Dating Neurological Injury: A Forensic Guide for Radiologists, Other Expert Medical Witnesses, and Attorneys

Dating Neurological Injury Jeff L. Creasy Dating Neurological Injury A Forensic Guide for Radiologists, Other Expert...

Author: Jeff L. Creasy

48 downloads 481 Views 7MB Size Report

This content was uploaded by our users and we assume good faith they have the permission to share this book. If you own the copyright to this book and it is wrongfully on our website, we offer a simple DMCA procedure to remove your content from our site. Start by pressing the button below!
Report copyright / DMCA form

DOWNLOAD PDF

Dating Neurological Injury

Jeff L. Creasy

Dating Neurological Injury A Forensic Guide for Radiologists, Other Expert Medical Witnesses, and Attorneys

Jeff L. Creasy Associate Professor of Neuroradiology Vanderbilt University Medical Center Nashville, TN USA [email protected]

ISBN 978-1-60761-249-0 e-ISBN 978-1-60761-250-6 DOI 10.1007/978-1-60761-250-6 Springer New York Dordrecht Heidelberg London © Springer Science+Business Media, LLC 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibil-ity for any errors or omissions that may be made. The publisher makes no warranty, express or im-plied, with respect to the material contained herein. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)

Preface

Why do we need a book on the dating of neurological injury? Over the last decade, I have personally reviewed more than 80 medical–legal cases related to neurological disease in which some aspect of the case involved imaging technology. Many cases – in clinical situations, such as alleged birthrelated hypoxia or ischemia, surgically-related injuries, or trauma-induced spinal cord or brain substance abnormalities, for example – shared the need both to detect the presence of an injury and to date the time it occurred. While a minority of cases involved the misdiagnosis of an aneurysm, a delayed diagnosis of spinal fracture, or orbital injury during a surgical procedure, the large majority of cases used modern imaging, first to detect if an injury had occurred to the brain substance or the spinal cord (collectively referred to as the central nervous system) and second to determine, if an injury did occur, at what time it occurred. In a medical–legal setting, the interplay between the radiographic findings and the clinical findings has several possible scenarios. On one extreme, the imaging findings may be so unequivocal that no doubt exists as to what occurred and even little doubt about when it occurred. On the opposite extreme, the radiologic findings may be either completely noncontributory or may show that an event occurred but offer no insight into when it occurred (and hence its proximate cause). In between is a gray area in which the clinical history can often be very helpful in delineating the imaging findings to more accuracy and specificity; and the reverse may also be true, i.e., that the radiology may help clarify the clinical picture. My hope is that this text will be helpful in all situations – from those in which radiology is clear, to those in which the findings are less certain though still present – by providing guidelines and principles for the application of imaging findings. The realm of this book is not to discuss specific clinical and radiographic findings at the level of the medical expert radiologist, nor is it intended to be an exhaustive treatise on recognizing the imaging signs of brain abnormality, as that is more appropriately covered in a textbook on medical imaging. Rather, I intend to represent in a systematic fashion the principles involved in the interpretation of images of the central nervous system specifically in a medical–legal setting where concern exists about the occurrence and timing of an injury. What this book uniquely presents is a new way to approach the dating of neurological injury as imaged by modern computed tomography (CT), magnetic resonance (MR), and ultrasound (US). Throughout the text, I describe dating by two distinct but complementary methods. In the first, I explain how knowledge of the dynamic and rapidly changing imaging findings that occur in the first few weeks after an injury permit dating in this acute period. In the second, I illustrate how patterns of injury with specific features can date with some accuracy the time an injury occurs, which may be much earlier than the time when the image was obtained. This tends to be dating that occurs in the chronic period. Chapters are presented in a logical progression beginning with the general appearance of normal brain and progressing to the way abnormalities manifest themselves on CT, MR, and US images. The emphasis in these discussions is on the appearance of edema and of hemorrhage, as these two findings are the brain’s most common response to injury. I discuss the role of contrast in central v

vi

Preface

nervous system (CNS) imaging, which will lead to a discussion of how infarction (death of tissue), ischemia (decreased blood flow to tissue that is still potentially alive and recoverable), and hemorrhage change with time as seen on CT, MR, and US images, and a dialog of what different patterns of injury tells us about the mechanism, severity, and duration of injury. This then permits a statement of what I consider the overriding principles of image interpretation as they relate to legal matters and a frank discussion, based on everything mentioned up to this point, of what can and what cannot be said in a medical–legal setting based on the imaging findings. The last chapter is on the root causes for uncertainty in dating neurologic events from imaging studies.

Acknowledgments

The following individuals were instrumental in helping me bring this book to publication. I wish to thank them all. • • • • • • • • •

Dr. James Scatliff and Dr. Robert Whaley - my Neuroradiology mentors at UNC in Chapel Hill The Vanderbilt radiology fellows and attending staff who assisted with case acquisitions The members of the Neuroradiology section at Vanderbilt who assisted me Dr. Jeanette Norton for her assistance in multiple revisions of the first chapter on anatomy. Janet Staley for her effort as an editorial and grammatical assistant who reviewed the entire manuscript several times prior to submission. Dominic Doyle for his preparation of the illustrations Administrative secretarial assistance from Tara Timmons, Debbie Holland and Dewain Patterson The Springer editorial staff in both New York and in India And most importantly, Lynn and our family, Erin, David, John and Carrie. They have continually supported me in my effort to write this book with their encouragement and understanding. It is to them that I dedicate this book.

