic tract lesion
¢ Right homonymous hemianopia
e May have RAPD
E
Optic tract
Lateral geniculate nucleus
Meyer loop
¢ Right superior homonymous
quadrantanopia
=
Medial geniculate nucleus
¢ Right inferior homonymous
Brachium of
superior colliculus
quadrantanopia
G
Total optic radiation lesion
¢ Right homonymous hemianopia
E
¢ Right inferior homonymous
quadrantanopia
G
Total optic radiation lesion
¢ Right homonymous hemianopia (also
seen in lesion of total primary visual
Gas)
_
¢ Right superior homonymous
quadrantanopia
F
Pulvinar
Pretectal nucleus
Optic radiations
—.
Cuneus
Lingual gyrus
Cuneus lesion
¢ Right inferior homonymous
quadrantanopia
{
=
:
Cuneus
' is
-
Calcarine sulcus
Lingual gyrus
Lingual gyrus lesion
¢ Right superior homonymous
quadrantanopia
Visual Field Deficits
Left
Right
ov
ay,
a6,
an,
Lesion
: }
Left
Right
<
the observer’s right
(coronal). In this case, when looking at MRI/CT,
t’s right. Underpatien
the
is
left
is the patient’s left and the observer’s
viewed in the
and
used
are
s
standing the reality of how these image
is of the
:
is absolutely essential to the diagnos
!
clinical environment
field
visual
onding
patient with visual system lesions and the corresp
deficits.
BLANK MASTER DRAWING
8-48
Blank master drawing for visual pathways. This illustration is
provided for self-evaluation of visual pathway understanding,
FOR VISUAL PATHWAYS
for the instructor to expand on aspects of the visual pathways not
covered in the Aclas, or both.
Tracts, Pathways, and Systems in Anatomical and Clinical Orientation |
AUDITORY
PATHWAYS
IN ANATOMICAL
The origin, course, and distribution of the fibers collectively
composing the auditory pathway. Central to the cochlear
nerve and dorsal and ventral cochlear nuclei, this system is, largely,
bilateral and multisynaptic, as input is relayed to the auditory cortex.
Synapse and crossing (or recrossing) of information can occur at several
levels in the neuraxis. Consequently, central lesions rarely result in a
total unilateral hearing loss. The medial geniculate body is the thalamic
station for the relay of auditory information to the temporal cortex. The
vestibulocochlear nerve (CN VIII) is a sensory nerve although it is well
known that there is an olivocochlear projection (efferent cochlear bundle)
that dampens the ossicles in response to excessive auditory stimuli.
Neurotransmitters
Glutamate (+) and aspartate (+) are found in some spiral ganglion cells
and in their central terminations in the cochlear nuclei. Dynorphincontaining and histamine-containing fibers are also present in the cochlear nuclei; the latter arises from the hypothalamus. A noradrenergic
projection to the cochlear nuclei and the inferior colliculus originates
from the nucleus locus ceruleus. Cells in the superior olive that contain cholecystokinin and cells in the nuclei of the lateral lemniscus that
contain dynorphin project to the inferior colliculus. Although the olivocochlear bundle is not shown, it is noteworthy that enkephalin is found
in some of the cells that contribute to this projection.
Clinical Correlations—Categories of Deafness
Conductive deafness is caused by problems of the external ear (obstruction of the canal, wax build up) or disorders of the middle ear (otitis
media, otosclerosis). Nerve deafness (sensorineural hearing loss) results
from diseases involving the cochlea or the cochlear portion of the vestibulocochlear nerve. Central deafness results from damage to the cochlear nuclei or their central connections.
Hearing loss may result from trauma (e.g., fracture of the petrous
bone), demyelinating diseases, tumors, certain medications (streptomycin), or occlusion of the labyrinthine artery. Damage to the cochlear
ORIENTATION
part of the eighth nerve (e.g., vestibular schwannoma) results in tinnitus
and/or deafness (partial or total) in the ipsilateral ear. High-frequency
hearing losses (presbyacusis), such as a woman’s voice or discrimination
between sounds, are more commonly seen in older patients.
The Weber test and Rinne test are used to differentiate between neural
hearing loss and conduction hearing loss, and to lateralize the deficit. In
the Weber test, a tuning fork (512 Hz) is applied to the midline of the
forehead or apex of the skull. In the normal patient, the sound (conducted
through the skull bones) is heard the same in each ear. In the case of nerve
deafness (cochlea or cochlear nerve lesions), the sound is best heard in the
normal ear, whereas in conductive deafness, the sound is best heard in the
abnormal ear. In the Rinne test, a tuning fork (512 Hz) is placed against
the mastoid process. When the sound is no longer perceived, the prongs
are moved close to the external acoustic meatus, where the sound is again
heard; this is the situation in a normal individual (positive Rinne test). In
middle ear disease, the sound is not heard at the external meatus after it
has disappeared from touching the mastoid bone (abnormal or negative
Rinne test). Therefore, a negative Rinne test signifies conductive hearing
loss in the ear tested. In mild nerve deafness (cochlea or cochlear nerve
lesions), the sound is heard by application of the tuning fork to the mastoid and movement to the ear (the Rinne test is positive). In severe nerve
deafness, the sound may not be heard at either position.
In addition to hearing loss and tinnitus, large vestibular schwannomas may result in nausea, vomiting, ataxia/unsteady gait (vestibular root
involvement), facial muscle weakness (facial root), altered facial sensations,
and a diminished corneal reflex (trigeminal root); the latter two in the case
of large schwannoma (<2 to 3 cm). There also may be general signs associated with increased intracranial pressure (lethargy, headache, and vomiting).
Central lesions (e.g., gliomas or vascular occlusions) rarely produce
unilateral or bilateral hearing losses that can be detected, the possible
exception being pontine lesions, which damage the trapezoid body and
nuclei. Injury to central auditory pathways and/or primary auditory cortex
may diminish auditory acuity, decrease the ability to hear certain tones, or
make it difficult to precisely localize sounds in space. Patients with damage
to the secondary auditory cortex in the temporal lobe experience difficulty
in understanding and/or interpreting sounds (auditory agnosia).
ABBREVIATIONS
AbdNu
ACNu
ALS
(AE
FacNu
IC
IC, Br
IC, Com
Abducens nucleus
Anterior (ventral) cochlear
IGSSE
Internal capsule,
sublenticular limb
nucleus
Anterolateral system
Crus cerebri
Facial nucleus
Inferior colliculus
Inferior colliculus,
brachium
Inferior colliculus,
commissure
RB
RetF
LGNu
LL
LL, Nu
MGNu
ML
MLF
Restiform body
Reticular formation
Lateral geniculate nucleus
Lateral lemniscus
Lateral lemniscus, nucleus
Medial geniculate nucleus
Medial lemniscus
Medial longitudinal
fasciculus
Posterior (dorsal) cochlear
nucleus
Pulvinar nuclear complex
SC
SCP, Dec
Superior colliculus
Superior cerebellar
peduncle, decussation
Superior olive
Spiral ganglion
Spinal trigeminal tract
Trapezoid body
Trapezoid nucleus
Transverse temporal gyrus
PCNu
PulNu
SO
SpGang
SpTTr
TrapB
TrapNu
TTGy
Review of Blood Supply to Cochlear Nuclei, LL (and Associated Structures), Pontine
Tegmentum, IC, and MGNu
Structures
Arteries
Cochlear Nuclei
Anterior inferior cerebellar (see Figure 6-16)
LL, SO in Pons
Long circumferential branches of basilar (see Figure 6-23)
Long circumferential branches (quadrigeminal branches) of basilar, superior cerebellar
(see Figure 6-30)
Thalamogeniculate branches of posterior cerebral (see Figure 6-41)
IC
MGNu
$$$
instr meont me,
NNN
8-49 AUDITORY
PATHWAYS
IN ANATOMICAL
ORIENTATION
Positions of LL and
related structures
=
own
a
as
|
iT
Bole
J .
1
N
PCNu
TrapNu
TrapB
RetF
ACNu
SpGang bo Be
Hair cells in
organ of Corti a
> date cia
272
figau Care
Le
senie ate:
: Tracts, Pathwaye, ran
dSys|
VESTIBULAR PATHWAYS
IN ANATOMICAL
The origin, course, and distribution of the main afferent and
- efferent connections of the vestibular nuclei (see also Figures
Be
8-16, 8-36, and 8-37). Primary vestibular afferent fibers may end in the
vestibular nuclei or pass to cerebellar structures via the juxtarestiform
body. Secondary vestibulocerebellar axons originate from the vestibular
nuclei and follow a similar path to the cerebellum. Efferent projections
from the vestibular nuclei also course to the spinal cord through vestibulospinal tracts (see Figures 8-16, 8-36, and 8-37), as well as to the motor
nuclei of the oculomotor, trochlear, and abducens nerves via the MLE.
Cerebellar structures most extensively interconnected with the vestibular nuclei include the lateral regions of the vermal cortex of anterior and
posterior lobes, the flocculonodular lobe, and the fastigial (medial) cerebellar nucleus. For our purposes, the vestibulocochlear nerve (CN VIII)
is considered a sensory nerve, all though it has the efferent olivocochlear
bundle that innervates the stapedius muscle which functions to dampen
the damaging effects of excessive noise.
Neurotransmitters
y-Aminobutyric acid (—) is the transmitter associated with many cerebellar corticovestibular fibers and their terminals in the vestibular complex; this substance is also seen in cerebellar corticonuclear axons. The
medial vestibular nucleus also has fibers that are dynorphin positive and
histamine positive; the latter arise from cells in the hypothalamus.
Clinical Correlations
The vestibular part of the eighth nerve can be damaged by many of
the same insults that affect the cochlear nerve. Damage to vestibular
ORIENTATION
receptors of the vestibular nerve commonly results in vertigo. The
patient may feel that his or her body is moving (subjective vertigo) or
that objects in the environment are moving (objective vertigo). They
have equilibrium problems, an unsteady (ataxic) gait, and a tendency to
fall to the lesioned side but do not have cerebellar signs such as dysmetria or an intention tremor. Deficits seen in nerve lesions, or in brainstem
lesions involving the vestibular nuclei, include nystagmus, nausea, and
vomiting, along with vertigo and gait problems.
Vestibular schwannoma represents about 8% to 10% of CNS tumors, commonly results in hearing loss (95%+), is frequently characterized by disequilibrium and tinnitus (65% to 70%), and is sometimes
related to headache and facial numbness (about 30%); the latter indicates that the lesion is large (generally >2.0 to 2.5 cm in size), and has
encroached on the trigeminal nerve root. Facial weakness (facial palsy)
occurs in about 10% of cases. These vestibular deficits, along with partial or complete deafness, are seen in Méniére disease. A patient that
presents with bilateral vestibular schwannomas should be evaluated
for neurofibromatosis type 2 (NF2). These lesions are genetic in origin
(autosomal dominant), may be accompanied by lesions elsewhere in the
body (but less than NF1), and are sometimes called bilateral acoustic
neurofibromatosis.
Lesions of those parts of the cerebellum with which the vestibular
nerve and nuclei are most intimately connected (flocculonodular lobe
and fastigial nucleus) result in nystagmus, truncal ataxia, ataxic gait,
and a propensity to fall to the injured/lesioned side. The nystagmus seen
in patients with vestibular lesions and the internuclear ophthalmoplegia
seen in some patients with MS are signs that correlate with the interruption of vestibular projections to the motor nuclei of III, IV, and VI
via the MLE.
ABBREVIATIONS
AbdNu
ALS
Cbl
Cbl-Co Ves
CbINu
HyNu
IC
InfVNu
JRB
LVesSp
LVNu
MesNu
ML
MLF
MVesSp
| MVNu
Abducens nucleus
Anterolateral system
Cerebellar
Cerebellar corticovestibular fibers
Cerebellar nuclei
Hypoglossal nucleus
Inferior colliculus
Inferior (spinal) vestibular nucleus
Juxtarestiform body
Lateral vestibulospinal tract
Lateral vestibular nucleus
Mesencephalic nucleus
Medial lemniscus
Medial longitudinal fasciculus
Medial vestibulospinal tract
OcNu
PAG
Py
RB
RNu
SG
SCP; Dec
SVNu
TroNu
VesGang
VesCbl, Prim
Medial vestibular nucleus
Oculomotor nucleus
Periaqueductal gray
Pyramid
Restiform body
Red nucleus
Superior colliculus
Superior cerebellar peduncle, decussation
Substantia nigra
Solitary nucleus
Solitary tract
Spinal trigeminal tract
Superior vestibular nucleus
Trochlear nucleus
Vestibular ganglion
Vestibulocerebellar fibers, primary
VesCbl, Sec
Vestibulocerebellar fibers, secondary
SN
SoINu
SolTr
SpTTr
Review of Blood Supply to Vestibular Nuclei, TroNu, and OcNu
Structures
Arteries
Vestibular Nuclei
Posterior inferior cerebellar in medulla (see Figure 6-16), long circumferential branches
of basilar in pons
(see Figure 6-23)
TroNu and OcNu
Paramedian branches of basilar bifurcation, medial branches of posterior cerebral
and posterior communicating,
short circumferential branches of posterior cerebral (see Figure 6-30)
$e
estou sitens
8-50 VESTIBULAR
PATHWAYS
IN ANATOMICAL
ORIENTATION
Position of vestibular nuclei,
MLF, and related structures
CbiINu
Cbl-CoVes
JRB
Ne aera
sie
VesCbl, Sec
Cbl cortex
:
VesCbl, Prim
Zz a,
{
\
\
/
2 ——
Crista ampullaris
Macula utriculi
Macula sacculi
VesGang
InfVNu
:
4
MVesSp in MLF
LVesSp
BLANK MASTER
8.5]
DRAWING
FOR AUDITORY OR VESTIBULAR PATHWAYS
Blank master drawing for auditory or vestibular pathway.
This illustration is provided for self-evaluation of auditory
or vestibular pathway understanding, for the instructor to expand on
aspects of these pathways not covered in the Atlas, or both.
:om aOptio,
8-51 BLANK MASTER
DRAWING
FOR AUDITORY
Auditory.
y, andVestibular systems ata
OR VESTIBULAR
PATHWAYS
(tSct
YA
Pit
a
p
e
Tracts, Pathways, and Systemsin Anatomical and Clinica
'
ae
ae
Se
rientation— nternal Cap:
;
ar
‘
THE INTERNAL CAPSULE: RELATIONSHIPS AND CONTENTS
The internal capsule, its relationship to the basal nuclei and
thalamus, and its major constituent fiber bundles in the axial
plane.
Pathways conveying sensory information (with the exception of olfaction) from the entire body and pathways influencing motor activity of cranial nerves and the extremities all traverse some part of the internal capsule.
The internal capsule is divided into five parts, called limbs, which
are most easily recognized in the axial plane (see facing page). Each
limb has a characteristic relationship to adjacent structures and largely
contains particular fiber groups.
Anterior limb: The anterior limb is located between the head of the
caudate nucleus and the lenticular nucleus. The major fiber populations
found in the anterior limb are frontopontine fibers, the anterior thalamic radiations (medial and anterior thalamic projections to the frontal and cingulate cortex), and, adjacent to the genu, small fascicles of
descending fibers from the frontal eye fields.
Genu: The positions of the column of the fornix, the interventricular
foramen, the venous angle, and the anterior tubercle of the thalamus indicate the location of the genu of the internal capsule. The most clinically
significant fiber bundles in the genu are corticonuclear fibers projecting
to the motor nuclei of cranial nerves (see also Figures 8-13 and 8-14).
Posterior limb: The posterior limb is the largest part of the internal
capsule, is located between the thalamus and the lenticular nucleus, and
contains a number of important fiber populations. These larger bundles include corticospinal fibers, superior thalamic radiations (ventral
anterior, ventral lateral, ventral posteromedial, and posterolateral projections to motor and sensory cortices), and, in its more caudal region,
parietopontine fibers. Smaller bundles of fibers including corticorubral,
corticoreticular, corticonigral, corticosubthalamic, the general category
of corticotegmental fibers, and pallidothalamic fibers that arise in the
medial segment of the globus pallidus, traverse the posterior limb.
Sublenticular limb: The sublenticular limb is difficult to identify,
although its trajectory and contents are well known. It extends between
the medial geniculate nucleus and the temporal lobe, particularly the
auditory cortex, and contains auditory radiations (genticulotemporal
radiations), temporopontine fibers, and corticotectal fibers.
Retrolenticular limb: The retrolenticular limb is the large mass of
fibers located immediately caudal the lenticular nucleus; hence its name,
retrolenticular. The larger fiber bundles within this limb are visual radiations (geniculocalcarine or optic radiations) and occipitopontine fibers;
the smaller bundles comprise corticotectal, corticotegmental, and some
corticorubral fibers.
Recall that the optic radiations are composed of fibers that arise in
the lateral geniculate nucleus and pass caudally directly to the primary
visual cortex, and of fibers that arise in the lateral geniculate nucleus,
arch forward into the temporal lobe, turn sharply caudal (as the Meyer
loop), and then proceed to the primary visual cortex. These two portions of the optic radiations are conveying information from different
parts of the visual fields; lesions of these parts result in specific visual
deficits (see Figures 8-44 through 8-47).
ABBREVIATIONS
F
Face
f.
Fibers
LE
Lower extremity
rad
Radiations
UE
Upper extremity
Trunk extremity
#i
:
General note: Most of the limbs of the internal capsule also contain
thalamocortical projections (other than those mentioned above), corticothalamic fibers (from all cortical areas to their respective thalamic
nuclei), and corticostriate fibers.
Neurotransmitters
re
a
There are no nuclei within the internal capsule, only fibers of passage
conveying a variety of motor and sensory information, and fibers that
are integrative in nature. The major transmitters associated with fibers
within the internal capsule are glutamate (most cortical efferent fibers,
thalamocortical fibers) and GABA (pallidothalamic fibers), and smaller
populations of cholinergic, dopaminergic, serotoninergic, histaminergic,
and GABA-ergic fibers.
Clinical Correlations
Lesions of the internal capsule are usually expressed as movement disorders related to involvement of corticospinal, pallidothalamic, or corticonuclear fibers (depending on the general location of the lesion), and
somatosensory losses related to damage to thalamocortical projections.
A general characteristic of forebrain lesions is that motor and sensory
deficits are all on the same side (the side of the body opposite the location of the lesion). Cranial nerve deficits are usually lacking unless the
damage involves the genu of the internal capsule.
A lesion in the genu of the internal capsule results in deficits that generally reflect damage to corticonuclear fibers to the facial and hypoglossal nuclei, and to the nucleus ambiguus. The facial muscles are weak on
the lower half of the face opposite the lesion (a central seven as opposed
to a Bell palsy), the tongue deviates to the opposite side on attempted
protrusion, and the uvula deviates toward the lesioned side when the
patient makes an “ah” sound. In addition, the patient may not be able to
elevate the ipsilateral shoulder against resistance (trapezius weakness) or
to rotate the head to the contralateral side against resistance (sternocleidomastoid weakness) assuming injury to fibers of the accessory nucleus.
This combination of deficits is unique to genu lesions and is clearly different from cranial nerve deficits resulting from brainstem lesions.
Damage to the posterior limb of the internal capsule may result in a
frank contralateral hemiplegia or hemiparesis (-plegia refers to paralysis
and -paresis refers to weakness or incomplete paralysis) affecting upper
and lower extremities and a hemianesthesia on the same side as the weakness. This sensory loss may affect the body only or the body plus the head.
The anterior choroidal artery syndrome (also called von Monakow
syndrome) is characterized by a hemiplegia and a homonymous hemianopia, both contralateral to the side of the lesion. If this lesion (which is
in the lower portion of the posterior limb) extends upward, it may also
involve thalamocortical fibers from sensory relay nuclei, producing a
hemianesthesia on the same side as the other deficits. This vessel serves
portions of the genu, and corticonuclear deficits may sometimes be seen.
of Blood Supply to the Internal Capsule
eReview
ee
Structures
Arteries
Anterior Limb
gee ’
Posterior Limb
Sublenticular Limb
Retrolenticular Limb
Lateral striate branches of middle cerebral; medial striate branches of anterior
cerebral (see Figure 6-41)
Lateral striate branches of middle cerebral; anterior choroidal artery (see Figure
6-41)
Lateral striate branches of middle cerebral; anterior choroidal artery (see Figure
6-41)
Penetrating branches of middle cerebral (temporal, angular branches)
Posterior cerebral; small branches from anterior choroidal
$$
eee
Internal Capsule and Thalamocortical Connections
8-52 THE INTERNAL CAPSULE: RELATIONSHIPS AND CONTENTS
Head of caudate nucleus (HCaNu)
Lateral ventricle,
anterior horn
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Anterior thalamic
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Temporopontine rad.
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Lateral geniculate nucleus
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RETROLENTICULAR LIMB | Corticotectal,
(RLintCap) | Corticorubral,
Corticotegmental f. and
Posterior thalamic rad.
~
Tapetum
HCaNu
Put
HCaNu
Put
GP
GP
Thalamus
|
PLIntCap
Thalamus
RLIntCap
Quadrigeminal cistern
Quadrigeminal cistern
ae
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BieTas
Clinic
Tracts, Pathways, and Systems in Anatomand
ica
lal Orientation See
sina
aia
THE TOPOGRAPHY
OF THALAMOCORTICAL
The major nuclei of the dorsal thalamus, commonly called the
thalamus, and their major cortical targets. The thalamic nuclei
may generally be divided into association nuclei, relay nuclei, and intralaminar nuclei. Association nuclei project to multiple cortical regions
and receive input from similarly diverse regions (e.g., pulvinar, centromedian). Relay nuclei are those which receive a specific type of information (discriminative touch, vision) and send this information on to
a precise cortical target (primary somatosensory cortex, primary visual
cortex); examples are: the ventral posterolateral nucleus and the lateral
geniculate nucleus. Intralaminar nuclei are located within the internal
medullary lamina; the most obvious is the centromedian nucleus; smaller
intralaminar nuclei include the central lateral, central medial, and the
parafascicular nuclei. The thalamic reticular nucleus is a group of neurons forming a shell around the thalamus, separated from it by the internal medullary lamina, and located medial to the internal capsule.
The thalamic nuclei receive information from many sources and project to the cerebral cortex. The more important thalamic nuclei, their
afferents, and the cortical areas/gyri to which they project are summarized below and illustrated in Figure 8-53 on the facing page. Some
generalizations are made for clarity.
Association nuclei:
Dorsomedial nucleus: afferents—amygdala, pallidum, temporal and orbitofrontal cortex, olfactory system, basal forebrain; efferents—orbital
cortex, medial and lateral frontal lobe (excluding the motor cortex)
Pulvinar: afferents—superior colliculus, visual cortex (areas 17, 18, 19),
temporal and occipital cortex; efferents—superior colliculus, visual cortex (areas 17, 18, 19), temporal and occipital cortex
Relay nuclei:
Anterior thalamic nuclei: afferents—medial mammillary nucleus, hippocampal formation; efferents—cingulate gyrus, small amount to limbic and orbitofrontal cortex
Ventral anterior nucleus: afferents—globus pallidus, substantia nigra,
cortical areas 6 and 8; efferents—frontal cortex (excluding area 4),
orbital cortex
Ventral lateral nucleus: afferents—globus pallidus, cerebellar nuclei,
motor cortex (area 4); efferents—motor cortex (area 4), supplemental
motor cortex
Ventral posterolateral nucleus: afferents—posterior column—medial
lemniscus system, anterolateral system; efferents—primary somatosensory cortex (areas 3, 1, 2)
Ventral posteromedial nucleus: afferents—spinal and principal sensory
nuclei, solitary nucleus (taste); efferents—face area of primary somatosensory cortex (areas 3, 1, 2), frontal operculum and adjacent insular
cortex (taste areas)
Medial geniculate nucleus: afferent—inferior
transverse temporal gyrus (of Heschl, area 41)
colliculus;
efferents—
Lateral geniculate nucleus: afferents—portions of both retina, visual
area 17; efferents—primary visual cortex (area 17, some to 18 and 19)
CONNECTIONS
Intralaminar nuclei:
Centromedian nucleus: afferents—frontal, limbic and motor cortex,
pallidum, cerebellar nuclei, reticular formation, spinal cord, sensory
cortex; efferents—corpus striatum (putamen, globus pallidus, caudate),
subthalamic nucleus, substantia nigra, frontal lobe
Other intralaminar nuclei: afferents—cerebral cortex, brainstem reticular formation, nucleus accumbens, olfactory tubercle; efferents—similar
to centromedian, cingulate gyrus
Other:
Thalamic reticular nucleus: afferents—collaterals of thalamocortical,
corticothalamic, thalamostriate, and pallidothalamic fibers; efferents—
thalamic nuclei
Clinical Correlations
The thalamus receives extensive sensory and motor and other messages, has an equally extensive projection to all parts of the cerebral
cortex (and many subcortical centers), and receives reciprocal connections from the cerebral cortex. Consequently, a variety of deficits
is seen resultant to lesions of the thalamus. While thalamic lesions
may present as tumors (such as astrocytoma), neural degenerative,
or encephalopathic, they are most commonly vascular in origin and,
therefore, respect structures located within the respective vascular
territories.
Hemorrhage into the thalamogeniculate territory damages the
sensory relay nuclei (VPM and VPL) and may result in the thalamic
syndrome (syndrome of Déjérine-Roussy). The characteristics of this
syndrome are: (1) loss of all somatic sensation on the contralateral side
of the body, or a dissociated sensory loss (position/vibratory loss greater
than pain/thermal loss, or vice versa); (2) with recovery, the occurrence
of a perception of pain (paresthesia, hyperpathia) sometimes intense
and/or long lasting; and, (3) may present with a homonymous hemianopia and/or hemiplegia of the UE and LE, all on the contralateral side;
these may resolve with time. The hemiplegia may relate to hemorrhage
impinging on the laterally adjacent posterior limb of the internal capsule or pressure from the primary lesion.
In addition to variations of the thalamic syndrome, hemorrhagic thalamic lesions may extend into the midbrain and produce various oculomotor deficits (third nerve or nucleus damage), pupil dilation, and an
absent or diminished pupillary light reflex. These hemorrhagic lesions
may also invade the subthalamic nucleus and contribute abnormal
movements to the overall clinical picture.
Lesions in more anterior and medial portions of the dorsal thalamus may produce deficits that are generally more global. The patient
may experience ataxia (thalamic ataxia) of a transient nature and possibly aphasia. In the case of a lesion in the thalamic territory of an azygos thalamoperforating territory (see Figure 2-44), the pathway of the
ascending reticular activating system is interrupted, and the patient may
be difficult to arouse, stuporous, or in a coma.
Review of Blood Supply to the Dorsal Thalamus
Structures
Arteries
Anterior Thalamic Areas
Thalamoperforating branches of P, (see Figure 6-41)
Thalamogeniculate branches of P, (see Figure 6-41)
Medial posterior choroidal artery, P; branch (see Figure 6-41)
Posterior Thalamic Areas
Caudomedial Thalamic Area
eee
8-53 THE TOPOGRAPHY
OF THALAMOCORTICAL
CONNECTIONS
Precentral gyrus
Postcentral gyrus
Superior parietal lobule
Superior frontal gyrus
Frontal eye field
Middle frontal gyrus
fz
Lateral occipital gyri
Superior temporal gyrus
Inferior frontal gyrus
Middle temporal gyrus
Orbita! cortex (gyri)
Inferior temporal gyrus
Primary auditory cortex
Posterior paracentral gyrus
Anterior paracentral gyrus
~<
Superior frontal gyrus (medial surface)
— Cingulate gyrus
Precuneus
Lingual gyrus
Parahippocampal gyrus
Occipitotemporal gyri
Dorsomedial nucleus
eee
Anterior nucleus
Magnocellular part,
rll UD
:
Ventral anterior nucleus
lif
c
“
‘
Parvocellular part
Centromedian nucleus
[
|
Internal medullary lamina
Pulvinar
Oral part
Ventral lateral nucleus
Caudal part
Internal medullary lamina
Lateral dorsal nucleus
Lateral posterior nucleus
Medial geniculate nucleus
:
Lateral geniculate nucleus
\ Ventral posteromedial nucleus
Ventral posteromedial nucleus
280i
. Tracts, Pat
Pa hways, and
Sy
1 Amygdala
a
HIPPOCAMPAL CONNECTIONS
"
BAX
nuclei.
Neurotransmitters
Glutamate (+)-containing cells in the subiculum and Ammon’s horn project to the mammillary body, other hypothalamic centers, and the lateral
septal nucleus through the fornix. Cholecystokinin (+) and somatostatin
(—) are also found in hippocampal cells that project to septal nuclei and
hypothalamic structures. The septal nuclei and the nucleus of the diagonal band give rise to cholinergic afferents to the hippocampus that travel
in the fornix. In addition, a y-aminobutyric acid (—) septohippocampal
projection originates from the medial septal nucleus. Enkephalin- and
glutamate-containing hippocampal afferent fibers arise from the adjacent entorhinal cortex; the locus ceruleus gives origin to noradrenergic
fibers to the dentate gyrus, the Ammon horn, and subiculum; and serotoninergic fibers arise from the rostral raphe nuclei.
Clinical Correlations
Dysfunction associated with damage to the hippocampus is seen in
patients with trauma to the temporal lobe, as a sequel to alcoholism, and
as a result of neurodegenerative changes seen in the dementing diseases
(e.g., Alzheimer disease and Pick disease). Bilateral injury (as in closed
head injury in automobile collisions) to the hippocampus results in loss
of recent memory (remote memory is unaffected), impaired ability to
remember recent (new) events, and difficulty in turning a new experience
(something just done or experienced) into a longer-term memory that can
be retrieved at a later time. Also, memory that depends on visual, tactile,
or auditory discrimination is noticeably affected. These represent visual
agnosia, tactile agnosia, and auditory agnosia, respectively.
In the Korsakoff psychosis (amnestic confabulatory syndrome, or
Korsakoff syndrome) there is memory loss, dementia, amnesia, and a
tendency to give confabulated responses. This type of response is fluent (the patient’s response is immediate, smooth, and in appropriate
cadence), but consists of a string of unrelated, or even made up, “memories” that never actually occurred or make no sense (hence, the confabulation). This may lead to an incorrect conclusion that the patient
is suffering from dementia. In addition to lesions in the hippocampus
in these patients, the mammillary bodies and dorsomedial nucleus of
the thalamus are noticeably affected. Korsakoff psychosis is irreversible.
Wernicke encephalopathy (Wernicke-Korsakoff syndrome, or Wernicke
syndrome) is seen in patients who are long-term alcoholics (with very poor
nutrition habits), and presents with a variety of eye movement deficits,
pupil changes, ataxia, confusion, and tremor. Degenerative changes, or cell
loss, are seen in many areas but especially in the hippocampus, mammillary nuclei, and dorsomedial nucleus of the thalamus. This condition is
treatable with therapeutic doses of thiamin and dietary improvements.
ABBREVIATIONS
AC
AmHrn
Amy
Anterior commissure
Ammon horn
Amygdaloid nucleus (complex)
A,
ORIENTATION
IN ANATOMICAL
Selected afferent and efferent connections of the hippocampus
(upper) and the mammillary body (lower) with emphasis on
the circuit of Papez. The hippocampus receives input from, and projects
to, diencephalic nuclei (especially the mammillary body via the postcommissural fornix), the septal region, and amygdala. The hippocampus
also receives cortical input from the superior and middle frontal gyri,
superior temporal and cingulate gyri, precuneus, lateral occipital cortex,
occipitotemporal gyri, and subcallosal cortical areas. Those corticohippocampal fibers from the cingulate gyrus are a particularly important
part in the Papez circuit of emotion. The mammillary body is connected
with the dorsal and ventral tegmental nuclei, anterior thalamic nucleus
(via the mammillothalamic tract), septal nuclei, and through the mammillotegmental tract, to the tegmental pontine and reticulotegmental
_
-
LT
MB
MedFCtx
AntNu
Anterior nucleus of thalamus
MedTh
CC, G
CC, Spl
Cing
CingGy
CorHip
DenGy
EnCtx
For
Corpus callosum, genu
Corpus callosum, splenium
Cingulum
Cingulate gyrus
Corticohippocampal fibers
Dentate gyrus
Entorhinal cortex
Fornix
MTegTr
MtIr
NuAcc
OpCh
Pi
RSpICtx
SepNu
SMNu
GyRec
Hip
Hyth
IC,G
Gyrus rectus
Hippocampus
Hypothalamus
Internal capsule, genu
Sub
TegNu
VmNu
Lamina terminalis
Mammillary body
Medial frontal cortex
Medial thalamus
Mammillotegmental tract
Mammillothalamic tract
Nucleus accumbens
Optic chiasm
Pineal
Retrosplenial cortex
Septal nuclei
Supramammillary nucleus
Subiculum
Tegmental nuclei
Ventromedial hypothalamic
nucleus
Review of Blood Supply to Hip, MB, Hyth, and CingGy
Structures
Arteries
Hip
Anterior choroidal (see Figure 6-41)
MB, Hyth
Branches of circle of Willis (see Figure 2-21)
AntNu
Thalamoperforating (see Figure 6-41)
CingGy
Branches of
anterior cerebral
EEE
RSplCtx
4
we
Amy e-
SE
c—- Hip
DenGy
AmHrn
Sub
a
CingGy ~,
Cing
TegNu
DenGy
AmHrn
pe
sb
=
AMYGDALOID
CONNECTIONS
ae The origin, course, and distribution of selected afferent and
efferent connections of the amygdaloid nuclear complex in
sagittal (upper) and coronal (lower) planes. The amygdala receives input
from, and projects to, brainstem and forebrain centers via the stria terminalis and the ventral amygdalofugal pathway. Corticoamygdaloid
and amygdalocortical fibers interconnect the basal and lateral amygdaloid nuclei with select cortical areas.
Neurotransmitters
Cells in the amygdaloid complex contain vasoactive intestinal polypeptide
(VIP, +), neurotensin (NT), somatostatin (SOM, —), enkephalin (ENK, -),
and substance P (SP, +). These neurons project, via the stria terminalis or
the ventral amygdalofugal path, to the septal nuclei (VIP, NT), the bed
nucleus of the stria terminalis (NT, ENK, SP), the hypothalamus (VIP,
SOM, SP), the nucleus accumbens septi, and the caudate and putamen
(NT). Serotonergic amygdaloid fibers originate from the nucleus raphe
dorsalis and the superior central nucleus, dopaminergic axons from the
ventral tegmental area and the substantia nigra—pars compacta, and
noradrenalin-containing fibers from the locus ceruleus. Glutamate (+) is
found in olfactory projections to the prepiriform cortex and the amygdaloid complex. Acetylcholine is present in afferents to the amygdala from
IN ANATOMICAL
ORIENTATION
the substantia innominata, as well as from the septal area. In patients
with Alzheimer disease and associated dementia, there is a marked loss
of acetylcholine-containing neurons in the basal nucleus of the substantia innominata, the cortex, and the hippocampus.
Clinical Correlations
oS
Dysfunctions related to damage to the amygdaloid complex are seen
in patients with trauma to the temporal lobes, herpes simplex encephalitis, bilateral temporal lobe surgery to treat intractable epileptic
activity, and in some CNS degenerative disorders (e.g., Alzheimer
disease and Pick disease). The behavioral changes seen in individuals with what are usually bilateral amygdala lesions collectively form
the Kliiver-Bucy syndrome. In humans these changes/deficits are: (1)
hyperorality; (2) visual, tactile, and auditory agnosia; (3) placidity;
(4) hyperphagia or other dietary manifestations; (5) an intense desire
to explore the immediate environment (hypermetamorphosis); and
(6) what is commonly called hypersexuality. These changes in sexual
attitudes are usually in the form of comments, suggestions, and inept
attempts at actual contact rather than blatant attempts at inappropriate behavior. These patients also may show aphasia, dementia, and
amnesia.
ABBREVIATIONS
AC
Amy
Anterior commissure
Amygdaloid nuclear complex
AmyCor
AmyFugPath
AntHyth
Ba-LatNu
CaNu
Amygdalocortical fibers
Amygdalofugal pathway
Anterior hypothalamus
Basal and lateral nuclei
Caudate nucleus
Cen-MedNu
Central, cortical and medial nuclei
CorAmy
DVagNu
EnCtx
For
GP
Hyth
LT
LHAr
MedThNu
MGNu
MidTh
NuAcc
Corticoamygdaloid fibers
Dorsal motor vagal nucleus
Entorhinal cortex
Fornix
Globus pallidus
Hypothalamus
Lamina terminalis
Lateral hypothalamic area
Medial thalamic nuclei
Medial geniculate nucleus
Midline thalamic nuclei
Nucleus accumbens
NuCen, s
Nucleus centralis, superior
NuCer
Nucleus ceruleus
NuRa, d
NuRa, m
NuRa, o
NuRa, p
NuStTer
OIfB
OpCh
PAG
PbrNu
PfNu
Pi
POpNu
PPriCtx
Put
SepNu
SNpce
SolNu
StTer
Sub
SubIn
VenTegAr
VmNu
Nucleus raphe, dorsalis
Nucleus raphe, magnus
Nucleus raphe, obscurus
Nucleus raphe, pallidus
Nucleus of the stria terminalis
Olfactory bulb
Optic chiasm
Periaqueductal (central) gray
Parabrachial nuclei
Parafascicular nucleus
Pineal
Preoptic nucleus
Prepiriform cortex
Putamen
Septal nuclei
Substantia nigra, pars compacta
Solitary nucleus
Stria terminalis
Subiculum
Substantia innominata
Ventral tegmental area
Ventromedial hypothalamic nucleus
Review of Blood Supply to Amy and Related Centers
Structures
Arteries
Amy
Anterior choroidal (see Figure 6-41)
Hyth
Branches of circle of Willis (see Figure 6-41)
Brainstem
See Figures 6-16, 6-23, and 6-30
Thalamus
Thalamoperforating, thalamogeniculate
(see Figure 6-41)
OO
hs RNS ONCSSIS SA Si SCE SO ace US Ae eG a
andAmygdala
| Limple system Hippocampu
s
DEES
8-55 AMYGDALOID
CONNECTIONS
IN ANATOMICAL
MedThNu
MidTh, Pf{Nu, MGNu
ee)
NuStTer
AC
—1)
LT
AntHyth
olfB —
cue
WS
PAG
&
SNopc, VenTegAr
NuRa,d
POpNu——~
AmyFugPath
Amy
ORIENTATION
ef
;
Cen-MedNu
< &
1 Ba-LatNu
(S| a
NN
PPriCtx
SolNu
NuRa,p
NuRa,o
DVagNu
Prefrontal cortex
Cingulate gyrus
certi
htmat
ERO
NuStTer
Insula
ea)
StTer
Temporal
lobe
Fa
at
Parahippocampal
gyrus
SepNu
Ag
N\
AmyCor
NuAcc
é
SS
aes
rg
of
to StTer
CZ.
a
Me
K
IES
a
For
|
Hyth
.
y
“0
p
a)
AmyFugPath
aA
Ba-LatNu
3=
Popa
Middle cerebral artery
Amygdalofugal pathway: to septal
nuclei, medial thalamic nuclei, preoptic nucleus, hypothalamus, substantia innominata, brainstem nuclei
Uncus
Amygdaloid
complex
Middle cerebral artery
Temporal horn,
lateral ventricle
Amygdaloid complex
Temporal horn,
lateral ventricle
Stria terminalis: to hypothalamus,
nucleus accumbens, preoptic
nucleus, putamen, caudate nucleus
Hippocampus
Hippocampus
Crus cerebri
Crus cerebri
Interpeduncular fossa
Stria terminalis
Midbrain tegmentum
Fornix
Fornix: to anterior thalamic
nucleus, hypothalamus,
septal nuclei, gyrus rectus +
Inferior colliculus
medial frontal cortex,
nucleus accumbens
Superior (quadrigeminal)
cistern
Anterior lobe of
cerebellum
wep. The principal efferent projections of the amygdaloid
nucleus and the hippocampal formation superimposed on
MRL in clinical orientation. This axial image is a T2-weighted MRI. The
arrowheads on the efferent fibers, and the targets indicated for these
fibers, indicate that these pathways have extensive and widespread
connections.