vii

Contents

Part I Fundamentals 1 The Structure of the Normal Brain and Its Imaging Appearance.................................. Introduction............................................................................................................................ The Layers of the Scalp, Skull, and Meninges...................................................................... The Scalp........................................................................................................................... The Skull............................................................................................................................ The Epidural Space............................................................................................................ The Dura............................................................................................................................ The Subdural Space........................................................................................................... The Arachnoid Membrane and Subarachnoid Space......................................................... The Pia............................................................................................................................... The Visible Outer Surface of the Brain.............................................................................. The Imaging Appearance of the Normal Scalp, Skull, and Meninges............................... Brief Overview of Brain Anatomy......................................................................................... The Blood Supply to the Brain.............................................................................................. The Arterial Vessels........................................................................................................... The Venous Vessels............................................................................................................ Methods for Imaging the Intracerebral Arteries and Venous Structures............................ The Cerebral Hemispheres..................................................................................................... The Lobes of the Cerebral Hemispheres............................................................................ The Cortical Gray Matter................................................................................................... White Matter of the Cerebral Hemispheres....................................................................... Deep Gray Matter Nuclei of the Cerebral Hemispheres.................................................... Imaging Appearance of the Normal Cerebral Hemispheres.............................................. Cerebellum............................................................................................................................. Gray Matter of the Cerebellar Hemispheres...................................................................... Deep Cerebellar White Matter........................................................................................... Imaging Appearance of the Cerebellar Hemispheres........................................................ Brainstem............................................................................................................................... The Imaging Appearance of the Normal Brain Stem........................................................ Ventricles................................................................................................................................ The Ventricles – Normal Shape, Size, and Position........................................................... The Nonventricular CSF Spaces (Cisterns)....................................................................... CSF Dynamics................................................................................................................... Imaging Appearance of the Normal Ventricles, CSF Spaces,and CSF Dynamics............ References..............................................................................................................................

3 3 4 4 4 5 6 6 7 8 8 8 9 10 10 14 16 20 20 22 22 23 24 27 32 32 32 32 35 35 35 37 38 40 40

ix

x

Contents

2 The General Appearance of Edema and Hemorrhage on CT, MR and US (Including a General Introduction to CT, MR and US Scanning).................................. Introduction............................................................................................................................ CT Scanning: The Absolute Basics....................................................................................... MR Scanning: The Absolute Basics...................................................................................... US Scanning: The Absolute Basics....................................................................................... Edema.................................................................................................................................... Edema on CT Scanning..................................................................................................... Edema on MR Scanning.................................................................................................... Edema on US Scanning..................................................................................................... The General Appearance of Hemorrhage.............................................................................. Hemorrhage on CT Scanning............................................................................................. Hemorrhage on MR Scanning........................................................................................... Hemorrhage on Ultrasound................................................................................................ Chapter Summary.................................................................................................................. References..............................................................................................................................

43 43 43 45 47 48 51 52 52 53 54 55 55 57 58

3 The Basics of Contrast and Its Role in Dating.................................................................. Introduction............................................................................................................................ Basic Principles to Understanding the Use of Contrast in the Brain..................................... For CT Contrast................................................................................................................. For MR Contrast................................................................................................................ MR Contrast Dose and Pulse Sequence Choice.................................................................... MR Contrast Effects vs. Flow Void Effects........................................................................... Clinical Importance of Contrast Enhancement...................................................................... References..............................................................................................................................

59 59 59 61 61 62 62 67 67

4 How the Imaging Appearance of Edema and Hemorrhage Change Over Time on CT, MR, and US: Dynamic (Acute) Dating................................ Introduction............................................................................................................................ Changes of Edema Over Time on CT................................................................................ Changes of Edema Over Time on MR............................................................................... Locations of Possible Intracerebral Hemorrhage................................................................... Changes of Hemorrhage Over Time on CT....................................................................... Changes of Hemorrhage Over Time on MR...................................................................... T1 Changes Over Time Within a Hemorrhage on MR Scanning.......................................... T2 Changes Over Time Within a Hemorrhage on MR Scanning.......................................... FLAIR Changes Over Time Within a Hemorrhage on MR Scanning................................... Gradient Echo (Magnetic Susceptibility-Weighted) Changes Over Time Within a Hemorrhage on MR................................................................................................. Changes of Edema and Hemorrhage Over Time on US.................................................... References..............................................................................................................................

85 85 86

5 Patterns of Parenchymal Injury: Pattern (Chronic) Dating............................................ Introduction............................................................................................................................ Beginning Principles.............................................................................................................. Factors Affecting the Outcome of a Region of Ischemia....................................................... Regional Variations in Perfusion....................................................................................... Variations in Severity of Insult........................................................................................... Variations in Duration of Injury......................................................................................... Variations in Metabolic Activity........................................................................................

89 89 89 90 90 91 91 92

69 69 70 71 74 75 76 81 81 84

Contents

xi

Patterns of Parenchymal Injury.............................................................................................. 92 Patterns Where There Has Been Total Loss of a Focal Region of Brain Parenchyma.......................................................................................................... 92 Injuries That Affect the Brain Diffusely............................................................................ 94 Common Patterns That Show Targeting, with Partial or Total Cell Loss.......................... 95 References.............................................................................................................................. 100 Part II Application to the Medical-Legal Setting 6 Principles of Dynamic Dating in the Medical Legal Setting............................................ Introduction............................................................................................................................ General Comments on Dating an Event by CT and/or MR and/or US in the First 2 Weeks................................................................................................................ Dating Edema by CT Alone................................................................................................... Dating Hemorrhage by CT Alone.......................................................................................... Dating Edema by MR Alone.................................................................................................. Dating Hemorrhage by MR Alone......................................................................................... Dating Edema by US Alone................................................................................................... Dating Hemorrhage by US Alone.......................................................................................... Dating Events by CT in Conjunction with MR, and with US...............................................

103 104 104 105 106 107 107 107

7 Principles of Pattern Dating in the Medical Legal Setting............................................... Introduction............................................................................................................................ Concerning Edema and Infarction..................................................................................... Concerning Hemorrhage.................................................................................................... Conclusion.............................................................................................................................