Limbic System:
Hippocampus
and Amygdala
HIPPOCAMPAL AND AMYGDALOID EFFERENTS IN CLINICAL ORIENTATION:
REPRESENTATIVE LESIONS AND DEFICITS
Amygdalofugal pathway: to septal
nuclei, medial thalamic nuclei, preoptic nucleus, hypothalamus, substantia innominata, brainstem nuclei
Middle cerebral artery
Middle cerebral artery
Amygdaloid lesion(s)
Amygdaloid complex
Temporal horn,
lateral ventricle
Stria terminalis: to hypothalamus,
nucleus accumbens, preoptic
nucleus, putamen, caudate nucleus
Hippocampus
Crus cerebri
-Kluver—Bucy syndrome consisting of
hyperorality, hyperphagia, agnosia
(visual, tactile, auditory), placidity,
hypersexuality, hypermetamorphosis:
seen only in bilateral lesions
-Aphasia, amnesia, dementia
-Stimulation = emotional outbursts
-Bilateral lesions more common and
correlated with more severe deficits
Hippocampal lesion(s)
-Severe/long-lasting memory deficits in
bilateral lesions
-Loss of short-term and immediate
memory, unable to turn these into long-
term memory; much of long-term (remote)
memory is intact
Interpeduncular fossa
Midbrain tegmentum
Fornix: to anterior thalamic
-Other related conditions: Korsakoff and
Wernicke—Korsakoff syndromes,
Alzheimer disease
-Confabulation, amnesia
Inferior colliculus
nucleus, hypothalamus,
septal nuclei, gyrus rectus +
medial frontal cortex,
nucleus accumbens
Superior (quadrigeminal)
cistern
Anterior lobe of
cerebellum
Alzheimer dementia
Representative lesions of the amygdaloid nucleus and hippocampal formation and the deficits (in pink boxes) that cor-
and medial
relate with each lesion. Damage to these regions of the rostral
s are
collision
vehicle
motor
;
bilateral
ly
frequent
temporal lobes is most
common causes. Although there may be damage to only one side, as in
stroke, deficits are most severe in situations of bilateral damage. The
lower MRI are examples of conditions that affect the hippocampus and/
or the amygdala; the enlarged ventricles signify loss of brain tissue.
BLANK MASTER
8-57
DRAWING
Blank master drawing for limbic pathways. This illustration is provided for self-evaluation of limbic pathways or
FOR LIMBIC PATHWAYS
connections, for the instructor to expand on aspects of these pathways
not covered in the Atlas, or both.
Tracts, Pathways, and Systems in Anatomical and Clinical Or
HYPOTHALAMIC
STRUCTURES AND CONNECTIONS:
STAINED SECTIONS
The structure of the hypothalamus in three representative coronal sections (A, B, C), and a drawing in sagittal (upper left)
axial plane (upper right), showing the general arrangement of the nuclei
and the relationships of immediately adjacent fiber bundles and nuclei.
The various hypothalamic nuclei that are labeled are generally representative of that coronal level; for a more detailed representation in the
axial plane, see Figure 8-59.
The hypothalamus is organized into three rostrocaudally oriented
zones (upper right). The comparatively narrow periventricular zone is
located in the ventricular wall, is of an irregular thickness, and contains a
number of small nuclei. Neurons within the periventricular zone function
in the synthesis of releasing hormones (RHs) that are conveyed to the pituitary via the tuberoinfundibular tract. The medial zone is located immediately lateral to the periventricular zone and is divided into three regions: a
supraoptic region (internal to the optic chiasm), a tuberal region (internal
to the location of the tuber cinereum), and a mammillary region (internal
to the mammillary body). For the large part, the medial zone is arranged
into a number of named nuclei. The lateral zone is an area of diffusely
arranged neurons commonly called the lateral hypothalamic area that contains relatively few named nuclei, but does contain the medial forebrain
bundle. The positions of the column of the fornix and the mammillothalamic tract indicate the border between the medial and lateral zones. See
Figure 8-59 for additional information on hypothalamic zones and nuclei.
preoptic nuclei, and the lateral hypothalamic area). Angiotensin II is in
a family of peptides that exhibits vasoconstrictive activity; these cells
are found in the paraventricular and supraoptic nuclei (and project to
the posterior pituitary), and fibers are found in the dorsomedial nucleus.
Releasing factors (RFs) and RHs: Many of these substances are associated with projection systems that originate in the hypothalamus and
travel to the pituitary. The main RFs and RHs are corticotrophin RF
(cells in the medial preoptic and paraventricular nuclei and the lateral
hypothalamic area); luteinizing RH (cells in supraoptic, medial preoptic, and infundibular nuclei [the latter projects to the posterior pituitary lobe]); somatostatin (cells in infundibular, suprachiasmatic, medial
preoptic, and paraventricular nuclei [these cells project to other hypothalamic nuclei]), and thyrotropin RH (cells in the median eminence;
ventromedial, dorsomedial, preoptic, and suprachiasmatic nuclei; and
the periventricular zone).
Dynorphin and enkephalin: These substances are found at many
locations in the CNS; one of their functions is related to pain modulation. Dynorphin (cells in the supraoptic, suprachiasmatic, ventromedial, dorsomedial, and paraventricular nuclei [all of these nuclei plus
the anterior nucleus and medial preoptic area also contain fibers]) and
enkephalin (cells in the supraoptic and paraventricular nuclei and the
preoptic region) are also found in cells located in many areas of the
forebrain, brainstem, and spinal cord.
Neurotransmitters
Clinical Correlations
The entire diencephalon constitutes only about 2% of the entire CNS
by weight and the hypothalamus, a small part of the diencephalon,
represents under 0.2% of the CNS. In spite of its minuscule size, the
hypothalamus has a widespread and powerful influence over the CNS,
and, indeed, the entire body. This is at least partially reflected by the
fact that numerous neurotransmitter substances are found in the cells
of the hypothalamus or in terminals ending in these nuclei that arise
in other locations. The following is not intended to be an all-inclusive
list of transmitters associated with the hypothalamus, but serves as a
representative example.
Due to its compact nature and location, deficits related to lesions involving the hypothalamus are frequently complicated by endocrine disorders,
visual field defects, and behavioral disorders. Only representative deficits
are mentioned here that would relate to lesions within the hypothalamus.
The medial mammillary nucleus receives extensive connections from
the hippocampus via the postcommissural part of the fornix. Lesions of
the mammillary nuclei result in an inability to process short-term events
into long-term memory. This may be seen in vascular lesions or in the
Korsakoff syndrome (Korsakoff psychosis).
The suprachiasmatic nucleus receives input from the retina and is
involved in the establishment and maintenance of circadian rhythms;
these are cycles consisting of a light phase and a dark phase collectively
forming about 24 hours. Damage to this area may modify, or abolish,
these rhythms.
The supraoptic and paraventricular nuclei synthesize oxytocin and
vasopressin and transmit these substances to the posterior lobe of the
pituitary via the supraopticohypophyseal tract. Damage to these nuclei,
or to this tract, as in a traumatic brain injury (TBI), may result in dia-
Monoamines: The monoamines histamine (cells in the dorsomedial
nucleus, posterior hypothalamic area, tuberal nuclei), dopamine (cells
in the caudal hypothalamus A11 cell group, periventricular area), and
serotonin (fibers in the dorsomedial, ventromedial, preoptic, suprachiasmatic, and infundibular nuclei) are found in the hypothalamus. Some of
these cells may project to other of the hypothalamic nuclei.
Peptides: These are sometimes referred to as gut-brain peptides
because they were initially isolated from brain and gut tissue. The
principal peptides found in the hypothalamus are neurotensin (cells in
rostral periventricular zone, the preoptic, paraventricular, and infundibular nuclei and lateral hypothalamic area; fibers in these nuclei and the
median eminence), cholecystokinin (cells in the paraventricular, medial
preoptic, supraoptic, and dorsomedial nuclei; fibers in the ventromedial
nucleus), vasoactive intestinal polypeptide (VIP) (cells in the suprachiasmatic nucleus; fibers in the dorsomedial, ventromedial, paraventricular,
anterior nucleus, and preoptic regions); and substance P (cells and fibers
in the supraoptic, paraventricular, dorsomedial, ventromedial, arcuate,
betes insipidus (DI); this condition is characterized by increased water
intake (polydipsia) and increased urination (polyuria).
Damage to the nuclei of the lateral hypothalamic area results in
a decrease in feeding behavior with a resultant weight loss, whereas
injury to the ventromedial nucleus (commonly called a satiety center)
will cause excessive eating and abnormal weight gain. The dorsomedial
nucleus, which is dorsally adjacent to the ventromedial nucleus, is a
behavioral center; stimulation causes sham rage; destruction results in
a
decrease in aggression and feeding behaviors.
Review of Blood Supply to the Hypothalamus
Structures
Arteries
Anterior Hypothalamus
Anteromedial group from A, and ACom (see Figure 2-21)
Posteromedial group from PCom and P, (see Figure 2-21)
Mid/Caudal Hypothalamus
Ss
OO
Soe
a "Hypothalamus and Pituitary —
wa
8-58 HYPOTHALAMIC
STRUCTURES AND CONNECTIONS:
STAINED SECTIONS
Axial plane
Medial and lateral preoptic n.
Column of fornix:
Hypothalamic
sulcus
Supraoptic n.
Anterior nucleus
Ventromedial n-
commissure
[|
Tuberal nuclei
Axial plane
Mammillothalamic tr.
Optic
:
chiasm
Mamumillary
body
Lateral nuclei
Tuberomammillary n.
;
Lateral mammillary n.
Paraventricular n.
Arcuate n.
Dorsomedial n.
Posterior n.
Medial mammillary n.
Lateral hypothalamic area/zone
Diagonal band (of Broca)
Medial preoptic area
Anterior nucleus
Third ventricle
Anterior commissure
Periventricular areas/zones
Supraoptic nucleus
Optic tract at chiasm
Supraoptic commissure
Stalk of infundibulum
Infundibular recess
Column of fornix
:
Lateral hypothalamic area/zone
Hypothalamic sulcus
P.araventricicular uclenuclei
Periventricular areas/zones
Dorsomedial nucleus
Ansa lenticularis
Supraoptic nucleus
Optic tract
Ventromedial nucleus
Arcuate nucleus
Tuberal nuclei
Third ventricle
Posterior nuclei
Zona incerta
Lenticular fasciculus
Lateral hypothalamic area/zone
Third ventricle
Optic tract
j y nucleus
Lateral mammillar
Principal mammillary fasciculus
(to mammillothalamic and
mammillotegmental tracts)
Subthalamic nucleus
Medial mammillary nuclei
eo
Aa
aa
see wl
ae ae
n
Tracts, Pathways, and Systemsin Anatomica and Clinical Orie
j
HYPOTHALAMIC
:
a
s
-
=a)
STRUCTURES AND CONNECTIONS:
The structure of the hypothalamus represented in the axial
plane showing the three zones, the regions of the medial zone,
and their major afferent and efferent connections. The connections of
the hypothalamus are complex and widespread within the brain. In
addition, many of these connections are reciprocal: structures that project to the hypothalamus frequently receive input from the hypothalamus. An effort is made here to illustrate the hypothalamus in axial
plane, its principal nuclei, and its major afferent and efferent pathways,
all in a semi-diagrammatic format. Hypothalamic afferents are shown
in red (on right), efferents in blue (on left).
Zones: The lateral zone (shaded blue) contains diffuse cell groups,
the tuberal nuclei, and the fibers of the medial forebrain bundle. The
medial zone is organized into the supraoptic region (shaded green), the
tuberal region (shaded red), and the mammillary region (shaded gray);
each region is composed of several named nuclei. The periventricular
zone (unshaded/white) is a thin sheet of cells in the wall of the hypothalamic portion of the third ventricle. See also Figure 8-58.
Retinohypothalamic fibers: Axons arising from ganglion cells of the
retina project bilaterally to the suprachiasmatic nucleus via the optic
nerve and tract. These projections are essential to the maintenance of
circadian rhythms.
Amygdalohypothalamic fibers: The amydgala projects to the hypothalamus via the ventral amygdalofugal pathway (VAF) and the stria
terminalis (ST). VAF fibers arise in the basolateral amygdala, course
medially and inferior to the lenticular nucleus, to end in the septal area,
lateral zone, and preoptic areas. Fibers forming the ST arise in the corticomedial amygdala, form a small bundle medial to the caudate and
accompanied by the thalamostriate vein, and distribute to the septal
area and nuclei of the supraoptic and tuberal regions.
Hippocampohypothalamic fibers: Cells of the hippocampal formation coalesce to form the fornix. The precommissural fornix is diffusely
arranged and distributes to septal, preoptic, and anterior hypothalamic
nuclei, whereas the primary target of the postcommissural fornix, which
is compactly arranged is the medial mammillary nucleus with lesser
projections to the dorsomedial nucleus and lateral hypothalamic zone.
A rostrocaudal line drawn between the postcommisural fornix and the
mammillothalamic tract generally separates the lateral from medial zones.
Brainstem-hypothalamic fibers: Afferents to the hypothalamus
that arise within the brainstem and ascend mainly in the mammillary
peduncle and posterior (dorsal) longitudinal fasciculus, with fewer
fibers traversing the medial forebrain bundle. These projections arise in
the tegmental and raphe nuclei of the midbrain, the locus coeruleus, and
the lateral parabrachial nucleus and terminate in the lateral zone and in
many of the nuclei of the medial and paraventricular zones. Serotinergic
fibers arise from the raphe nuclei, and monoaminergic projections originate from the locus coeruleus.
ABBREVIATIONS
nucleus
tract
=} -,
PROJECTIONS
Other afferent fibers: The hypothalamus also receives spinohypothalamic fibers via the anterolateral system and corticohypothalamic fibers
from widespread areas of the cerebral cortex including occipital, frontal, and parietal, and from the cortices of the limbic lobe.
Efferent hypothalamic connections: The double-headed arrows on
the left signify the fact that the amygdaloid nuclear complex and the
hippocampal formation receive input from the hypothalamic nuclei to
which they project. This also applies to the fact that many of the cortical areas that give rise to a corticohypothalamic projection also receive
hypothalamocortical fibers.
The posterior (dorsal) longitudinal fasciculus contains fibers arising
in various nuclei of the periventricular and medial zones and projects to
the midbrain tegmentum, tectum, and the central gray of the brainstem;
some of these fibers target visceral motor nuclei.
The principal mammillary fasciculus is the bundle that passes out of
the mammillary nuclei, then immediately divides into the mammillothalamic tract and the mammillotegmental tract. The former projects to the
anterior thalamic nucleus, and the latter projects mainly to the midbrain
tegmental nuclei.
Descending fibers that arise in the paraventricular and posterior
hypothalamic nuclei (emphasis on the paraventricular) and in the lateral hypothalamic zone, influence brainstem visceral motor and sensory nuclei, parts of the nucleus ambiguus, the ventrolateral medullary
regions, and the spinal cord (specifically the interomediolateral cell column). Through these descending fibers to visceral nuclei of the brainstem, the hypothalamus influences a wide range of essential activities
controlled by these brainstem regions. Damage to these hypothalamospinal fibers may result in a Horner syndrome (ptosis, myosis, anhydrosis
on the ipsilateral side) along with other deficits characteristic of the
lesion be it in the midbrain, lateral pontine tegmentum, lateral medulla,
or cervical spinal cord.
The medial forebrain bundle is diffusely arranged and contains fibers
arising in the lateral zone and ascending to hypothalamic, olfactory,
and other basal forebrain areas and of some descending fibers to the
brainstem.
Clinical Correlations
i
ee
ee
In addition to the clinical comments made above, a number of further
clinical examples of hypothalamic lesions are described in Figure 8-58.
It is important to recall that hypothalamic lesions may initially present with the patient complaining of various visual deficits or of a variety of endocrine (visceromotor) disorders; a thorough examination
and evaluation will reveal the hypothalamic source of the primary
lesion.
Review of Blood Supply to the Hypothalamus
Structures
Arteries
Anterior Hypothalamus
Anteromedial group from A; and ACom (see Figure 2-21)
Posteromedial group from PCom and P, (see Figure 2-21)
Mid/Caudal Hypothalamus
—_—_—_———————————————————
a
| Seba
ooo
8-59 HYPOTHALAMIC
STRUCTURES AND CONNECTIONS:
bees Eee
201
PROJECTIONS
Retina
7
Basolateral amygdala
Amygdalofugal pathway
Anterior commissure
Stria terminalis
Septal nuclei
?
Corticomedial amygdala
Precommissural fornix
Hippocampal formation
Postcommisural fornix
To preoptic, supraoptic,
and suprachiasmatic nuclei
To anterior thalamic nucleus
via mammillothalamic tract
To brainstem tegmentum; tegmental,
superior central, dorsal motor vagal, and
Third ventricle
solitary nuclei; nucleus ambiguus;
ventrolateral medulla; and
From tegmental, raphe, superior
central, and parabrachial nuclei;
locus coeruleus; central gray;
midbrain and pontine tegmentum;
and reticular formation
intermediolateral cell column
Key for nuclei
Medial and lateral preoptic n.
Column of fornix
Key for zones and regions
Supraoptic n.
:
Anterior nucleus
Suprachiasmatic n.
Ventromedial n.
Periventricular nuclei
Tuberal nuclei
Paraventricular n.
Mammillothalamic tr.
Lateral
| nuclei
nu
Tuberomammillary n.
Lateral mammillary n.
Medial mammillary n.
(ears |Periventricular zone
Supraoptic region
Arcuate n.
Tuberal region
A
Dorsomedial n.
Mammillary region
Posterior n.
Ea
Lateral zone
Medial zone
BLANK MASTER
8-60
DRAWING
FOR HYPOTHALAMIC
Hypothalamic structures and connections are complex. This
illustration is provided in the recognition that the instructor
STRUCTURES AND CONNECTIONS —
—may wish to provide a less detailed, or a more detailed, treatment of the
structure and connections of the hypothalamus than is covered in this Atlas.
8-60 BLANK MASTER
DRAWING FOR HYPOTHALAMIC
AND CONNECTIONS
STRUCTURES
ft ae
baa
.
Tracts, Pathways,
and Syster
es
é
¢
oF
THE PITUITARY GLAND
The structure, relationships, and major pathways of the pituitary gland in the sagittal plane. The pituitary gland, also called
the hypophysis, consists of two parts: one that arises from the developing
oral cavity (adenohypophysis, anterior lobe) and the other that arises
from the developing neural tube (neurohypophysis, posterior lobe).
The adenohypophysis, commonly called the anterior lobe of the
pituitary, consists of a larger portion called the pars distalis (or pars
anterior), a small portion, the pars intermedia, and the pars tuberalis,
which is a small extension of the anterior lobe that wraps around the
infundibular stalk. The neurohypophysis, also called the posterior lobe
of the pituitary, consists of a neural lobe, the pars nervosa, and the
infundibulum, or infundibular stalk, which joins the neural lobe with
the hypothalamus.
The pituitary gland sits in the sella turcica of the sphenoid bone; the
diaphragma sellae, a small extension of the dura, forms a donut-shaped
structure through which the infundibular stalk passes. The anterior and
posterior intercavernous sinuses pass across the midline (and between
the cavernous sinuses) at the attachment of the diaphragma sellae to the
sphenoid bone.
Hormones
There are numerous hormones and neuroactive substances associated
with the hypothalamus and pituitary. Of particular importance to the
pituitary gland are those substances found in the supraopticohypophyseal and the tuberoinfundibular (or tuberohypophyseal) tracts.
The peptides oxytocin and vasopressin (antidiuretic hormone) are
synthesized in the paraventricular and supraoptic nuclei and transported to the posterior lobe via the supraopticohypophyseal tract. Oxytocin is released during coitus, parturition, suckling, and regression of
the uterus after birth. Vasopressin (ADH) is involved in the regulation
of fluid homeostasis within the body and may either increase or reduce
the production of urine.
A variety of RHs are synthesized in the periventricular zone and in
the arcuate nucleus, with further contributions coming from the paraventricular, medial preoptic, tuberal, and suprachiasmatic nuclei. These
hormones are transported to the hypophyseal portal system and to the
anterior lobe where they enter the vascular system.
Clinical Correlations
Due to its location, lesions of the pituitary may present as endocrine
disorders, visual deficits (bitemporal hemianopia is most common), features of increased intracranial pressure, diplopia, and headache related
to activation of nerves of the diaphragma sellae. In addition, lesions of
the pituitary may be classified according to size: microadenomas (less
than or equal to 1 cm in size) or macroadenomas (greater than 1 cm), or
as secreting (excess hormone production) or nonsecreting (no hormone
production/secretion). Hypersecreting tumors are those commonly seen
in the clinical setting.
Excessive production of growth hormone may produce either gigantism or acromegaly. In the former, excessive hormone is produced before
the growth plates have closed; the patient is abnormally tall and has
large, but weak, muscles. In the latter, excessive hormone is produced
after the growth plates have closed; the patient has large facial features,
a large nose and thick lips, large hands and feet, and cardiac problems
(hypertension, heart failure).
A female patient that presents with headache (common), visual deficits, amenorrhea, and vertigo (“dizziness”) may have an empty sella
syndrome. This may result from increased intracranial pressure, an
untreated pituitary tumor, or arachnoid herniation into the sella. The
pituitary may be compressed or displaced.
Excessive production of corticotropin results in Cushing disease. The
patient has truncal obesity, a rounded (“moonlike”) face, hypertension,
acne, osteoporosis, violet stretch marks, and diabetes mellitus. Excessive production of luteinizing hormone may result in hypogonadism in
males (testes may be present, but may not function normally) or disruption of the ovarian cycle in females.
Excessive production of prolactin in females results in gallactorrhea
(milk production when not pregnant) and amenorrhea (absent menstrual cycles). Hyperprolactinemia in men may be signaled by infertility,
decreased libido, or a combination of these signs and symptoms.
A patient presents with frequent urination (polyuria) and the need for
large amounts of water (polydipsia), particularly cold water, following
an automobile collision. CT reveals a TBI and consequent brain swelling within the skull. Shearing of the infundibular stalk and resultant DI,
in this case, may relate to: (1) sudden violent movement of the brain
within the skull; (2) brain swelling in a supratentotrial compartment
with a shift from one side to the other; or (3) transtentorial (central)
herniation, in which the brain is extruded downward through the tentorial notch and the integrity of the infundibular stalk is compromised
(see Chapter 9). Basal skull fracture involving the sella turcica or the
clivus may cause DI due to vascular compromise; clivus fractures may
also damage the larger vertebrobasilar arteries. In addition, DI may be
a consequence of hemorrhage into the pituitary, or into a tumor located
within the pituitary.
Excessive production of vasopressin (antidiuretic hormone) produces hyponatremia (low blood sodium levels and decreased urine
excretion) and natriuresis (enhanced excretion of sodium in the urine).
These patients may have hypotension, dehydration, headache, or may
have more serious problems, such as coma and seizures.
Review of Blood Supply to the Pituitary Gland
aerated sie eee eee
EE
The arterial blood supply to the pituitary comes from the inferior hypophyseal arteries (branches of the cavernous part of the internal carotid)
and from the superior hypophyseal arteries (branches of the cerebral
part of the internal carotid, A,, and P,). The venous drainage is via the
hypophyseal portal system and inferior hypophyseal veins into locally
adjacent dural sinuses.
ieee
:.
— —
—.
-
ee ee
_
Hypothalamus and Pituitary
8-61 THE PITUITARY GLAND
,
reaant
Lamina terminalis
Paraventricular nucleus
Arcuate nucleus
Supraoptic nucleus
=...
Supraoptic recess
nucleus
Infundibular recess of third ventricle
Optic chiasm
(/
tract
Infundibulum
Superior hypophysial artery
¥ |
Diaphragma sellae
ZS
Anterior intercavernous sinus
or
Pars tuberalis (of i
Supraopticohypophysial tract
|
(TY|
Diaphragma sellae
\
—_
Q
Neurohypophysis (posterior lobe, pars nervosa)
Inferior hypophysial artery
Inferior hypophysial veins
©)
Adenohypophysis (anterior lobe, pars distalis)
»>——— Veins to dural sinuses
<a
Dura of sella
Pars intermedia (of adenohypophysis)
Hypothalamus
e
osterior intercavernous sinus
wa
ey oo
:
P< Bone of sella
Mammillary body
Optic chiasm
—Interpeduncular
Infundibulum
cistern
Adenohypophysis
Stalk of
2
Adeno-
pituitary
a
:
pos
Infundibulum
=
Neuro-
Neurohypophysis
hypophysis
g
E
5
Optic chiasm
Empty sella
Adenohypophysis
Infundibulum
Sar
Stalk of
Neurohypophysis
= NOTES.
Q&A for this chapter is available online on (@Point.
296
dc
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ed
©.
Clinical Syndromes of the CNS
©
ne
J
Part |
Herniation Syndromes of the Brain and Spinal Discs
INTRODUCTION
AND COMPARTMENTS
The cranial cavity contains brain, cerebrospinal fluid (CSF), and blood
(within vessels), all within a vault of unforgiving bone. This is good in that
it offers essential protection to the soft, almost gelatinous, brain when
there is a minor bump to the head. However, when there is trauma to
the skull that may result in brain damage (resultant edema, bleeding) or
an intracranial event (hemorrhage, rapidly growing mass), these spaceoccupying lesions may increase intracranial pressure that attempts to displace the brain. Recall that when the physician views a coronal MRI, his/
her right is the patients left, and the physician’s left is the patients right;
this is an essential clinical distinction.
As a mass increases in size within a particular intracranial compartment,
it displaces CSF and, to a lesser extent, blood within vessels, raising the
pressure within that compartment when compared to the adjacent compartments. When a mass increases to the point where the CSF space is exhausted,
the pressure differential between the compartment containing the mass
(higher) and the adjacent compartments (lower) may result in a herniation
of brain from the region of higher pressure into one of lower pressure. These
events, and resultant deficits, are called herniation syndromes.
A wide variety of clinical events may precede the development of a
herniation syndrome, such as hemorrhage (epidural, subdural, parenchymatous), mass lesion/tumor (primary or metastatic), trauma, brain
infarcts or abscess, infections, and a variety of metabolic conditions. One
thing that is common, to varying degrees, to all of these occurrences, is
(Coronal
T2 MRI)
Right supratentorial
compartment
Left supratentorial
compartment
the brain edema that usually accompanies these events; it can be a major
element in the resulting herniation or its propagation.
The supratentorial space, the space above the tentorium cerebelli, is
divided into right (Figure 9-1, pink) and left (Figure 9-1, blue) compartments by the midline position of the falx cerebri. The space below the
tentorium cerebelli is not subdivided but presents as a single infratentorial
compartment (Figure 9-1, green). The continuation of the supratentorial
compartments with the infratentorial compartment is through the tentorial
notch, which contains the midbrain and large vessels. Although not specifically described as a compartment, the cranial subarachnoid space, and its
CSE, is continuous with the spinal subarachnoid space and represents the
anatomical basis for herniation through the foramen magnum (Figure 9-2).
While brain herniation syndromes may be characterized on the basis
of their own specific features, one herniation may morph, with clinical
deterioration, into another. For example, a subfalcine herniation may, as
the mass enlarges, become a central herniation, or a central herniation
may contribute to a tonsillar herniation. In a real sense, brain herniation
is a dynamic process that may change as the clinical picture changes.
Spinal cord injuries, or damage to the cauda equina (a cauda equina syndrome), particularly damage resulting from extruded intervertebral discs,
or trauma, share similarities with brain herniations: mechanical impingement on neural structures with predictable deficits. Recognizing these features in common, selected samples of intervertebral disc extrusions and
other spinal cord syndromes or lesions are included within this chapter to
offer a more complete picture of this important clinical problem.
(Sagittal
T2 MRI) 5
Quadrigeminal cistern
Cerebellum
Lateral
ventricle
Position of
falx cerebri
Tentorial notch
Cisterns:
Interpeduncular
Prepontine
Premedullary
Position of
tentorium
cerebelli
Cisterna
ae
magna
Infratentorial compartment
297
A (Coronal)
Falx eerebri
B (Axial CT)
Superior sagittal sinus
pea
yV
Anterior cerebral artery
Swollen brain,
sulci effaced
Hemorrhage
in brain
Falx cerebri
C (Axial CT)
Falx cerebri
Brain herniated under falx
Hemorrhage
Enlarged lateral ventricle—§
Falx cerebri
Subfalcine (cingulate or falcine) herniation. An expanding mass
2
in the supratentorial compartment on one side may force the cingulate gyrus against, and/or under, the edge of the falx cerebri (A). These
lesions are frequently located in the more superior area of the hemisphere,
such as the parietal lobe, but may also occur in the superior aspect of the
frontal lobe. Segments of the ACA are particular candidates for injury.
Several features generally characterize a subfalcine herniation. First,
with the exception of the general symptoms of increased intracranial pressure (headache, nausea, vomiting), the event may be initially
“silent” in that the patient has no long tract or focal signs. Second, this
herniation may compromise the anterior cerebral artery (ACA) against
the falx cerebri on the side of the mass, on the opposite side, or on both
sides (A, B). The resulting deficits reflect damage to the lower extremity
Edematous brain, sulci effaced
regions of the primary motor and somatosensory cortices (weakness,
loss of proprioception and exteroceptive sense in a lower extremity).
Depending on which ACA is occluded, the deficits may be on the side
of the mass, the opposite side, or bilateral. Third, as the herniation
progresses, the brain is pushed underneath the edge of the falx cerebri
(A, C). When this event takes place, the superior areas of the diencephalon may be involved and the internal cerebral veins may be compressed,
resulting in venous stasis, edema, or venous infarcts in the areas served
by these veins. Fourth, with enlargement of the mass, a subfalcine herniation may evolve into a central, or transtentorial, herniation with the
consequent clinical deficits. Fifth, damage to the cingulate gyrus may
also result in alterations in behavior, but these may be masked by other
more obvious clinical deficits.
A (Coronal)
SS
Falx cerebri
ae
Hemorrhage
in brain
sinus
Anterior cerebral artery
WL
~-
-Inferior sagittal sinus
Thalamus
Brainstem
B (Axial CT)
Left anterior horn,
absent on right
Hemorrhage with edema
Basal nuclei
Right thalamus
impinged on
left thalamus
Blood in posterior horn
Sulci effaced a.
Falx cerebri
9.4
Diencephalic stage of central herniation. Expanding masses in
frontal, parietal, and, to a lesser degree, occipital lobes, or in
the central region of the hemisphere (basal nuclei, internal capsule, lateral thalamus) may result in brain displacement toward the opposite
side; this is the diencephalic (thalamic) stage of central herniation (A, B).
A supratentorial mass within the hemisphere that enlarges and
impinges on the contralateral side of the brain will result in a cascade of
deficits characteristic of the structures damaged during this event. The
hemisphere may be affected by tumor growth to a critical stage, stroke, a
hemorrhagic event such as traumatic hematoma, or bleed from an arteriovenous malformation (AVM); the hemisphere is significantly swollen,
sulci are usually obliterated, and the midline is clearly effaced (A, B).
These signs and symptoms include a decrease in the level of consciousness (reflecting compromise of the ascending reticular activating system),
potential onset of diabetes insipidus (if the pituitary stalk is damaged
as the brain shifts), a general increase in muscle tone, and respiratory
changes that accompany these motor symptoms. Breathing may initially
be normal with occasional yawns or sighs but followed by the potential onset of ascending and descending rhythmic patterns characteristic
of Cheyne-Stokes respiration (breathing that increases in depth then
decreases followed by a period of apnea). In this stage, the pupils are
small but minimally reactive, both eyes rotate to the side opposite a head
rotation (doll’s eyes maneuver), and both eyes look toward the ear irri-
gated by cold water (cold caloric test). A noxious stimulus results in a
movement of the upper extremity to deflect the offending source. Based
on the extent of the damage, the patient may have unilateral, contralateral, or bilateral Babinski reflexes (extension, fanning of the toes), and a
hemiparesis of upper and lower extremities (compromise of corticospinal
fibers; the Babinski sign is on the same side as the weakness).
A likely outcome of an enlarging supratentorial mass is decorticate rigidity (also called decorticate posturing). The level of consciousness, alertness, and arousability is decreased. The lower extremities,
trunk and neck musculature are extended (opisthotonos), representing
increased activity in reticulospinal and vestibulospinal fibers to extensor motor neurons in the spinal cord), and the upper extremities are
flexed (increased activity in rubrospinal fibers to flexor motor neurons
in the cervical spinal cord). With the removal of cortical modulation
(decortication), brainstem nuclei are driven to higher levels of activity
by infratentorial centers such as the cerebellum, vestibular nuclei, retic-
ular nuclei, and spinal cord.
300
9/
B (Sagittal)
A (Coronal)
aN
~~
Straight sinus
ce Ae oO
:
Brainstem
Midbrain ee
Pons
Medulla
Brainstem
C (Axial CT)
D (axial CT)
+—
=
aN
Lesion impinges
into brainstem
:
SS
L
\
~
Bs
a
Cerebellum
E (Axial CT)
Lesion in
midbrain
Hemorrhage
* with edema
Brain shift
Midbrain
right to left
Cerebellum
Blood in
posterior
horn
fi Quadrigeminal
cistern
Blood in
posterior
horn
Tentorium cerebelli
Falx cerebri
Transtentorial or central herniation. As a supratentorial mass
2-5
enlarges, and in the absence of an opportunity to control or
reverse the pressure, the brain will be displaced downward through the
tentorial notch; this is transtentorial or central herniation (A, B). The
brain is displaced from a region of greater pressure (above the tentorium) into a region of lower pressure (below the tentorium).
When the capacity of the supratentorial compartments is exceeded,
the brain will herniate downward and compromise the midbrain and
even eventually lower levels. In this example, a large supratentorial mass
(A, B, C) extends through the tentorial notch and into the brainstem
(D, E). This sequelae of events may happen suddenly or unexpectedly, or be predictable based on the clinical deterioration during the
diencephalic/thalamic stage.
The decorticate rigidity, which may appear during the diencephalic
stage, may convert to decerebrate rigidity (also called decerebrate posturing). In this situation, there is total body rigidity; the lower extremities,
trunk and neck, and the upper extremities are extended. This posturing
reflects increased influence of vestibulospinal and reticulospinal tracts,
especially the latter, on extensor spinal motor neurons, and loss of the
red nucleus (midbrain damage) and its influence on cervical flexor spinal motor neurons. Consequently, spinal extensor motor neuron activity
prevails.
Respiratory patterns are irregular and may range from tachypnea
(rapid breathing) to Cheyne-Stokes (breathing that increases in depth
then decreases followed by a period of apnea). The pupils are fixed,
dilated to midposition, or irregular in size and shape, and there may
be visual losses (difficult/impossible to detect) resultant to compression
of the posterior cerebral artery within the tentorial notch. Head rotation or cold caloric irrigation of an ear generally results in dysconjugate
eye movements. After central herniation has occurred, the chance of a
meaningful recovery is low (less than 5%) even if a treatment can be
instituted and is successful.
A
(axial)
Crus cerebri (CC)
NV WIA
7
,
B
~Oculomotor
nerve (OcNr)
Hem
Hemorrhage aN
(Hem)
7
/
Corticospinal
fibers (CSp)
Tentorium cerebelli (Ten)
s
Spinal
ix
| 8—~
Spinal
motor neuron
| 3—~<
motor neuron
E (Axial CT)
Crural
cistern
effaced
Herniated
brain
CE
Hem
Crus
against
Ten
Herniated
brain
Ambient
Cisterns
cistern
effaced
9-6
Uncal herniation. A rapidly expanding mass, such as a
S
hematoma, neoplasm, or infarction with resultant edema,
located in the temporal lobe may result in uncal herniation. The
uncus, and frequently portions of the parahippocampal gyrus,
are extruded over the edge of the tentorium cerebelli, through the
tentorial notch, and impinge on the midbrain (A). An early sign is
a dilated pupil that responds slowly; if unilateral, the side of the
dilated pupil predicts the side of the herniation in about 90% of
cases. The dilated pupil may also be fixed, unresponsive to stimuli.