111 111 111 113 115

103 103

8 Therefore, What Can Be Said Based on the Images, and What Can’t Be Said Based on the Images.................................................................. 117 Introduction............................................................................................................................ 117 9 The Root Causes of Uncertainty in Dating Neurologic Events Based on Imaging Findings............................................................................................................ Introduction............................................................................................................................ The Interpretation of the Available Images Varies from Expert to Expert, with Disagreement as to Whether Certain Findings Are Present or Not............................... Image Findings Are Acknowledged to be Present by All Observers; However, the Interpretation of the Findings Varies from Expert to Expert........................................... Multiple Findings are Present for Which the Neuroradiological Dating Methods We Have Discussed Produce Conflicting Time Periods as to the Probable Occurrence of the Injury........................................................................... Radiographic Findings Which Are at Odds with the Clinical Picture................................... Conclusion.............................................................................................................................

119 119 120 120 121 121 121

Index............................................................................................................................................ 123

Part I

Fundamentals

Chapter 1

The Structure of the Normal Brain and Its Imaging Appearance

Abstract This chapter is an introduction to the anatomy and terminology necessary for understanding the remainder of the book. It presents the names of the regions and structures of the brain, the various spaces of the intracranial compartment, the significant anatomy of the major structures that surround the brain, and the spaces that contain cerebrospinal fluid both within and around the brain. Because infarctions and hemorrhage are major topics discussed later in the book, this chapter places heavy emphasis on the vessels of the brain, normal vascular anatomy of the brain, normal vascular territories, and the various means of imaging these vascular structures. Keywords Brain • Brainstem • Cerebellum • Computed tomography (CT) • Magnetic resonance (MR) • Meninges • Neuroanatomy • Scalp • Skull • Spinal cord • Ventricles • Ultrasound (US)

Introduction This chapter’s anatomic discourse is intended to introduce to those unfamiliar with neuroanatomy the basic concepts necessary to understand the more detailed discussion which will follow. Topics to be covered in this chapter are: (1) layers of the scalp, skull, and meninges (the tissue coverings of the brain and spinal cord); (2) blood supply (arterial and venous); (3) the cerebral hemispheres; (4) the cerebellum; (5) the brainstem; and (6) the ventricles (fluid-filled cavities within the brain) and cerebral spinal fluid (CSF) dynamics. Clinicians, experts, or others with an existing, solid knowledge of neuroanatomy and the normal appearance of the brain on computed tomography (CT), magnetic resonance (MR), and ultrasound (US) may need only to skim this chapter as a review before beginning in earnest in Chap. 2. However, regardless of one’s level of familiarity with these topics, individuals who are unfamiliar with the basic terminology used to describe CT, MR, and US should briefly read the first section of Chap. 2 before tackling this chapter on introductory anatomy and the imaging appearance of the brain. Finally, before we proceed, we must briefly discuss the standard nomenclature for orientation of images. When referring to different cross-sectional images of the brain, three standard orientations are used. As a reference, if one uses a person standing, facing you, the viewer, then an axial plane is a section parallel to the floor – that is, perpendicular to the long axis that runs from the head to the feet. A coronal plane is at right angles to an axial plane and results in thin sections, as though one were viewing a small slice of the brain from the front. A sagittal plane is perpendicular to both of the previous planes and results in a thin section of the patient’s brain viewed from the side (Fig. 1.1). If images of a patient are initially obtained in one plane and then used to produce images in a different plane, the second set of images is said to be reformatted.

J.L. Creasy, Dating Neurological Injury: A Forensic Guide for Radiologists, Other Expert Medical Witnesses, and Attorneys, DOI 10.1007/978-1-60761-250-6_1, © Springer Science+Business Media, LLC 2011

3

4

1 The Structure of the Normal Brain and Its Imaging Appearance

Fig. 1.1 Anatomic planes. Oblique view of the head showing standard anatomic orientation of a coronal, a sagittal, and an axial (or transverse) plane

The Layers of the Scalp, Skull, and Meninges A discussion of normal brain and skull anatomy is best started with an explanation of the layers of tissue related to the skull, beginning most superficially and extending sequentially into the deeper and deeper tissues. Figure 1.2 is a graphical representation of the layers.

The Scalp The scalp is the outermost layer of the tissues of the head. Beginning superficially and progressing to successively deeper tissues encountered are the skin (epidermis and underlying dermis), a layer of fat, a layer of dense fibrous tissue (the aponeurosis), another thin layer of fat, and the periosteum, covering the outer surface of the bony skull. Clinical Note: Blood can collect between any of these layers. If it is located in the skin and underlying fat above the aponeurosis, it is termed a caput succedaneum. If located between the aponeurosis and the periosteum, it is a subgaleal hemorrhage. Lastly, if between the periosteum and the outer table, it is termed a subperiosteal hemorrhage – or, alternatively, a cephalohematoma [1].

The Skull The cranial portion of the skull, composed of bone, has a dense outer layer – the outer table – and a second dense inner layer, the inner table. Between the inner and outer tables is the diploic space, which contains fat and myeloproliferative elements – unlike the thicker, denser bone on either side. The myeloproliferative elements are constituents of the body which produce and are the precursors of white blood cells, red blood cells, and platelets.

The Layers of the Scalp, Skull, and Meninges

5

Fig. 1.2 Layers of the scalp, skull, and meninges. Intracranially, the space between the skull and the dura is the epidural space, the space between the dura and the arachnoid membrane is the subdural space, and the space between the arachnoid membrane and the pia membrane closely applied to the brain surface is the subarachnoid space. Cerebral spinal fluid (CSF) fills the subarachnoid space normally

The major bones comprising the sides and top portion of the skull are the frontal, parietal, temporal, and occipital bones. The underlying lobes of the brain take their names from the bones which overlie them. Sutures are the point of contact between adjacent bones. The paired coronal sutures are the line of connection between the frontal and parietal bones; the single midline sagittal suture is where the two parietal bones meet in the midline at the top of the skull and the posteriorly located, paired lambdoid sutures are where the occipital bone meets the parietal bone on either side. In the neonate the region in the anterior midline at the front of the sagittal suture is not yet completely fused, and this anterior fontanelle permits US examination of the brain up to about 1 year of age (when the fontanelle closes completely) (Fig. 1.3).

The Epidural Space The epidural space is a potential space; meaning that it has the possibility of existing, but in many normal individuals, does not. It is the space between the inside of the skull (or inner table) and the endosteal layer of the dura (the outermost connective tissue covering the brain) which has produced a periosteum, which is normally closely and firmly applied to the inner surface of the skull. In order for anything to occupy this space, this periosteum must be stripped (separated) from the inner table. Clinical Note: Blood collections in the epidural space most commonly occur as the result of a skull fracture, which ruptures blood vessels either in the skull or in the dura. As arterial pressure builds behind the blood and strips the periosteum from the inner table, a clot forms within the epidural space. Characteristically, blood in the epidural space has a biconvex shape, meaning both sides of the clot bow outward. This is due to the difficulty the clot has in stripping the dura from the inner table, so that the size of the hematoma is restricted and the margins of the hematoma are sharply defined.

6


Fig. 1.3 Bones and sutures of the skull. Side and top view of the skull showing the major flat bones which make up the calvarium – the frontal, parietal, temporal, and occipital bones; and the major connecting sutures – the coronal, sagittal, and lambdoid sutures

Since the dura is very tightly applied to the skull at the coronal, sagittal, and lambdoid sutures, epidural hemorrhages rarely cross cranial suture lines (Figs. 2.12 and 2.13).

The Dura The dura is the outermost, toughest, thickest layer of the meninges, which collectively are the three connective tissue layers that cover the brain. The meninges consist of the dura, the arachnoid membrane, and the pial membrane. The dura is further subdivided into an endosteal layer (firmly applied to the bone and producing a periosteum as described above) and a meningeal layer. These two portions of the dura are normally closely applied to each other throughout most of the inside of the skull. However, along the top of the skull and the rear of the skull on either side, the two layers separate and produce a venous drainage passage or dural sinus deep in the skull (Fig. 1.2). The inner portion of the dura also subdivides the major compartments of the brain. The inner meningeal layer of the dura is reflected inward, toward the center of the skull and forms two principal septae. The first, the tentorium cerebelli, runs horizontally, separating the occipital lobe of the cerebral hemispheres from the cerebellum and brainstem. The second, the falx, is a midline, vertically oriented layer of meningeal dura that separates the right from the left hemisphere. This separation is partial, as a side-to-side connection remains, represented by the major white matter tract of the corpus callosum (Fig. 1.4).

The Subdural Space The subdural space is the space between the meningeal layer of dura and the arachnoid membranes. This space is normally very small, with the potential to enlarge.

The Layers of the Scalp, Skull, and Meninges

7

Fig. 1.4 Dura. The dura consists of an endosteal layer and a meningeal layer. The endosteal layer is applied to the inner surface of the skull and forms the periosteum. The meningeal layer is normally fused to the endosteal layer, but is separated from the latter at locations of dural venous sinuses. It is the meningeal layer that turns inward toward the center of the skull, forming the two major septae – the midline falx cerebri structure which is attached superiorly to the skull but is open inferiorly, and the horizontally oriented tentorium cerebelli which separates the occipital lobe above the tentorium from the cerebellum and brainstem below

Clinical note: Hemorrhage within the subdural space can flow more freely over the cerebral hemispheres, but it does not flow down into the sulci (troughs) between the cortical gyri (the rounded, curved linear structures on the surface of the brain). It is not limited by suture lines and has a characteristic convex/concave shape – that is, the convex side hugs the inner table and dura and the concave side faces the brain below (Figs. 2.12 and 2.13).

The Arachnoid Membrane and Subarachnoid Space The arachnoid membrane is normally closely applied to the meningeal layer of dura. The subarachnoid space is located between the arachnoid membrane and the pia (which is closely applied to the brain surface) and is filled with cerebrospinal fluid. This space is important for several reasons. First, the arteries and cortical veins on the surface of the brain lie within this space. Second, it is the space into which aneurysms most commonly rupture. Next, it is also the space into which nonaneurysmal hemorrhage occurs, most commonly due to trauma. Finally, it is the space in which purulent material accumulates in a meningeal infection. Clinical Note: The most common cause (occurring 80–90% of the time) of subarachnoid hemorrhage in the nontraumatic patient is rupture of an intracerebral aneurysm (a weakened portion of an artery that has abnormally ballooned) [2]. However, overall, the most common cause of subarachnoid hemorrhage is trauma, as trauma is a much more common entity than aneurysmal rupture. Therefore, the CSF can become bloody both from aneurysm rupture and from head trauma. The subarachnoid space can also be filled with inflammatory cells in cases of meningitis (infection or inflammation of the meninges) and in most cases of cerebritis (infection or inflammation of the brain). Other causes of dense CSF include proteinaceous inflammatory fluid or frank pus from a truly fulminate bacterial infection. The subarachnoid space over the hemispheres freely communicates with the subarachnoid space around the spinal column and with the CSF within the ventricles (fluid-containing cavities

8


within the brain) via small holes in the fourth ventricle, called the foramen of Magendie and Luschka (see Fig. 1.37). Finally, the arterial vessels that supply the brain, as well as the cortical veins that drain blood from the brain, run within the subarachnoid space. As the incoming arterial vessels branch progressively smaller, they remain on the surface of the brain until they reach a small size, at which point they penetrate the surface of the brain, carrying with them in a circumferential fashion a contiguous extension of pia and the subarachnoid space. This extension of the subarachnoid space around the penetrating arteries and draining veins is called the Virchow–Robin space. The fluid within this space is CSF.

The Pia This, the last and deepest layer of the meninges, is a thin layer closely applied to the surface of the brain.