Respiration is usually normal (eupnea) in early stages, and there is
an appropriate response to noxious stimuli; the patient may hyperventilate as herniation progresses. Consequent to pupillary dilation,
most eye movement is absent (third nerve palsy), and eye movements
in head rotation or cold caloric irrigation may be dysconjugate. In
the same interval, the patient may become hemiparetic (damage to
corticospinal fibers in the crus cerebri) with a Babinski reflex on the
hemiparetic side, may experience visual deficits (compression of the
posterior cerebral artery serving the visual cortex), and may have
a decreased level of consciousness or arousability (somnolence or
stupor).
There are two variations in this theme. The first is a herniation that
damages the midbrain (oculomotor nerve [CN III] crus cerebri) on the
side of the herniation resulting in oculomotor deficits on the side of the
herniation and hemiparesis on the contralateral side (with additional
symptoms) (B, D). This result is essentially a Weber syndrome (a superior crossed, or alternate, hemiplegia). The second is a herniation that
shifts the midbrain from one side toward the other, damaging the root
of CN III on the side of the herniation and causing damage to the crus
cerebri (and corticospinal fibers) on the opposite side (C, E) sometimes
by impinging on the edge of the tentorium cerebelli (E). This herniation
results in CN III deficits on the side of the herniation and a hemiparesis
of the upper and lower extremities on the same side. The damage to the
crus opposite the herniation is the cause of the corticospinal deficits on
the same side as the CN III deficits (C). This is a Kernohan syndrome,
also called the Kernohan phenomenon. In this case, the corticospinal
deficits are a false localizing sign.
{
+
RS
Necrotic cyst with fluid level
B (Sagittal T1 MRI )
A tae
Lesion
OD
ae wD
i Ny)
Midbrain (Mid) SS
Pons
S
Enlarged third and
Fourth ventricle (ForVen)”
lateral ventricles
=
Medulla (Med)
Cerebellum (Cbl)
Cisterna magna
C (Coronal T2 MRI)
Right supratentorial
compartment
Mid”
Pons
ForVen
‘Med
)
Cbl
Cisterna magna
Left supratentorial
compartment
Necrotic cyst
Tentorium cerebelli
Tentorium cerebelli
Cerebellum
Upward cerebellar herniation. A posterior fossa (infratentoor ie_ rial) mass, particularly one in the cerebellum, may force brain
structures upward through the tentorial incisure (notch) (A). A lesion
in the posterior fossa may present with the cardinal signs/symptoms
of increased intracranial pressure: headache, nausea, and/or vomiting.
In addition, an abducens palsy and papilledema (the latter seen after
4 to 6 days) may be present; both are exacerbated by further increasing intracranial pressure. In this example, the lesion involves primarily
medial cerebellar structures with a consequent presentation of a widebased gait, titubation, and vertigo (B, C).
Additional potential consequences of this type of lesion include the
following: entrapment of the PCA (potential visual deficits, homonymous
hemianopia), compression of the SCA between the tentorium and the
cerebellum (infarct of cerebellar cortex and nuclei, cerebellar motor
signs/symptoms), occlusion of the cerebral aqueduct (increased intracranial pressure, hydrocephalus), and compression of the caudal midbrain
(impaired voluntary upward gaze, horizontal gaze intact; the Parinaud
syndrome). Recognizing that about 450 cc of cerebrospinal fluid is
produced every 24 hours in a normal healthy individual, and much of
this in the lateral and third ventricles, a sudden occlusion of the cerebral aqueduct may quickly become a medical emergency. The medical
urgency is created because only about 150 cc (of the 450 cc) of cerebrospinal fluid is needed at any given time; the remainder must circulate
and be reabsorbed, or significant complications may occur.
A (Sagittal)
B (Sagittal M1 MRI)
Chl
ForVen
Cerebellum (Cbl)
Tonsil (Ton)
C (axial T2 MRI)
Mid
Vertebral arteries (VA)
Pons—-
ax
Midbrain (Mid)
Pons
Fourth ventricle (ForVen)~
Medulla (Med)
Med
\\
Lesion
Cisterna magna
Spinal cord (SpCd)-
D (Sagittal T1 MRI)
F(
G (Axial CT)
Normal foramen magnum
)
H (Axial CT
Se
Herniated
Herniated Ton over SpCd
Tonsils in foramen
Tonsillar herniation. Herniation of the cerebellar tonsils
through the foramen magnum may be a sequel to an enlarging
cerebellar mass (A) or to a supratentorial lesion descending through
the tentorial notch and resulting in a pressure cone directed toward
the foramen magnum. There are, however, situations where the tonsils
may be found in the foramen, and below, without neurologic signs or
symptoms. This may be the case where the tonsils descended during
development or slowly over long periods of time.
Normally the posterior fossa cisterns are open and the foramen magnum contains the medulla, vertebral and posterior inferior cerebellar
arteries, and CSF (B, C, G). With herniation, the tonsils descend through
:
Tonsils in foramen
the cisterna magna and into the foramen and eventually into the spinal
subarachnoid space (D-F, H).
Sudden herniation may compress the medulla, compromise cardiac and respiratory centers therein, and result in rapid clinical
deterioration. Initially, there is an immediate increase in blood pressure, followed by equally rapid increases in heart rate (tachycardia) and respiratory rate (tachypnea), followed by an equally rapid
decline. Tonsillar herniation may occur suddenly and may be rapidly fatal if not treated as a medical emergency. Lumbar puncture
(LP) should generally be avoided if elevated intracranial pressure is
suspected.
Anterior root
VertBd
Vertebral body (VertBd)
Anterior spinal a.
A
Anterior
ramus
Transverse foramen
(TraFor)
;
{e)=—-
Posterior J
ramus
Osteophyte
)
a
\)
7S
ae
ia
Intervertebral foramen
Posterior root y.
and ganglion
(InterFor)
Posterior spinal a.
C (Axial CT cisternogram
TraFor
VertBd
A
InterFor
sie
Cervical cord
Central cord syndrome. The normal cervical spinal cord is
oval shaped, located within the dural sac, and separated
from the bony vertebral canal by an epidural space (A, C). The central cord syndrome is an incomplete spinal cord injury (some motor/
sensory function survives three or more segments below the level of
the injury) and is the most commonly seen incomplete spinal cord
injury. A complete spinal cord injury is a loss of all motor and sensory function beginning at about three spinal levels below the level
of the spinal lesion. About 3% of patients that initially present with
a complete lesion may regain some function within 24 hours. Complete lesions lasting 72+ hours have basically a zero probability of
recovery. Contributing factors to an incomplete spinal cord injury
syndrome are hyperextension of the vertebral column (common in
cervical levels) in older patients with stenosis of the vertebral canal
complicated by osteophytes or hypertrophy of the ligamentum flavum (B, D). In younger patients, the hyperextension may occur
Osteophyte
Spinal cord damaged
during sport injuries or blows to the face/forehead with, or without,
fractures.
A central cord syndrome presents as weakness of the extremities
(greater in the upper extremity [UE], less in the lower extremity [LE]),
irregular sensory deficits (pain and thermal sense), and urinary reten-
tion. These deficits correlate primarily with damage to the anterior horn
at cervical levels and to the medial fibers of the lateral corticospinal
tract (bilateral weakness of the UEs), damage to the anterolateral system taking into account its somatotopy (irregular loss of pain and thermal sense), and descending visceromotor fibers in the central areas of
the cord (sphincter dysfunction/urine retention). Compromise of the
anterior spinal artery may be a contributing factor in some cases. As
these patients recover (about 90% may ambulate with assistance in 4 to
6 days), the LEs come back first, the bladder next, followed by the UEs,
with sensation returning intermittently. Younger patients fare much bet-
ter than elderly patients (about 95%+ vs. 40%+ recovery).
Anterior root
Vertebral body (VertBd)
Anterior spinal a.
Transverse foramen
rd
Anterior
Nie
=
(SY¥OSSA
Us
Posterior va
\
hen «
~
B (Axial CT cisternogram)
(TraFor)
es
VertBd
Cervical
d “oh
spinal cord
i
ramus
Posterior root
and ganglion
i
f)
Intervertebral foramen
(InterFor)
Posterior spinal a.
\
.
=¥
aH
oh
Fractured vertebral body
\ ai
>>
ve
=
q
lA
2
Bone protrude into
vertebral canal
Damage to anterior
and lateral cord
Posterior columns intact
Anterior cord syndrome. The morphological features of the
9-10
cervical spinal cord and its relationships are described in Figure 9-9 and further shown here (A, B). The anterior cord syndrome
(ACS) not only involves the territory of the anterior spinal artery, but is
more inclusive in that it involves all cord regions except the posterior
columns. This is also classified as an incomplete spinal cord injury since
there is surviving sensory function (discriminative touch, vibratory sense,
proprioception in the posterior columns) below the level of the lesion;
this is also called a dissociated sensory loss (loss of somatosensory, pain
and thermal sense, but preservation of proprioception, below the level
of the lesion). A common cause of ACS is vascular surgery, particularly
that which may compromise branches of the aorta that ultimately serve
the spinal cord. Precipitating events may also include anterior spinal
cord compression pursuant to trauma resulting in intervertebral disc or
bone fragments (from a fracture of a vertebral body) that impinge on
the cord (C). This pattern of compression may compromise the anterior
spinal artery, the arterial vasocorona on the anterolateral surface of the
cord, and/or the cord itself.
The deficits present as paralysis below the level of the lesion (bilateral corticospinal fiber damage): paraplegia if at thoracic cord levels and
below, quadriplegia if at cervical cord levels. Additional deficits include
a bilateral loss of pain and thermal sensation (bilateral ALS damage)
and bowel and bladder dysfunction (descending visceromotor fibers).
Posterior column function (proprioception, discriminative touch, vibratory sense) remains intact. The prognosis is grave for this incomplete
spinal injury; only about 15% recover to a functional level. A minimal
amount of motor control may return, and enough sensory function to
help the patient avoid further injury.
Anterior root
A (Sagittal)
Nucleus pulposus
Vertebrae:
Annulus fibrosus
Anterior
Z
ramus
Transverse foramen
Ly
(TraFor)
Posterior
ramus
Disc impinging
Intervertebral foramen
Posterior root
(InterFor)
and ganglion
Posterior spinal a.
yg Right portion of
spinal cord
Extruded disc
into InterFor
Right portion
of spinal cord
E (Axial T2 MRI)
Disc herniated
into InterFor
(exiting roots)
——I|ntervertebral disc
TraFor
Disc herniated
into InterFor
(exiting roots)
“
Open InterFor
Spinal cord
Exiting roots at cervical levels. The cervical spinal nerves exit
9-11
the spinal cord and course laterally, and just slightly caudad,
to their respective intervertebral spaces (see Figures 2-1 and 2-2). This
relationship means that the vast majority of disc herniations in cervical
levels involve the exiting root. The cervical spinal nerves exit the cord
superior to their respectively numbered vertebrae; C1 between the C1
vertebrae and skull base, the C4 root above the C4 vertebrae at the
C3-C4 interspace, the C6 root above the C6 vertebrae at the C5—C6
interspace, and so on (A). The C8 root exits between the C7 and the T1
vertebrae; consequently, below T1 all spinal nerves exit caudal to their
respectively numbered vertebrae (e.g., the T1 root below the T1 vertebrae at the T1-T2 interspace).
An example of a lesion involving an exiting root is a disc protrusion at
the C5—C6 interspace that impinges on the C6 root (B-D). The extruded
disc clearly invades the intervertebral space on the right side, especially
when compared to the left (D, E). In this case, the deficits reflect damage to
the Cé root and include weakness of forearm and wrist extensors, inability
to flex (dorsiflex) the wrist, and sensory loss in the C6 dermatome (back
of the shoulder, lateral aspect of UE, thumb). The losses reflect the damage
to the root at that level, not above or below the root exiting at that level.
Nucleus pulposus (NucPul)
A (Sagittal)
Annulus fibrosus
Anterior root
Anterior ramus
Cauda equina
Filum terminale internum
Disc impinging on
exiting roots
Disc impinging on
traversing roots
\
Posterior ramus
Posterior root and ganglion
€)
Lumbar cistern
C (axial T2 MRI) J
Disc impinging
on exiting roots
9-12, Exiting and traversing spinal nerve roots at lumbosacral levels.
9-12
Depending on the direction of the disc extrusion, herniations
at the lumbosacral levels may damage either exiting or traversing spinal
nerve roots (A, B).
A herniated lumbar disc that protrudes superiorly or laterally and
into the subarticular space of one intervertebral level damages the exiting root at that level; this root has a limited distribution. For example,
a herniation superiorly or far laterally at the L3-L4 interspace damages the L3 root resulting in weakness of knee extension, pain over the
anterior thigh and decreased sensation on the medial distal thigh, and a
diminished knee jerk (patellar tendon) reflex (A, C).
Lesions that may damage traversing spinal nerve roots are commonly
seen at lumbosacral levels; most disc extrusions occur at L4—-LS or LS-S1;
D (Axial T2 MRI)
Disc impinging
on traversing
those herniaticn’s extending posterolaterally may compress traversing
roots. This reflects the descending nature of spinal nerve roots at these levels to form the cauda equina (see Figure 2-4). For example, a disc extruded
medial to the subarticular zone/space at the L4—LS intervertebral space
may avoid the L4 root (the root at that level) and compress roots that
are descending to exit at lower levels such as LS and S$1-SS (A, D). In this
example, the deficits reflect damage to these traversing roots resulting in
weakness of knee flexion, plantar flexion of the ankle and extension of the
great toe, loss of the ankle jerk (Achilles), bulbocavernosus, and anocutaneous (anal wink) reflexes, and a loss of sensation in these respective
dermatomes (buttock, posterior thigh and leg, lateral leg, and most of the
foot). These losses reflect damage to nerve roots descending and exiting at
lower levels, not to roots at the level of the extruded disc.
308
9/
A (Sagittal)
Nucleus pulposus
Cauda equina
Midline herniation
»
Midline herniation impinging
on cauda equina
0
°
002.09 0
p00
oo O od
o
Impingement on dural
sac and cauda
D (Axial T2 MRI)
Ex Sagittal T2 MRI) —
Nucleus
pulposus
equina
eg!
Herniated
isc
impinging
Cauda
equina
Calida
Vertebral
body
Lumbar
Herniation
on cauda
equina
Cauda equina syndrome. The lumbar cistern is located
9-13
between about the L1/L2 and S82 vertebral levels and contains
descending anterior and posterior spinal nerve roots that collectively
form the cauda equina (A, B). This cistern is the primary avenue for
retrieving a sample of cerebrospinal fluid for diagnostic purposes.
Intervertebral disc extrusions take place at the L4—LS and at the L5S1 intervertebral levels in about the same numbers (about 45% each
level). Large disc ruptures at the midline at L4-L5 are a major cause
of cauda equina syndrome, followed by other events such as metastatic
tumors, bone fragments from spinal trauma, spinal epidural hematoma,
or the complication of infections (vascular compromise, compression).
The protruded disc, or other mass/fragments within the vertebral column, may compress the dural sac and the roots located therein (C-E).
Bladder and bowel problems (urinary retention, overflow incontinence; decreased anal sphincter tone) are early and usually consistent
findings. Other characteristic features include saddle anesthesia (sensory
loss over perineum, genitals, anus, buttocks, and inner thighs, reflecting
the coccygeal [Coc 1] root and $2-SS5 roots), lower extremity weakness (damage to multiple motor roots), potential loss of the ankle jerk
(Achilles reflex) ($1 level), pain in the lower back or sciatica (pain radiating down the posterior thigh and leg), and sexual dysfunction (a later
finding).
Clinical Syndromes of the CNS
Part Il
Representative Stroke Syndromes
ollowing heart disease, as broadly defined, and cancer, stroke is
the third most common cause of disability and/or death in the
waem United States. Of all patients presenting with a sudden onset of
neurologic dysfunction, about 90% to 95% are of vascular origin; the
remaining are related to tumors, seizure, or are of psychogenic origin.
Stroke is an interruption of blood supply to a localized area of the brain,
resulting in neurologic deficits that frequently may signal the type, location, extent, and severity of the event. In about 80% to 85% of cases,
the stroke is ischemic (sometimes referred to as occlusive); in about
15% to 30% of cases, they are hemorrhagic in origin.
Ischemic stroke may result from arterial blockage by a thrombus
(clot of blood products, attached or not attached to a vessel wall) or
embolus (clot of detached thrombi, bacteria, vegetation, or other foreign matter). Ischemic strokes produce a localized area of decreased
circulation of blood, which will likely transform into a frank infarct.
Occlusive stroke may be treated with tissue plasminogen activator (tPA,
or recombinant tissue plasminogen activator, rtPA) generally within
3 to 4.5 hours of the onset of symptoms; hemorrhagic stroke cannot
be treated with tPA due to the very real probability of exacerbating
the hemorrhage. There are specific guidelines for the administration of
tPA/rtPA. Following an ischemic stroke, there may be a central area of
permanent brain tissue loss and an immediately surrounding area of
salvageable brain; this region is the penumbra. If treated quickly, the
penumbra may be recruited into the externally located normal brain
that should survive and return to normal or relatively normal neurologic function. Rapid treatment with rtPA/tPA is an important element
in reclaiming the penumbra.
Hemorrhagic strokes may result from leak or rupture, usually
of an artery, into brain substance (parenchymatous or intracranial),
brainstem (midbrain, pons, medulla), meninges (extradural, subdural,
subarachnoid), and other examples. Hemorrhage into the meninges
and associated spaces is frequently related to trauma, and may present
with specific and unique signs and symptoms. Rupture of an intracranial aneurysm in the subarachnoid space is a source of blood in about
75% of cases.
A transient ischemic attack (TIA) is a sudden loss of function that
generally resolves in 5 to 60 minutes, many times within minutes, but
certainly in less than 24 hours; TIA is a sudden temporary decrease or
blockage of blood supply to a particular vascular territory that results in
deficits that are temporary, but characteristic to specific brain regions or
systems. These TIAs vary widely based on whether the temporary occlusion is in the internal carotid system, posterior cerebral artery system,
or in the vertebrobasilar system. TIA may be a harbinger of impending
stroke. For example, about 15%+ of ischemic strokes are preceded by
a TIA. This sequelae of events is a particular issue in crescendo TIA in
which 2+ attacks take place within a 24-hour time frame; this constitutes a medical emergency.
A systemic drop in blood pressure (hypoperfusion) may result in a
decrease of perfusion of the distal parts of arterial territories (the watershed zones) and may produce a watershed infarct. Watershed infarcts
of the distal MCA-ACA territories may result in weakness of proximal
UE and LE and cause a man-in-a-barrel syndrome. Watershed lesions in
the overlap of distal branches of MCA-PCA may result in visual agnosia, cortical blindness, and the Balint syndrome (optic ataxia, ocular
apraxia, simultanagnosia). Deficits usually present suddenly, and may
be accompanied by headache of various severity, possibly syncope, and/
or focal signs that may reflect damage to cranial nerve roots or nuclei,
hemiplegia, sensory loss, and cognitive compromise.
309
Lesions Involving the ICA, ACA, and MCA
Clinical Syndromes of the CNS—Part Il: Representative Stroke Syndromes—Vascular
" LentStr
BrsofMi
of MCA
Vascular lesions involving the internal carotid artery (ICA) and
its main branches, the anterior (ACA) and middle (MCA) cerebral arteries. The patient in A has significant vascular pathology (seen as
irregular rather than smooth vessel contour) in the right ICA (cavernous,
and carotid parts, with narrowing); the vascular damage extends into the
ACA and MCA (A). It is highly likely that the right ICA in this patient will
eventually occlude. A large infarct in the lateral portion of the right cerebral hemisphere (the middle cerebral artery, MCA territory) is the result
of obstruction of the right MCA (B). The MCA, ACA, and PCA vascular
territories (B, D, E) represent the three main vascular regions within the
hemisphere. Since the PCA originates from the vertebrobasilar system, portions of the caudal and medial occipital cortex may be spared. The ACA
and MCA
vascular territories (B, C, E) represent two of the three main
vascular territories in the cerebral hemisphere. A variation on this theme
is when the occlusion of the ICA may result in significant damage to all
three vascular territories (ACA, MCA, PCA: B, D, E). Two explanations
are possible. First, the patient may have had simultaneous occlusions of the
ICA and of the P1 segment of the PCA, a possible occurrence in the case of
severe systemic vascular disease. A second explanation is an ICA occlusion
in a patient with a persistent fetal PCA (see Figure 2-43) on that side. The
fetal PCA arises from the intracranial segment of the ICA and persists in
22% to 25% of adults. Some particularly important functions represented
in these respective territories are: somatomotor and somatosensory for face,
hand, and upper extremity, trunk to the hip (B, MCA); somatomotor and
somatosensory for the hip and lower extremity (D, ACA); and visual loss
(E, PCA). The respective deficits would be: (1) weakness and sensory deficits of the UE, trunk, and face on the right (B); (2) weakness and sensory
deficits for the LE on the left (B); and (3) a left homonymous hemianopia.
The vascular cases in B and C share certain similarities: one involves cortical branches of MCA with sparing of portions to the internal capsule and
basal nuclei (B), and the other involves a lesion within the basal nuclei (C)
with sparing of the cortex. These lenticulostriate vessels arise from M1;
damage to that vascular territory may not involve the parent vessel M1,
and the cortex is spared.
Vascular
Lesions
in the Thalamus,
B
Vascular lesions in the thalamus, subcortical white matter,
and the basal nuclei. The territory of the thalamoperforating
artery (A, arrow) includes the anterior thalamic nucleus, the ventral
anterior nucleus, and significant anterior regions of the dorsomedial
nucleus. This vessel arises from P1, enters the posterior perforated
substance, and serves those parts of the thalamus involved in arousal
of the cerebral cortex. Unilateral damage may cause lethargy or somnolence; bilateral lesions may result in coma. The caudal portions of
the thalamus, such as the pulvinar, geniculate nuclei, and the ventral
posterolateral nucleus (B, arrow) are served by the thalamogeniculate
artery, which is usually a branch of P). In this particular case (C), a male
patient underwent heart surgery and during the postoperative period
Subcortical
White
Matter, and the Basal Nuclei
C
experienced systemic hypoperfusion and multiple small infarcts in the
MCA-ACA watershed zones on right and left sides. It is also likely that
an embolic shower contributed to this man’s situation. The vascular territory (D, arrow) of the medial posterior choroidal artery is in the caudomedial dorsal thalamus. This vessel arises primarily from P3, encircles
the midbrain aad caudal thalamus, enters the caudal roof of the third
ventricle, and serves the choroid plexus of the third ventricle, pineal,
caudal dorsomedial thalamus, and the habenula. This vascular lesion
(E, arrows) is in the territory of the lateral striate branches of M, (E). It
is in the same territory as Figure 9-14D, but spares the thalamus and is
located primarily in the putamen and the anterior limb of the internal
capsule.
the Basal Nuclei, Cerebral Hemis; phere, and Watershed Zones
Clinical Syndromes of the CNS —Part Il: Representative Stroke Syndromes —Vascular Lesions in
B
Vascular lesions in the basal nuclei, cerebral hemisphere, and
watershed zones. Bilateral hypodense areas in this CT (A,
arrows) are in the head of the caudate nucleus and extend into portions
of the anterior limb of the internal capsule (A); this vascular territory
is supplied by the medial striate artery (artery of Heubner). This vessel
is usually a branch of proximal A). This intrahemispheric hemorrhage
(B, arrows) into the frontal lobe resulted from rupture of an aneurysm
located at the ACA—Acom junction with subsequent dissection into the
orbitofrontal cortex. This location for aneurysmal formation is fairly
common in the internal carotid circulation. The bilateral hyperintense
areas (C, arrows) at the junction of the distal territories of ACA and
MCA illustrate watershed infarcts. The anticipated deficits of an ACAMCA watershed infarct are discussed in Figure 9-15C. This axial diffusion—weighted image (DWI) shows a bright area (D, arrow) in about
the posterior half of the posterior limb of the internal capsule. This is
the location of the corticospinal fibers for the body, sans the head. This
lesion resulted in a weakness of UE and LE on the side opposite the
lesion: lesion on left, deficits on right. For practice (E); (1) what structure(s) are likely damaged by this lesion; (2) what are the likely deficits;
and (3) what is the vascular territory?
Vascular
Lesions
Related to Variant Artery Development
B
Vascular lesions related to variant artery development and
lacunar stroke. Coronal (A) section through the caudal portions of the hemisphere and through the cerebellum showing bilateral
lesions in the ACA territory, likely A;. In most cases, the ACA arising from
each side serves its respective hemisphere. In rare situations (B, arrows),
about 2% of cases, a single ACA (azygos or unpaired) arises from the
general area of the ICA-MCA junction and branches to serve both hemispheres (B). In such instances, damage to, or occlusion of, this azygos
vessel will result in bilateral deficits. The angiogram (B, labels/arrows)
shows an azygos ACA arising from the left MCA as a stem vessel and
immediately branching, one branch to the right hemisphere, the other to
the left. It is not uncommon for a patient with one vascular abnormality
to have additional ones. The patient with the vascular abnormalities in B
also presented with a fetal PCA (C, arrows). This pattern, seen in about
and Lacunar Stroke
C
25% of individuals, is a retention of the fetal pattern where the PCA
arises from the MCA and, as development progresses, does not join the
vertebrobasilar system characteristic of most adults. The two PCAs arise
at the bifurcation of the basilar artery. Each PCA has proximal branches
that largely serve the thalamus, intermediate branches that serve temporal areas, and distal branches that serve the visual cortex and adjacent
temporal regions. The small lacunar lesion (D, upper arrow) is likely
an occlusion of distal branches of the thalamogeniculate artery and the
lower defect (D, lower arrow) in the optic radiations and adjacent cortex
is from damage to distal PCA branches. The effacement of gyri and sulci
(E), almost complete obliteration of the anterior horn of the lateral ventricle and third ventricle, and the small size of the quadrigeminal cistern,
indicate a likely increase in intracranial pressure (E), which may present
as headache, nausea, vomiting, and change in mentation.
Clinical Syndromes
of the CNS—Part
Il: Representative
B
Vascular lesion in the brainstem. The small lesion in the right
crus cerebri (A, arrow) is the resuit of damage to penetrating
vessel in the immediate area; likely candidates in this case are small
branches from P, and/or from similar branches of the quadrigeminal
artery, also a P; branch. Lesions of the middle portions of the crus cerebri will damage corticospinal fibers (right hemiplegia in this case) and
corticonuclear fibers (tongue, facial, uvula, shoulder shrug, head turning
weakness when attempting movements). Vascular damage to the midbrain (B) may result from a large supratentorial lesion herniating downward through the tentorial notch into the midbrain. In such cases, the
patient may present with dilated pupils, eye movement disorders, and
respiratory irregularities, and a decorticate patient may exhibit decerebrate posturing. Lesions in the brainstem can be quite small (C, small
lesion in axial MRI and in detail) as in this case involving primarily
the trochlear nucleus; the main deficit is weakness of the contralateral
Stroke Syndromes—Vascular
Lesion
in the Brainstem
C
superior oblique muscle. The causes of a locked-in syndrome (D, arrows)
include occlusion of the basilar artery with infarct of basilar and various
portions of the tegmental pons, and central pontine myelinolysis. The
basic lesion destroys the motor tracts in the basilar pons and the lower
cranial nerves, but largely spares the ascending sensory tracts and upper
cranial nerves. On initial examination, the patient appears unresponsive,
but careful observation reveals that sensation is intact and the patient
can communicate via eye movements. Small lesions in the brainstem
(E) may be the result of small vessel occlusion/disease, or brainstem
distortion resultant to central herniation (Duret hemorrhage) or demyelination. In this case, the small lesion is in the area of corticospinal fibers
causing the left-sided weakness of UE and LE. A small lesion is centered
in the right pontine tegmentum (F), mainly in the paramedian pontine
reticular formation (PPRF) and the medial lemniscus. This results in a
variety of eye movement disorders in both eyes in the horizontal plane.
9-19
Examples of small lesions in the medulla. A female patient
presents with intractable vomiting and has an MRI in an
attempt to identify the source of the problem. This case required vigilance. A meticulous review of every MRI image revealed two small
lesions (arrows in detail from A point to small bilateral medullary
lesions), in just one MRI image; the lesions were bilateral in the caudal
medulla in the area postrema, the brainstem emetic (vomiting) center.
In (B, arrow), the vascular lesion in the caudal and lateral medulla
resulted in an alternating sensory deficit: a loss of pain and thermal
sense on the left side of the face and oral cavity and a loss of pain and
thermal sense on the right side of the body. Although there are additional deficits seen in larger lateral medullary syndromes, the alternating
sensory deficits are the most commonly seen in combination. This is
the arterial territory of the posterior inferior cerebellar artery; consequently, it is commonly called a PICA syndrome (lateral medullary or
Wallenberg syndrome). The medial medulla is served by penetrating
branches (one to the right, next to the left, and so forth) of the anterior
spinal artery. Occlusion of one penetrating branch results in infarct of
the medial medulla on one side; this results in a medial medullary syndrome (Déjérine syndrome) (see Figs. 1-16 and 8-12A, B). In this case,
the lesion is on the left, so there is a right hemiplegia (corticospinal
fibers), a loss of vibratory sense and proprioception on the right side
of the body (medial lemniscus), and deviation of the tongue to the left
on protrusion (hypoglossal nerve).
Clinical Syndromes of the CNS—Part II: Representative Stroke
Vascular lesions of the medulla and the cerebellum. The posterior inferior cerebellar artery (PICA) arises from the vertebral
artery, passes around the medulla to which it sends important penetrating branches, and continues on to serve the medial and inferior aspects
of the cerebellar cortex. Depending on where the vascular obstruction is
located, different patterns/deficits may be seen. Obstruction of the vertebral artery at the origin of PICA results in a lesion of all PICA territories
distal to that point plus a loss of vertebral territories. Alternatively, the
lesion may be proximal (A, arrow) resulting in loss of medullary and
cortical territories with the range of anticipated deficits, a PICA syndrome. On the other hand, in the case of the more distal obstruction
of PICA, the medulla is spared (B, F) and the damage is sequestered in
the medial and inferior cerebellar cortex. The resulting deficits include
dysmetria, ataxia, intention tremor, rebound phenomenon, and others.
The territory of the anterior inferior cerebellar artery (AICA) occupies
the inferior and more lateral portion of the cerebellar hemisphere (C)
Syndromes —Vascular Lesions of the Medulla and Cerebellum
sparing the most medial cortex, which is the PICA territory (C, arrow).
PICA and AICA serve their respective cortical areas but provide no significant blood supply to the cerebellar nuclei. The superior cerebellar
artery (SCA) serves the superior surface of the cerebellar cortex (D, E)
and is also a major source of arterial blood to the cerebellar nuclei. Vascular lesions of the SCA ( D, arrow; E, large dark area) compromise the
cerebellar nuclei plus cortex and result in deficits on the same side as the
lesion; in D deficits on the left, in E deficits on the right. Recalling that
the SCA branches from the basilar artery just before it bifurcates into
the two P1 segments, it is not surprising that some PCA branches may
be recruited into a large SCA lesion (E). Vascular lesions involving distal
PICA and AICA territories (only cortex damaged)
more
likely result
in transient deficits that resolve quickly, usually within just a very few
weeks. On the other hand, vascular lesions in the SCA territory (involving cerebellar cortex + nuclei) result in deficits that may last months or
years or, to varying degrees of disability, especially in the elderly patient.
Q&A for this chapter is available online on
Point.
NS
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EATERY
See eee
SEES
_Anatomical-Clinical
Correlations: Cerebral
Angiogram, MRA, and MRV
chapter
317
Anatomical—Clinical
Correlations: Cerebral Angiogram,
MRA, and MRV—Cerebral
Angiogram,
MRA, and MRV
Callosomarginal branch
(of ACA)
Parietal branches
(of MCA)
Pericallosal branch
(of ACA)
Angular branch
(of MCA)
Anterior cerebral artery
(ACA)
Middle cerebral artery
(MCA)
Internal carotid artery
Ophthalmic artery =)
Internal carotid artery
(cavernous part)
Internal carotid artery
(petrous part)
— Internal carotid artery
(cerebral part)
Internal carotid angiogram (left lateral projection, arterial phase)
showing the general patterns of the internal carotid, middle, and
anterior cerebral arteries (A, B) and an image with especially good filling of
the ophthalmic artery (B). The ophthalmic artery leaves the cerebral part of
the internal carotid and enters the orbit via the optic canal.
This vessel gives rise to the central artery of the retina, which is an
important source of blood supply to the retina. Occlusion of the ophthalmic artery may result in blindness in the ipsilateral eye; occlusion of
smaller branches of the ophthalmic artery may result in a scotoma with
a corresponding visual loss in that part of the visual field. The terminal
branches of the ophthalmic artery anastomose with superficial vessels
around the orbit. The venous drainage of the orbit generally mirrors
that of the arteries serving the orbit. Orbital veins receive tributaries
from the face and coalesce to form the superior and inferior ophthalmic
veins, which end in the cavernous sinus. These ophthalmic veins represent a potential route through which infections of the “danger triangle
of the face,” or within the orbit, may directly access the central nervous
system. Compare with Figures 2-12, 2-21, 2-24, and 2-27,
Cerebral Angiogram,
MRA, and MRV
Superior sagittal sinus
Superior cerebral veins
Inferior sagittal sinus
Straight sinus
Thalamostriate vein
Transverse sinus
Internal cerebral vein
Great cerebral vein (of Galen)
Venous angle
Sigmoid sinus
Inferior cerebral veins
Inferior anastomotic vein
(of Labbé)
Superficial middle
Basal vein
cerebral vein
(of Rosenthal)
B
Superior cerebral
veins
Superior anastomotic vein
(of Trolard)
Straight sinus
Inferior anastomotic vein
(of Labbé)
Superficial middle
cerebral vein
Two internal carotid angiograms (left lateral projection, venous
phase). Superficial and deep venous structures are clear, including the inferior anastomotic vein of Labbé, in (A), but (B) shows a particu-
larly obvious superior anastomotic vein of Trolard. The thalamostriate vein
(A) at this location is also called the superior thalamostriate (terminal) vein.
The junction of the superior thalamostriate vein with the internal
cerebral vein is called the venous angle (A). The interventricular foramen
is located immediately rostral to this point; small tumors at this location (such as a colloid cyst, or a small choroid plexus papilloma) may
block the flow of cerebrospinal fluid from one or both lateral ventricles
and result in an increase in intracranial pressure and hydrocephalus (see
Figure 2-26 for a colloid cyst and enlarged ventricles). Compare these
images with the drawings of veins and sinuses in Figures 2-13, 2-19,
and 2-28.
Anatomical-Clinical
Correlations: Cerebral Angiogram,
MRA, and MRV
A
Middle cerebral artery
(M,-cortical branches)
Anterior cerebral artery
(Aq, As)
Middle cerebral artery
(Mo-insular branches)
Anterior cerebral artery
(As)
(Az)
(A;)
Lenticulostriate branches
(of M,;)
Middle cerebral artery
(Mj)
Internal carotid artery
(cavernous part)
Internal carotid artery
(cerebral part)
Internal carotid artery
(petrous part)
Internal carotid artery
Internal carotid angiogram (A) in the arterial phase of an
anterior-posterior projection. Note general distribution
patterns of anterior (ACA) and middle (MCA) cerebral arteries and
the location of lenticulostriate branches. The A, segment of the ACA
is located between the internal carotid bifurcation and the anterior
communicating artery. The distal portion of the ACA immediately
rostral to the anterior communicating artery and inferior to the rostrum of the corpus callosum is the A; segment (infracallosal). The
remaining portions of the ACA include: (1) the A; segment (precallosal) arching around the genu of the corpus callosum; (2) the Ay
segment(supracallosal) located above the corpus callosum; and (3)
the As (postcallosal) segment, which is located caudal to the corpus
callosum.
The M, segment of the MCA is located between the internal carotid
bifurcation and the point at which this vessel branches into superior
and inferior trunks on the insular cortex. As branches of the MCA pass
over the insular cortex, they are designated as M3, as M; when these
branches are located on the surface of the frontal, parietal, and temporal
opercula, and as My where they exit the lateral sulcus and fan out over
the lateral aspect of the cerebral hemisphere.
An aneurysm of the cavernous portion of the internal carotid artery
(B, arrows) may compromise blood flow through the ACA (quite narrow in this patient) and the MCA. The aneurysm (in C, arrows) is
located in the rostral portion of the temporal lobe, arises from M,, and
its laminated appearance suggests it may be of long standing. Compare
with vascular figures in Chapter 2.
Cerebral Angiogram,
MRA, and MRV
Arachnoid villi
Superior cerebral
veins
Superior sagittal sinus
Superior sagittal
Inferior sagittal sinus
sinus
Confluence of sinuses
Transverse
sinus
Transverse sinus
Sigmoid sinus
Internal
carotid
angiogram
(anterior—posterior
projection,
venous phase). The patient’s head is tilted slightly; this image
shows the arching shapes of the superior and inferior sagittal sinuses (A).
In many individuals, the superior sagittal sinus (SSS) turns predom-
inately to the right at the confluence to form the right transverse sinus,
and the straight sinus turns mainly to the left to form the left transverse
sinus (TS). In some individuals, there is a true confluence of sinuses.
Occlusion of the superior sagittal sinus (B, arrows) may result in reduced
venous
outflow, brain edema, potential venous infarct (dotted circle)
or hemorrhage, and eventual increase in intracranial pressure. The SSS
and TS are the most common sites of dural venous sinus thrombosis
(~70%). Arteriovenous malformations
(AVMs) (C, left temporal lobe)
may go undetected in some cases until they express clinical manifestations. Note the other venous structures in this image and compare with
the arterial phase shown in Figure 10-3 (facing page) and the images in
Figures 10-5 and 10-6. Also compare with Figure 2-28.
——
Superior sagittal sinus
Superficial cerebral veins
Sigmoid sinus
Jugular bulb
Digital subtraction image of an internal carotid angiogram
10-5
(anterior—posterior projection, venous phase).
Image (A) is early in the venous phase (greater filling of cortical veins),
whereas image (C) is later in the venous phase (greater filling of the dural
venous sinuses and internal jugular vein). Both images are of the same patient.
The patient in (B, arrows) has a partially occluded, or stenotic, right
transverse sinus (TS). Few or no deficits may result from TS occlusion
unless the opposite TS is hypoplastic or otherwise reduced in size or
partially occluded.
The jugular bulb is a dilated portion of internal jugular vein (IJV)
in the jugular fossa at the point where the sigmoid sinus is continuous
with the IJV; this continuity is through the jugular foramen. The
jugular foramen also contains the roots of cranial nerves 1b.ee >.G
and XI, the continuation of the inferior petrosal sinus with the IJV,
and several small arteries. There are several syndromes that signify
damage to the contents of the jugular foramen in various combinations of the nerves that traverse the foramen
(such as the Vernetor
Jackson syndromes), or damage to these structures plus the hypo-
glossal root (Collet-Sicard or Villaret syndromes). Recall that the
jugular foramen and the hypoglossal canal are immediately adjacent,
one to the other, in the posterior fossa. Compare with Figures 2-16
and 2-19.
Anterior cerebral artery (ACA)
(e
Ap segment
Sean
wil
Anterior communicating artery
Posterior cerebral artery (PCA)
Superior sagittal sinus (SSS) -———
Superior cerebellar artery (SCA)
Middle cerebral artery (MCA)
My segment
M, segment
Internal carotid artery (ICA):
Cerebral part
Sigmoid sinus
cea
Cavernous part
Petrous part
Transverse sinus (TS)
Anterior inferior cerebellar artery (AICA)
Confluence of sinuses (CS)
Vertebral artery (VA)
Basilar artery (BA)
Magnetic
resonance
angiography
(MRA)
is a noninvasive
method for imaging cerebral arteries, veins, and dural venous
10-6
sinuses simultaneously.
A three-dimensional phase contrast MRA (A) and an inverted
video image window
dural venous sinuses from anterior to posterior.
C shows the relative
position of the major vessels and dural venous sinuses as imaged in
(A) and (B). The superior sagittal sinus, as seen in (A) and (B), is usually continuous with the right transverse sinus at the confluence of
(B) of the same view show major vessels and _ sinuses.
Anatomical-Clinical
Correlations:
MRA, and MRV
Cerebral Angiogram,
:
:
ae
=
!
l Posterior choroidal arteries
I
| Posterior cerebral arteries
\
Parieto-occipital
branches (of PCA)
Calcarine branch
(of PCA)
(PCA)
Thalamoperforating
arteries
\
\
\
Basilar bifurcation
Posterior communicating
N
ys
i
LC
= wartery eee
ie
Posterior inferior
cerebellar artery
(PICA)
Superior cerebellar
artery (SCA)
YU
7
4
7
Vertebral artery
Basilar artery (BA)
(VA)
LF
Se.
Parieto-occipital
branches
f
Calcarine branch
PCA
- Basilar bifurcation—
eRe
sent
THF
TURIN
ep)O >
wearer
”
erent
a
jee)>
Anterior inferior
\, cerebellar artery
X
\
rica
VA
A vertebral artery angiogram (left lateral projection, arterial
phase) is shown in (A), and the same view, but in a different
patient, is shown in (C), using digital subtraction methods. Note the
characteristic orientation of the major vessels, particularly the loop of
PICA around the medulla and through the cisterna magna. The patient
in (B) also has a left lateral projection showing the basilar artery anda
small basilar tip aneurysm (B, arrow). This aneurysm is in the immediate vicinity of the oculomotor nerve (CN III). The bright white structure
inferior to the splenium of the corpus callosum is a calcified pineal gland
(B). Compare with Figures 2-21 and 2-24.
PCA, cortical branches
PCA
Thalamoperforating
arteries
SCA
AICA
Basilar artery (BA)
Vertebral artery (VA)
é
:
PCA,
i
;
Posterior
cerebral
arteries
cortical
r
8
branches
.
(PCA)
Superior
-— Thalamopentorating
cerebellar
artery
(SCA)
BA
AICA
PICA
“arteries
soit
rrr
(of the basilar
bifurcation)
SCA
:
Anterior inferior
cerebeiiar
artery (AICA)
ie
es
Posterior inferior
cerebellar
artery (PICA)
VA
A vertebral artery angiogram (anterior—posterior projection,
' arterial phase) is shown in (A); the same view, but in a different patient, is shown in (B), using digital subtraction methods.
Even though the injection is into the left vertebral artery, there is bilat-
:
Me che
bs
eral filling of the vertebral arteries and branches of the basilar artery.
The thalamoperforating arteries are important branches of P; that
generally serve rostral portions of the diencephalon which are involved
in cortical arousal. Bilateral occlusion of the thalamoperforating arteries, or occlusion of the stem of an azygos (single, unpaired) thalamoperforating artery (seen in about 8% of patients) that serves both thalami,
results in a comatose state.
interpeduncular cistern and between the superior cerebellar and posterior cerebral arteries en route to its exit from the skull through the
superior orbital fissure.
In this position, the oculomotor nerve may be damaged by aneurysms (C) of the rostral end of the basilar artery (called the basilar
tip, or basilar head) that impinge on the oculomotor nerve. Unlike
third nerve damage from other etiologies, external compression from
an aneurysm results initially in a dilated pupil followed by muscle
weakness as the compression increases. In this case, the aneurysm
(C, arrow) is likely located at the junction of P, with the posterior communicating artery. Aneurysms are commonly located at the branch
The root of the oculomotor (CN III) nerve, after exiting the inferior aspect of the midbrain, characteristically passes through the
points of the cerebral
and 3-3C.
arteries.
Compare
with
Figures
2-21,
3-2B,
Middle cerebral
artery (MCA):
Anterior cerebral artery:
Ag segment
M4 segment
Ap segment
My segment
A, segment
MCA, insular branches
Basilar artery (BA)
Posterior cerebral
artery (PCA)
MCA, cortical branches
(M4 segment)
PCA, temporal branch a
<n.
*
Internal cerebral vein
Superior petrosal sinus
Lateral ventricular
vein
Great cerebral vein
(of Galen)
Straight sinus (SS)
Transverse sinus (TS)
TS
B
——
Superior sagittal sinus
Anterior cerebral artery:
Great cerebral vein
(Aa)
(Ao)
MCA, Mp segment
Ss
Internal carotid
artery
‘i
Posterior communicating artery —
PCA
TS
Superior cerebellar
artery
MRA images arteries, veins, and dural venous sinuses simul-
10-9 taneously, based on the movement of fluid in these structures.
These are inverted video images of three-dimensional phase contrast
MRA images as viewed in the axial plane (A) and from the lateral
aspect, a sagittal view (B). The portion of the anterior cerebral artery
(ACA) located between the internal carotid artery and the anterior communicating artery is the Ay segment (precommunicating). The part of
the ACA immediately rostral to the anterior communicating artery and
inferior to the rostrum of the corpus callosum is the Ay segment (infracallosal). The portion of the ACA arching around the genu of the corpus
callosum is the A; segment (precallosal) and the A, (supracallosal) and
As (postcallosal) segments are located superior to (above), and caudal
to, the corpus callosum. Compare these images with arteries and veins
as depicted in Figures 2-18 and 2-19, 2-21, and 2-24, 2-27, and 2-28.
Cerebral Angiogram,
MRA, and MRV
Anterior cerebral artery:
Cortical branches
A1 segment
Internal carotid artery
Branches of middle
cerebral artery
Middle cerebral artery:
Branches 9n insula (Mo)
Internal carotid artery
M4 segment
Posterior communicating
artery
Cortical branches (Mg)
Posterior cerebral artery:
Posterior communicating
artery
Po segment
P4 segment
i
Posterior cerebral artery
ltofmtr/20
363 —
Parieto-occipital artery
Calcarine artery
W:14xig
}. Othk/ 0120:
Anterior communicating artery
if
= (ae
Orbit
Anterior cerebral artery
(Ay segment)
Ophthalmic artery
Middle cerebral artery
(branches on insula)
Cavernous sinus
(containing internal
carotid artery)
Petrosal segment of
internal carotid artery
Superior cerebellar artery
Middle cerebral artery
(M, segment) -
Tumor (vestibular schwannoma)
Posterior communicating
artery
Posterior cerebral artery
Basilar artery
Calcarine artery
Posterior cerebral
artery -
MRA images, in the axial plane, of the vessels at the base
of the brain forming much of the cerebral arterial circle (of
Willis) (A, B).
Note the anterior, middle, and posterior cerebral arteries as they
extend outward from the arterial circle.
The upper image (A) is from a normal individual, and the lower image
(B) is from a patient with a vestibular schwannoma (VS). These tumors
are generally slow growing, may become symptomatic after 30 years of
age, usually present (95%+ of the time) with hearing deficits (difficulty
discriminating sounds, hearing loss), and, if especially large (generally,
>2.5 cm in size), may involve the trigeminal nerve (CN V) root with a corresponding sensory loss on the ipsilateral face and scalp. Additional deficits include tinnitus, dysequilibrium, headache, facial numbness (about
30%
of cases), and facial weakness
(interestingly enough, only about
10% to 14% of cases). A patient with bilateral VS, or with unilateral VS
and less than 30 years of age, should be evaluated for neurofibromatosis
type 2. Descriptions of the segments of the anterior, middle, and posterior
cerebral arteries are found in Chapters 2 and 10.
Superior sagittal sinus
Callosomarginal branch
of ACA
Superficial cerebral veins
Pericallosal branch
of ACA
Anterior cerebral artery
Internal cerebral vein
(ACA)
Middle cerebral
artery
Great cerebral vein (of Galen)
Ophthalmic artery
or vein
Straight sinus
Carotid artery
Vein of Labbé
(cavernous portions)
Transverse sinus
Basal vein (of Rosenthal)
Confluence of sinuses
Sigmoid sinus
Basilar artery —
Internal jugular vein
Superficial cerebral veins
Superficial cerebral
veins
Superior sagittal sinus
Middle cerebral artery
on insular cortex
Superficial cerebral vein
Transverse sinus
Sigmoid sinus
Inferior petrosal sinus
Internal jugular vein
_ Magnetic resonance venography (MRV) primarily demon10-11
strates veins and dural venous sinuses, although arteries
(seen in A and B) may also be visualized. Many veins and venous sinuses
can be seen in this sagittal view (A) and in the anterior—posterior, or
coronal, view (B).
The superficial cerebral veins provide venous outflow from the more
external areas (cortex, subcortical white matter) while deep venous
Confluence of sinuses
Basilar artery
Internal carotid artery
Vertebral artery
channels, such as the internal cerebral vein (A), provide egress for venous
blood from deep structures (thalamus, caudate). The superior sagittal
sinus and the transverse sinus (more frequently the right) are the most
common sites (~70% of cases) of venous sinus thrombosis. Note that
the continuation of the superior sagittal sinus is most prominent into
the right transverse sinus (B, compare with Figure 10-6). Compare with
Figures 2-13, 2-16, 2-19, and 2-28.
Overview
Anterior cerebral artery
of Vertebral
and
Carotid
Arteries
Middle cerebral artery
Internal carotid artery
Cerebral part
Cavernous part
Basilar artery (BA)
Petrosal part
Anterior inferior
cerebellar artery
(AICA)
Cervical part
Vertebral artery
Posterior inferior
cerebellar artery
Maxillary artery
(br. of external
carotid artery)
Internal carotid artery
Vertebral artery (VA)
External carotid artery
Common carotid artery
Posterior cerebral
artery (PCA)
Superior
cerebellar artery
Position of
oculomotor
nerve
BA
AICA
(intercranial portion)
AICA
VA
(passing caudally and
medially around the lateral
mass of the atlas)
VA
(passing through transverse
foramen of the atlas)
MRA overview (A-C) of the arteries in the neck that serve
the brain (internal carotid and vertebral) and of their main
terminal branches (anterior cerebral artery and middle cerebral artery,
vertebrobasilar system) as seen in an anterior—posterior view.
In approximately 40% to 45% of individuals, the left vertebral
artery (VA) is larger, as seen here, and in about 4% to 7% of individuals,
one or the other of the vertebral arteries may be hypoplastic as seen here
on the patient’s right. Basically, the right VA ends at the origin of PICA
(A) with only a very narrow hypoplastic portion (seen in about 6% to
7% of cases, more frequently on the right) continuing to the basilar
artery. The MRA in (B) is a detailed view of the vertebrobasilar system
from the point where the vertebral arteries exit the transverse foramina
of the cervical vertebrae to where the basilar artery bifurcates into the
posterior cerebral arteries. The rostral portion of the basilar (C) gives
rise to the superior cerebellar artery (SCA), then immediately bifurcates
into the two P; segments of the posterior cerebral artery. Note the narrowing of the left P; segment (C) in this patient. Compare this image
with Figure 2-21.
The vertebral artery (VA) is generally described as being composed of
four segments sometimes designated as V, to V4. The first segment (V;)
is between the VA origin from the subclavian artery and the entrance
of VA into the first transverse foramen of the cervical vertebra (usually
C6); the second segment (V3) is that part of VA ascending through the
transverse foramen of C6—C2; the third segment (V3) is between the exit
of VA from the transverse foramen of the axis and the dura at the foramen magnum (which includes the loop of the VA that passes through
the transverse foramina of C1/the atlas); the fourth segment (V4) enters
the posterior fossa and joins its counterpart to form the basilar artery.
Anatomical—Clinical
Correlations:
Cerebral Angiogram,
MRA,
and MRV
B
Angiogram in the coronal plane of an aneurysm (A, arrows)
at the point where the M, segment branches into the M,
segments.
In about 75% of cases, there is a true bifurcation at this location; in
about 25%, there may be a branching into 3, 4, 5 or more M) segments.
Many MCA aneurysms occur at these branch points; aneurysms are commonly at branch points of vessels or at points where a vessel makes an
abrupt turn in its course. Small bilateral vascular lesions in the midbrain
(B, arrows, larger view below) may compromise the medial longitudinal fasciculus and portions of the oculomotor complex. This patient may
present with internuclear ophthalmoplegia, weakness of some eye movement, and probable pupillary dilation due to damage to the visceromotor
preganglionic parasympathetic Edinger-Westphal nucleus. In such a case,
the unaffected postganglionic sympathetic fibers to the eye prevail. The
small AVM in the right cerebellopontine angle (C) is characterized by flow
voids in the vessels within the structure. AVMs are congenital lesions that
may enlarge with age; may present with hemorrhage, seizure, and potentially mass effect; and are slightly more common in male patients. The
peak age for hemorrhage is 15 to 20 years of age. Aneurysm may coexist
with AVM. Occlusion of the basilar artery with resultant bilateral infarction of the basilar (plus) pons (D, arrows) may result in a locked-in syndrome. In this case, motor function for the LE and the UE and for most
of the lower cranial nerves is absent (descending motor tracts damaged
in the basilar pons), while sensory pathways (sensory tracts and upper
cranial nerves are not damaged in the pontine tegmentum) and some eye
movements are intact. Within the internal carotid system, aneurysms are
frequently discovered in the vicinity of ACom and its junction with A,
and A, (E, arrow). If an aneurysm at this location ruptures, it may dissect into the orbitofrontal cortex (see Figure 9-16B) and possibly into the
anterior horn of the lateral ventricle.
Q&A for this chapter is available online on
Point.
Q&As: A Sampling of Study and
Review Questions, Many in the USMLE
Style, All with Explained Answers
here are two essential goals of a student studying human neurobiology, or, for that matter, the student of any of the medical sciences.
wemneee The first is to gain the knowledge base and diagnostic skills to
become a competent health care professional. Addressing the medical needs
of the patient with insight, skill, and compassion is paramount. The second
is to successfully negotiate whatever examination procedures are used in a
given setting. These may be standard class examinations, Subject National
Board Examination
(now used/required in many courses), the USMLE
Step 1 Examination (required of all U.S. medical students), or simply the
desire, on the part of the student, for self-assessment.
The questions in this chapter are prepared in two general styles. First,
there are study or review questions that test general knowledge concerning the structure and function of the central nervous system. Second,
there are single one-best-answer questions in the USMLE Style that use a
patient vignette approach in the stem. These questions have been carefully
reviewed for clinical accuracy and relevance as used in these examples. In
order to make this a fruitful learning exercise, some answers may contain
additional relevant information to extend the educational process.
chapter
In general, the questions are organized by individual chapters,
although Chapters 1 and 2 are combined. Reference(s) to the page (or
pages) containing the correct answer are usually to the chapter(s) from
which the question originated. However, recognizing that neuroscience
is dynamic and three dimensional, some answers contain references to
chapters other than that from which the question originated. This provides a greater level of integration by bringing a wider range of information to bear ona single question. Correct diagnosis of the neurologically
compromised patient may also require inclusion of concepts gained in
other basic science courses. In this regard, a few questions, and their
answers, may include such additional basic concepts.
This is not an all-inclusive list of questions, but rather a sampling
that covers a variety of neuroanatomical and clinically relevant points.
There is certainly a much larger variety of questions that can be developed from the topics covered in this Atlas. It is hoped that this sample
will give the user a good idea of how basic neuroscience information
correlates with a range of clinically relevant topics and how questions
on these topics may be developed.
PRINT AND ONLINE Q&AS
The following is a sampling of Questions and Answers that are random
and not divided according to chapters. This sample of 60 Q&As plus
about 250 additional (for a total of over 310) are all available online as
one of the several Bonus Materials available for this Atlas. This entire
set of Q&As is organized according to chapter and follows the other
general guidelines described above.
of a sudden excruciating headache and then became stuporous (difficult to arouse). Suspecting a ruptured aneurysm, the
physician orders a CT. Which of the following would specify
the appearance of acute blood in the subarachnoid space in this
patient?
1. A 69-year-old woman is brought to the Emergency Department. The
daughter reports that her mother suddenly seemed unable to speak
but seemed to understand her difficulty. The examination reveals that
the woman has a nonfluent (Broca) aphasia. A sagittal MRI would
most likely show a lesion in which of the following gyri?
(B)
(C)
(D)
(E)
(A)
(B)
(C)
(D)
(E)
Angular
Inferior frontal
Lingual
Middle frontal
Supramarginal
2. A 71-year-old morbidly obese man is brought to the Emergency
Department by his son. The son reports that the man complained
(A) Black (hypodense)
Black to gray
Light gray
Medium gray
White (hyperdense)
3. Which of the following venous structures is found deep in the
lateral sulcus on the surface of the insular cortex?
(A) Anterior cerebral vein
(B) Basal vein of Rosenthal
(C) Deep middle cerebral vein
(D) Superficial middle cerebral vein
(E) Vein of Labbé
331
Q&As: A Sampling of Study and Review Questions, Many in the USMLE Style, All wi
4. A 47-year-old man presents with an intense pain on his face arising from stimulation at the corner of his mouth. The diagnosis is
trigeminal neuralgia (tic douloureux). MRI shows a vessel impinging on the root of the trigeminal nerve. Aberrant branches of which
of the following vessels would most likely be involved?
(A) Anterior inferior cerebellar artery
(B) Basilar artery
(C) Posterior cerebral artery
(D) Posterior inferior cerebellar artery
(E) Superior cerebellar artery
5. A 22-year-old man is brought to the Emergency Department from the
site of a motor vehicle collision. The examination reveals facial lacerations, a dilated right pupil, and loss of most eye movement on the right.
He has no other motor or sensory difficulties. CT reveals fractures of
the face and orbit. A fracture that traverses which of the following, and
damages its contents, would most likely explain this man’s deficits?
(A) Foramen ovale
(B) Foramen rotundum
(C) Inferior orbital fissure
D) Superior orbital fissure
(D)
(E) Stylomastoid foramen
6. A 71-year-old woman is diagnosed with a one-and-a-half syndrome
resultant to a lesion on the right side of the pons. Movement of
which of the following muscles is preserved in this patient?
(A)
B)
(B)
(C)
D)
(D)
Left lateral rectus
Left medial rectus
Left superior rectus
Right lateral rectus
(E) Right medial rectus
7. Bacterial meningitis is an inflammation of the meninges that generally is found in which of the following locations?
(A)
(B)
(C)
(D)
(E)
Epidural space
Subarachnoid space
Subdural space
Subpial space
Ventricular space
8. An 85-year-old woman is brought to the Emergency Department
by her family because she suddenly became confused and lethargic. The examination revealed a left homonymous hemianopia. CT
shows a hemorrhagic event in the vascular territory serving the
medial and lateral geniculate bodies. Which of the following structures would also likely be involved in this vascular lesion?
(A)
(B)
(C)
(D)
(E)
Anterior thalamic nucleus
Rostral dorsomedial nucleus
Globus pallidus
Pulvinar nucleus(i)
Subthalamic nucleus
9. A 16-year-old boy is brought to the Emergency Department following a diving accident at a local quarry. The initial examination
reveals a bilateral loss of motor and sensory function from about
T4 down including the lower extremities. At 36 hours after the accident, the boy is able to dorsiflex his toes, slightly move his right
lower extremity at the knee, and is able to perceive pinprick stimulation of the perianal skin (sacral sparing). Which of the following
most specifically describes the spinal cord lesion in this patient?
(A) Central cord
(B) Complete
(C)
Hemisection
(D) Incomplete
(E) Large syringomyelia
10. A 71-year-old man is brought to the Emergency Department by his wife.
She explains that he suddenly became weak in his left lower extremity.
She immediately rushed him to the hospital, a trip of about 20 minutes.
The examination reveals an alert man who is obese and hypertensive.
He has no cranial nerve deficits, is slightly weak on his left side, and
has no sensory deficits. Within 2 hours the weakness has disappeared.
A CT and MRI obtained within 5 hours shows no lesions. Which of
the following most specifically describes this man’s medical experience?
(A) Central cord syndrome
(B) Small embolic stroke
(C) Small hemorrhagic stroke
(D) Syringobulbia
(E) Transient ischemic attack
11. An 81-year-old woman is brought to the Emergency Department by
her adult grandson. He explains that during dinner she slumped off
of her chair, did not lose consciousness, but had trouble speaking.
The examination in the ED revealed weakness of the left upper and
lower extremities, deviation of the tongue to the right on protrusion, and loss of vibratory sense on the left. Which of the following
most specifically describes the deficits in this elderly patient?
(A)
(B)
(C)
(D)
(E)
Alternating (crossed) hemianesthesia
Hemihypesthesia
Inferior alternating (crossed) hemiplegia
Middle alternating (crossed) hemiplegia
Superior alternating (crossed) hemiplegia
12. Which of the following structures is located immediately internal to the
crus cerebri, appears as a dark shade of gray (hypointense) in a sagittal
T1-MRI, and when its cells are lost a pill-rolling tremor is seen?
A) Brachium of the inferior colliculus
(A)
(B) Periaqueductal gray
(C) Pretectal area
(D)
Red nucleus
(E) Substantia nigra
i133 A 15-year-old boy is brought to the Emergency Department after
an accident on his father’s farm. The examination reveals significant
weakness (a hemiparesis) of the left lower extremity. There is a loss of
pinprick sensation on the right side beginning at the T8 dermatome
(about half way between the nipple and umbilicus), and dorsiflexion of the left great toe in response to plantar stimulation. Based on
this examination, which of the following represents the most likely
approximate location of this lesion?
(A)
(B)
(C)
(D)
(E)
T6 on the left side
T6 on the right side
T8 on the left side
T8 on the right side
T10 on the left side
14. The physician is conducting a routine neurologic examination of a
16-year-old boy in preparation for summer football camp. As part
of this examination, he taps the patellar tendon and elicits a knee-
jerk reflex. The functional integrity of which of the following spinal
levels is tested by this reflex?
(A) CS5-C6
(B) C7-C8
(C) T8-T10
(D) L2-L4
(E) L5-S1
mpling of Study and Review Questions, Many in the USMLE
Style, All with Explained Answers
15. During a busy day in the Emergency
Department, the neurology
resident sees three patients with brainstem
lesions. The first is an
83-year-old woman with a lesion in the territ
ory of the midbrain
served by the quadrigeminal and lateral poster
ior choroidal arteries.
The second is a 68-year-old man with a posterior
inferior cerebellar
artery (lateral medullary or Wallenberg) syndr
ome. The third is a
47-year-old woman with a presumptive gliob
lastoma multiforme
invading the mid to lateral portions of the pontine tegme
ntum and
adjacent portions of the middle cerebellar peduncle. Which
of the
following would most likely be seen in all three patients
assuming a
thorough neurologic examination?
(A) Claude syndrome
(B) Contralateral hemiplegia
(C) Facial hemiplegia
(D) Horner syndrome
(E) Medial medullary syndrome
16. Somatovisceral reflexes are those in which the afterent limb arises
from a cutaneous
receptor (a somatic afferent), and the efferent
limb is mediated through pre- and postganglionic visceromotor fibers. A grain of sand blown into the eye results in increased secretions of the lacrimal gland in an effort to flush the offending object.
In the tearing (or lacrimal) reflex, which of the following represents
the location of the postganglionic cell bodies that innervate the
lacrimal gland?
A)
(A)
(B)
(C)
(D)
Dorsal motor vagal nucleus
Geniculate ganglion
Otic ganglion
Pterygopalatine ganglion
(E) Superior salivatory nucleus
17. A 23-year-old man is brought to the Emergency Department from an
accident at a construction site. CT shows a fracture of the left mastoid bone with total disruption of the stylomastoid foramen. Which
of the following deficits would most likely be seen in this man?
(A) Alternating hemianesthesia
(B) Alternating hemiplegia
(C) Central seven
(D) Facial hemiplegia
(E) Hemifacial spasm
18. A 59-year-old man, who is a family physician, confides in a neurology colleague that he believes he has early-stage Parkinson disease.
The neurologic examination reveals a slight resting tremor of the
left hand, slow gait, and subtle change in the normal range of facial
expression. Which of the following is the most likely location of the
degenerative changes, at this stage, of this physician’s disease?
(A) Bilateral substantia nigra
(B) Left globus pallidus
(C) Left substantia nigra
(D) Right globus pallidus
(E) Right substantia nigra
19. An inherited (autosomal recessive) disorder may appear early in the
teenage years. These patients have degenerative changes in the spinocerebellar tracts, posterior columns, corticospinal fibers, cerebellar cortex, and at select places in the brainstem. The symptoms of
these patients may include ataxia, paralysis, dysarthria, and other
clinical manifestations. This constellation of deficits is most charac-
teristically seen in which of the following?
(A) Friedreich ataxia
(B) Huntington disease
(C) Olivopontocerebellar degeneration (atrophy)
(D) Parkinson disease
(E) Wallenberg syndrome
20. A 20-year-old man is brought to the Emergency Department from
the site of a motorcycle accident. The examination reveals multiple
head injuries, facial lacerations, and a broken humerus. Cranial CT
shows a basal skull fracture extending through the jugular foramen. Assuming that the nerve, or nerves, that traverse this opening
are damaged, which of the following deficits would most likely be
seen in this man?
(A)
(B)
(C)
(D)
(E)
Deviation of the tongue to the injured side on protrusion
Diplopia and ptosis
Drooping and difficulty elevating the shoulder
Drooping of the face on the ipsilateral side
Loss of the efferent limb of the corneal reflex
Ail Which of the following represents a relay nucleus of the thalamus?
(A)
(B)
(C)
(D)
(E)
Centromedian
Dorsomedial
Medial geniculate
Pulvinar
Thalamic reticular
. A 39-year-old woman presents with sustained and oscillating muscle contractions that have twisted her trunk and extremities into
unusual and abnormal postures. This woman is most likely suffering from which of the following?
(A)
B)
(B)
(C)
D)
(D)
Dysarthria
Dysmetria
Dysphagia
Dyspnea
(E)
Dystonia
23. The concerned mother of a 16-year-old girl brings her to the family
physician. The girl explains that she occasionally has drops of a
white fluid coming from her breasts. Further examination confirms
that the girl is not sexually active and is not pregnant. An MRI
reveals a small tumor in the area of the pituitary and hypothalamus. Based on this girl’s signs and symptoms, she is most likely
suffering from which of the following?
(A) Excessive corticotropin production
(B) Excessive growth hormone production
(C) Excessive luteinizing hormone production
D) Excessive prolactin production
(D)
(E) Excessive vasopressin production
24. The neurologist on call sees three patients in the Emergency Department. The first is a 61-year-old woman with a superior alternating
hemiplegia, the second a 12-year-old boy with an ependymoma of
the fourth ventricle that is impinging on the facial colliculus, and
the third a 72-year-old man with a vascular infarct in the territory
of the paramedian branches of the basilar artery at the pontomedullary junction. Which of the following do all of these patients have
in common?
A) Aphasia
B) Agnosia
) Diplopia
)
Q&As: A Sampling of Study and Review Questions, Many in
piey. A 44-year-old woman presents to her family physician with the complaint of persistent headache and difficulty seeing out of her left eye.
The examination reveals that the woman has significantly impaired
vision in her left eye. When a light is shined into her left eye there
is no direct or consensual pupillary light reflex; the afferent limb is
compromised. Magnetic resonance angiography (MRA) shows a
large aneurysm at the origin of the ophthalmic artery. Which of the
following represents the likely point of origin of this vessel?
(A)
(B)
(C)
(D)
Cavernous part of the internal carotid artery
Cerebral part of the internal carotid artery
First segment (A;) of the anterior cerebral artery
First segment (M;) of the middle cerebral artery
(E) Petrous part of the internal carotid artery
Questions 26 and 27 are based on the following patient.
A 59-year-old woman presents with the complaint of a sudden severe
headache that did not respond to OTC medications, but cleared after
several hours. Upon questioning her physician discovers that she had
similar prior episodes over the last 3 months and he orders an MRI. This
series of images reveals a large fusiform aneurysm of the P; segment.
LO Based on its location, which of the following gyri would most likely
be impinged upon by this aneurysm?
(A) Cuneus
(B)
(C)
(D)
(E)
Lingual
Orbital
Parahippocampal
Superior temporal
Wife Assuming the neurosurgeon decides that this is a serious vascular
lesion that requires treatment, based on its location which of the
following deficits might this patient experience?
(A)
(B)
(C)
(D)
(E)
Blindness in one eye
Partial bilateral hearing loss
Partial bilateral visual loss
Somatomotor loss of the body
Somatosensory loss of the body
Questions 28 and 29 are based on the following patient.
A 63-year-old man has hearing loss, tinnitus (ringing or buzzing sounds
in the ear), vertigo, and unsteady gait; all of these deficits developed
slowly, but progressively, over several years. MRI reveals a large tumor
(3 cm in diameter) at the cerebellopontine angle, most likely a vestibular
schwannoma (incorrectly called an acoustic neuroma).
28. What additional deficit could this patient also have?
(A) Anosmia
B) Hemianopsia
(B)
(C) Numbness on the face
D) Visual field deficits
(D)
(E) Weakness of the tongue
He). In addition to the vestibulocochlear nerve, which of the following
structures would most likely also be affected by the tumor in this man?
(A) Anterior inferior cerebellar artery
(B) Facial nerve
(C) Glossopharyngeal nerve '
(D) Posterior inferior cerebellar artery
(E) Vagus nerve
Questions 30 and 31 are based on the following patient.
A 23-year-old man is brought to the Emergency Department from the
site of an automobile collision. The neurologic examination reveals
weakness of the right lower extremity and a loss of pain and thermal
ous |
sensations on the left side beginning at the level of the umbilicus. GT
shows a fracture of the vertebral column with displacement of bone
fragments into the vertebral canal.
30. Damage to which of the following tracts would correlate with
weakness of the lower extremity in this man?
(A)
(B)
(C)
(D)
(E)
Left lateral corticospinal tract
Reticulospinal fibers on the right
Right lateral corticospinal tract
Right rubrospinal tract
Vestibulospinal fibers on the right
31. Which of the following represents the most likely level of damage
to the spinal cord resulting from the fracture to the vertebral column in this man?
(A)
B)
(B)
(C)
D)
(D)
T6 on the left
TS8 on the left
T8 on the right
T10 on the left
(E) T10 on the right
Questions 32 and 33 are based on the following patient.
A 71-year-old woman presents to her family physician with the complaint that “food dribbles out of my mouth when IJ eat.” The examination reveals a unilateral weakness of muscles around the eye (palpebral
fissure) and the opening of the mouth (oral fissure). She also has a loss
of pain and thermal sensations on the opposite side of the body excluding the head. CT shows an infarcted area in the lateral portion of the
pontine tegmentum.
32. Damage to which of the following nuclei would most likely explain
the muscle weakness experienced by this woman?
(A)
(B)
(C)
(D)
Abducens
Arcuate
Facial motor
Hypoglossal
(E) Trigeminal motor
33. The loss of pain and thermal sensations experienced by this woman
would most likely correlate with a lesion involving which of the
following structures?
(A)
(B)
(C)
(D)
Anterior (ventral) trigeminothalamic tract
Anterolateral system
Lateral lemniscus
Medial lemniscus
(E) Spinal trigeminal tract
Questions 34 and 35 are based on the following patient.
A 41-year-old man is brought to the Emergency Department after an
accident at a construction site. The examination reveals a weakness
(hemiplegia) and a loss of vibratory sensation and discriminative touch
all on the left lower extremity, and a loss of pain and thermal sensations on the right lower extremity. CT shows a fracture of the vertebral
column adjacent to the T8 level of the spinal cord.
34. Damage to which of the following fiber bundles or tracts would
most likely explain the loss of vibratory sensation in this man?
(A ) Anterolateral system on the right
B) Cuneate fasciculus on the left
(B)
(C) Cuneate fasciculus on the right
D) Gracile fasciculus on the left
(D)
(E) Gracile fasciculus on the right
he USI ALE Style, All with Explained Answers
35. The loss of pain and thermal sensation in this man reflects damage
to which of the following fiber bundles or tracts?
(A) .Anterolateral system on the left
(B) Anterolateral system on the right
(C) Cuneate fasciculus on the left
(D) Gracile fasciculus on the left
(E) Posterior spinocerebellar tract on the left
40. Injury to which of the following structures in this man is most specifically related to the loss of pain and thermal sensations on the
body below the neck?
A
(A)
B)
(B)
(C)
D
(D)
Anterolateral system
Cuneate fasciculus
Gracile fasciculus
Medial lemniscus
(E) Spinal trigeminal tract
Questions 36 through 38 are based on the following patient.
An 88-year-old man is brought to the Emergency Department by
his daughter. She indicates that he complained of sudden weakness of his
and “leg” (upper and lower extremities) on
the right side and of “seeing two of everything” (double vision—
diplopia). CT confirms an infarcted area in the medial area of the pons
at the pons—medulla junction. The infarcted area is consistent with
the vascular territory served by paramedian branches of the basilar
artery.
“arm”
36. Weakness of the extremities on the right can be explained by damage to which of the following structures?
(A) Corticospinal fibers on the left
(B) Corticospinal fibers on the right
(C) Middle cerebellar peduncle on the left
(D) Rubrospinal fibers on the left
(E) Rubrospinal fibers on the right
j
37. The diplopia (double vision) this man is having is most likely the
result of damage to which of the following structures?
(A) Abducens nerve root
(B) Facial nerve root
(C) Oculomotor nerve root
(D) Optic nerve
(E) Trochlear nerve or root
38. Recognizing that this patient’s lesion involves the territory served
by paramedian branches of the basilar artery, which of the following structures is also most likely included in the area of
infarction?
(A) Anterolateral system
(B) Facial motor nucleus
(C) Hypoglossal nucleus
(D) Medial lemniscus
(E) Spinal trigeminal tract
Questions 39 through 42 are based on the following patient.
A 69-year-old man is brought to the Emergency Department with the
complaint of a sudden loss of sensation on his face and in his mouth.
The history and examination reveals that the man is overweight,
hypertensive, and does not regularly take medication. When the man
speaks his voice is gravelly and hoarse. The examination further
reveals a loss of pain and thermal sensations on the right side of his
body and on the left side of his face. CT shows an infarcted area in the
medulla.
39. Damage to which of the following structures would most likely
explain the man’s hoarse, gravelly voice?
(A)
(B)
(C)
(D)
Facial nucleus
Gracile nucleus
Hypoglossal nucleus
Nucleus ambiguus
(E) Spinal trigeminal nucleus
41. Damage to which of the following structures would most specifically explain the loss of pain and thermal sensations on this man’s
face?
(A)
(B)
(C)
(D)
(E)
Anterolateral system
Medial lemniscus
Medial longitudinal fasciculus
Solitary tract
Spinal trigeminal tract
42. The CT shows an infarcted area in the medulla in this man. Based
on the combination of deficits experienced by this man, which of
the following vessels is most likely occluded?
(A) Anterior spinal artery
(B) Posterior spinal artery
(C) Posterior inferior cerebellar artery
(D) Anterior inferior cerebellar artery
(E) Penetrating branches of the vertebral artery
Questions 43 through 45 are based on the following patient.
A 73-year-old man is brought to the Emergency Department after
losing consciousness at his home. CT shows a large hemorrhage
in the right hemisphere. The man regains consciousness, but is not
fully alert. After 3 to 4 days the man begins to rapidly deteriorate.
His pupils are large (dilated) and respond slowly to light, eye movement becomes restricted, there is weakness in the extremities on the
left side, and the man becomes comatose. Repeat CT shows an uncal
herniation.
43. Based on its location, which of the following parts of the brain is
most likely to be directly affected by this herniation, especially in
its early stages?
(A)
(B)
(C)
(D)
(E)
Diencephalon/thalamus
Mesencephalon/midbrain
Myelencephalon/medulla
Pons and cerebellum
Pons only
44. Damage to corticospinal fibers in which of the following locations would most likely explain the weakness in this man’s
extremities?
(A) Left basilar pons
(B) Left crus cerebri
(C) Right basilar pons
(D) Right crus cerebri
(E) Right posterior limb of the internal capsule
45. The dilated, and slowly responsive, pupils in this man are most
likely explained by damage to fibers in which of the following?