The Visible Outer Surface of the Brain The outermost part of the brain surface is composed of a thin mantle of cortex. The cortex is made up of cells, both neurons and their supporting elements of several different cell types, all collectively referred to as glial cells. Because in the fresh brain the neurons on the surface appear gray, the cortex is also referred to as gray matter. Just below the cortex, the tissue that is the axons of neurons – each one surrounded by a fatty sheath – interconnects different portions of the brain. Since these nerve sheaths appear “white” in the fresh brain, they are referred to as white matter. The cellular organization of the brain will be discussed in more detail in the section on the cerebral hemispheres, below.

The Imaging Appearance of the Normal Scalp, Skull, and Meninges In general, different elements of the scalp, skull and meninges show up differently on the two major imaging methods: CT and MR. CT demonstrates bony structures better than MR scans. MR is superior in the demonstration of the soft tissues of the scalp superficially and of the meningeal structures that are deep to the cranium. On CT, beginning most superficially in the scalp, a thin, dense (bright) line represents the skin or dermis. Deep to this is a predominantly fat layer of variable thickness that has low density – a CT number of less than zero (for more information on CT numbers, see the introduction to CT at the beginning of Chap. 2). Immediately deep into the subcutaneous fatty tissue is another dense, fibrous layer that is intimately applied to the outer surface of the skull. Due to its thinness, this structure is usually not discretely imaged. The thick, protective top and sides of the skull consist of both an inner and an outer layer (or table) of dense bone, which appear on CT as an inner and an outer white line, separated by an interposed lower density, more lucent (darker) line that is the diploic or marrow space. The contents of the diploic space are cellular and may represent fatty marrow, and thus the CT numbers can be fairly low. Even if a contrast agent is administered, it is difficult to image the dura on the inner surface of the inner table. Similarly, the pia and arachnoid are not easily visualized on CT scanning. The subarachnoid space, with the black (i.e., low density) CSF filling

Brief Overview of Brain Anatomy

9

Fig. 1.5 Appearance of layers of scalp and skull. Axial computed tomography (CT) with (a) brain windows, (b) soft tissue windows, and (c) bone windows. Even with intravenous contrast (not given in this case), the dura is not visible. Axial magnetic resonance (MR) scans – (d) T2-weighted, (e) FLAIR, (f) T1-weighted without contrast, and (g) T1-weighted with contrast. The major layers of the scalp including the fat-containing dermis, the outer table of the skull (ot), the diploic space (ds), the inner table of the skull (it), and the dura on the inside surface of the skull. In G, the enhancing dural structures are visible

the cortical sulci (clefts between the gyri) as well as the basilar cisterns, is usually well seen (CT of these structures – Fig. 1.5a–c). MR scanning is unlike CT in that no radiation is used, only radio waves and a high-strength magnet. On MR, the soft tissues of the scalp will be bright on both T1- and T2-weighted imaging. (The terms T1- and T2-weighted refer to specific types of MR sequences. A more complete introductory description of MR will be given at the beginning of Chap. 2.) If fat saturation is employed with either of these pulse sequences, the fatty tissues will appear dark. As for bone, on all pulse sequences bone has no signal, so both the inner and outer tables will show up as black lines. The diploic space contains cellular elements (including fatty tissue) and, therefore, will have some brightness on both T1- and T2-weighting. The dura is best seen only after a contrast agent has been administered. It is important to note that mild degrees of dural enhancement are much better visualized on MR than CT, as in MR one is trying to visualize an enhancing white line next to the black inner table – this is markedly easier to see than the thin, white enhancing line on CT next to another white line of the inner table dense bone (MR of these structures – Fig. 1.5d–g).

Brief Overview of Brain Anatomy Before beginning a discussion of intracranial arteries and veins, and later CSF spaces – even before a more detailed discussion of the cerebrum, cerebellum, and brainstem – it is appropriate to briefly name the major brain substructures. The accompanying diagram shows the CNS

10


Fig. 1.6 Basic layout of the brain and skull base. (a) View from the side and (b) view from the top, with the top of the skull and the brain removed – looking down at the bony skull base. The cerebrum, brainstem, cerebellum, and spinal cord are labeled and shown in relation to the head and skull. For reference, other key intracranial structures such as the foramen magnum (the opening at the base of the skull where the brainstem meets the spinal cord and enters the spinal column), the pituitary fossa or sella (within which is the pituitary gland), the three (anterior, middle, and posterior) paired intracranial fossae, and the eyes or orbits are indicated. Lastly, directional terms are included, such as anterior (to the front), posterior (to the rear), midline (in the sagittal center of the body), and lateral (extending away from the midline)

structures of cerebrum, brainstem, cerebellum, and spinal cord in relation to the head and skull. For reference, other key intracranial structures, such as the foramen magnum (the opening at the base of the skull where the brainstem meets the spinal cord and enters the spinal column), the pituitary fossa or sella (within which is the pituitary gland), and the eyes, or orbits, are drawn. Lastly, directional terms, such as anterior (to the front), posterior (to the rear), midline (in the sagittal center of the body), and lateral (extending away from the midline) are demonstrated (Fig. 1.6).

The Blood Supply to the Brain The Arterial Vessels The vessels that bring blood to the brain consist of a system of larger arteries steadily narrowing to medium vessels, to progressively smaller caliber vessels, all of which lie in the subarachnoid space around the brain. At some point, when arterial vessels are small enough, they penetrate the brain surface, traveling radially from the outside in an inward direction to supply the brain tissue. Upon reaching their target, the arteries continue to branch into smaller and smaller arteries, then arterioles and, finally, a capillary system. Nutrients pass from the blood stream to the cells of the brain at the capillary level. These small blood vessels then reaggregate into venules, small veins, and then progressively larger veins. The arterial supply to the brain is divided into the anterior circulation, made up of the right and left internal carotid arteries (or ICAs) and their branches on either side and the posterior circulation, or vertebro-basilar system (Figs. 1.7 and 1.8) [3, 4].

The Blood Supply to the Brain

11

Fig. 1.7 Major intracerebral arteries. These four views are diagrammatic representations of the appearance of the intracranial major arteries as viewed from an anterior (from the front) projection (a, c) and from a lateral (from the side) projection (b, d). Major intracranial branches of the right internal carotid artery (R ICA) viewed from the front (in (a)) and from the side (in (b)). Major posterior vessels viewed from the front (in (c)) and from the side (in (d))

The anterior intracranial circulation is made up of the right and left ICAs, which enter the skull base, passing up through the cavernous sinus (a venous structure located on either side of the pituitary gland in the very central aspect of the skull base). Just above the cavernous sinus each ICA bifurcates into an anterior cerebral artery (ACA) and a middle cerebral artery (MCA). The MCA passes laterally into the Sylvian fissure and, near its lateral extent, bifurcates into multiple branches which supply the lateral aspect of the brain. The ACA passes antero-medially forward from the terminus of the ICA and, immediately in front of the pituitary region, a short linking artery, the anterior communicating artery (AComm), connects the right and left ACAs. Beyond this the ACAs continue, first forward and then up over and posteriorly over the corpus callosum (Fig. 1.7). Posteriorly, the major arteries are the right and left vertebral arteries and the single artery they create when they fuse at or near the base of the brain: the basilar artery. The basilar artery then proceeds superiorly in front of the brainstem until it reaches its terminus, the basilar summit. The blood supply for the cerebellum, brainstem, the rear of the cerebral hemispheres (the occipital and temporal lobes), and a portion of the deep structures within the cerebral hemispheres arises from this vertebrobasilar system. At, roughly, the level of the foramen magnum at the base of the skull, before they join to create the basilar artery, each vertebral artery gives rise to a posterior inferior cerebellar artery (PICA), which supplies the inferior portions of the cerebellar hemispheres and a portion of the medulla. The basilar artery gives rise to the anterior inferior cerebellar artery (AICA), supplying the midportion of the cerebellar hemispheres and, just below the terminus of the basilar artery, to the bilateral superior cerebellar arteries (SCAs) that feed the superior aspects of the cerebellar hemispheres. At its terminus, the basilar tip bifurcates into the two posterior cerebral arteries (PCAs). Between the major arteries of the anterior and posterior circulations, one pair of connecting vessels, the right and left posterior communicating arteries (or PComm), travels from the distal portion of

12


Fig. 1.8 Circle of Willis. The circle of Willis, if complete, is a ring of vessels that connect the internal carotid (anterior) to the vertebro-basilar (posterior) circulation. This ring is often incomplete, as different segments of the ring may be absent in the normal individual. The right half of the circle, beginning posteriorly, starts at the tip of the basilar artery (ba) and proceeds clockwise through the proximal portion of the right posterior cerebral artery (PCA) or P1 segment (R P1), the right posterior communicating artery (PComm), the top end of the R ICA, the proximal portion of the right anterior cerebral artery (ACA) or A1 segment (R A1) and, finally, in the midline anteriorly, the anterior communicating artery (AComm). Similar labels apply to the left half of the circle of Willis. The shaded regions (A1 segment, PComm, P1 segment) denote the most commonly absent segments

the ICA backward to the early portion of the PCA on the same side. In this fashion, potentially, a circle of blood vessels lies at the base of the brain. Known as the circle of Willis, it is composed of the basilar tip itself and then, presuming one were viewing the circle of Willis from above, would consist of the proximal portion of the PCA and the PComm on the left, the distal aspect of the left ICA, the left ACA between the ICA terminus and the AComm (otherwise known as the A1 segment of the ACA). Following the AComm itself are the right A1 segment of the right ACA, the terminus of the right ICA, the right PComm and, finally, the proximal portion of the right PCA, which once again connects to the basilar artery terminus (Fig. 1.8 – Line drawing of circle of Willis). However, it should be noted that, in the vast majority of patients, the circle of Willis is incomplete, with the most common absences being lack of a P1 segment of the PCA (from the basilar terminus to the PComm), lack of a PComm, or lack of an A1 segment of the ACA (from the ICA terminus to the AComm) (see shaded vessel portions in Fig. 1.8). In fact, only about 30% of people have an absolutely, completely intact circle of Willis [5]. This fact is relevant to our discussion of ischemia and infarction, as an intact circle of Willis allows shunting of blood to a region of brain that would otherwise progress to infarction. For example, an individual may have a sudden occlusion of the right ICA in the neck, but if, via an intact circle of Willis, blood can flow into the right ACA via the AComm from a normal left ACA, or into the very superior right ICA (and, thence, into the right ACA and right MCA), from a patent right PComm, then an infarction may not occur. On the other hand, a person with an acute right ICA occlusion, who has absence of the right A1 segment of his right ACA and an absent right PComm, is doomed to have a large infarction of the effectively isolated entire MCA territory. Preexisting vascular anatomy