(A)
(B)
(C)
(D)
(E)
Abducens nerve
Corticonuclear fibers in the crus
Oculomotor nerve
Optic nerve
Sympathetic fibers on cerebral vessels
Q&As: A Sampling of Study and Review Questions, Many in the USMLE Styl o
46. A newborn baby girl is unable to suckle. The examination reveals
that muscles around the oral cavity and of the cheek are poorly
developed and some are absent. A failure in proper development of
which of the following structures would most likely contribute to
this problem for the baby?
(A)
(B)
(C)
(D)
(E)
Head mesoderm
Pharyngeal arch 1
Pharyngeal arch 2
Pharyngeal arch 3
Pharyngeal arch 4
Questions 47 and 48 are based on the following patient.
A 62-year-old woman presents with tremor and ataxia on the right side
of the body excluding the head, and with a loss of most eye movement
on the left; the woman’s eye is rotated slightly down and out at rest.
The left pupil is dilated. There are no sensory losses on her face or body.
47. Based on the deficits seen in this woman, which of the following
represents the most likely location of the causative lesion?
(A) Cerebellum on the left
B) Cerebellum on the right
(B)
(C) Medulla on the left
D) Midbrain on the left
(D)
(E) Midbrain on the right
48. The dilated pupil in this woman is most likely a result of which of
the following?
(A)
(B)
(C)
(D)
(E)
Intact parasympathetic fibers on the left
Intact parasympathetic fibers on the right
Intact sympathetic fibers on the left
Intact sympathetic fibers on the right
Interrupted hypothalamospinal fibers on the left
Questions 49 and 50 are based on the following patient.
A 69-year-old man is diagnosed with dysarthria. The history reveals
that the man has had this problem for several weeks. MRI shows an
infarcted area in the brainstem on the right side.
49. Damage to which of the following structures would most likely
explain this deficit in this man?
(A) Cuneate nucleus
(B) Nucleus ambiguus
(C) Solitary tract and nuclei
(D) Spinal trigeminal tract
(E) Vestibular nuclei
50. Assuming that the infarcted area in the brain of this man is the
result of a vascular occlusion, which of the following arteries is
most likely involved?
(A)
(B)
(C)
(D)
(E)
Anterior inferior cerebellar
Labyrinthine
Posterior inferior cerebellar
Posterior spinal
Superior cerebellar
Questions 51 through 53 are based on the following patient.
An 80-year-old woman is brought to the Emergency Department from
an assisted care facility. The woman, who is in a wheelchair, complains
of not feeling well, numbness on her face, and being hoarse, although
she claims not to have a cold. The examination reveals a loss of pain and
thermal sensations on the right side of her face and the left side of her
body. CT shows an infarcted area in the lateral portion of the medulla.
ot A lesion of which of the following structures in this woman would
explain the loss of pain and thermal sensations on her body excluding the head?
(A)
(B)
(C)
(D)
(E)
Anterolateral system on the left
Anterolateral system on the right
Medial lemniscus on the left
Spinal trigeminal nucleus on the left
Spinal trigeminal tract on the left
oP The hoarseness in this woman
following?
(A)
(B)
(C)
(D)
(E)
Lesion
Lesion
Lesion
Lesion
Lesion
is most likely due to which of the
of the facial nucleus
of the hypoglossal nucleus/nerve
of the nucleus ambiguus
of the spinal trigeminal tract
of the trigeminal nucleus
D)ahc Assuming this woman suffered a vascular occlusion, which of the
following vessels is most likely involved?
(A)
(B)
(C)
(D)
(E)
Anterior inferior cerebellar artery
Anterior spinal artery
Posterior inferior cerebellar artery
Posterior spinal artery
Superior cerebellar artery
Questions 54 and 5S are based on the following patient.
A 37-year-old man is brought to the Emergency Department from the site
of an automobile collision. He was unrestrained and, as a result, has extensive injuries to his face and head. CT shows numerous fractures of the facial
bones and skull and blood in the rostral areas of the frontal lobes and in
the rostral 3 to 4 cm of the temporal lobes, bilaterally. After several weeks
of recovery the man is moved to a long-term care facility. His behavior is
characterized by: (1) difficulty recognizing sounds such as music or words;
(2) a propensity to place inappropriate objects in his mouth; (3) a tendency
to eat excessively or to eat nonfood items such as the leaves on the plant in
his room; and (4) a tendency to touch his genitalia.
54. Which of the following most specifically describes the tendency of
this man to eat excessively?
A) Aphagia
(A)
B) Dysphagia
(B)
(C) Dyspnea
(D)
(E) Hyperphagia
Dic Based on the totality of this man’s deficits he is most likely suffering
from which of the following?
(A) Kliiver-Bucy syndrome
(B) Korsakoff syndrome
(C) Senile dementia
(D) Wallenberg syndrome
(E) Wernicke aphasia
Questions 56 and S57 are based on the following patient.
A 23-year-old man is brought to the Emergency Department from the
site of an automobile collision. CT shows fractures of the facial bones
and evidence of bilateral trauma to the temporal lobes including blood
is the parahippocampal gyri and hippocampus.
56. As this man recovers, which of the following deficits is likely to be
the most obvious?
(A) A bilateral sensory loss in the lower body
(B) A loss of immediate and short-term memory
JS | MLE Style, All with Explained Answers
(C) A loss of long-term (remote) memory
‘
\
D) Dementia
(E) Dysphagia and dysarthria
OE Assuming that this man also has sustained bilateral injury to the
Meyer—Archambault loop, which of the following deficits would he
also most likely have?
(A) Bitemporal hemianopsia
(B)
(C)
(D)
(E)
Bilateral inferior quadrantanopia
Bilateral superior quadrantanopia
Left superior quadrantanopia
Right superior quadrantanopia
Questions 58 through 60 are based on the following patient.
A 67-year-old man is brought to the Emergency Department by his wife.
She explains that he fell suddenly, could not get out of his bed, and
complained of feeling nauseated, but did not vomit. The examination
revealed a left-sided weakness of the upper and lower extremities, a lack
of most movement of the right eye, and a dilated pupil on the right. MRI
shows an infarcted area in the brainstem.
58. The weakness of this man’s extremities is explained by damage to
the axons of cell bodies that are located in which of the following
regions of the brain?
(A)
(B)
(C)
(D)
Left somatomotor cortex
Right anterior paracentral gyrus
Right crus cerebri
Right precentral gyrus
of an intracranial aneurysm frequently complain of an intense,
sudden headache (“the most horrible headache I have ever had”).
Acute blood in the subarachnoid space will appear white to very
white on CT; this blood is hyperdense. This will contrast with the
medium gray of the brain and the black of cerebrospinal fluid (CSF)
in the ventricles. The degree of white may vary somewhat, based on
the relative concentration of blood, from very white (concentrated
blood) to white (mostly blood, some CSF), to very light gray (mixture of blood and CSF).
. Answer C: The deep middle cerebral vein is located on the insular cortex and, by joining with the anterior cerebral vein, forms
the basal vein of Rosenthal. The superficial middle cerebral vein
is located on the lateral aspect of the hemisphere in the vicinity of
the lateral sulcus, arches around the temporal lobe, and joins the
cavernous sinus. The vein of Labbé drains the lateral aspect of the
hemisphere into the transverse sinus.
. Answer E: Branches of the superior cerebellar artery are most
frequently involved in cases of trigeminal neuralgia that are presumably of vascular origin. The posterior cerebral artery and its
larger branches serve the midbrain—-diencephalic junction or join
the medial surface of the hemisphere. The basilar artery serves the
basilar pons and the anterior inferior cerebellar artery serves the
caudal midbrain, inner ear, and the inferior surface of the cerebellar surface. The basal vein drains the medial portions of the hemisphere and passes through the ambient cistern to enter the great
cerebral vein (of Galen).
(E) Right somatomotor cortex
. Answer D: This man’s deficits, loss of most (but not all) eye move-
Dek This man’s dilated pupil is due to damage to which of the following
fiber populations?
(A)
(B)
(C)
(D)
(E)
Preganglionic fibers from the Edinger—Westphal nucleus
Preganglionic fibers from the inferior salivatory nucleus
Postganglionic fibers from the ciliary ganglion
Postganglionic fibers from the geniculate ganglion
Postganglionic fibers from the superior cervical ganglion
60. Which of the following descriptive phrases best describes the constellation of signs and symptoms seen in this man?
(A)
(B)
(C)
(D)
(E)
Alternating hemianesthesia
Brown-Séquard syndrome
Inferior alternating (crossed) hemiplegia
Middle alternating (crossed) hemiplegia
Superior alternating (crossed) hemiplegia
ANSWERS
i Answer B: The inferior frontal gyrus consists of the pars orbitalis
(Brodmann area 47), pars triangularis (area 45), and pars opercularis (area 44). A lesion located primarily in areas 44 and 45 in the
dominant hemisphere will result in a nonfluent (Broca, or motor)
aphasia. The supramarginal (area 40) and angular (area 39) gyri
represent what is called the Wernicke area, and the middle frontal
gyrus contains areas 6 and 8. The lingual gyrus 1s located below the
calcarine sulcus; the superior quadrant of the opposite visual fields
is represented in this gyrus (area 17).
_ Answer E: The most common cause of blood in the subarachnoid
space is resultant to trauma; the second most common cause Is rupture of an intracranial aneurysm. Patients who experience rupture
ment and dilation of the pupil, are on the right side. These losses,
with no other deficits, indicate damage to the oculomotor nerve;
this nerve exits the cranial cavity via the superior orbital fissure.
This fissure also transmits the ophthalmic nerve. The foramen ovale
transmits the mandibular nerve (plus fibers to the masticatory muscles) and the foramen rotundum transmits the maxillary nerve.
After the maxillary nerve passes through the rotundum, it shifts
course and enters the orbit via the inferior orbital fissure. The facial
nerve passes through the stylomastoid foramen.
. Answer A: In this patient the pontine lesion is on the right side.
This results in a paralysis of the right lateral rectus (abducens lower
motor neurons) and of the right and left medial recti on attempted
lateral gaze (damage to the axons of interneurons entering the
medial longitudinal fasciculus on both sides). The surviving muscle
is the left lateral rectus.
. Answer B: The inflammation in meningitis generally occupies the
subarachnoid space and its minute extensions into the sulci; the
infection may also extend into cisterns. The commonly used clinical
terms leptomeningitis (signifying arachnoid + pia) or pia-arachnitis
reflect the fact that this infection is frequently sequestered within
the subarachnoid space. Meningitis may involve the dura (pachymeningitis) and, by extension, invade the minute spaces between
the pia and brain surface (subpial space). However, these are not
the main locations of this disease process. Epidural and subdural
spaces are the result of trauma or some pathologic process and,
around the brain, are not naturally occurring spaces.
. Answer D: The geniculate bodies are tucked-up under the caudal
and inferior aspect of the pulvinar nucleus(i). The groove between
the medial geniculate body and pulvinar contains the brachium
of the superior colliculus. The geniculate bodies and the pulvinar
Q&As: A Sampling of Study and Review Questions, Many in the USML
have a common blood supply from the thalamogeniculate artery,
a branch of P;. None of the other choices have a close apposition
with the geniculate bodies. The anterior thalamic, rostral dorsomedial, and subthalamic nuclei do not share a common blood supply
with the pulvinar.
Answer D: Although this patient initially presented with complete
motor and sensory losses, some function had returned by 36 hours;
in this case, the lesion is classified as an incomplete lesion of the
spinal cord. Patients with no return of function at 24+ hours and
no sacral sparing have suffered a lesion classified as complete and
it is unlikely that they will recover useful neurologic function. In a
central cord and a large syringomyelia, there is generally sparing of
posterior column sensations and in a hemisection the loss of motor
function is on the side of the lesion and the loss of pinprick is on
the opposite side.
10. Answer E: The short-term loss of function, frequently involving a
specific part of the body, is characteristic of a transient ischemic
attack (commonly called a TIA). The follow-up MRI shows no
lesion because there has been no permanent damage. TIAs are
caused by a brief period of inadequate perfusion of a localized
region of the nervous system; recovery is usually rapid and complete. However, TIAs, especially if repeated, may be indicative of an
impending stroke. Hemorrhagic strokes frequently result in some
type of long-term or permanent deficit, and the central cord syndrome has bilateral deficits. A small embolic stroke would be visible on the follow-up MRI and, in this patient, would have resulted
in a persistent deficit. Syringobulbia (cavitation within the medulla)
may include long tract signs as well as cranial nerve signs.
ik. Answer C: Weakness of the extremities accompanied by paralysis of
muscles on the contralateral side of the tongue (seen as a deviation
of the tongue to that side on protrusion) indicates a lesion in the
medulla involving the corticospinal fibers in the pyramid and the
exiting hypoglossal roots. This is an inferior alternating (crossed)
hemiplegia. Middle alternating (crossed) hemiplegia refers to a lesion
of the pontine corticospinal fibers and the root of the abducens nerve,
and superior alternating (crossed) hemiplegia specifies damage to the
oculomotor root and crus cerebri. Alternating (alternate, or crossed)
hemianesthesia and hemihypesthesia are sensory losses.
2, Answer E: The substantia nigra is located internal to the crus cerebri and, in T1-weighted MRI, appears as a darker shade of gray
(hypointense) than does the crus. Loss of the dopamine-containing
cells of the nigra results in characteristic motor deficits, including a
pill-rolling (resting) tremor. The red nucleus and the periaqueductal
gray are located in the midbrain, but do not border on the crus cerebri. The brachium of the inferior colliculus is found on the lateral
surface of the midbrain, and the pretectal area is adjacent to the
cerebral aqueduct at the midbrain—diencephalic junction.
13% Answer A: The combination of weakness on the left side (corticospinal involvement) and a loss of pain sensation on the right side specifies components of Brown-Séquard syndrome. The motor loss is
ipsilateral to the damage and the sensory loss is contralateral; second
order fibers conveying pain information cross in the anterior white
commissure ascending about two spinal segments in the process. In
this patient, the lesion is on the left side at about the T6 level; this
explains the left-sided weakness and the loss of pain sensation on
the right beginning at the T8 dermatome level. Lesions at T8 or T10
would result in a loss of pain sensation beginning, respectively, at
dermatome levels T10 or T12 on the contralateral side.
14. Answer D: A tap on the patellar tendon stretches the muscle spindles in the quadriceps muscles, results in contraction of the same
muscle group of the thigh, and the knee abruptly swings forward;
this is mediated through spinal levels L2-L4. This is a monosynaptic reflex (and a muscle stretch reflex) with excitation of the extensor muscles of the leg and, through an interneuron, inhibition of
leg flexors. The biceps reflex is mediated through C5-C6, and the
triceps through C7—-C8. The abdominal reflex is mediated through
spinal levels T8—-T10; level $1, with contributions from LS and S82,
mediates the ankle reflex.
NS) Answer D: Lesions in the lateral portions of the brainstem damage
descending projections from the hypothalamus to the ipsilateral
intermediolateral cell column at spinal levels T1-T4, these being the
hypothalamospinal fibers. The result is Horner syndrome (ptosis,
myosis, anhydrosis on the face) on the side ipsilateral to the lesion.
Horner syndrome also may be seen following cervical spinal cord
lesions. A contralateral hemiplegia is not seen in lesions in lateral
areas of the brainstem. The other choices are syndromes or deficits
specific to medial brainstem areas or to only a particular level.
16. Answer D: The afferent limb of the tearing (lacrimal) reflex is via
the trigeminal nerve (pain receptors in the conjunctiva and cornea),
and the efferent limb travels on the facial nerve; the preganglionic
parasympathetic cells are in the superior salivatory nucleus, and the
postganglionic cells are in the pterygopalatine ganglion. The dorsal
motor vagal nucleus contains preganglionic parasympathetic cells
that distribute to ganglia in the thorax and abdomen. The geniculate ganglion contains the cell bodies of somatic afferent (SA) and
visceral afferent (VA) fibers that enter the brain on the facial nerve;
the otic ganglion contains postganglionic parasympathetic cell
bodies that serve the parotid gland.
1
Answer D: The paralysis of facial muscles on one side of the face
(left in this case) with no paralysis of the extremities is a facial hemiplegia; this is also commonly known as Bell palsy or facial palsy.
Hemifacial spasms are irregular contractions of the facial muscles,
and a central seven (also called a supranuclear facial palsy) refers
to paralysis of muscles on the lower half of the face contralateral
to a lesion in the genu of the internal capsule. Alternating (crossed)
hemiplegia describes a motor loss related to a cranial nerve on one
side of the head and motor deficits of the extremities on the contralateral side of the body. A similar pattern of sensory losses is
called an alternating (alternate or crossed) hemianesthesia.
18. Answer E: Degenerative changes in the dopamine-containing cells
of the substantia nigra pars compacta on the right side correlate
with a left-sided tremor. The altered message through the lenticular
nucleus and thalamus and on to the motor cortex on the side of the
degenerative changes will result in tremor on the opposite (right)
side via altered messages traveling down the corticospinal tract.
The initial symptoms of Parkinson disease appear on one side in
about 75% to 80% of patients and extend to bilateral involvement as the disease progresses. Bilateral changes in the substantia nigra correlate with bilateral deficits. The globus pallidus does
not receive direct nigral input but rather input via a nigrostriatal—
striatopallidal circuit.
19: Answer A: This inherited disease is Friedreich ataxia; it initially
appears in children in the age range of 8 to 15 years and has the
characteristic deficits described. Huntington disease is inherited,
but appears in adults (age range at onset 35 to 45 years); olivopontocerebellar atrophy is an autosomal dominant disease and gives
tyle, All with Explained Answers
rise to a totally different set of deficits. The cause of Parkinson
disease is unclear, but it is probably not inherited and generally
seen in patients 45+ years of age. The Wallenberg syndrome is a
brainstem lesion resulting from a vascular occlusion and most commonly characterized by an alternating (crossed) hemianesthesia.
20. Answer C: A fracture through the jugular foramen would potentially damage the glossopharyngeal (IX), vagus (X), and spinal
accessory (XI) nerves. The major observable deficit would be a loss
of the efferent limb of the gag reflex and paralysis of the ipsilateral
trapezius and sternocleidomastoid muscles (drooping of the shoulder, difficulty elevating the shoulder especially against resistance,
difficulty turning the head to the contralateral side). The patient
would also experience difficulty swallowing (dysphagia) and speaking (dysarthria). Involvement of facial muscles would suggest damage to the internal acoustic or stylomastoid foramina; this would
also be the case for the efferent limb of the corneal reflex. Diplopia
and ptosis would suggest injury to the superior orbital fissure, as all
three nerves controlling ocular movement traverse this space. The
hypoglossal nerve (which supplies muscles of the tongue) passes
through the hypoglossal canal.
Zt. Answer C: A relay nucleus is one that receives a specific type of
information from a comparatively specific source, and sends this
information on to an equally specific cortical target. The medial
geniculate nucleus receives mainly auditory information from the
cochlear nuclei and brainstem auditory relay nuclei and projects to
the transverse temporal gyrus. The dorsomedial, centromedian, and
pulvinar are association nuclei; these receive input from diverse
sources and project to equally diverse cortical targets. The thalamic
reticular nucleus, while not specifically classified as either a relay
nucleus or an association nucleus, basically functions as an association nucleus.
Dap. Answer E: Dystonia is a movement disorder characterized by
abnormal, sometimes intermittent, but frequently sustained, contractions of the muscles of the trunk and extremities that force the
body into a twisted posture. Dystonia may be seen in patients with
diseases of the basal nuclei. Dysmetria, the inability to judge the
distance and trajectory of a movement, is a feature of cerebellar
disease or lesions. Dyspnea is difficulty breathing; this may result
from heart and/or lung disorders as well as from neurologic disorders, which may include central or nerve root lesions. Dysphagia
is difficulty swallowing, dysarthria is difficulty speaking, and both
may be seen together in several central or peripheral lesions.
Le: Answer D: Prolactinoma, a tumor that produces excessive amounts
of prolactin (a hypersecreting tumor), may result in milk production in females in the absence of pregnancy. In females, excess luteinizing hormone may disrupt the ovarian cycle but not result in
milk production. Overproduction of corticotropin results in Cushing disease; excessive growth hormone results in either gigantism
(before growth plates close) or acromegaly (after growth plates
close). Overproduction of vasopressin influences urine excretion.
24 ° Answer C: These three involve the roots of the oculomotor and
abducens nerve and the nucleus of the abducens nerve, all of which
innervate extraocular muscles. Each of these patients would experience some form of diplopia, one of their complaints would be
seeing “double” or “two of everything.” Aphasia and agnosia are
usually associated with lesions of the forebrain. Dysarthria and
dysphagia are frequently seen in medullary lesions, lesions involving the nuclei or roots of some cranial nerves of the medulla, but
may also be seen in patients with large hemispheric strokes. Hemianesthesia may be present in patients with lesions at many levels of
the central nervous system, but not in medially located lesions as is
the case with these three patients.
2S. Answer B: In most instances (approximately 80% to 85%), the
ophthalmic artery originates from the cerebral portion of the internal carotid artery just after this parent vessel leaves the cavernous
sinus and passes through the dura. In a small percentage of cases,
the ophthalmic artery may originate from other locations on the
internal carotid artery, including its cavernous portion (about 7%).
This vessel does not originate from the petrous portion of the internal carotid or from anterior or middle cerebral arteries.
26. Answer D: The P3; segment lies along the orientation of, and adjacent to, the parahippocampal gyrus as this part of the posterior
cerebral artery courses around the midbrain. Branches of the P;
segment serve the inferior surface of the temporal lobe, which
includes much of the laterally adjacent occipitotemporal gyri, and
lower portions of the optic radiations. The lingual gyrus and the
cuneus are in the territory of the Py segment and the orbital gyri are
served by branches of the anterior and middle cerebral arteries. The
superior temporal gyrus is served by My, branches of the inferior
trunk of the middle cerebral artery.
AU: Answer C: Treating fusiform aneurysms (in this case on the P3 segment) present special considerations and complications and may
result in blockage of all blood flow to targets distal to this point.
Distal portions of the posterior cerebral artery (the P, segment)
serve the primary visual cortex. Somatosensory, somatomotor,
and auditory regions of the cerebral cortex are served by terminal
branches of the middle cerebral artery (Mz, in the case of motor and
sensory, M3/M, in the case of auditory). Blindness in one eye would
result from a lesion rostral to the optic chiasm; in the case of a vascular cause, this may relate to damage to the ophthalmic branch of
the internal carotid.
28. Answer C: Vestibular schwannomas larger than 2 cm in diameter
may enlarge rostrally, impinge on the sensory root of the trigeminal nerve and, cause loss of sensation on the same side of the face.
Although the other deficits listed (olfactory loss, visual deficits,
tongue weakness) are not seen in these patients, diplopia (involvement of oculomotor, abducens, or trochlear nerves, singularly or in
combination) may be present, in fewer than 10%, of patients with
vestibular schwannoma.
wy). Answer B: The internal acoustic meatus contains the vestibulocochlear nerve, the facial nerve, and the labyrinthine artery, a branch
of the anterior inferior cerebellar artery. A vestibular schwannoma
located at the meatus may affect the facial nerve and result in facial
weakness. Large schwannomas usually produce sensory loss on
the face (30%+ of the time) while facial weakness may be seen in
about 10%+ of cases. The vagus and glossopharyngeal nerves exit
the skull via the jugular foramen (along with the accessory nerve).
The cerebellar arteries originate within the skull and distribute to
structures within the skull.
30. Answer C: In this patient the weakness of the right lower extremity
is related to a lesion of lateral corticospinal tract fibers on the right
side of the spinal cord. The left corticospinal tract serves the left
side of the spinal cord and the left lower extremity. Rubrospinal,
reticulospinal, and vestibulospinal fibers influence the activity of
spinal motor neurons; however, the deficits related to corticospinal
All with Explai ned A
Q&As: A Sampling of Study and Review Questions, Many in the USMLE Style,
tract damage (significant weakness) will dominate over the lack of
excitation to flexor or extensor motor neurons in the spinal cord
via these tracts. These latter tracts are dominant in cases of decorticate and decerebrate posturing.
. Answer C: The loss of pain and thermal sensations beginning at the
level of the umbilicus (T10 dermatome) on the left side results from
damage to fibers of the anterolateral system at about the T8 level on
the right. These fibers ascend about two spinal levels as they cross
the midline. Damage at the T6 level would result in a loss beginning
at the TS level on the contralateral side and damage at the T10 level
would result in a loss beginning at about the T12 level.
O2e Answer C: Weakness of the muscles of the face, particularly when
upper and lower portions of the face are involved, indicates a
lesion of either the facial motor nucleus or the exiting fibers of
the facial nerve; both are located in the lateral pontine tegmentum
at caudal levels. The hypoglossal nucleus, which is located in the
medial medulla, innervates muscles of the tongue. The trigeminal
nucleus innervates masticatory muscles and is present in the mid
to more rostral pontine tegmentum. The abducens nucleus is found
internal to the facial colliculus and innervates the lateral rectus
muscle. These nuclei innervate muscles on the ipsilateral side. The
arcuate nucleus is a group of cells located on the surface of the
pyramid.
3)3%5 Answer B: The fibers of the anterolateral system are located in the
lateral portion of the pontine tegmentum anterior (ventral) to the
facial motor nucleus; these fibers convey pain and thermal inputs
from the contralateral side of the body. The spinal trigeminal tract
and the anterior trigeminothalamic tract also convey pain and thermal input but from the ipsilateral and contralateral sides of the
face, respectively. The lateral lemniscus is auditory in function and
the medial lemniscus conveys proprioception, vibratory sense, and
discriminative touch also from the contralateral body.
34. Answer D: Damage to the gracile fasciculus on the left (at the T8
level this is the only part of the posterior columns present at this
level) accounts for the loss of vibratory sensation (and discriminative touch). Injury to the gracile fasciculus on the right would
result in this type of deficit, but on the right side. The level of the
cord damage is caudal to the cuneate fasciculi and the anterolateral
system conveys pain and thermal sensations from the contralateral
side, not proprioceptive information.
30 Answer A: The loss of pain and thermal sensations on the right
side of the body correlates with a lesion involving the anterolateral
system on the left side of the spinal cord. The axons carrying this
sensory information cross the midline ascending about two spinal
levels as they do so. A lesion of the right anterolateral system would
result in a left-sided deficit. The gracile and cuneate fasciculi convey
discriminative touch, vibratory sensation, and proprioception from
the ipsilateral side of the body. The posterior spinocerebellar tract
conveys similar information, but it is not perceived/recognized as
such (consciously) by the brain.
36. Answer A: In this case the weakness of the upper and lower extremities on the right, in association with the diplopia (abducens injury),
reflects damage to corticospinal fibers on the left side of the basilar
pons. A lesion of these fibers on the right side of the pons would
produce a left-sided weakness after they cross in the motor decussation. Rubrospinal fibers are not located in the territory of paramedian branches of the basilar artery. Also, lesions of rubrospinal
fibers and of the middle cerebellar peduncle do not cause weakness
but may cause other types of motor deficits, particularly in lesions
causing decorticate and decerebrate rigidity.
STs Answer A: The best localizing sign in this case is the diplopia; along
with the corticospinal deficit and vascular territory, it specifies a
lesion at the pons—medulla junction on the left. The exiting fibers
of the abducens nerve (on the left) are in the territory of the paramedian branches of the basilar artery and are laterally adjacent to
corticospinal fibers in the basilar pons. Diplopia may result from
lesions of the oculomotor and trochlear nerves, but these structures
are not in the domain of the paramedian basilar branches. A lesion
of the optic nerve results in blindness in that eye and damage to the
facial root does not affect eye movement but may cause a loss of
view of the external world if the palpebral fissure is closed due to
facial muscle weakness.
38. Answer D: At caudal pontine levels most, if not all, of the medial
lemniscus is located within the territory served by paramedian
branches of the basilar artery. Penetrating branches of the anterior
spinal artery serve the hypoglossal nucleus. The other choices are
generally in the territories of short or long circumferential branches
of the basilar artery. The hypoglossal nucleus and its root are in the
territory of the anterior spinal artery.
3h) Answer D: The vocalis muscle (this muscle is actually the medial portion of the thyroarytenoid muscle) is innervated, via the vagus nerve,
by motor neurons located in the nucleus ambiguus. The gracile
nucleus conveys proprioception and vibratory sense from the body
and the spinal trigeminal nucleus relays pain and thermal sensory
input from the face. The hypoglossal nucleus is motor to the tongue
and the facial nucleus is motor to the muscles of facial expression.
40. Answer A: Fibers comprising the anterolateral system convey pain
and thermal sensations from the body, excluding the face. These
fibers are located in lateral portions of the medulla adjacent to the
spinal trigeminal tract; this latter tract relays pain and thermal sensations from the face. Both of these tracts are in the territory of the
posterior inferior cerebellar artery. The gracile and cuneate fasciculi
convey proprioception, discriminative touch, and vibratory sense in
the spinal cord and the medial lemniscus conveys this same infor-
mation from the medulla to the dorsal thalamus.
41. Answer E: The loss of pain and thermal sensations on one side of
the face correlates with damage to the spinal trigeminal tract; in
this case the loss is ipsilateral to the lesion. The anterolateral system
relays pain and thermal sensations from the contralateral side of
the body, the solitary tract conveys visceral sensory input (general
visceral sense and taste), and the medial lemniscus contains fibers
relaying information related to position sense and discriminative
touch, also from the contralateral side. The medial longitudinal fasciculus does not contain sensory fibers.
42. Answer C: The posterior inferior cerebellar artery (commonly called
PICA by clinicians) serves the posterolateral portion of the medulla,
which encompasses the anterolateral system, spinal trigeminal tract,
and nucleus ambiguus plus other nuclei. This combination of deficits
is variably called the PICA syndrome, lateral medullary syndrome, or
Wallenberg syndrome. The anterior and medial areas of the medulla
(containing the pyramid, medial lemniscus, and hypoglossal nucleus/
nerve) are served by the anterior spinal artery and the anterolateral
area of the medulla (the region of the olivary nuclei) is served by pen-
etrating branches of the vertebral artery. The posterior spinal artery
serves the posterior column nuclei in the medulla and
the anterior
inferior cerebellar artery (commonly called AICA) serves
caudal portions of the pons and cerebellum,
Answer B: The uncus is at the rostral and medial aspect of the
parahippocampal gyrus, and, in this position, is directly adjacent to
the
anterolateral aspect of the midbrain. The diencephalon is rostral
to
this point and the medulla, the most caudal part of the brainstem, is
located in the posterior fossa. Late stages of uncal herniation may,
but not always, result in damage to the rostral pons; this is especially the case if the patient becomes decerebrate. The cerebellum is
not involved in uncal herniation but may participate in upward or
downward cerebellar herniation.
44. Answer D: Herniation of the uncus through the tentorial incisura
compresses the lateral portions of the brainstem, particularly the
midbrain, eventually resulting in compression of the corticospinal
fibers in the crus cerebri. Weakness on the patient’s left side indicates damage to corticospinal fibers in the right crus. In situations
of significant shift of the midbrain due to the herniation, the contralateral crus also may be damaged, resulting in bilateral weakness. Although all other choices contain corticospinal fibers, none
of these areas are directly involved in uncal herniation.
45. Answer C: The root of the oculomotor nerve conveys (general)
somatic efferent (SE) fibers to four of the six major extraocular
muscles and (general) visceral efferent (VE) parasympathetic
preganglionic fibers to the ciliary ganglion from which postganglionic fibers travel to the sphincter muscle of the iris. Pressure on
the oculomotor root, as in uncal herniation, will usually compress
the smaller diameter, and more superficially located VE fibers first
(pupil dilation) followed by eventual compression of the larger
diameter motor fibers (muscle weakness), Optic nerve damage
results in blindness in that eye, injury to sympathetic fibers to the
eye results in constriction of the pupil, and an abducens root injury
results in an inability to abduct that eye or in diplopia. A lesion of
corticonuclear fibers in the crus results primarily in motor deficits
related to the facial, hypoglossal, and accessory nerves.
46
Answer C: The absence of, or the aberrant development of, muscle
around the oral cavity and over the cheek (muscles of facial expression, innervated by the facial [VII] nerve) indicate a failure of proper
differentiation of the second pharyngeal arch. Arch 2 also gives rise
to the stapedius, buccinator, stylohyoid, platysma, and posterior
belly of the digastric. Mesoderm of the head outside of the pharyngeal arches gives rise to the extraocular muscles and muscles of the
tongue. The muscles of mastication (plus the tensor tympani, tensor
veli palatini, mylohyoid, anterior belly of the digastric) arise from
arch 1, the stylopharyngeus from arch 3, and striated muscles of the
pharynx, larynx, and upper esophagus from arch 4.
47. Answer D: The best localizing sign in this patient is the paucity of
eye movement and dilated pupil on the left; this indicates a lesion
of the midbrain on the left at the level of the exiting oculomotor
fibers. The red nucleus is found at the same level and, more importantly, immediately lateral to the red nucleus is a compact bundle of
cerebellothalamic fibers. The ataxia and tremor are related primarily
to damage these cerebellar efferent fibers. The motor deficit is contralateral to the lesion because the corticospinal fibers, through
which the deficit is expressed, cross at the motor (pyramidal) decussation. Lesions at the other choices would not result in a paucity
of eye movement, or result in these deficits on the wrong side, and,
therefore, are not potential candidates.
48. Answer C: The lesion on the exiting oculomotor fibers (on the
left) damages the preganglionic parasympathetic fibers from the
Edinger—Westphal preganglionic nucleus. Activation of these fibers
produces pupil constriction; when their influence is removed the
pupil dilates. Consequently, the intact postganglionic sympathetic
fibers from the ipsilateral superior cervical ganglion predominate,
and the pupil dilates. Choices describing deficits on the right side
are not correct, the surviving fibers are on the left side and will
result in a dilated pupil on that side when activated. Damage to
hypothalamospinal fibers would remove sympathetic influence at
the intermediolateral cell column, and the pupil would constrict
(parasympathetic domination).
49. Answer B: Cell bodies in the nucleus ambiguus innervate muscles
of the pharynx and larynx, including what is commonly called the
vocalis muscle. One result of damage to this nucleus is dysarthria;
another is dysphagia. The solitary tract and nuclei are concerned
with visceral afferent information, including taste, and the spinal
trigeminal tract is made the central processes of primary sensory
fibers conveying (general) somatic afferent (SA) information from
the ipsilateral side of the face and oral cavity. Proprioceptive information from the ipsilateral upper extremity is transmitted via the
cuneate nucleus; the vestibular nuclei are related to balance, equilibrium, and control of eye movement.
50. Answer C: The area of the brainstem that contains the nucleus
ambiguus is served by branches of the posterior inferior cerebellar
artery (PICA). Occlusion of this vessel usually gives rise to the PICA
(lateral medullary or Wallenberg) syndrome. The anterior inferior
cerebellar artery (AICA) serves the lateral and inferior cerebellar
surface and the superior cerebellar artery serves the superior surface and much of the cerebellar nuclei. The labyrinthine artery, a
branch of AICA, serves the inner ear. The posterior spinal artery
serves the posterior columns and their nuclei.
Syile Answer B: The lesion in this woman is in the medulla, and the
sensory loss on the body (excluding the head) is on her left side; a
lesion in the medulla on the right side, involving fibers of the anterolateral system (ALS), accounts for this sensory deficit. The overall
sensory deficits in this case may be called an alternate (or crossed)
hemianesthesia. A lesion of the ALS on the left side of the medulla
would result in sensory deficits on the right side of the body. The
spinal trigeminal tract and nucleus convey pain and thermal sensations from the ipsilateral side (right side in this case) of the face,
and the medial lemniscus conveys vibratory and discriminative
touch sensations from the contralateral side of the body.
es Answer C: The woman is hoarse because the lesion involves the
region of the medulla that includes the nucleus ambiguus. These
motor neurons serve, via the glossopharyngeal (IX) and vagus (X)
nerves, the muscles of the larynx and pharynx, including the medial
portion of the thyroarytenoid, also called the vocalis muscle. Paralysis of the vocalis on one side will cause hoarseness of the voice.
This patient will, most likely, also experience difficulty swallowing (dysphagia). Hypoglossal nucleus or nerve, or facial nucleus
lesions, may cause difficulty with speech (altered movements of
the tongue or muscles around the mouth) but not hoarseness. The
spinal trigeminal tract conveys sensory input from the ipsilateral
side of the face. There are no historical or examination findings to
support a diagnosis of upper respiratory viral findings (cold or flu).
5546 Answer C: The posterior inferior cerebellar artery (PICA) serves
the lateral area of the medulla that contains the anterolateral sys-
Q&As: A Sampling of Study and Review Questions, Many in the USMLE Style, All wi
tem, spinal trigeminal tract (loss of pain and thermal sensations
from the ipsilateral side of the face), the nucleus ambiguus, and
other structures. Many patients that present with a PICA (Wallenberg or lateral medullary) syndrome may also have involvement of
the vertebral artery on that side. The posterior spinal artery serves
the posterior column nuclei in the medulla, and the anterior spinal
artery serves the pyramid, medial lemniscus, and exiting roots of
the hypoglossal nerve. The anterior inferior cerebellar artery and
the superior cerebellar artery distribute to the pons and midbrain,
respectively, plus significant portions of the cerebellum.
54. Answer E: Excessive eating (gluttony), which may also include, in
the case of this patient, a propensity to attempt to eat things not
considered food items, is hyperphagia. Dysphagia is difficulty in
swallowing and frequently related to medullary damage. Aphagia is
the inability to eat; this may reflect dysfunction of the masticatory
apparatus or the lack of desire to eat. Hyperorality is the tendency
to put items in the mouth or to appear to be examining objects
by placing them in the oral cavity. Dyspnea is difficulty breathing.
2)5% Answer A: The constellation of deficits experienced by this man
is characteristic of the Kliiver-Bucy syndrome; this may be seen
following bilateral damage to the temporal poles particularly that
which includes the amygdaloid complex. The Korsakoff syndrome
(psychosis) is seen, for example, in chronic alcoholics, and senile
dementia is a loss of cognitive and intellectual function associated
with neurodegenerative diseases of the elderly (e.g., Alzheimer disease). Wernicke (receptive or fluent) aphasia is seen in patients with
a lesion in the area of the inferior parietal lobule, and the Wallenberg syndrome results from a lesion in the medulla and is characterized by alternating (crossed) hemisensory losses and, depending
on the extent of the damage, other deficits.