13

is, therefore, one important factor in determining both if an infarction occurs and, if so, the severity of the injury. The vascular territories of the supratentorial portion of the brain (that portion of the brain – the cerebrum – that sits above the tentorium cerebelli) are supplied by the anterior, the middle and the PCAs. The ACAs normally supply a wedge-shaped portion of the frontal lobe, beginning at the midline, and extending laterally to involve a wedge-shaped region of the brain. This ACA territory begins inferiorly at the floor of the frontal fossa and then extends up superiorly, narrowing as it gets more posterior and ending in a stripe several centimeters wide that extends posteriorly in a parasagittal location to near the level of the rear of the corpus callosum. The PCA, similarly, mainly supplies a triangular-shaped region of brain occupying the occipital lobe, beginning at the midline and extending laterally, and then extending up over the posterolateral surface of the brain to meet the rear portion of the ACA distribution. The inferior surface of the temporal lobe, beginning just behind the temporal tip and extending all the way back to the occipital lobe, is also supplied by posterior temporal branches of the PCA. The MCA territory occupies the area laterally in the hemisphere bounded by the anterior circulation anteriorly and superiorly, and the posterior circulation posteriorly and inferiorly. The MCA territory includes the majority of the posterior portions of the frontal lobe, lateral portions of the parietal lobe, and the anterior and superior portions of the temporal lobe. The MCA, therefore, supplies the majority of the lateral portion of the cerebral hemispheres (Fig. 1.9 – Line drawing of supratentorial vascular territories). In the posterior fossa (that portion of the brain – brainstem and cerebellum – that lies under the tentorium cerebelli), the PICA vessels supply portions of the medulla, as well as the inferior portions of the cerebellar hemispheres. The SCA supplies the superior portion of the cerebellar hemispheres. The AICA arteries supply the midequatorial portions of the cerebellar hemispheres. The blood supply to the majority of the brainstem comes directly from the basilar artery itself (Fig. 1.10 – Line drawing of infratentorial vascular territories). Clinical Note: Occlusions of any one of these named vessels or one of their branches above or below the tentorium cerebelli result in a geographic, sharply demarcated infarction (region of cell death), which includes all the tissues (grey and white matter) in the involved vascular supply. Such an

Fig. 1.9 Supratentorial arterial vascular territories. The anterior, middle, and PCA territories are indicated by shading. The ACA territory begins inferiorly as a wedge-shaped portion of the frontal lobes and extends superiorly as a band along the midline medial portion of the hemisphere. The middle cerebral artery (MCA) territory is the lateral aspect of the hemisphere beginning at the temporal tip and extending upward and backward until it reaches the anterior circulation territory anteriorly and superiorly and the posterior circulation posteriorly. The posterior cerebral territory is a wedge at the rear of the brain in the occipital lobe extending forward to meet the anterior and MCA territories. It includes the inferior aspect of the temporal and occipital lobes except for the temporal tip

14


Fig. 1.10 Infratentorial arterial vascular territories. The major vascular territories in the posterior fossa are those supplied by the right and left posterior inferior cerebellar artery (PICA), anterior inferior cerebral artery (AICA), and superior cerebellar artery (SCA) and by smaller vessels arising directly from the basilar artery. The PICA territory is the inferior aspect of the cerebral hemispheres and portions of the postero-lateral medulla. The AICA supplies the midportion of the cerebellar hemispheres, while the SCA supplies the superior aspect of the cerebellar hemispheres. The majority of the blood to the brainstem (midbrain, pons, and medulla) itself is from small vessels that originate directly from the basilar artery

infarct is said to be arterial in nature, as it follows well-defined arterial vascular territories. The severity of a total arterial occlusion also depends on the amount of collateral blood flow that reaches the region deprived of blood by occlusion of its normal primary supplying vessel. Additional factors affecting the extent of the infarction will be discussed in Chap. 5.

The Venous Vessels Venous vascular anatomy is a complement to the arterial system, but does not merely duplicate each vessel. The venous drainage system is different in two important ways. First, there is no venous intracranial counterpart to the major arteries comprising the anterior, middle, and cerebral arteries. In order words, the arterial territories supplied by the arteries are different from the venous territories drained by the veins and dural sinuses. Second, unlike the feeding arteries which all follow the same general pattern, once the blood is collected into medium and large veins, two functionally and anatomically distinct venous drainage systems exist – the deep, central midline venous system and the system that consists of the cortical veins and dural venous sinuses [6, 7].


15

Fig. 1.11 Deep (midline) venous system. The major components, directly in the midline, with blood flowing from anterior to posterior, are the internal cerebral veins, the short vein of Galen, and the straight sinus. Contributing to these midline veins, the paired thalamostriate veins flow forward in the lateral ventricle, going through the foramen of Monro and then joining the septal veins to create the internal cerebral vein. More posteriorly, the basal veins of Rosenthal drain the lateral ventricles and, together with the internal cerebral veins, form the Vein of Galen

In the deep system (Fig. 1.11), as the blood collects from the capillaries into small venules and then into larger veins, the brain drains centrally inward at right angles to the surface of the ventricles in the medullary veins. These veins, in the walls of the body of the lateral ventricles, collect blood that flows forward toward the foramen of Monro and then posteriorly in the roof of the third ventricle as the internal cerebral vein. This system is duplicated on both sides. Upon reaching the rear of the third ventricle, these veins are joined by the right and left basal veins of Rosenthal, which drain the temporal lobes, and this set of four veins collectively form the vein of Galen. This midline, normally short, one-centimeter vein swings upward and posteriorly and continues inferiorly and posteriorly as the straight sinus that extends all the way to the rear of the skull, joining the superior sagittal sinus at the confluence of the sinuses. The second venous drainage pattern involves veins that radiate outward toward the surface of the brain (Fig. 1.12). On the surface of the brain, the cortical veins collect to form increasingly larger veins. These larger cortical veins then drain superiorly into the superior sagittal sinus and laterally and posteriorly into the transverse sinus. For these cortical veins to reach the dural sinuses (channels formed between the endosteal and meningeal layers, or twofolds of meningeal dura), they must cross the intervening subarachnoid space. The veins which traverse these spaces are the bridging veins, which are susceptible to injury from a number of causes and which, if injured, can result in bleeding into the subarachnoid space. Thus, whether the cortical veins are small or one of the larger, named cortical veins, they all, via bridging veins, drain into the superior sagittal sinus, other dural sinuses or smaller venous plexuses around the skull base centrally. The largest dural venous sinus is the superior sagittal sinus, which runs from the frontal region to the confluence of the sinuses in the midline of the skull posteriorly. This superior sagittal sinus has a triangular cross-section, with all three sides formed by layers of dura (Fig. 1.2).