56. Answer B: Bilateral damage to the temporal lobes, as in this case, may
result in damage to the hippocampus by any one of several mechanisms. While remote memory, the ability to recall events that happened
years ago, is intact, the man will have difficulty “remembering” recent
(last few days/weeks) or immediate (last few minutes/hours) events.
That is, he will find it difficult, if not impossible, to turn a new experience into longer-term memory (something that can be recalled in its
proper context at a later time). Dysphagia (difficulty swallowing) and
dysarthria (difficulty speaking) are deficits usually seen in brainstem
lesions. Bilateral sensory losses of the lower portion of the body could
be seen with bilateral damage to the posterior paracentral gyri (falcine
meningioma) or to the antezior white commissure of the spinal cord.
Dementia is a multiregional symptom that usually involves several
areas of the brain, cortical as well as subcortical.
Dc Answer C: The Meyer-Archambault loop (sometimes called
the Meyer loop) is composed of optic radiation fibers that loop
through the temporal lobe. These fibers, on each side, convey visual
input from the contralateral superior quadrant of the visual field.
Consequently, a bilateral lesion of these fibers results as a bilateral
superior quadrantanopia. Bilateral inferior quadrantanopia is seen
in bilateral lesions that would involve the superior portion of the
optic radiations. Right or left superior quadrantanopia is seen in
cases of unilateral damage to, respectively, the left or right Meyer—
Archambault loop. A bitemporal hemianopsia results in a lesion of
the optic chiasm.
58. Answer C: The combination of eye movement disorders and a contralateral hemiplegia localizes this lesion to the midbrain on the side
of the ocular deficits (right side); the best localizing signs are the third
nerve deficits. This also specifies that corticospinal fibers on the right
(in the crus) are damaged, and places the location of the cells of origin for these fibers in the somatomotor cortex on the right side. The
right crus contains the axons of these fibers but not the neuronal cell
bodies. The left somatomotor cortex influences the right extremities.
The right precentral gyrus does not contain cells projecting to the left
lumbosacral spinal cord (left lower extremity), and the right anterior
paracentral gyrus does not contain the cells that project to the left
cervical spinal cord (left upper extremity).
SY), Answer A: The lesion in this man is in the central (brainstem/midbrain) and involves the third nerve and adjacent structures, such
as the red nucleus and cerebellothalamic fibers. Consequently, the
damage is to the preganglionic parasympathetic fibers in the root of
the oculomotor (III) nerve; this removes the parasympathetic influence (pupil constriction) that originates from the Edinger—-Westphal
preganglionic nucleus. Fibers from the superior cervical ganglion
are intact, hence the dilated pupil. Fibers from the geniculate ganglion and inferior salivatory nucleus distribute on the facial (VII)
and glossopharyngeal (IX) nerves, respectively. Postganglionic fibers from the ciliary ganglion, although involved in this pathway, are
not damaged in this lesion.
60. Answer E: The loss of most eye movement on one side (oculomotor
nerve root involvement) coupled with a paralysis of the extremities
on the contralateral side is a superior alternating (crossed) hemiplegia (this is also known as the Weber syndrome): superior because it
is the most rostral of three; alternating (crossed) because it is a cranial nerve on one side and the extremities on the other; and hemiplegia because one-half of the body below the head is involved.
A middle alternating (crossed) hemiplegia involves the abducens
(VI) nerve root and adjacent corticospinal fibers (Raymond syndrome), and an inferior alternating (crossed) hemiplegia involves
the hypoglossal (XII) nerve root and corticospinal fibers in the pyramid (Déjérine syndrome). Alternating hemianesthesia is a sensory
loss, and a Brown-Séquard syndrome is a spinal cord lesion with
no cranial nerve deficits.
Index
Note: Page numbers in italics denote figures;
those followed by t refer to table; those
followed by Q denote questions; and those
followed by A denote answers.
Ambient cistern, 48, 64, 65
Amenorrhea, 294
Amiculum of olive, 116, 118, 120
Ammon horn, 280, 281
Amnesia, 280, 282, 285
A
Abdominal muscles, 236, 236
Abdominal reflex, 210, 236, 332Q, 338A
loss of, 210
Amnestic confabulatory syndrome, 280
Amygdala, lesions and deficits, 285
Amygdalocortical fibers, 282, 283
Amygdalofugal fibers, 166
Amygdalofugal pathway, 282, 284-285,
290,291
Amygdalohypothalamic fibers, 290
Amygdaloid connections, 282-283, 283
Abducens internuclear neuron, 53
Abducens nerve, 20, 22-25, 33, 44t, 49-53,
130; 132, 138,226, 227-229
Abducens nucleus, 53, 122, 123, 128,
130=132, 138, 139, 179, 228, 229,
232-233, 272, 334Q, 340A
blood supply of, 226
contralateral, 214
lesion of, 53
Abducens root, lesion of, 53
Amygdaloid efferents, 284, 284-285, 385
lesions and deficits of, 285, 285
projections of, 284
Accessory cuneate nucleus, 114, 116, 118
Amygdaloid nuclear complex, 68, 69, 78, 91,
162-475,282
blood supply to, 282
connections of, 282, 283, 290
Accessory nerve (XI), 22, 23, 31, 51
Accessory nucleus, 106-107, 112-113, 214,
lesions of, 285
Amygdaloid nucleus, 187, 187
216-217, 238, 238, 276
Accessory olivary nucleus
dorsal, 250, 251
medial, 114, 116, 118, 120, 250, 251
posterior, 116, 118, 120
Acetylcholine, 192, 210, 226, 262, 282
Acoustic neuroma. See Vestibular schwannoma
Acromegaly, 294
Acute central cervical spinal cord syndrome,
108
Acute subdural hematomas, 58, 63
Adamkiewicz, artery of, 9
A-delta and C fibers, 236
Adenohypophysis, 294, 295
Afferent fibers, 244, 245
clinical correlations in, 244
Amyotrophic lateral sclerosis, 210, 226, 230
Anatomical orientation, 4, 5-6, 189
anterolateral system in, 196, 197-198, 201
neurotransmitters in, 244
Ageusia, 206
Agnosia, 192, 270, 280, 282, 333Q, 339A
Alar plate, 96
Alcoholic cerebellar degeneration, 244
Alcoholic dementia and cerebellar atrophy, 285
Alternating (or crossed) hemiplegia, 53, 210,
214, 226
inferior, 124, 226, 337A, 341A
middle, 138, 337A, 341A
superior, 152, 333Q, 337A, 341A
Alternating deficits, 95
Alternating hemianesthesia, 202, 338A, 342A
Alveus of hippocampus, 156, 160, 162
Alzheimer dementia, 285
Alzheimer disease, 280, 282
of auditory pathways, 270, 271
of cerebellar efferent fibers, 248-251
clinical correlations, 190, 192, 196, 202
medial lemniscus system in, 192, 193
neurotransmitters, 190, 196, 202, 242
nigral connections, 256, 257
orientation drawing for, 190, 191
pallidal efferents, 256, 257
postsynaptic-posterior (dorsal) column
system, 200, 201
solitary pathways, 206, 207
spinocerebellar tracts, 242, 243
spinocervicothalamic pathway, 200, 201
trigeminal pathways, 202, 203, 204
of vestibular pathways, 272, 273
Anesthesia dolorosa, 174
Aneurysms, 22, 40
basilar tip, 47
in infratentorial area, 47
rupture of, 46, 47
supratentorial, 46
treatment of, 65
Angiography
digital subtraction, 322
internal carotid, 320-322
magnetic resonance, 323, 334
vertebral artery, 324-325
Angular gyrus, 12, 16
Anhidrosis, 6, 124, 195, 199, 205, 213, 262
Anosmia, 206
Ansa lenticularis, 158, 166, 181, 256, 257,
289
Anterolateral system (ALS), 196
Anterior cerebral artery (ACA), 14-15, 18-19,
21-22, 23, 27, 33, 37-38, 46, 298,
298, 313
anterior cerebral arteries, 21, 23, 27, 29,
33, 38
azygos ACA, 313
branching patterns of, 15
callosomarginal branch, 27
frontopolar branches, 27
infarction in territory, 14
internal frontal branches, 27
internal parietal branches, 27
medial striate artery, 40
occlusion of distal branches of, 174
orbital branches of, 19, 27
origin of, 38
paracentral branches, 27
pericallosal branch, 27
A, segment of, 21
A> segment of, 21, 27
A3 segment of, 27
temporal branches of, 19
terminal branches of, 27
vascular lesions, 310, 313
watershed infarcts, 312
Anterior cerebral vein, 19, 37
Anterior choroidal artery, 23, 46, 72, 174, 175
Anterior choroidal artery syndrome, 25, 46,
174, 276
Anterior cochlear nucleus, 120, 122, 125,
126, 2H
Anterior commissure, 29, 68, 69, 77, 77,
Tey Cs ed, HOS US WEY, 1S IAS,
W/O USM eSDel SZ Sie
eee
DS, LA
Anterior communicating artery, 21-23, 27,
33, 38, 40, 40, 46, 46, 323, 323, 327
anteromedial branches, 175
magnetic resonance imaging of, 27, 33, 38
Anterior cord syndrome, 305, 305
Anterior corticospinal tract, 100, 102, 104,
L106, 109 ea
Anterior forceps, 86
Anterior funiculus, 9
Anterior horn, 70, 70, 99-105
of lateral ventricle, 68-70, 71, 76-77,
86-89, 168, 170, 172, 178, 180-181,
BY DAD)
at levels C3—C7, 109
Anterior hypothalamus, 283
343
344
Index
vestibular pathways and, 272, 273
Sige
DON
esiloNelonoeos Se
aberrant loop of, 230
branch to choroid plexus, 72
magnetic resonance angiography of, 323
medulla territory served by, 125
origin of, 42
Anterior inferior cerebellar artery occlusion, 196
Anterior intercavernous sinus, 21, 295
Anterior interposed cerebellar nucleus.
See Emboliform nucleus
Anterior lobe of cerebellum, 48-49, 284-285
Anterior median fissure, 9, 22, 94, 100,
102, 104
Anterior medullary velum, 25, 29, 30, 31, 33,
243, 249
Aphasia, 12, 278, 339A
nonfluent (Broca), 331Q
Wernicke, 342A
Aqueduct, cerebral, 5, 18, 48, 66, 68, 69,
82, 90-92, 140, 142, 144, 146, 148,
150; 153, 194, 198; 212, 216-217,
228-229, 302
blood in, 74
magnetic resonance imaging of, 29, 33
Arachnoid, 8, 10, 58t, 59
Arachnoid mater, 59, 60
Arachnoid trabeculae, 58, 58t, 59
Arachnoid villus, 59
Arbitrary continuation, 11
Arcuate nucleus, 114, 116, 118, 120, 289,
Anterior nucleus of thalamus. See Anterior
thalamic nucleus
295, 334Q, 340A
Area postrema, 116
Anterior paracentral gyrus, 12, 13, 26, 28,
Area X, 104
211-213, 279, 337Q, 342A
Anterior perforated substance, 23, 25, 41,
168, 175
Anterior quadrangular lobule, 34
Anterior radicular artery, 9, 109
Anterior root, 9, 9, 234-236, 263, 304-307
Anterior root fibers, 100, 102
Anterior spinal artery, 8, 9, 21, 23, 25, 33, 42,
SiS
occlusion of, 108, 124
thrombosis of, 108
Anterior spinal medullary artery, 8, 9, 109
Anterior spinocerebellar tract, 102, 104, 196,
OD, TA, MAA, TING, TUES, TAOS, WS
130, 132, 134
Anterior tegmental decussation, 219, 221
Anterior thalamic nucleus, 79, 87-88, 162, 164,
166, 175, 178-181, 182, 183, 289, 291
Anterior thalamic radiations, 276
Anterior trigeminothalamic fibers, 236, 236-238
Anterior tubercle of thalamus, 78
Anterior vertebral venous plexus, 21
Anterior watershed infarcts, 174
Anterior white commissure, 102, 104, 109,
G5 ENS, DDS OAD
Anterolateral cordotomy, 200
Anterolateral sulcus, 104
Anterolateral system, 54t, 95, 98, 100, 102,
Areflexia, 234
Arnold-Chiari deformity, 246
Arterial vasocorona, 9, 9, 109
Arteriovenous malformation (AVM), 108
bleeding from, 58, 71
of cerebellar vessels, 246
in spinal cord, 108
Artery(ies)
Adamkiewicz, 9
occlusion of, 108
anterior cerebral
anterolateral branches of, 175
anteromedial branches of, 175
callosomarginal branch, 15, 27, 318, 328
frontopolar branches, 15, 27
infarction in territory, 14
internal frontal branches, 27
internal parietal branches, 15, 27
magnetic resonance imaging, 21, 23, 27,
DIESE) Sis
medial striate branch of, 175
orbital branches, 19, 27
paracentral branches, 15, 27, 318, 328
pericallosal branch, 27
anterior choroidal, 23, 46, 72, 175
anterior communicating, 21, 23, 27, 33, 38,
40, 46, 70, 320, 323
magnetic resonance imaging of, 27, 33, 38
104, 106, 109, 112, 114, 116, 118, 120,
122, 125-126, 128, 130, 132, 134, 136,
138, 139-140, 142, 144, 146, 148, 150,
anterior inferior cerebellar, 21, 23, 25, 31,
US3; 156,158, 196199203, 211,219;
anterior spinal, 8, 9, 21, 23, 25, 33, 42
DIYS PDEs PASN=
PIBY.,ASS, DH Bin PN OOD
medulla territory served by, 125
335Q, 340A, 341A
auditory pathways and, 270, 271
blood supply to, 196
cerebellar efferents and, 248, 249-251
335 50), 72
anterior radicular, 9, 109
occlusion of, 108, 124
anterior spinal medullary, 8, 9, 109
system, 192, 193-195
basilar, 9, 21-23, 25, 29, 33, 38, 39, 42, 47,
47, 49, 50, 64, 72, 78, 93, 323-329
angiography of, 324, 325
magnetic resonance angiography, 323,
326-327, 329
occlusion of, 138
pons territory served by, 139
calcarine, 324, 327
carotid, common, 328, 329
carotid, external, 329
reticulospinal tract and, 218, 219
carotid, internal, 19, 21-25, 27, 33, 37, 38, 40,
in spinal cord, 198, 199
tectospinal tract and, 218, 219
41, 47, 49, 72, 318, 320, 323, 326-329
labyrinthine, 23, 25, 33, 42
lateral posterior choroidal, 31, 72
trigeminal pathways and, 202, 203-205
lenticulostriate, 19, 21, 23, 41
cranial nerve efferents and, 230, 231-233
damage to, 334Q, 335Q, 340A
lesions and deficits of, 199, 199
in medulla, 5, 194, 195, 204
in midbrain, 198-199, 204-205
in pons, 198-199
and posterior column—medial lemniscus
spinocerebellar tract and, 242, 243
maxillary, 329
medial posterior choroidal, 72
medial striate artery, 23, 40, 40, 72
middle cerebral artery, 33, 37, 47, 48, 60, 72,
170, 174917538 18,320; 323, 3262824
angular branches of, 15, 17, Bi, ules
anterior parietal branches OMe 1, BY
anterior temporal branches, 17, 37
anterolateral branches of, 175
branching patterns of, 15, 17
cortical branches, 326-327
inferior trunk of, 19, 37
insular branches, 320, 326
on insular cortex, 328
lateral striate arteries, 41, 175
magnetic resonance imaging of, 37, 38,
47, 48
middle temporal branches, 17
M, segment of, 19, 23, 37
M, segment of, 37
M; segment of, 23, 37
M, segment of, 37
orbitofrontal branches, 15, 17, 19, 37
posterior parietal branches of, 17, 37
posterior temporal branches, 17, 37
prerolandic branches, 15, 17, 37
rolandic branches, 15, 17, 37
superior trunk of, 19, 37
temporal branches, 17
ophthalmic, 21, 23, 318, 327-328
occlusion of, 318
origin of, 334Q, 339A
polar temporal, 23
pontine, 23
posterior cerebral, 21-23, 25, 33, 38, 42, 47,
48, 72, 78-80, 91, 152, 160, 323-327
(See also Posterior cerebral artery)
anterior temporal branch of, 19, 27
branching patterns of, 15
calcarine branch of, 19, 27
fetal, 38
origin of, 38
parieto-occipital branch of, 19, 27
posterior temporal branch of, 19, 27
P; segment of, 19
segments P\—P, of, 19
temporal branches of, 19
thalamoperforating arteries, 39
posterior choroidal, 23, 25, 33
posterior communicating artery, 19, 21-23,
255275395 4/2 ele
magnetic resonance imaging, 47
posterior inferior cerebellar artery, 9, 21-23,
25, 29, 32-33, 42, 72, 324-325, 329
origin of, 42
posterior radicular artery, 9, 9, 109
posterior spinal, 8, 10, 21, 23, 23, 25, 31,
33, 42
quadrigeminal, 19, 23, 25, 31, 33
segmental, 9
sulcal, 9, 109
superior cerebellar artery,
21-23, 25, 31, 33,
47-49, 72, 323-327, 329
superior hypophysial, 295
thalamogeniculate, 25, 31, 33, 153, 324
thalamoperforating, 39, 324, 325
uncal, 23
vertebral artery, 9, 2.1, 23, 25-33, 42,
323--325, 327-329
Index
Areflexia, 234
Artery of Heubner. See Medial striate artery
Aspartate, 192, 220, 244, 248, 270
Association nuclei, 278
Astereognosis, 192
Asterixis, 254
Ataxia, 56, 138, 192, 242, 244, 246, 278
Ataxia telangiectasia, 244
Atrium of lateral ventricle, 68-70, 88-90,
154, 178, 182, 187
Auditory agnosia, 270, 280, 282
Auditory cortex, 12, 270, 279
Auditory pathways, 56, 56, 270, 271
in anatomical orientation, 270, 271
blank master drawing for, 274-275
Auditory radiations, 276
Autosomal recessive disorder, 333Q, 338A
Azygous ACA, 38
B
Babinski reflexes, 299
Babinski sign, 192, 210
Bacterial meningitis, 58, 332Q, 337A
Balint syndrome, 309
Basal nucleus(ei), 166, 168, 258, 299
internal distribution of arteries to, 174, 175
lesions of, 259
of Meynert, 166, 168
MRI of, 155-173
vascular lesions in, 311, 312
Basal plate, 96
Basal skull fracture, 294
Basaleveins 1952743743
Oe 82/3315 337A
Basilar artery (BA), 9, 21-23, 25, 29, 33, 47,
49, 50, 64, 72, 78, 93, 316, 323-329
angiography of, 324-325
anterior and posterior inferior cerebellar
arteries, 42
MRA of, 323, 326-327, 329
occlusion of paramedian branches of, 138,
314, 314
vascular sprouts, 38
Basilar bifurcation, 22, 23, 324, 325
Basilar plexus, 21
Basilar pons, 5, 20, 22-24, 28, 29, 32, 34,
35, 46-50, 64, 70, 79, 80, 81, 92-93,
92-93, 136, 139, 140, 142, 144, 160,
179, 1815 204, 210; 2125216; 222, 223,
D239 2327233; 258;259;335Q, 340A
Basilar tip aneurysm, 47
Basolateral amygdala, 290, 291
Bell palsy, 230, 338A
Benedikt syndrome, 54, 152
Biceps reflex, 338A
Bilateral acoustic neurofibromatosis, 272
Bilateral flaccid paraplegia, 108
Bilateral for upper face, 215
Bilateral superior quadrantanopia, 337Q, 342A
Binasal hemianopia, 267
Bitemporal hemianopia, 262, 267, 294
Biventer lobule, 34
Bladder and bowel problems, 308
Blank master drawing
for connections of basal nuclei, 260-261, 261
for efferent cerebellar connections, 252-253,
253
for limbic pathways, 286-287, 287
for visual pathways, 268-269, 269
Blindness, 46, 262, 318
Rlood
in atrium of lateral ventricle, 71
in brain, 71, 74
in cerebral aqueduct, 74
to choroid plexus, 72
in frontal lobe, 74
intraventricular, 71
in lateral ventricles, 70, 71
in posterior horn, 73
in subarachnoid space and cisterns, 65
in temporal horn, 73
in third ventricle, 71, 74
Body
of caudate nucleus, 68-69, 79-82, 86, 154,
156, 160, 164, 175, 250-251
of corpus callosum, 28, 68-69, 76-82, 86,
156, 162, 164, 166, 168, 170, 172
of fornix, 29, 79-81, 87, 156, 160, 162, 164,
175, 258
juxtarestiform, 30, 30, 118, 122, 128, 130,
246, 247, 250, 272, 273
of lateral ventricle, 68, 69
mammillary, 18, 22, 23, 25, 29, 33, 46, 48,
Coe CITT SR
795 OI 1A Ol ALSO S158,
162, 175, 179186; 186,228;)229-280,
2392295
restiform, 5, 25, 30-33, 51, 52, 94, 94, 114,
LUGS A QOD 2512 6128 h 305193,
194, 197, 198, 204, 205, 212, 216, 232,
242, 243, 246, 247, 273
Bone of sella, 295
Brachium
of inferior colliculus, 25, 30-33, 35
of superior colliculus, 25, 30, 31, 89, 148,
150, 239, 264-265
Brachium conjunctivum. See Superior
cerebellar peduncle
Brachium pontis. See Middle cerebellar
peduncle
Brain, median sagittal MRI of, 64
Brain edema, 297
Brainstem, 4-5, 96, 181, 241
function components in, 96
hemorrhage, 74
inferior (ventral) view of, 20-25
lateral view of, 24-25, 32-33, 35
of left side, 32
lesions of, 54t
level of inferior colliculus, 142, 142
median sagittal view of, 48
at pons—midbrain junction, 140, 140
superior (dorsal) view of, 30-31
SVE and GSA components of, 96
vascular lesions in, 314
Brainstem cranial nerve, medial-to-lateral
positions of, 97, 97
Brainstem-hypothalamic fibers, 290
Breves gyri, 36
Bridging veins, 58
Broca aphasia, 12
Brodmann areas, 12
Brown-Séquard syndrome, 108, 190, 192,
196, 210, 242, 337Q, 338A, 342A
Bulb of eye, 46
C
Cajal, nucleus of, 150
Calcar avis, 69
Calcarine artery, 327
345
Calcarine sulcus, 11, 12, 13, 26, 28, 69, 187,
262, 265-267
Calcitonin gene-related peptide (CGRP), 196,
210, 226, 230
Callosomarginal branch, 27
Capsule
external, 76-80, 88, 160, 162, 164, 166,
168, 170, 172, 175, 180
extreme, 76-79, 88, 160, 162, 164, 166,
168, 170, 172
internal, 31, 41, 41, 46, 62, 76, 76, 78, 78,
88, 156, 174, 190, 191, 276, 277
Carotid artery, 327
Cauda equina, 10, 10, 59, 99, 307-308,
307-308
roots of upper portions of, 100
Cauda equina syndrome, 10, 308, 308
Caudal basilar pontine lesion, 53
Caudal diencephalon, dorsal view of, 30-31
Caudal pons, 130, 130
Caudate nucleus, 69, 77, 154, 178, 178, 180,
180, 182, 182, 184, 185, 185, 283
blood supply to, 254
body of, 68, 69, 79, 80, 81, 82, 86, 86, 87,
154, 156, 160, 162, 164, 175, 187, 250,
ZOIRZ SS
head of, 68, 69, 76, 76, 77, 78, 86, 87, 88,
89, 90, 166, 168,170; 1725075. 78;
178, 180, 182, 183, 194, 212, 216, 217,
Dies
tail of, 68, 69, 79, 80, 81, 87, 88, 154, 156,
160, 164, 175, 178, 180, 184, 186
veins of, 27
Cardiorespiratory portion of solitary nucleus,
207
Cavernous sinus, 19, 21, 37, 318
Central cord syndrome, 304, 304, 332Q, 338A
Central deafness, 270
Central gray, 112, 114, 136, 140, 142, 144,
146, 182, 249
Central herniation, 297, 300, 300
diencephalic stage of, 299, 299
Central lesions, 270
Central midbrain lesion, 152
Central nucleus, 140, 142
Central nervous system and associated
meninges, 59
Central pontine myelinolysis, 314
Central sulcus, 11, 11, 14, 16, 17, 26, 28, 36
of insula, 36
Central tegmental tract, 116, 118, 120, 122,
128713 0;132393
413
6,140,142,
144, 146, 148, 150
Centromedian nucleus, 178, 178, 180, 180
of thalamus, 87, 88, 158, 178, 180, 182,
183, 249, 257
Cerebellar, 273
Cerebellar artery
anterior inferior, 21, 23, 23, 25, 31, 33,
50; 72125, 1B 99230023, 245325),
329;33208334Q, 3350 93380;3394,
341A, 342A
posterior inferior, 9, 21, 23, 23, 25,29, 31,
82°93). 725125,202, 206,324; 325,
329, 333Q, 335Q, 338Q, 340A, 341A,
342A
superiom 20, 22) 23925,
1195147, 48, 49,
72, 78993, 230, 3259, S245 25,026;
327, 329, 332Q, 338Q, 337A, 342A
346
Index
Cerebellar corticonuclear fibers, 246, 247
Cerebellar corticovestibular fibers, 246, 247,
VID RIT©)
Cerebellar efferent fibers, 248-251
in anatomical orientation of, 248, 249
clinical orientation of, 250, 250-251, 251
lesions of, 246
deficits of, 246, 251, 251
neurotransmitters in, 248
Cerebellar nuclei, 127, 128, 129, 246, 247,
248, 273
blood supply to, 248
efferent fibers of, 248, 249-253
medulla at level of, 126, 126
Cerebellar nucleocortical fibers, 246, 247,
MTs LTS!
Cerebellar peduncles, 34
Cerebellar projections to pons and medulla,
250, 251
Cerebellar tonsil, 50
Cerebellar veins, 17
Cerebellar vermis, 50
Cerebello-olivary fibers, 248, 249
Cerebellopontine angle (CPA), 24
Cerebellorubral fibers, 148, 150, 164, 248,
249, 251
Cerebellothalamic fibers, 148, 150, 164, 248,
249, 251
Cerebellum, 17, 18, 20, 23, 24, 28, 47,
Sonja
N90. 9 t 20) 194, OL OT,
185, 185
afferent fibers to, 244, 245
anterior lobe of, 48, 284, 285
blood supply to, 246
inferior (ventral) view of, 20-24
median sagittal view of, 35
middle cerebellar peduncle, 34
rostral, caudal, and inferior view, 34
superior cerebellar peduncle, 33
tonsil of, 50-52
vascular lesions of, 316
vermis of, 50
Cerebral aqueduct, 5, 18, 29, 33, 48, 66, 68,
69, 82, 90, 91, 92, 136, 140, 142, 144,
146, 148, 150, 153, 194, 198, 212,
DIGA2178 2282295302
blood in, 74
magnetic resonance imaging of, 29, 33
and periaqueductal gray, 228. 229
Cerebral arterial circle, 22, 38
Cerebralicortéx, 555 191521000852 502 251.
254, 255, 258, 278, 334Q, 339A
Cerebral hemisphere
arteries of, 18, 19, 22, 27, 37
Brodmann areas, 12
cross-sectional representation of, 37
gyri, 14, 16, 17, 26, 27
inferior (ventral) view of, 18-21
lateral and medial views, 11, 12
lateral view of left, 16-17, 36, 37
midsagittal view of right, 26-29
somatomotor and somatosensory
cortices, 13
sulci, 14, 16, 17, 26, 27
superior (dorsal) view of, 14-15
vascular lesions in, 312
Cerebral hemorrhage, 74
Cerebral meninges, 58t
Cerebral vessel and branch, 59
Cerebropontine fibers, 245, 299, 304, 305
at C7-C8, 212, 213
morphological features of, 304
Cerebrospinal fluid, 59
Cerebrum, 59
Ceruleocerebellar fibers, 244, 245
Cervical cord, 97
Cervical spinal cord, 204, 205
Cheyne-Stokes respiration, 299, 300
Chiasmatic cistern, 64
Cholecystokinin, 196, 202, 206, 264, 280,
288
Chordoma, 230
Choreiform movements, 254
Choroid plexus, 22, 23, 66, 69, 72, 73, 126,
154, 156, 160, 162, 178, 182
AICA branch to, 72
in atrium, 66
of lateral ventricle, 72
blood supply to, 72
in body of lateral ventricle, 72
cerebrospinal fluid production, 59
in foramen of Luschka, 42
in fourth ventricle, 25, 31, 33, 72
lateral and dorsal views, 68
of lateral ventricle, 31, 72
PICA branch to, 72
in temporal horn of lateral ventricle, 72
in third ventricle, 25, 29, 31, 33, 72, 77-79
tumors of, 71, 73
Choroid plexus papilloma, 73, 319
Chronic subdural hematomas, 58
Ciliary ganglion, 226, 239, 239, 263
Cingulate gyrus, 28, 76, 154, 156, 160, 162,
166,168; 170; 4729279) 283
isthmus of, 26
Cingulate sulcus, 11, 26, 28, 191
Cochlea, 50
damage to, 56
Cochlear nerve, 120, 270, 272
Cochlear nuclei, 32, 185, 185, 270
blood supply to, 270
medulla at level of, 126, 126
Cochlear portion of eighth nerve, 50
Collateral sulcus, 11, 18, 20
Collet-Sicard syndrome, 51, 52, 230, 322
Colliculi, 34
Colloid cyst, 26, 26, 319
Column of fornix, 29, 77, 78, 88, 89, 158,
175sA825 2897 291
in hypothalamus, 78
Common carotid artery, 329
Computed tomography angiography (CTA), 1
Computed tomography cisternogram, 4-S, 5,
304, 305, 308
medulla: A13. 105n09
79119) 1215 123
medulla—pons junction, 120, 122
midbrain, 141, 145, 147
pons, 131, 391355 137
pons—midbrain junction, 140
Computed tomography (CT), 1
acute blood in subarachnoid space, 331Q,
337A
advantages of, 2
axial, 2
brain and related structures in, 2t
of choroid plexus tumors, 73
cranial, 333Q
disadvantages of, 2
of epidural hematoma, 62, 63, 71
fractures of face and orbit, 332Q, 333Q,
333A, 341A
fractures of vertebral column, 333Q, 334Q,
339A
Cingulum, 76, 154, 156, 160, 162, 168, 170,
172, 281
Circle of Willis, 38
Circuit of Papez, 280
hyperdense lesion in, 1
hypodense lesion in, 1
of intraventricular hemorrhage, 70
Circular sulcus, 11
Cisterna magna, 64
Cistern(s), 59, 64, 65
ambient, 64
blood in, 65
chiasmatic, 64
crural, 64
lesion involving cerebellar nuclei, 249
of medulla, 335Q, 336Q, 340A
of patient following injection of radiopaque
inferior cerebellopontine, 64
interpeduncular, 64
lamina terminalis, 64
paracallosal, 64
premedullary, 64
prepontine, 64
quadrigeminal, 64
superior cerebellopontine, 64
sylvian, 64
Claude syndrome, 54t, 152, 220, 246
Claustrum, 76, 77, 78, 79, 80, 87, 88, 89,
160, 162, 164, 166, 168, 170, 172,
175,178, 180, 182
Clinical orientation, 4, 5, 5, 189
anterolateral system, 196, 198-199
corticospinal tracts, 212
medial lemniscus system in, 194, 194
posterior column, 195
trigeminal pathways, 205
Coccygeal ligament, 59
Coccyx, 10, 59
isodense in, 1
contrast media, 5
of pons—medulla junction, 335Q, 340A
of pontine tegmentum, 334Q, 340A
stylomastoid foramen, 333Q, 339A
of subarachnoid hemorrhage, 3, 59, 64, 65
of subdural hematoma/hemorrhage, 62, 63
uncal herniation, 335Q, 340A
Computed tomography myelogram, 98
cervical
C1 level, 106
C7 level, 104
lumbar, 98-100, 102
sacral, 98-99
thoracic, 102
Conductive deafness, 270
Confluence of sinuses, 321, 321, 322, 323,
328
Constrictor muscles, 238
Contralateral hemiplegia, 25, 152, 174, 276
Contralateral motor deficit, 110
Contrecoup injury, 63
Conus medullaris, 10, 10, 59
Convexity meningioma, 66, 66
Corona radiata, 77-79, 80, 86, 87
Corona radiate, 77, 78, 79, 80, 86, 87
Index
Corneal reflex, 236, 236
Corpus callosum, 11, 26, 28, 47, 67, 69, 86,
178, 191, 258
Decorticate rigidity, 223, 299, 300
Deep middle cerebral vein, 19, 37
Déjerine-Roussy syndrome, 210, 278
body of, 28, 69, 76, 77, 78, 79, 80, 81, 86, 156,
Déjérine syndrome, 124, 315. See also Medial
160, 162, 164, 166, 168, 170, 172, 179
genu of, 28, 68, 87, 179, 180, 280, 281
medullary syndrome
Dementia, 238, 254, 259, 280, 282, 337Q, 342A
Denticulate ligament, 8
posterior vein of, 27
rostrum of, 28, 69, 76, 172
splenium of, 25, 28, 68, 69, 83-84, 83, 84,
O78
14803 154,179,181, 183,248,
249, 280, 281
sulcus of, 26, 28
thinning of, 26
Cortical blindness, 309
Corticoamygdaloid fibers, 282, 283
Corticohypothalamic fibers, 290
Corticomedial amygdala, 290, 291
Corticonuclear fibers, 54t, 214, 215, 216, 217,
246, 247,276
Corticonuclear pathways, 55, 55
Corticonuclear system, 212, 216
Corticorubral fibers, 276
Corticospinal deficits, 138
Corticospinal fibers, 53, 54t, 81, 92, 98, 102,
112, 120, 122, 125, 126, 130, 140, 148,
156, 158, 160, 162, 204, 210, 216,
PIT PAKS
Corticospinal tracts, 201, 211, 213
Corticostriatal fibers, 106, 110, 112, 254,
NSE Ons 26
Corticotectal fibers, 276
‘Corticothalamic fibers, 276
Corticovestibular fibers, 246, 247
Cranial nerve motor nuclei, 95
Cranial nerves (CNs), 24, 97
efferents of, 56, 56
functional components of, 55, 55
magnetic resonance imaging, 46-52, 55, 64
at pons—mediulla junction, 50
reflex pathways, 56, 56
striated muscles innervated by, 96
synopsis of, 44t—4St
Crossed extension reflex, 235, 235
Crural cistern, 64, 65
Crus cerebri, 18, 22, 23, 25, 30-33, 35, 46,
48, 49, 181, 181, 183, 186, 186, 193,
LOANS A2040205,2 1082105227,
239, 248, 258, 264, 266, 284, 285,
301, 301, 338A
corticospinal fibers in, 212, 213, 216, 217,
DSO, PS DE:
magnetic resonance imaging, 22, 23, 25,
30-33
vascular lesions in, 314
Crus cerebri damage. See Contralateral
hemiplegia
Cuneate fasciculus, 30, 31, 102, 104, 106,
HAD, WMA NG, TES. SIS, AO
Cuneate tubercle, 25, 30-33
Cuneus, 12, 26, 28, 262-267, 279
Cuneus lesion, 267
Cushing disease, 294
D
Dandy Walker Syndrome, 246
Darkschewitsch, nucleus of, 150, 196, 197, 248
Deafness, 270
Decerebrate rigidity, 218, 220, 223
Decerebrate posturing, 314
Diabetes insipidus (DI), 294
Diaphragma sellae, 294, 295
Diencephalon, 183, 183, 185, 185, 187, 187
caudal, 30-31
inferior (ventral) view of, 18-21, 25
internal distribution of arteries to, 174, 175
median sagittal view of, 48
midsagittal view of, 26-29
MRI off1552157,159, 1615163; 165,167,
ISYy
TAL, 1/3
Diminished knee jerk, 307
Diplopia, 22, 48, 53, 138, 333Q, 339A
abducens nerve root damage and, 335Q
and ptosis, 339A
Dissociated sensory loss, 278
Distal posterior inferior cerebellar artery, 70
Doll’s eyes maneuver, 299
Dopamine, 288
Dopaminergic nigrostriatal fibers, 256, 257
Dorsal accessory olivary nucleus, 244, 245,
248-251
Dorsal cerebellomedullary cistern, 68
Dorsal motor nucleus of vagus, 114, 116,
12552302231
Dorsal nucleus of Clarke, 102, 242, 243
Dorsal thalamus, 25, 29, 33, 46, 47, 69, 258,
278
Dorsomedial nucleus, 79, 80, 87-89, 158,
160, 162, 164, 178, 178, 179, 180,
(81,183,279
Dura, 8, 10, 58t, 59, 63
Dural tail, 66
Dura mater, 8, 10, 58t, 59, 63
Duret hemorrhage, 74, 314
Dynorphin, 288
Dysarthria, 4St, 230
Dysconjugate eye movements, 300
Dysarthria, 45t, 51, 199, 205, 206, 217, 226,
230, 233, 242, 244, 246, 251, 254,
259, BOSQV SIA:
Dysphagia, 45t, 51, 54t, 124, 199, 205, 206,
217, 2265230, 233; 24452545252,
333Q, 339A
Dyspnea, 230, 254
and tachycardia, 124
Dystonia, 254, 259, 333Q, 339A
E
Edinger--Westphal complex, 146, 148, 148,
239,
Edinger—Westphal centrally projecting nucleus, 226, 239
Edinger-Westphal preganglionic nucleus
(EWpgNu), 226, 239
Efferent hypothalamic connections, 290
Emboliform nucleus, 126, 128, 183, 249-251
Embolization, 174
Embolus, 309
Empty sella syndrome, 294
Enkephalin, 288
Enophthalmos, 262
Epidural hematoma, 58, 62, 63
347
Epidural space, 59
Epilepsy, intractable, 285
Exiting roots
at cervical levels, 306, 306
at lumbosacral levels, 307, 307
External capsule, 76-80, 88, 160, 162, 164,
UGG MGSi Oa
External medullary lamina, 156, 160, 162,
187, 187
Eye movements
deficits of, in horizontal plane, 55, 55
dysconjugate, 300
Eye movement disorders, 335Q, 342A
F
Facial colliculus, 30, 30, 31, 32, 32, 128, 130,
216,217, 227,228,229
abducens nucleus in, 334A, 340A
ependymoma and, 334Q, 339A
Facial hemiplegia, 230, 333Q, 338A
Facial motor nucleus, 335Q, 340A
Facial muscles, 230, 236, 238, 339A
facial nucleus response to, 238
paralysis of, 214, 217, 338A
weakness, 276
Facial nerve (VII), 22-24, 25, 29, 30, 44t, 49,
S0=§2,122, 128, 130013251398 155%
213, 232-233, 236-238, 334Q, 337A
Facial nucleus, 123, 128, 129, 130, 132, 139,
1813 18152023. 2039214,27 5,220,
230, 231-233, 236,238; 270,271;
335Q, 340A
Facial palsy, 230, 272
Falcine meningiomas, 67
Falx cerebri, 14, 59, 60, 61, 63, 67, 297, 297
Fasciculus cuneatus, 8, 9
Fasciculus gracilis, 8, 9
Faucial reflex, 238
Fetal PCA, 38
Fiber bundles, 335Q, 340A
Filum terminale internum, 10, 10, 99
Fimbria, 81, 82, 88-90, 154, 156, 178, 182,
186, 187
Finger-nose test, 246
Finger-to-finger test, 246
Flapping tremor (asterixis), 254
Flexed posture, 254
Flexor reflex, 235
Flocculonodular lobe, 242, 243, 272
Flocculus, 20, 22, 24, 32, 35, 49, 51, 81, 94,
246, 247
Fluent aphasia, 12
Foix-Alajouanine syndrome, 108
Foramen of Luschka, 32, 68, 70, 72
Forebrain, 154, 154, 156, 156, 158, 160, 162,
164, 164, 166, 166, 168, 168, 170,
470; 172: 172, 186, 186
vascular syndromes or lesions of, 174
leone, fil, AS5 YOR, SS, tore, OL), NV, 1727, IO).
191, 280, 281, 282, 283-285
Fourth ventricle, 20, 29, 35, 47-49, 51, 64, 70
choroid plexus of, 31, 72
lateral recess of, 30, 50, 68, 70
medial eminence of, 32
PICA branch to choroid plexus in, 72
rostral part of, 65
striae medullares of, 30
Foville syndrome, 138, 210 See also Raymond
syndrome
348
Index
Fractures, of face and orbit, 332Q
Frenulum, 30, 136
Friedreich ataxia, 242, 333Q, 339A
Frontal eye fields, 12, 16, 214, 215, 276, 277
Frontal lobe, 17, 40, 40, 46, 47, 71, 74
blood in, 74
breves, 36
cingulate, 26, 26, 28, 76, 154, 156, 160, 162,
166; 168; 170997292 78927 93282,1283
inferior frontal, 12, 16, 279, 331Q, 337A
Frontal pole, 18, 20, 71
lingual, 12, 18, 26, 28, 264-267, 279
middle frontal, 12, 14, 16, 36, 279
middle temporal, 16, 279
occipital, 14, 16, 18
occipitotemporal, 18, 20, 26, 279
orbital, 18, 20, 172
parahippocampal, 18, 20, 22, 26, 279, 283
paraterminal, 26, 170
parolfactory, 26
postcentral, 12-14, 12-16, 36, 194, 195,
197-199, 204, 205, 279
posterior paracentral, 12, 13, 26, 28, 194,
HOS, INS, WDD, 2D
precentral, 12-14, 16, 36, 111, 212, 213,
DNS DIN. DYE
inferior temporal, 18, 279
isthmus of cingulate, 26
Frontopontine fibers, 142, 144, 146, 148, 150,
212, 216, 217, 228, 244, 245, 276
Functional components, concepts of, 96
Fusiform aneurysm, 334
G
Gag reflex, 51, 206, 238, 240
Gallactorrhea, 294
y-Aminobutyric acid (GABA)
in globus pallidus, 256
in Purkinje cells, 246
striopallidal and strionigral fibers, 254
terminals in vestibular complex, 272
Ganglia of cranial nerves, 204, 205
Ganglion cells of retina, 263, 264
Geniculate bodies, 337A
Geniculate nuclei, 184
Geniculocalcarine fibers, 264
Genioglossus muscle, 52, 228, 229
Genu
of corpus callosum, 28, 68
of internal capsule, 78, 87, 88, 190, 191,
194, 198, 204, 205, 214, 215-217, 229
lesions in, 229, 233
Gigantism, 294, 339A
rectus, 18, 20, 22, 69, 284, 285
superior frontal, 14, 16, 26, 28, 36, 66, 279
superior temporal, 16, 279
supramarginal, 12, 14, 16
Habenula, 29, 31
Habenular commissure, 158, 180
Habenular nucleus, 158, 178
Habenulopeduncular tract, 148, 150, 158,
182
Hair cell in organ of Corti, 271
22D
3
Globose nucleus, 126, 128, 248, 249-251
Globus pallidus, 77-79, 88-89, 158, 160,
162, 164, 166, 168, 170, 178, 180,
Head of caudate nucleus, 68, 76-78, 86-90,
75, USE OMS, HIN, ON hy PLIETE
Hearing loss, 230, 270
Heel-to-shin test, 246, 251
Hemianesthesia, 46, 276
Hemiballismus, 174, 256
Hemiballistic movements, 256
Hemifacial spasm, 230, 333Q, 338A
lateral segment, 158, 160, 162, 164, 166,
168, 170, 180, 185, 187, 255, 257
medial segment, 158, 160, 162, 185, 187,
DSSyDSH
Glomus, 68
Glossopharyngeal nerve (IX), 22-24, 31, 45t,
Sil, Sil, MA, P30, AB2, YES, 23S
Glossopharyngeal neuralgia, 51, 206
Glutamate, 196, 200, 202, 210, 214, 218,
220, 242, 244, 245, 248, 254, 256,
262, 264, 280, 282
Glycine, 220, 256
Gracile fasciculus, 30, 31, 98, 100, 102, 104,
106, 112, 114, 124, 125, 193-195,
201, 340A
Gracile lobule, 34
Gracile nucleus, 112, 114, 116, 193-195, 201
Gracile tubercle, 25, 31-33
Hemihypesthesia, 174
Hemiplegias, 210
contralateral, 46
Hemisphere, inferior view of
exiting fibers of oculomotor nerve (III), 47
optic nerve (II), chiasm, tract, 46
Hemorrhage, 256
of lenticulostriate arteries, 41
in spinal cord, 108
splinter, 74
subdural, 63, 65
subependymal, 71
Hemorrhagic stroke, 74, 309
Hereditary cerebellar ataxia, 244
Herniation syndromes, 297-308
anterior cord syndrome, 305, 305
Cauda equine syndrome, 308, 308
central cord syndrome, 304, 304
Gray matter, 102
central herniation, 297, 300, 300
Great cerebral vein, 19, 27, 319, 326, 327
diencephalic stage of, 299, 299
cerebrospinal fluid and, 297
Gubler syndrome, 54t, 138
Gustatory nucleus, 206, 207
Gyri breves, 36
Gyri longi, 36
Gyrus(i)
angular, 12, 16
anterior paracentral, 12, 13, 26, 28, 210,
ZUI—21 3,279
projections of, 284
Hippocampal formation, 68, 69, 79, 80,
81-83, 88=91, 154, 156, 162, 175,
178, 180, 182, 184-187, 291
Hippocampohypothalamic fibers, 290
Hippocampus, 187, 187, 280, 281,
284-285, 336Q, 342A
Hippocampus
lesions and deficits, 285
Histamine, 244, 270, 272, 276, 288
Hoarseness, 54t, 124, 204, 205, 206,
272253
Homonymous hemianopia, 46, 262, 278,
3320}
Homonymous quadrantanopia, 267
Horizontal fissure, 34
Horizontal gaze center, 53
Horizontal gaze palsies, 214
Horner syndrome, 124, 138, 262, 290, 333Q,
338A
H
Gigantocellular reticular nucleus, 218, 219,
182, 184, 185, 187, 254, 258, 277, 283
blood supply to, 256
external segments, 258
internal segments, 258
uncal herniation, 301, 301, 341A
upward cerebellar herniation, 302, 302
Hilum of dentate nucleus, 126
Hippocampal commissure, 83, 154, 178
Hippocampal connections, 280-281, 281
Hippocampal efferents, 284-285
lesions and deficits of, 285, 285
exiting roots
and traversing roots at lumbosacral
levels, 307, 307
at cervical levels, 306, 306
mesencephalon/midbrain, 335Q, 341A
subfalcine herniation, 297, 298, 298
tonsillar herniation, 297, 303, 303
Hounsfield units, 1
Huntington disease, 76, 254, 255, 259, 333Q,
338A
Hydrocephalus, 319
noncommunicating, 74
obstructive, colloid cyst with, 26
in Parinaud syndrome, 152
Hydromyelia, 108, 196
Hyperextension of neck, 108
Hyperintense lesion, 3, 3
Hypermetria, 246, 251
Hyperorality, 282, 285
Hyperphagia, 282, 285, 337Q, 342A
Hyperprolactinemia, 294
Hyperreflexia, 234
Hypermetamorphosis, 282
Hypersexuality, 282
Hypoglossal nerve (XII), 22-24, 25, 33,
50-52, 54t, 114, 118, 125, 226,
227-229, 238
Hypoglossal nucleus, 30, 52, 114-119, 125,
179, 203, 207, 219-217,22 7-229:
231, 288 n272
Hypoglossal root, lesion of, 52
Hypoglossal trigone, 30, 32
Hypokinesia, 174, 254, 256, 259
Hypometria, 246, 251
Hypoperfusion, 309, 311
Hyporeflexia, 234
Hypotensive crisis, 108
Hypothalamic nuclei, 166, 288
Hypothalamic structures and connections,
288-293
blank master drawing for, 292-293, 293
lateral hypothalamic area, 288
iateral zone, 288
mamumillary region, 288
mammillothalamic tract, 288
medial forebrain bundle, 288
medial zone, 288
neurotransmitters in, 288
periventricular zone, 288, 289
Index
projections, 290-291, 291
stained sections, 288-289, 289
supraoptic region, 288
tuberal region, 288
tuberoinfundibular tract, 288
zones of, 290
Hypothalamic sulcus, 29
Hypothalamocerebellar fibers, 244, 245
Hypothalamus, 18, 25, 29, 33, 46, 48, 67, 69,
184, 186, 186, 288, 295
I
Indusium griseum
lateral longitudinal stria of, 156, 162, 166
medial longitudinal stria of, 154, 160, 168,
179472
Infarct in internal capsule, 111
Inferior alternating hemiplegia, 124, 337Q,
342A
Inferior anastomotic vein, 17, 319
Inferior cerebellar peduncle, 30
Inferior cerebellopontine cistern, 64
Inferior colliculus, 5, 25, 29-35, 47, 64, 83,
91, 140, 142, 144, 146, 153-154, 156,
179, 181, 183-184, 194, 249, 271,
284-285
Inferior fovea, 30, 32
venous phase, 321, 321
digital subtraction image of, 322, 322
Internal carotid artery (ICA), 19, 21-25, 27,
OSPI
OSHA SAIS 2 1313) 31 BYS19,
320, 323, 326-329
vascular lesions, 310
Internal carotid bifurcation, 22
Internal cerebral vein, 19, 26, 27, 29, 30, 66 >
67,319, 326, 328
Internal jugular vein (IJV), 17, 19, 21, 322,
322
Internal medullary lamina, 80, 88, 160, 162,
164, 178, 278, 279
Internal occipital veins, 27
Internuclear ophthalmoplegia (INO), 53, 272
Interpeduncular cistern, 64, 65
Interpeduncular fossa (IPF), 18, 25, 29,
46-49, 79, 80, 90, 144, 153, 216-217,
228-229, 284, 285
Interventricular foramen, 26, 29, 68, 69, 179 )
1D)
Intervertebral disc extrusions, 308
Intervertebral ligament, 59
Intracerebral hemorrhage, 71, 74
Intracranial compartment, 297, 297
Intracranial pressure (ICP), 6
increase in, 313
Inferior frontal gyrus, 16, 279
lesion, 331Q, 337A
Intrahemispheric hemorrhage, 312
Inferior frontal sulcus, 16
Inferior horn of lateral ventricle, 68, 69,
Intraparietal sulcus, 16
Intraventricular blood. See Intraventricular
hemorrhage
Intraventricular hemorrhage, 70, 71
Ipsilateral cerebellar nuclei, 246
Ipsilateral oculomotor palsy, 152
Ischemic stroke, 74, 309
Isthmus of cingulate gyrus, 26
79-82, 91
Inferior petrosal sinus, 17, 19, 21
Inferior pulvinar nucleus, 150
Inferior sagittal sinus, 29, 295, 297
Inferior salivatory nucleus, 126, 127, 237
Inferior semilunar lobule, 34
Inferior temporal gyrus, 18
Intralaminar nuclei, 255, 257, 278
Inferior visual quadrant, 13
J
Infratentorial compartment, 297, 297
Infundibular recess, 29, 48, 68
Infundibulum, 18, 22, 23, 29, 32, 46, 47, 294,
Jaw-jerk reflex, 202, 237, 237
295
Insula, 11, 36, 37, 65, 76-79, 89, 156, 160,
162, 166, 168, 170, 175
Insular cortex, 11, 23, 36, 37, 258-259
Jugular bulb, 322, 322
Jugular foramen, fracture in, 333Q, 339A
Jugular foramen syndromes, 51, 52, 230
Jugular vein, internal, 17, 19, 21, 322, 328
Juxtarestiform body, 30, 30, 118, 122, 128,
130, 246, 247, 250,272, 273
Internal blood supply, to spinal cord, 108, 109
Internal capsule, 31, 41, 41, 46, 62, 180, 180,
182, 276-277, 277
anterior limb, 39, 76-78, 88-89, 168, 170,
D724 TS S194, 198, 212, 216-217, 276;
K
Kayser—Fleischer ring, 254, 259
Kernohan syndrome, 152, 301
Kliver-Bucy syndrome, 282, 285, 336Q,
342A
Knee-jerk reflex, 333Q
Korsakoff psychosis, 280, 285, 288
posterior limb, 79-81, 88, 89, 111, 158, 160,
162, 164, 175, 178, 193-195, 197-199,
203-205, 211-214, 216-217, 222-223,
250,258,276) 277
retrolenticular limb, 156, 175, 276, 277
sublenticular limb, 156, 244, 245, 276, 277
thalamocortical projections, 276
Internal carotid angiogram, 318-322
anterior—posterior projection, 320-322
arterial phase, 318, 318, 320, 324, 325
left lateral projection, 318, 319, 324
Lateral corticospinal tract, 98, 100, 102, 104,
LOG AOI 1D UZOS ASIA D273)
219221
Lateral dorsal nucleus of thalamus, 80, 181,
133, 2
Lateral geniculate body, 25, 30-33
Lateral geniculate nucleus, 81, 89, 90, 148,
150, 156, 164, 175, 184, 186, 187,
239, 263, 265=267, 276, 277; 279
Lateral horn, 103
Lateral hypothalamic area, 166, 282, 288,
289
Lateral lacunae, 59
Lateral lemniscus, 130, 132, 134, 136, 139-140,
142, 153) 18351865270, 274
Lateral longitudinal stria, 154, 156, 160, 162,
166, 168, 170,172
Lateral mammillary nucleus, 289
Lateral medullary syndrome, 54t, 94, 124,
alls)
Lateral nuclei, 282, 283, 291
Lateral olfactory stria, 168, 170
Lateral optic chiasm lesion, 267
Lateral pontine syndrome, 138, 244
Lateral posterior choroidal artery, 31, 72
Lateral posterior nucleus, 279
Lateral recess of fourth ventricle, 30, 50, 68,
70
Lateral rectus motor neuron, 53
Lateral rectus muscle, 53, 228, 229
Lateral reticular nucleus, 114, 116, 118, 244,
245, 249
Lateral segment, 158, 160, 164, 166, 168, 170
Lateral striate arteries, 41
Itererall cuilens, Wil, iL, 13, 16, 174 37 UST
Lateral ventricle, 74, 83, 87, 166
anterior horn of, 68-70, 168, 170, 172, 178,
180, 181, 277
atrium of, 68, 70
blood in, 71
body of, 68, 69, 156, 160, 162, 164
choroid plexus in body of, 72
posterior horn of, 68, 70
temporal horn of, 65, 70
venous structures in, 331Q,
Left internuclear ophthalmoplegia, 53
Left lateral rectus, 332Q, 337A
Lemniscus
lateral, 130, 132, 134, 139, 140, 153, 183,
186, 270, 271
IGT
genu of, 166, 168, 178, 194, 198, 204, 205,
DEG NZI
6427OF277infarct in posterior limb of, 110, 111
Laryngeal and pharyngeal muscles, 238
Lateral cervical nucleus, 200, 201
Lateral cortex, 246, 247
Lateral corticospinal fibers, 106
inferior horn of, 68, 69
Intercavernous sinuses, 19
Intermediate nerve, 22
Intermediolateral cell column, 262
349
IL
Labbé, vein of, 15, 17, 319, 328
Labyrinthine artery, 22, 23, 25, 33, 42
occlusion of, 270
Lacrimal gland, 207, 231, 237, 333Q
Lacrimal reflex, 202, 231
Lacunar strokes, 210, 214
Lamina
external medullary, 156, 160, 162, 164
internal medullary, 80, 88, 160, 162, 278,
LYS)
Lamina terminalis, 29, 40, 48, 68, 70, 182,
TSAOUSOR 25 ON2 SINS2 2833295,
Lamina terminalis cistern, 64, 65
nucleus, 134, 271
medial, 92-94, 114, 116, 118, 120, 122,
125, 130, 132, 134, 136, 140, 142, 144,
146, 148, 150, 179, 181, 183, 192-195,
DVI, POS WS, AUN AI 35,AUD, DPI, PONS,
228;.231; 232,247, 249,263, 204, 271,
273
in medulla, 192-195, 204-205, 228,
232-233
in midbrain, 191, 194-195, 198-199,
204-205
in pons, 191, 194-195, 198-199, 204,
228-229
at pons—medulla junction, 232-233
350
Index
Lenticular fasciculus, 158, 160, 162, 164, 166,
181, 183, 185, 258, 289
Lenticulostriate arteries, 19, 21, 23, 41
Lenticulostriate branches, 37
Lenticulostriate vessels, 310, 311
Leptomeningitis, 58, 60, 61
Level of obex, 30, 116
Lid reflex, 236, 236
Limbic lobe, 11
Limbic pathways, blank master drawing for,
286-287, 287
Limen insulae, 36, 37
Lingual gyrus, 12, 18, 26, 28, 264, 265, 267,
DUS)
lesion, 267
Lobe
flocculonodular, 238, 239
frontal, 40, 46, 47, 71, 74
insular, 11
limbic, 11
Oceipitaleel deel 72/093
Panletalaial alee
ae
temporal, 11, 17, 18, 27, 32, 46, 47, 49, 61
Lobules
IV, 35
VI-IX, 34
X, 34
Localizing sign, 95
Locked-in syndrome, 314, 314
Locus ceruleus, 136
Longitudinal fissure, 14, 20
anterior tubercle of thalamus, 78
anterolateral system, 5, 115, 117, 119, 121,
123) 137; 138 NsSie Za
atrium of lateral ventricle, 82-83, 87-90
axial, 4, 34, 38, 39-42, 46-50, 52, 64,
86-94
basilar artery, 21, 33, 38, 47, 49, 50, 93
basilar pons, 20, 28, 29, 35, 46-50, 79-81,
92698
brain and related structures in, 3t
bulb of eye, 46
calcarine sulcus, 26, 28
caudate nucleus, 86, 87
body of, 69, 79-81, 86
head of, 68, 69, 76-78, 86, 87, 89
central sulcus, 26, 28, 36
of insula, 36
cerebellar hemisphere, 50
cerebellar tonsil, 50
cerebellar vermis, 50
cerebellum, 18, 20, 28, 47, 49-52, 90, 91
anterior lobe of, 34, 48-49
median sagittal view of, 35
middle cerebellar peduncle, 34
rostral, caudal and inferior view of, 34
superior cerebellar peduncle, 33
tonsil of, 28, 34, 50-52
vermis of, 34, 50
cerebral aqueduct, 29, 33, 81, 82, 90, 91
cervical
C7 level, 105
Lumbar cistern, 10, 59, 308, 308
Lumbar puncture, 10, 10
Lumbar spinal cord, 100
Lumbosacral cord, 97
of choroid plexus tumors, 73
of cingulate gyrus, 26, 28
cingulate sulcus, 28
Luschka, foramina of, 32, 59, 68, 70, 72
cochlea, 50
Luteinizing hormones, 288
excessive production of, 333Q, 342A
cochlear portion of eighth nerve, 50
M
Macula, 261
Magendie, foramen of, 59
Magnetic resonance angiography (MRA), 1,
8235323
anterior cerebral artery, 323
anterior inferior cerebellar artery, 323
basilar artery, 323
confluence of sinuses, 323
internal carotid artery, 323
posterior cerebral artery, 323
superior cerebellar artery, 323
superior sagittal sinus, 323
vertebral artery, 323
Magnetic resonance imaging (MRI), 1-3
cisterns, 64
colloid cyst, 26, 26
column of fornix, 29, 77, 78, 88, 89
coronal, 76-84
coronal radiata, 77-80, 86-87
corpus callosum, 26, 76, 86
body of, 28, 76-83
genu of, 28, 68
rostrum of, 28
sulcus of, 26, 28
corticonuclear fibers, 145, 147, 149
corticospinal fibers, 52, 123, 131, 133, 135,
137, 141, 145, 149
cranial nerves, 46-52, 55, 64
crus cerebri, 22, 23, 25, 30-33, 46, 48, 49,
79, 80-82, 90, 91, 149, 151
crus of fornix, 82, 83, 87
cuneate nucleus, 115, 117
abducens nerve, 52
cuneus, 26, 28
advantages of, 3
dentate nucleus, 93, 129, 131
anterior cerebral arteries, 21, 23, 27, 29, 33,
disadvantages of, 3
38
anterior commissure, 29, 77, 78, 89, 90
anterior communicating artery, 27, 33, 38,
46
anterior horn of lateral ventricle, 68-70, 76,
dorsal thalamus, 25, 29, 33
dorsomedial nucleus, 80, 87-89
Edinger—Westphal preganglionic nucleus,
149
emboliform nucleus, 127, 129
77, 86-89
anterior inferior cerebellar artery, 50
external capsule, 76-78
anterior lobe of cerebellum, 48, 49
anterior median fissure, 9, 22, 94
facial motor nucleus, 129
extreme capsule, 76, 77
anterior medullary velum, 31, 33
facial nerve, 50
facial nucleus, 133
anterior nucleus of thalamus, 79, 87
anterior paracentral gyrus, 26, 28
fastigial nucleus, 129
fimbria of fornix, 81-82
forebrain, 155, 157, 159, 161, 163, 16S,
1G AUGIE Iles
HOVADUDSGAo) Oy ES)Tl
body of, 29, 79-81
column of, 29
fourth ventricle, 29, 34, 48-51, 83, 92-95
frontal lobe, 46, 47
genu of internal capsule, 87-88
globose nucleus, 127, 129
globus pallidus, 77-79, 88-89
gracile nucleus, 113, 115
gyri breves, 36
gyri longi, 36
habenular nucleus, 88
hemisphere
of anterior lobe of cerebellum, 92
of posterior lobe of cerebellum, 93-94
hippocampal commissure, 83
hippocampal formation, 68, 69, 79-83,
88-91
hyperintense lesion, 3, 3
hypoglossal nerve, 52
hypoglossal nucleus, 52, 115, 117, 119
hypointense areas in white matter of hemisphere, 3, 3
hypothalamus, 18, 25, 29, 46, 69, 78-79, 90
interpeduncular fossa, 48
inferior colliculus, 5, 29, 47, 83, 91, 141,
143, 155
inferior horn of lateral ventricle, 79-82, 91
inferior (spinal) vestibular nucleus, 119, 127
infundibulum, 29, 46, 77
insula, 71-79, 89
internal capsule, 78, 87
internal carotid artery, 38, 47, 49
internal cerebral vein, 26
internal medullary lamina, 80, 88
interpeduncular fossa, 29, 46-49,
79-80, 90
juxtarestiform body, 129
lateral geniculate nucleus, 81, 89, 90, 149,
US, USS
lateral recess of fourth ventricle, 50, 70
lateral thalamic nuclei, 88-89
lateral ventricle, 87
body of, 79-82, 86
limen insulae, 36
lingual gyrus, 26, 28
mammillary body, 33, 46, 48, 79, 90
marginal sulcus, 26, 28
medial geniculate nucleus, 81, 89, 90,
147, 151
medial lemniscus, 92-94, 115, 122, 131,
133, 135, 137, 141, 143, 145, 147,
149, 151
medial longitudinal fasciculus, 117, 119,
1235127129913 TALS OR IST
143, 145, 147
medial vestibular nucleus, 119, 123,
WAY, USI
medulla, 5, 28, 52, 64, 82, 83, 113, 115,
IZ, HAS, UAL, WAS
meningitis, 60, 61
mesencephalic nucleus and tract, 133, 137,
143, 145, 147
mesencephalic tract and nucleus, 145, 149
midbrain, 18, 34-35, 46, 48, 64, 65, 141,
143, 145, 147, 149, 151
midbrain—diencephalon junction, 151
Index
midbrain tegmentum, 46, 48, 49
middle cerebellar peduncle, 20, 49, 82-83,
92-93
middle cerebral artery, 18, 33, 38, 48
middle frontal gyrus, 14, 16, 36
nucleus accumbens, 76
nucleus prepositus, 121
occipital lobe, 38
oculomotor nerve, 47, 48
oculomotor nucleus, 147, 149
third ventricle, 47, 77-79, 88-90
tonsil of cerebellum, 50-52, 94, 127
Medial midbrain (Weber) syndrome, 152
Medial motor nuclei, 98, 100, 102, 104,
trigeminal ganglion, 49, 93
trigeminal motor nucleus, 135
Medial nucleus, 156, 158, 160, 162, 164
106, 112
trigeminal nerve, 49, 80, 93
trochlear nerve, 48
uncus, 18, 46, 47
vagus nerve, 50, 52
vermis, 5O
of anterior lobe of cerebellum, 34, 35
olfactory tract, 76
olivary eminence, 52, 94
of ophthalmic artery, 334Q, 339A
optic chiasm, 29, 46, 47, 77
optic nerve, 46, 48, 76
of posterior lobe of cerebellum, 93, 94
vestibular portion of eighth nerve, 50
vestibulocochlear nerve, 50
Magnetic resonance venography (MRV), 1,
328, 328
optic radiations, 83, 84, 87
optic tract, 18, 46, 48, 77, 78, 90, 149, 151
Mamumillary body, 18, 23, 25, 29, 33, 46, 48,
xs, GO), Hes, 72), HO); QUASI GS, 1.
periaqueductal gray, 81, 82
parieto-occipital sulcus, 26, 28
parolfactory gyri, 26
pineal, 29-31
pituitary tumor in, 2, 3
pons; 20,429,731, 133, 135, 137,141
136, 086722 99230,1287,2895295
Mammillotegmental tract, 180, 181
pons—medulla junction, 50, 52
pontine tegmentum, 28, 49, 50
postcentral gyrus, 36
posterior cerebral artery, 33, 48, 90
posterior communicating artery, 33
posterior forceps, 86
posterior horn of lateral ventricle, 84, 87-89
posterior limb of internal capsule, 79, 80,
Mammillothalamic tract, 79, 89, 150, 158,
162, 164, 179, 181, 182, 184, 280, 281
Mandibular division of trigeminal nerve,
202, 203
Mandibular reflex, 237
Man-in-a-barrel syndrome, 309
Marginal sulcus, 11, 26, 28
Massa intermedia, 29, 68, 69
Masseter muscles, 237
Mastoiditis, 60
120, 244, 245, 249-251
posterior paracentral gyrus, 26, 28
postolivary sulcus, 51
Medial cerebellar nucleus, parvocellular
precentral gyrus, 14, 16, 36
Medial
Medial
Medial
Medial
Medial
precuneus, 26, 28
preolivary sulcus, 51, 94
pyramid, 49, 51, 52, 80, 82, 94, 113, 115,
iz
1523
quadrigeminal cistern, 29
red nucleus, 33, 80, 90, 147, 149, 151
restiform body, 51, 52, 94, 115, 117, 119,
PADI
I27 129, 131
semicircular canals, 50
septum, 77, 86, 87
septum pellucidum, 29, 77, 86, 87
spinal trigeminal nucleus, 113, 115, 117,
HANDS, WA, WAS 5PATS OL ily5)
spinal trigeminal tract, 113, 115, 117, 119,
Pith
on 127,129, 151
spinothalamic fibers, 145, 147, 149, 151
splenium of corpus callosum, 28, 82, 83, 88
substantia nigra, 80, 90, 91, 143, 145, 147
superior cerebellar artery, 47, 49
superior cerebellar peduncle, 20, 83, 91-93,
Poet
2
Peds Pts, 1352137
superior colliculus, 29, 47, 82, 89, 90, 145,
147, 149
superior frontal gyrus, 14, 26, 28
T1-weighted image, 2
T2-weighted image, 2, 4, 5
tapetum, 83, 84, 89
tegmentum of pons, 49, 93
temporal lobe, 18, 36, 46, 49, 76, 93
thalamus, 79
dorsal, 29, 46, 47
ventral anterior nucleus of, 78-79
ventral lateral nucleus of, 80
ventral posterolateral nucleus of, 80
region, 246, 247
division fibers, 100
division fibers of posterior root, 102
eminence of fourth ventricle, 32
forebrain bundle, 290
geniculate body, 25, 30- 33, 35, 180,
18SOL132) £82, 270,271
Medial geniculate nucleus, 25, 81, 89, 90,
146, 148, 150, 156, 175, 180, 182,
184, 185, 185, 239, 262, 263-267,
DLO oils 277s 279
Medial lemniscus, 5, 52, 54t, 92-94, 114,
1G, IES, HAO), WAZ, WAS, USS US,
134, 136, 140, 142, 144, 146, 148,
LIOMPO MS teal Son OQ LIS 195.
201-203, 211=213, 219, 221, 227;
228, 231, 232, 243, 245, 249, 263,
264, 271, 273, 324Q, 340A
in medulla, 193, 194, 195, 198, 199, 204,
QOS 22502325 259
in midbrain, 193, 194, 195, 198, 199, 204,
205
in pons, 193, 194, 195, 198, 199, 204, 228
at pons—medulla junction, 222, 223, 232, 233
Medial longitudinal fasciculus (MLF), 53,
53, 82, 100, 102, 104-106, 109, 112,
HEL WG, HAS, TAMPA,
Medial olfactory stria, 170
Medial pontine syndrome, 138
Medial posterior choroidal artery, 31, 72,
(5356) 75311
Medial
Medial
Medial
Medial
rectus motor neuron, 53
rectus muscle, 53
segment, 158, 160, 166
striate artery, 23, 40, 40, 72, 312,
ot?
Medial thalamus, 31, 280, 281
Medial vestibular nucleus, 114, 116, 118,
122, 124, 126, 203, 215, 217-218,
243, 245, 269
Medial vestibulospinal fibers, 220
Medial vestibulospinal tract, 220, 221,
246, 273
Medulla, 5, 28, 33-35, 52, 64, 82, 83, 181,
fhesil, Wtss335 tess, II
nuclei in, 187
lesion in, 315, 316
at pons—medulla junction, 222-223, 232
transverse section of, 112-123
vascular syndromes or lesions of, 124
Medulla oblongata, 97, 113, 115, 117, 119,
LATA
Maxillary artery, 329
Medial accessory olivary nucleus, 114, 116,
87-89
351
LAs, AGS,
128, 130, 132, 134, 136, 138-140,
142, 144, 148, 150, 153, 179, 186,
NO, WY, Pilile AGE BUS, QU, PAs
227=229, 249, 271, 273
blood supply to, 220
rostral interstitial nucleus of, 214
Medial mammillary nuclei, 284, 289
Medial medullary syndrome, 52, 54t, 124,
DUO 315:
ZS
2S)
Medulla—pons junction, 120-122
Medullary feeder arteries, 9
Medullary reticulospinal fibers, 100,
222-223
Medullary reticulospinal tract, 102, 104,
106
Méniére disease, 272
Meninges, 58, 58t, 59
infections of, 58
tumors of, 58, 58
Meningiomas, 2, 24, 58, 66, 67
Meningitis, 58-61
bacterial, 332Q, 338A
Mesencephalic nucleus, 130, 132, 134-137,
139, 141-149, 153, 202, 203, 231,
237i gp2435 273
Mesencephalic tract, 130, 132, 134-137, 139,
141-149, 153, 237
Mesencephalon, 191
Metencephalon, 191
Meyer-Archambault loop, 262, 337Q, 342A
Midbrain, 18, 25, 33-35, 48, 52, 64, 97,
144, 144, 146, 146, 148, 148, 183,
183, 263
affected by uncal herniation, 335Q, 341A
arterial territories in, 153
lesions of, 152
nuclei in, 183
transverse section of, 144-149
vascular damage to, 314, 314
Midbrain-diencephalon junction, 25,
150, 150
Midbrain tegmentum, 28, 46, 48, 49, 194,
198, 212, 216, 217, 228, 284-285
blood supply to, 262
Middle alternating hemiplegia, 138
Middle cerebellar peduncle, 20, 22, 23,
25, 30-3549 SoS noe mes
IBAMIGOMUISSeal Sos
204-205, 232-233, 245
Onela/s
352
Index
Middle cerebral artery, 17, 18, 22, 23, 33, 38,
ANIA
ZTASS OO 72, 10,
lL LOMAS
284-285, 313, 318, 320, 323, 326-328
angular branches of, 17, 37, 276
anterior parietal branches of, 17, 37
anterior temporal branches, 17, 37
anterolateral branches of, 175
branches of, 15, 17, 327
stylohyoid, 231-233
stylopharyngeus, 230, 232, 233, 238
superior oblique, 228, 229
superior rectus, 227
temporalis, 237, 237
tensor tympani, 227-229
trapezius, 45, 226
vocal 2801232) 3400N84
Myasthenia gravis, 210, 226, 230
Myelencephalon, 191
Myotatic reflex. See Muscle stretch reflex
M, segment of, 37
M; segment of, 23, 37
M, segment of, 37
occlusion of, 174
N
N-acetyl-aspartyl-glutamate, 262
Nasal glands, 237
posterior parietal branches of, 17, 37
posterior temporal branches, 17, 37
prerolandic branches, 15, 17, 37
rolandic branches, 15, 17, 37
superior trunk of, 19, 21, 37
temporal branches, 17
vascular lesions, 310
watershed infarcts, 312
Middle frontal gyrus, 12, 14, 16, 36, 279
Middle temporal gyrus, 16, 279
Midline thalamic nucleus, 282, 283
Midpontine base syndrome, 138
Millard—Gubler syndrome, 138, 210
Monoamines, 288
Monosynaptic reflex, 237
Motor cortex precentral gyrus, 111, 215
Motor decussation, 22, 106
Motor pathways, 221-224
Motor (pyramidal) decussation, 212
Movement disorders, 276
Mucous membranes of nose and mouth,
231
Multilayered fibers, 244
Multiple sclerosis, 226
Muscle(s)
abdominal, 236, 236
Muscle stretch reflex, 192, 234, 234
Natriuresis, 294
Nausea, 47, 54t, 73, 124, 138
Neostriatum, 254
Nerve deafness, 270
Neural tube, function components in, 96
Neurohypophysis (posterior lobe, pars
nervosa), 294
Neurotransmitters, 190
Nigroamygdaloid fibers, 256, 257
Nigrocollicular fibers, 256, 257
Nigrostriatal fibers, 146, 148, 164, 254, 255,
258-259
Nigrosubthalamic fibers, 256, 257
Nigrotectal fibers, 256, 257
Nigrothalamic fibers, 256, 257
Nociceptive reflex, 235, 235
Nodulus, 34, 126
Nonfluent (Broca) aphasia, 331Q, 337A
Nuclei and efferent fibers of CNs, 232, 232
Nuclei of lateral lemniscus, 136
Nucleocortical fibers, 246, 247
Nucleus
abducens, 30, 80, 94, 179, 195, 271, 273
ambiguus, 114-121, 124, 125, 199, 205,
buccinator, 231, 232, 233
206, 207, 215-217, 230-233, 238, 240,
291, 335Q, 336Q, 340A, 341A
blood supply to, 230
of Cajal, 150
centralis, 136, 140, 282, 283
cardiac, 231
ciliary,227, 239
ceruleus, 134, 136, 140, 142, 282, 283
of Darkschewitsch, 150, 196, 197, 249
deep back, 236, 236
gracilis, 179, 181
digastrics, 23.1, 232233
facial
452175230, 031,232, 2330236,
238, 238, 276, 333Q, 338A, 339A
paralysis of, 152, 214
genioglossus, 52, 215, 228, 229
hyoglossus, 227
inferior oblique, 227
intrinsic tongue, 227-229
lateral rectus, 227-229
lateral rectus, 53, 53, 228, 229
levator palpebrae, 227
masseter, 237, 237
masticatory, 232, 233
medial rectus, 53, 53, 227
mylohyoid, 231-233
platysma, 231, 232
sphincter of iris, 227
of stapedius, 231-233
sternocleidomastoid, 226
striated, 96, 231-233, 341A
148, 150, 244, 245
Occipitotemporal gyri, 18, 20, 26, 279
Occipitotemporal sulcus, 20
Oculomotor deficits, 278
Oculomotor nerve (III), 22-25, 29, 33, 44t,
47, 48, St, 239
tensor veli palatini, 227-229
cortical branches, 320, 326
inferior trunk of, 19, 21, 37
lateral striate arteries, 41
magnetic resonance imaging of, 18, 38
M, segment of, 19, 23, 37, 310, 311
orbitofrontal branches, 15, 17, 19, 37
parietal branches of, 15, 17, 37, 318
Occipitopontine fibers, 140, 142, 144, 146,
damage to, 48, 336Q
magnetic resonance imaging, 47, 48
Oculomotor nuclei, 53, 146, 148, 153, 164,
226, 227=229,-2397203
Occlusive stroke. See Ischemic stroke
Olfactory bulb, 18, 20, 282, 283
Olfactory groove meningiomas, 67, 67
Olfactory nerve (I), 44t
Olfactory sulcus, 18, 20, 76, 172
Olfactory tract, 18, 20,22523, 250172
Olivary eminence, 20, 22-24, 32, 50-52, 80, 94
Olive, 5, 20, 22-24, 51
Olivocerebellar fibers (OCDIF), 116, 118, 120,
183, 244, 245
Olivopontocerebellar degeneration, 244
One-and-a-half syndrome, 53, 214, 229,
3320, 3374
Ophthalmic artery, 21, 23, 318, 327, 328
Ophthalmic division of trigeminal nerve, 202,
203
Ophthalmic vein, 19, 21
Optic chiasm, 18, 22, 23,25;29532; 46,472
68, 69, 77, 170, 239, 262-267, 280,
PES PUSS, Ako ODS
Optic chiasm lesion, 267
Optic nerve (II), 18, 22, 23, 25, 29, 32, 40, 46,
48> S65 /On 21s 179,239, 262,9263—2 67;
lesion of, 46, 267
Optic radiations, 68, 69, 82-84, 87, 88, 90,
154, 156, 178, 180, 182, 186, 187,
262, 264-267
Optic tract, 18, 22, 23, 25, 32, 33, 46-48,
64, 69, 77-79, 90, 148, 150, 160, 162,
164, 166, 168, 175, 181, 184-187,
239, 263-267, 289
Optic tract damage. See Contralateral
hemianopia
Optic tract lesion, 267
Orbicularis oculi muscle, 236, 236
Orbit, 318, 327
intralaminar, 178, 190, 191, 197, 255, 257
Orbital cortex, 279
Orbital gyri, 18, 20, 172
Orbital sulci, 20
prepositus, 120, 125-126
proprius, 98, 100, 102, 104
Oxytocin, 294
raphe
dorsalis, 132, 136, 138, 196, 197, 283
macnus,, 1227130; 132) 196, £97 83
obscurus, 116, 118, 120, 122, 283
pallidus, 118, 120, 122, 283
pontis, 134
of stria terminalis, 282, 283
Nucleus ambiguus, 335Q, 336Q, 340A, 341A
Nucleus ambiguus lesion, 336Q, 340A
Nystagmus, 124
O
Obex, level of, 30, 116
Occipital gyri, 14, 16, 18
Occipital lobe, 11, 11, 38
Occipital pole, 18
Occipital sinus, 17, 21, 27
Otitis media, 60
Ie
Pachymeningitis, 58, 60
Pain receptors in cornea, 236
Palatal muscles, 238
Pallidal efferents, 256-259
Pallidonigral fibers, 146, 148, 164, DSO, 2S
Pallidosubthalamic fibers, 256, 257
Pallidothalamic fibers, 258, 258
Pantothenate kinase-associated
neurodegeneration (PKAN), 255
Parabrachial nuclei, 206, 207, 283, 291
Paracallosal cistern, 64
Paracentral sulcus, 11, 26, 28
Parafascicular nucleus, 282, 283
Parahippocampal gyri, 333Q, 342A
Parahippocampal gyrus, 18, 20, 22, 26, 279, 283
Index
Paralysis, 305
Paralysis agitans. See Parkinson disease
Paramedian pontine reticular formation, 214, 215
Paramedian reticular nuclei, 244, 245
Paraphasia, 12
Paraplegia, 305
Parasagittal meningiomas, 66, 66
Parasympathetic preganglionic fibers, in CN
Pontine gliomas, 202, 226
Pontine (medial) reticulospinal fibers,
218-219
Pontine nuclei, 122, 130, 132, 134, 136, 140,
141, 244, 245, 249
Pontine reticular nuclei, 218-219
Paraterminal gyrus, 26, 170
Paraventricular nuclei, 288, 289
Parenchymatous hemorrhage, 71
Pontobulbar nucleus, 120, 122
Pontocerebellar axons, 244
Pontocerebellar fibers, 130, 132, 134, 136,
Parietal lobe, 11, 17, 27
140, 244, 245
Pontoreticulospinal (medial reticulospinal)
fibers, 218
Pontoreticulospinal (medial reticulospinal)
tract, 100, 104, 106
Pontoreticulospinal tract, 102
Ill, 239
Parietofrontal areas, 298
Parieto-occipital sulcus, 11, 15, 26, 28
Parieto-occiptal artery, 327
Parietopontine fibers, 140, 142, 144, 146,
148, 150, 244, 245, 276
Pontine tegmentum, 28, 49, 50, 194, 198,
204,.21252289291
lesion in, 314
Parinaud syndrome, 152, 302
Parkinson disease, 174, 254, 259, 333Q, 338A
Parolfactory gyri, 26
Position of tentorium cerebelli, 61
Parotid gland, 207, 231
Pars distalis, 294, 295
Pars intermedia, 294, 295
Postcentral sulcus, 11, 14, 16
Postcommissural fornix, 280
Posterior accessory olivary nucleus, 116,
Iss. TAC
Posterior and anterior horns, 100, 102
Posterior cerebral artery (PCA), 21-23, 25,
Pars opercularis, 12, 16
Pars orbitalis, 12, 16
Pars triangularis, 12, 16
Pars tuberalis, 294, 295
Patellar reflex, 234
Pathways
motor, 221-224
sensory, 208, 209
solitary, 206, 207
spinocervicothalamic, 200, 201
trigeminal, 55, 202-205
Pedunculopontine nucleus, 256, 257
Penumbra, 309
Peptides, 288
Periaqueductal gray, 81, 82, 90, 140, 142,
144, 146, 153, 182, 196, 197, 249, 273
Peripeduncular nucleus, 148, 150
Periventricular areas/zones, 289
Periventricular nuclei, 291
Pharyngeal arch 2, failure in proper
development of, 336Q, 341A
Pharyngeal muscles, 238
Phrenic nerve, 109
Phrenic nucleus, 109
Pia mater, 58t, 59, 60
PICA syndrome, 202, 315, 316
Pick disease, 280, 282
Pineal, 29-31, 68, 69, 82, 88, 89, 150, 154,
1Yee, 17)
Pineal recess, 68
Pituitary gland, 294-295, 295
blood supply to, 294
Placidity, 282, 285
Polar temporal arteries, 23
Polysynaptic reflexes, 234
Pouset7, 97,179,179, 181, 181, 183, 183,
HESS, 11S)
arterial territories in, 135
nuclei in, 185
transverse section of, 132-134
vascular syndromes or lesions of, 138
Pons-medulla junction, 22, 22, 33, 44t, 50,
O25 2570 02225223) 2520233
Pons-midbrain junction, 140, 141
Pontine arteries, 23
Postcentral gyrus, 12-14, 16, 36, 192,
193-197, 204, 205, 279
33, 38, 42, 47, 48, 72, 160, 175, 313,
323, 325-327, 329
anterior temporal branch of, 19, 27
branches of, 15
calcarine branch of, 19, 27, 324
cortical branches of, 320, 325-327
fetal, 38, 313
magnetic resonance angiography of, 323
magnetic resonance imaging of, 33, 42
parieto-occipital branch of, 19, 27, 324
phalamogeniculate branch, 175
posterior temporal branch of, 19, 27
posteromedial branches of, 175
P, segment of, 23
P; segment of, 19
temporal branches of, 19
thalamoperforating arteries, 39
vascular lesions, 310
Posterior inferior cerebellar artery, 315, 316
distal PICA lesion (cortex), 247
PICA syndrome, 315, 316
Posterior choroidal arteries, 23, 25, 31, 33, 324
Posterior cochlear nucleus, 185
Posterior column, 192, 193-195, 200
Posterior column-medial lemniscus pathway,
Sy OA
OS
Posterior commissure, 29, 68, 81, 150, 179,
23
262,269
Posterior communicating artery, 19, 21-23,
ZIAD 33, Als 7
2p LON OLAS 320, S27,
magnetic resonance imaging of, 33
Posterior horn of lateral ventricle, 68, 68—70,
69, 70, 84, 87-90
Posterior hypothalamus, 162
Posterior inferior cerebellar artery (PICA),
Dil 25 29591, 935 A293 24, 325,
329-3350, 336Q, 340A, 341A
branch to choroid plexus in fourth ventricle,
72.
occlusion of, 124
Posterior inferior cerebellar artery syndrome,
196
353
Posterior intercavernous sinus, 21, 295
Posterior intermediate sulcus, 30, 102, 104, 106
Posterior (dorsal) longitudinal fasciculus, 114,
PGE
Se IZOD
2 S013
2, 01345
140, 142, 144, 146, 148
Posterior median sulcus, 30, 100, 102, 104, 106
Posterior nuclei, 289
Posterior paracentral gyrus, 12, 13, 26, 28,
192, 193-195
Posterior quadrangular lobule, 34
Posterior radicular artery, 9, 109
Posterior root, 101-103, 105, 109
Posterior root ganglia, 194, 195, 198, 199,
234, 240
Posterior spinal artery, 21, 23, 25, 31, 33, 42,
109, 125
Posterior spinal medullary artery, 9, 109
Posterior spinocerebellar tract, 102, 104, 106,
LOD MAZR TAI:
Posterior superior fissure, 34
Posterior tegmental decussation, 218, 219, 221
Posterior thalamic nuclei, infarction of, 174
Posterior watershed infarcts, 174
Posterolateral fissure, 35
Posterolateral sulcus, 30, 102, 104
Posterolateral tract, 235
Posteromarginal nucleus, 98, 100, 102, 104
Postganglionic sympathetic fibers, 262, 263
Postolivary sulcus, 51, 52
Precentral gyrus, 12-14, 16, 36, 210,
212135 219-21 7272
Precentral sulcus, 11, 14, 16, 26
Precommissural fornix, 290, 291
Precuneus, 26, 26, 28, 28, 279
Prefrontal cortex, 283
Premedullary cistern, 64
Preoccipital notch, 11, 16
Preolivary sulcus, 22, 51, 52, 94, 114, 116
Preoptic area of hypothalamus, 168
Prepiriform cortex, 282, 283
Prepontine cistern, 64
Pretectal area, 81
Pretectal nucleus, 239, 262, 263-264, 266-267
Primary auditory cortex, 279
Primary fissure, 34, 35
Primary vestibular afferent fibers, 272, 273
Primary visual cortex, 13
Primitive reflexes, 238
Principal (chief) sensory nucleus, 130, 132,
134, 135, 183, 202, 203, 231, 243
Principal mammillary fasciculus, 290
Principal olivary nucleus, 114, 114, 116, 118,
120, 122, 179, 181, 202, 203-204, 231,
342
Prolactin, 294
Propriospinal fibers, 98, 100, 102, 104, 106,
109
Pterygopalatine ganglion, 237, 333Q, 338A
Pulvinar, 25, 69, 182, 182
Pulvinar nuclear complex, 30, 148, 148, 150,
ISG, USS, UID, XP AG HED 2H
Pulvinar nuclei, 31, 180, 180, 332Q, 338A
Pupillary light reflex, 46, 48, 56, 239, 262,
265) 278
Pupillary pathways, 262, 263
Pupillary reflex. See Pupillary light reflex
Putamen, 76-80, 87-89, 160, 162, 164, 166,
168,01 708 172217
597SAS OL S25
184, 185, 187, 187
354
Index
Pyramid, 5, 22-24, 32, 49, 50, 51, 52, 80, 82,
94, 106, 112, 114, 116, 1178, 120, 122,
125, 179, 192, 193, 194, 198, 204,
IB
PUN PS
PSY APS WER aioe
DAS 2458
of medulla, 212, 213, 258
Pyramidal decussation, 106, 112, 125,
DAO 212
Q
Quadrigeminal artery, 19, 23, 25, 31, 33
Quadrigeminal cistern, 29, 64, 65
Quadriplegia, 108
R
Radiculopathy, 8
Radiofrequency pulse (RP), 2
Retrolenticular limb, of internal capsule, 81,
82, 88, 156, 175, 245
arteriovenous malformation in, 108
C2-C4 and C7-T1 levels, 8
Retro-olivary sulcus, 5, 22, 51, 114, 194,
DN, 2x
G@3=C7 levels39
C2-T1 levels, &
Retrosplenial cortex, 280, 281
Rheumatic chorea. See Sydenham chorea
Rhinal sulcus, 26
Right lateral corticospinal tract, damage to,
334Q, 339A
coccygeal, 10
function components in, 96
hemorrhage in, 108
incomplete lesion of, 332Q, 338A
internal blood supply to, 108, 109
Rinne test, 270
Rolandic vein, 15, 17
Rostral interstitial nucleus, of medial
lamina I, 98, 100, 104
lamina II, 98, 100, 104
lamina III, 98, 100, 104
lamina IV, 98, 100, 104, 200
lamina VI, 100, 102, 104
lamina VII, 98, 100, 102, 104, 243
lamina VIII, 100, 104
lamina IX, 98, 100, 102, 104
lamina X, 100
lumbar, 4, 10, 100
sacral, 10, 98
thoracic LOM 7AMO 220)
longitudinal fasciculus, 214, 215
Rostral part of fourth ventricle, 65
Rostrum of corpus callosum, 28, 76
Rubrospinal fibers, 222, 223
Rubrospinal tract, 100, 102, 104, 106, 109,
Raphecerebellar fibers, 244, 245
Raphe nuclei, 202, 244, 255, 257
112, 114, 116710851120; 1224125;
130, 132, 134, 136, 140, 144, 146,
Raphespinal fibers, 197
Raphestriatal fibers, 254, 255
Raymond syndrome, 54t, 138
Receptive aphasia, 12
Receptors in caudal mouth, 258
DAS, DNS), DRY, P2I, LS
Recombinant tissue plasminogen activator
(rtPA), 309
Red nucleus, 5, 25, 33, 80, 90, 146, 148,
ISO, NS? USD, MSO, MGS ITS, ee
181, 182, 183, 192, 193-195, 198,
NEED, PASAY, 21), DIY), APA, 723%
227-229, 243, 240-251, 263-264,
273
blood supply to, 220
caudal aspect, 146
Reflex(es) 234, 234-240
afferent limb, 46, 205, 206, 230, 233, 234,
236, 237, 238, 239, 333Q, 338A
S
Salivatory nuclei, 207, 230
Salivatory reflexes, 237
Schizophrenia, 256
Sciatica, 10
Secondary cochlear fibers, 122
Segmental artery, 9, 9, 109
Segmental medullary arteries, 9
Sellar meningioma, 67, 67
Sella turcica, 294
Sensory aphasia, 12
Sensory ataxia, 192
Sensory decussation, 114, 116, 192, 194-195
Sensory deficit, alternating, 315
Sensory pathways, 208, 209
Septal nuclei, 168, 280, 282, 284, 285, 291
baroreceptor, 240
efferent limb, 48, 56, 206, 234, 339A
Septal veins, 27
Septum, 28
in infants, 238
sneezing, 202
swallowing, 51, 240, 339, 342
Septum pellucidum, 27, 29, 68, 69, 76-79,
vagovagal, 240
vomiting, 202, 240
Relay nuclei, 278
intralaminar, 248
Releasing factors (RFs), 288, 294
Releasing hormones (RHs), 288
Restiform body, 25, 30; 31; 32;335 51, 52,
Was WANES HAG, ILLS, AAO, BH, WAS WANS
128, 130, 139, 193, 194, 197-199,
ROSS IXO)S., NO PANE, AIM, 25}
245, 247, 249-250, 271, 273
Reticular formation, 53, 116, 118, 120, 122,
130, 132, 136, 140, 144, 146, 196, 197,
199, 202, 203, 214, 215, 218, 234, 238 5)
240, 244, 249-251, 271, 278, 291
Reticular nuclei, 187, 219, 244
Reticulocerebellar fibers, 244, 245
Reticulospinal fibers, 100, 112, 114, 120,
222220,
Reticulospinal tract, 98, 100, 102, 104, 106,
IPALAL, DEMOS DIE,
Reticulotegmental nucleus, 134, 244, 245
Reticulothalamic fibers, 196, 197
Retina, 239, 266, 278, 290, 291, 318
Retinal disorders/trauma, 267
Retinogeniculate fibers, 264
Retinohypothalamic fibers, 290
86-88, 166, 168, 170, 172, 175
Serotonergic amygdaloid fibers, 282
Short ciliary nerves, 239, 239
Sigmoid sinus, 17, 19, 21, 24, 60, 319,
overall shape of, 102
transverse section of
appearance at lower cervical levels, 104
appearance at lumbar levels, 100
appearance at thoracic levels, 102
at Cl level, 106
sacral level, 98
vascular syndromes or lesions of, 108
Spinal cord—brainstem transition, 96
Spinal cord lesions, 332Q, 338A
general concepts of, 108
high cervical, 109
Spinal cord nuclei, medial-to-lateral positions
of 97,97
Spinal meninges, 58t
Spinal nerves, 59
functional components of, 55, 55
motor nuclei, 95
root damage, 8
Spinal reflexes, 234
Spinal trigeminal fibers, 204, 205
Spinal trigeminal nucleus, 237, 237
gelatinosa portion of, 106, 107
321-323, 328
magnocellular portion of, 106, 107, 279
Sinus confluens, 15, 17, 19
Skull, 247-5, 52; 58,59
pars caudalis, 97, 112, 114, 204, 205,
2310; 25/7,
Sneezing reflex, 202
Solitariospinal tract, 207
Solitary nuclei, 115, 117, 120, 121, 123, 129
Solitary nuclei and tract, 114, 116, 118, 121,
125, 12651307175 081
Solitary nucleus, 202, 203, 269, 279
Solitary pathways, 206-207
Solitary tract, 55, 96, 120, 122, 206, 207, 273
Somatic afferent, 95, 96, 338
Somatic efferent, 95
Somato-visceral reflex, 237, 237
Special somatic afferent, 44, 96, 97
Special visceral afferent, 44, 45, 96, 97, 206, 207
Special visceral efferent, 96, 97
Sphenoparietal sinus, 19, 21
Sphincter muscle
of ciliary body, 263
of iris, 263
Sphincter pupillae, 48, 239
Spinal and cranial nerve reflexes, 234
Spinal cord, 96, 97, 241
arteries of, 8-9
pars interpolaris, 97, 116, 118, 202, 204
Spinal nerves, 59
Spinal tracts, 95
Spinal trigeminal tract, 55, 106
Spinal vessel, 59
Spinocerebellar tracts, 102, 104, 106, 109,
112, 114, 116,118, 203120825
130, 132, 242, 243
blood supply to, 242
Spinocervicothalamic pathway, 200, 201
Spino-olivary fibers, 102, 104, 106, 112
Spinoreticular fibers, 196, 220
Spinotectal fibers, 144, 196, 197
Spinotectal tract, 146, 148
Spinothalamic fibers, 144, 146, 148, 150,
UDG, D7
Spiral ganglion, 270, 271
Splenium of corpus callosum, 25, 28, 68, 83
84, 87, 88
Stalk of infundibulum, 289
Stereoagnosis, 192
Stereoanesthesia, 192
t)
Index
Sternocleidomastoid muscles, 45, 214, 226, 238
Sternocleidomastoid weakness, 276
Straight sinus, 17, 19, 27, 319, 326, 328
Stretch. See Muscle stretch reflex
Striae medullares, 30, 32, 120
Stria medullaris thalami, 29, 160, 162, 164, 179
Striatal connections, 254, 255
Stria terminalis (ST), 69, 79, 80, 87, 154, 156,
160, 164, 166, 168, 175, 282, 283, 290,
Doi
Striatonigral fibers, 254, 255
Striatopallidal fibers, 254, 255, 258, 258, 259
Strionigral projection, 254
Striopallidal fibers, 254, 255
Stroke, 309
hemorrhagic, 309
ischemic, 309
lacunar, 313
lesions/syndromes, 310-316
Stylopharyngeus muscle, 232, 233, 238
Subarachnoid blood on tentorium
cerebella, 71
Subarachnoid hemorrhage (SAH), 29, 58, 65
Subarachnoid space (SAS), 59
of elder obese male, 331Q,
Subcallosal area, 279
Subcallosal gyrus, 76, 172
Subcortical white matter
vascular lesions in, 311
Subdural hematoma, 58, 62, 63
Subdural hemorrhage, 63, 65
Subiculum, 280, 281, 283
Subependymal! hemorrhage, 71
Subfalcine herniation, 63, 297, 298, 298
Sublenticular limb, 156, 276, 277
Sublingual gland, 231
Submandibular gland, 230
Substance P, 196, 200, 202, 206, 210, 254,
282, 288
Substantia gelatinosa, 97, 98, 100, 102, 104
Substantia nigra, 5, 18, 80, 90, 91, 142, 146,
148, 160, 164, 175, 181, 181, 183,
184, 192, 193, 194,198, 204, 205,
216, 20702197228, 22992455279,
DSi a6e 257 2589259926352 0451283
marginal, 11, 26, 28
Supraoptic commissure, 289
occipitotemporal sulcus, 20
Supraoptic decussation, 166, 168
Supraoptic nucleus, 150, 168, 183, 289,
295,
olfactory, 18, 20, 172
orbital, 20
paracentral, 11, 26, 28
parieto-occipital, 11, 15, 26, 28
postcentral, 11, 14, 16
posterior intermediate, 8, 30, 102, 104, 106
posterior median, 8, 30, 100, 102, 104, 106
posterolateral sulcus, 30, 102, 104
postolivary, 22, 51, 52, 94, 114, 116
precentral, 11, 14, 16, 26
preolivary, 22, 51, 52, 94, 114, 116, 216
retro-olivary, 5, 22, 51, 52, 94, 114, 116,
194, 216
superior frontal sulcus, 14, 16
superior temporal sulcus, 16
Superficial cerebral vein, 17, 37, 322, 328
Superficial middle cerebral vein, 17, 19, 21,
Sisto
Superior alternating hemiplegia, 152, 226
Superior anastomotic vein, 15, 17
Superior cerebellar artery (SCA), 21-23, 25,
31, 33, 47-49, 72, 316, 323-327, 329
lesion of cortex plus nuclei, 247
vascular lesions of, 316
Superior cerebellar peduncle decussation, 142,
144, 146, 179, 186, 186, 226, 227,
DUS, PLY Pays)
Superior cerebellar peduncles, 20, 34, 35,
83, 138
Superior cerebellar vein, 27
Superior cerebellopontine cistern, 64
Superior cerebral veins, 15, 17, 319, 321
Superior cervical ganglion, 262, 263
Superior cistern, 154, 156
Superior colliculus, 25, 29, 29-33, 30, 31, 33,
35, 47, 144, 146, 148, 150, 156, 179,
179, 180, 180; 196,197, 221, 227,
228, 249, 257, 263
Superior fovea, 30, 32
Superior frontal gyrus, 14, 16, 26, 28, 36,
66, 279
blood supply to, 254
Superior frontal sulcus, 14, 16
Superior ganglion of CN IX, 238
Superior hypophysial arteries, 295
pars compacta, 254, 282
Superior medullary velum, 122, 130, 132,
pars reticulata, 254, 256
Subthalamic fasciculus, 257
Subthalamic lesion, 259
Subthalamic nucleus, 184, 185, 185
lesions of, 174, 259
Subthalamonigral fibers, 256, 257
Subthalamopallidal cell/fiber, 258
Sulcal arteries, 9
Sulcus(1)
anterolateral, 104
calcarine, 11, 12, 13, 26, 28, 69, 187,
265-267
central, 11, 14, 16, 17, 26, 28, 36
cingulate, 11, 26, 28, 191
circular sulcus, 11
collateral sulcus, 11, 18, 20
of corpus callosum, 26
hypothalamic, 29, 289
inferior frontal, 16
intraparietal, 16
lateral sulcus, 11, 13, 16, 17, 37, 191
limitans, 30, 32, 97, 118, 228
134, 139
Superior oblique muscle, 228, 229
355
Supraoptic recess, 29, 48, 65, 68, 77,
186, 295
Supraopticohypophysial tract, 295
Suprapineal recess, 29, 68
Sydenham chorea, 254
Sylvian cistern, 64, 65, 65
Sylvian sulcus. See Lateral sulcus
Syndrome(s)
acute central cervical cord, 196
amnestic confabulatory, 280
anterior choroidal artery, 25, 25, 46,
TAT
Benedikt, 54, 152
Brown-Séquard, 95, 108, 190, 192, 196,
210, 242, 338A
cauda equina, 10
Claude, 54t, 152, 220, 229, 251
Collet-Sicard, 51, 52, 230, 322
Dandy-Walker, 246
Foix-Alajouanine, 108
Foville, 54t, 138, 210
Gubler, 54t
Horner, 124, 138, 262, 290, 338A
jugular foramen, 51, 52, 226, 230
Kernohan, 152, 301
Kliiver—Bucy, 282, 285, 342A
Korsakoff, 280, 285, 288, 342A
lateral medullary, 54t, 95, 124
lateral pontine, 138, 244
medial medullary, 52, 124
medial midbrain (Weber), 152
medial pontine, 138, 192
Millard-Gubler, 138, 210
one-and-a-half syndrome, 53, 214, 229
Parinaud, 152, 214, 302
posterior inferior cerebellar artery,
196, 341A
Raymond, 54t
Vernet, 51, 230, 322
Weber, 54t, 210, 226, 229
Wernicke—Korsakoff, 280, 285
Syringobulbia, 124, 226, 230
Syringomyelia, 108, 196
Syrinx, 108
Superior olive, 122, 130, 132, 271
Superior orbital fissure, 24, 44, 47, 325
T
Tactile agnosia, 192, 280
Superior parietal lobule, 14, 16, 279
Superior peduncle, 181, 181
Tail of caudate nucleus, 68, 79, 81, 87, 88,
Superior petrosal sinus, 17, 19, 21, 24, 326
Superior (quadrigeminal) cistern, 284, 285
Superior sagittal sinus, 15, 15, 17, 27, 58, 59,
61, 66, 319, 321-323, 326, 328
Superior salivatory nucleus (SSN), 128-133,
2315 237
Superior semilunar lobule, 34
Superior temporal gyrus, 16, 279
Superior temporal sulcus, 16
Superior thalamic radiations, 276
Superior thalamostriate vein, 27, 319
Superior visual quadrant, 13, 13
Superior vestibular nucleus, 128, 130, 132
Superior visual quadrant, 13
Suprachiasmatic nuclei, 288, 29 029i
Supramarginal gyrus, 12, 14, 16
175
“Talk and die,” 58
Tapetum, 68, 69, 82-84, 87-89, 154
Tectospinal fibers, 218
Tectospinal tract, 104, 106, 112, 114, 116,
IMS OO 12212
CD) Salis OS25
134, 136, 140, 142, 144, 219, 221, 231
Tectum, 28, 68
Tegmental nuclei, 245, 280, 281
Tegmentum of pons, 49, 70, 93
Tela choroidea, 30, 32, 126
Telencephalon, 190, 191
Temporal horn, lateral ventricle, 65, 70,
284, 285
Temporalis muscle, 237, 237
Temporal lobe, 11, 18, 27, 32, 36, 46, 47, 49,
Vs Vio D3
356
Index
Temporal pole, 18, 20, 26, 212, 216, 217,
228, 244, 245
Temporomandibular joint, 203
Temporopontine fibers, 140, 142, 144, 146,
148, 150, 276
Tentorial meningiomas, 66, 66
Tentorium cerebelli, 29, 59, 60, 61, 66, 67,
DOE RYE
Tentorium cerebelli meningioma, 66, 66
Terminal vein, 27, 78, 79
Thalamic fasciculus, 158, 160, 162, 164, 181,
USES, PED, AS), PSO, PSIG PSG, 2585
Thalamic nuclei, 178, 178, 183, 278
Thalamic reticular nuclei, 278
Thalamic syndrome, 196, 278
Thalamocortical fibers, 194, 195, 198, 199,
204, 205, 248, 249, 250, 258, 259
Thalamogeniculate arteries, 25, 31, 33, 324
Thalamoperforating arteries, 39, 324, 325
Thalamoperforating vessels, origin for, 39
Thalamostriatal fibers, 255
Transverse sinus, 17, 19, 21, 27, 59, 321-323,
326, 328
Transverse temporal gyrus, 36, 271
Trapezius muscles, 45, 226, 227, 238
Trapezoid body, 130, 132, 270, 271
Trapezoid nucleus, 270, 271
Traumatic brain injury (TBI), 74, 288, 294
Traversing roots, at lumbosacral levels,
307, 307
Trigeminal cutaneous receptors, 238
Trigeminal ganglion, 202-205, 236, 237, 238
Trigeminal motor nucleus, 130, 132, 134,
1355 18352089 215,23 1-238 2o75
238, 243, 249
Trigeminal motor root, 237
Trigeminal nerve (V), 20, 22, 25, 49, S4t, 55,
64, 80, 935 13091325 134,136, 138;
139,-2022204, 205, 2132 232393,237
maxillary division of, 203
motor root, 32, 33, 35
sensory root, 32, 33, 35, 49
of caudate nucleus and septum pellucidum, 27
cerebellar, 17, 27
corpus callosum, posterior vein of, 27
to dural sinuses, 323
deep middle cerebral, 19
of Galen, 19, 25, 27, 35, 66, 67, 89, 319,
BAG, Soh, DO
great cerebral, 19, 27, 319, 326, 328
inferior anastomotic, 17
inferior cerebral, 319
inferior hypophysial, 295
internal cerebral, 19, 26, 27, 29, 30, 66,
Of, BUD
internal jugular, 17, 19, 21, 322, 328
internal occipital, 27
Lalo, 15),, 17, 31D, SAS
ophthalmic, 19, 21
Rolandic, 15, 17
septal, 27
superficial cerebral, 322, 328
superficial middle cerebral, 17, 19, 37, 319
superior anastomotic, 15, 17, 319
Thalamostriate vein, 319
Trigeminal neuralgia (tic douloureux), 49,
Thalamogeniculate artery, 311, 313
Thalamoperforating artery, 311
Trigeminal nuclei, 6, 139, 195, 199
superior cerebral, 15, 17, 319, 321
Trigeminal pathways, 55, 202-205
Trigeminal root, 202, 205, 230, 233, 270, 327
Trigeminal sensory root, 236, 237
superior thalamostriate, 27, 319
Thalamus, 212, 277, 278
anterior nucleus of, 79, 87, 162, 164, 175,
178-181, 183, 257, 281, 289
dorsal, 29, 46, 47, 69, 166, 204, 216, 217,
258, 278
dorsomedial nucleus of, 79, 80, 87, 88, 158,
CO SA. UC, TSS, TRS, PEED, TLCS tecsee
MOI, BI BED, RSS,
Magnocellular part, 279
Parvocellular part, 279
lateral view of, 25, 31, 33
lateral dorsal nucleus of, 80, 160, 175, 181,
USS, AH
medial, 31, 281, 283
vascular lesions in, 311
ventral anterior nucleus of, 79, 87, 88, 166,
178, 180; 181, 183, 257,279
ventral lateral nucleus of, 80, 87, 88, 160,
162, 164, 178, 180, 181, 182, 185,
187
ventral posterolateral nucleus of, 80, 87, 88,
USS, HO), MIA, SH, DIL, WD UME DOS.
235, 248, 249
ventral posteromedial nucleus of, 80, 89,
LI SPISO; 1825183. 985, 295,199,203,
D06e207 2860272
ventromedial nucleus of, 257, 288, 289
Third ventricle, 49, 65, 68, 69, 70, 77-79,
88-90, 150, 158, 162, 164, 166, 168,
BSD, ADIN, ADS:
blood in, 71, 74
choroid plexus, 25, 29, 31, 33, 72
tumor in, 73
Thrombosis of anterior spinal artery, 108
Thrombus, 309
Tinnitus, 230
Tissue plasminogen activator (tPA), 309
Tonsil, 34
Tonsillar herniation, 124, 297, 303, 303
Tonsil of cerebellum, 28, 50-52, 94, 126
Trachyphonia, 254
Transient ischemic attack (TIA), 174, 309
crescendo, 309
Transition from crus cerebri (CC) to internal
capsule, 150
202; 230, 332Q,337A
Trigeminal tubercle, 30, 31, 32
Trigeminothalamic fibers, 202, 203, 237, 237
Trigeminothalamic tracts, blood supply to, 200
Trochlear decussation, 226, 227
Trochlear nerve exit, 136, 186, 228, 229
Trochlear nerve (IV), 22-25, 31-35, 44t, 48,
83, 91, 136, 139, 140, 154, 179, 186,
20607
exit of, 35
Trochlear nucleus, 142, 143, 144, 145, 153,
IS)5 ZD),. AA PS, AUD MIS
Tuberal nucleus, 288, 289, 290, 291
Tuberculum cinereum (trigeminal tubercle),
30-32
Tuberculum cuneatum (cuneate tubercle), 30
Tuberculum gracile, 30
Tuberoinfundibular tracts, 288, 294
Tuberomammillary nucleus, 291
Tumor
in atrium, 73
of choroid plexus, 73, 73
in third ventricle, 73
U
Uncal artery, 23
Uncal herniation, 152, 301, 301
Uncus, 18, 20, 22, 26, 46, 47, 77, 91, 163,
186, 279, 284
Upper motor neuron, 210
Upward cerebellar herniation, 302, 302
Uvula, 122
V
Vagal trigone, 30-32
Vagus nerve (X), 20, 22-25, 33, 50-52, 81,
118, 230, 231-234, 238
Vernet syndrome, 230
Vasoactive intestinal polypeptide, 288
Vasopressin, in pituitary gland, 294
Vein(s)
anterior cerebral, 17, 19, 37
basal, 19, 27, 37, 319, 328
superior cerebellar, 27
terminal, 27, 78, 79
Venous angle, 27, 319, 319
Ventral amygdalofugal fibers, 166
Ventral amygdalofugal pathway (VAF),
282, 290
Ventral anterior nucleus of thalamus, 79, 87,
88, 178, 180, 181, 183
Ventral lateral nucleus of thalamus, 87, 88,
160, 162, 164, 178, 180, 181, 182,
183, 185, 187, 248, 249, 250, 251,
278, 279
Ventral pallidum, 77
Ventral posterolateral nucleus of thalamus,
87, 88, 158, 180, 182, 187, 187, 190,
UL WIS, UDI AOS, BAS)
Ventral posteromedial nucleus of thalamus, 158
180, 1825 182) 185)1859191,.203, 207,
Ventral spinocerebellar tract, 242, 249
Ventral striatum, 77
Ventral tegmental area, 256, 282, 283
Ventral thalamic nucleus, 181, 181
Ventral trigeminothalamic fibers, 95, 139,
ISX, 153, 202
Ventral trigeminothalamic tract, 114, 116,
118, 120, 122,930, d32 13451368
140, 142, 144, 146, 148, 150
Ventricles, 64-67
blood in, 71, 74
Ventromedial hypothalamic nucleus, 280,
280, 283
Ventromedial nucleus of thalamus, 256, 257
Vermal cortex, 246, 272
Vermis, 34
of anterior lobe of cerebellum, 34
of posterior lobe of cerebellum, 34, 93
Vernet syndrome, 51, 322
Vertebra, 59
Vertebral artery, 21, 23, 25, 33, 72, 323-325,
3285329
magnetic resonance angiography of, 323
Vertebral artery angiogram
anterior—posterior projection, arterial phase,
SS),, 35)
left lateral projection, arterial phase, 324, 324
>
Index
Vertical gaze palsies, 214
Vertigo, 50, 124, 199, 205, 230, 272
Vestibular area, 30, 31, 32
Vestibular ganglion, 272
Vestibular nuclei, 32, 54, 97, 119, NAL, HAS,
P27 ALD 13151335139, 220, 246,
272,
Vestibular pathways, 56, 56, 272-275
Vestibular portion of eighth nerve, 50
Vestibular schwannoma, 24, 50, 230, 272
Vestibulocerebellar fibers, 272
Vestibulocochlear nerve (VIII), 20, 22, 23-25,
33, 35, 49-52, 80, 81, 94
Vestibulospinal fibers, 114, 222, 223
Vestibulospinal tracts, 100, 102, 221, 272
Vibratory sense, 6, 98, 100, 102, 104, 106,
Ms 112114, 018, 120, 122, 124,
Dor 2S ISON 1325 136, 1405 144.
MOI AS IONS 2. 195. 19952 13%
DUG)
Viral meningitis, 58
Visceral afferents, 95
Visceral efferent, 96, 341A
Visual agnosia, 280, 309
Visual cortex, 28, 56, 218, 262, 264, 265,
266, 276, 278
Visual field deficits, 262, 266, 267
Visual fields, 46, 262, 264, 265, 266, 267,
276, 288
Visual nerve (II), 44t
Visual pathways, 264-269
Vocalis muscle, 230, 232, 340A
Vomiting reflex, 202, 240
Vomiting, intractable, 315
von Monakow syndrome, 25, 46, 174, 276
357
Wallerian (anterograde) degeneration, 110
Watershed infarct, 174, 309
Watershed zones, 309
MCA-ACA, 311, 312
vascular lesions in, 311, 312
Weber syndrome, 54t, 210, 226, 301,
337Q, 342A
Weber test, 270
Wernicke aphasia, 12
Wernicke area, 337A
Wernicke-Korsakoff syndrome, 280, 285
White matter, 100, 258
White ramus communicans, 262
Willis, circle of, 21, 22, 23, 38, 319
Wilson disease, 254, 255, 259
Withdrawal reflex. See Nociceptive reflex
W
Wallenberg syndrome, 124, 315. See also
Posterior inferior cerebellar artery
syndrome
Ve
Zona incerta, 158, 160, 162, 164, 185, 185,
248, 249, 253, 257, 289
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