16


Fig. 1.12 Major cortical veins and dural venous sinuses. The diagram demonstrates the major dural venous sinuses: the superior sagittal sinus, the inferior sagittal sinus, the transverse sinuses, the sigmoid sinuses, and the straight sinus. In addition to these major dural venous sinuses are numerous cortical veins, the largest of which are the superiorly located and draining vein of Trolard, which drains in the superior sagittal sinus, and the laterally oriented vein of Labbe, which drains into the transverse sinus

The other significant large dural venous sinus begins where the sagittal sinus joins the straight sinus at the confluence of the sinuses, then splits and runs horizontally on both sides at the junction of the tentorium and the inner table as the left and right transverse sinus. Upon reaching the postero-lateral corner of the skull, this sinus turns downwards in an “S” shaped curve (hence called the sigmoid sinus) and forms the jugular bulb, which is the beginning of the internal jugular vein on each side. Clinical Note: Occlusions of dural venous sinuses have a propensity to cause venous infarcts due to blockage of venous outflow. Unlike a typical arterial occlusion, a clot within the superior sagittal sinus can cause an infarct on both sides of the midline. Similarly, a clot of a transverse sinus can cause infarcts or ischemia (decreased blood flow that has not yet progressed to infarction) in territories that cross the MCA and PCA territories, or even cause infarctions both above (in the occipital lobe) and below (in the cerebellum) the tentorium. Venous infarcts are also more prone to hemorrhage than arterial infarcts. An interesting imaging correlation of venous occlusion is that symptomatic venous thrombosis (occlusion of a blood vessel caused by an intraluminal blood clot) in the head is almost always accompanied by signal changes on MR [8]. Occlusions and thromboses of the central deep venous system cause abnormalities involving the deeper, more centralized portions of the brain, usually including the basal ganglia.

Methods for Imaging the Intracerebral Arteries and Venous Structures One has a number of options in imaging the intracerebral arteries and veins, including traditional catheter angiography, routine CT scanning, computed tomography angiography (CTA), routine MR imaging and magnetic resonance angiography (MRA), and magnetic resonance venography (MRV). Each of these modalities has strengths and weaknesses, relative indications and, consequently, each images the intracerebral arteries and veins to different degrees and clarities. Table 1.1 compares these five methods of imaging based on whether contrast is utilized or radiation is employed


17

Table 1.1 Five methods of angiographic imaging Method

Imaging used

Contrast

Invasive

Best used for

Significant artifacts

Catheter angiography

X-rays

Yes

Arterial anatomy

No

CTA CTV MRA MRV

CT CT MR MR

Yes Yes No No

Yes, requires vessel catheterization Yes, IV only Yes, IV only No No

Arteries Veins Arteries Veins

No No Yes No

and provides a relative rating of ease of visualization of the major veins, dural venous sinuses, and arterial structure. Traditional catheter angiography is performed by the sterile and fluoroscopically guided introduction of a small tube into a peripheral artery, usually the femoral artery at the groin. The catheter is directed retrograde up the descending aorta and then selectively into the vessels in the neck that feed blood to the brain, either the ICAs or the vertebral arteries. Following contrast injection, films are made about the head in various projections. This oldest and most traditional method of examining the vascular system in the brain carries with it several risks which fall into three categories: (1) risks associated with the contrast agent, (2) risks associated with injury to the femoral artery at the site of the puncture, and (3) risks associated with embolic or thrombolic processes occurring from the end of the catheter. A true anaphylactic reaction (i.e., a life-threatening, heart stopping, hard-to-breathe reaction to a chemical agent) can conceivably occur with any iodinated contrast (a contrast agent containing iodine – used for traditional catheter angiography, CTA and contrasted CT exams) administration. Complications that can arise at the site of the puncture include transection of the femoral artery, laceration of the femoral artery resulting in local hematoma, and induced arterio-venous fistulas (an abnormal direct connection between an artery and a vein). Complications occurring from the end of the catheter usually relate to the catheter tip displacing plaque or producing distal emboli (any substance – clot or arterial wall plaque – that forms in one part of the arterial system and travels along the blood vessel, eventually lodging and completely occluding the vessel more distally). Thrombus (arterial occlusion that occurs by a clot forming at a stationary place in the blood vessel without traveling distally) can also occur at the end of the catheter and can distally embolize into the brain, causing strokes or infarctions. Traditional catheter angiography excels at visualizing arteries of the intracranial vasculature. It is relatively less efficient at visualizing the cortical veins and the dural venous sinuses. CT, when not performed in a way to specifically image the vessels (that would be CTA), can, nevertheless, provide visualization of the intracranial vasculature. Gross lesions of the dural sinuses or arteries often cannot even be seen on routine CT without contrast, but the sensitivity is markedly increased by performing CT with contrast. However, the best manner in which to use CT to visualize the vasculature is to perform a specialized CTA examination. This employs a bolus administration of contrast material injected into a peripheral vein (as opposed to directly injecting it into an intracerebral artery) and using the special capabilities of a modern rapid CT scanner to image multiple thin sections through the region of interest, in this case the brain. This type of examination eliminates complications associated with the arterial puncture and with the catheter, though it retains the possibility of complications due to contrast administration and the ionizing radiation. Because of the relative lack of complications, CTA is becoming the method of choice for visualization of the intracranial vasculature. Numerous reports are now citing the utility of CTA for detecting atherosclerosis, vasospasm, arterial injury, arterial thrombosis, and intracranial aneurysms.

18


Routine MR (without using specialized MRA sequences) is also useful for visualizing gross vascular anatomy. On a routine MR sequence, patent (open) vessels with good flow will show up as areas of signal flow voids (the lumens of patent vessels will appear black). This aspect of MR can be used to demonstrate that a vessel is not occluded. This is velocity sensitive and works best for rapidly flowing blood; hence, flow voids are easier to visualize in intracerebral arteries than they are in intracerebral venous structures. If specific visualization of the vasculature is required, it is helpful to perform a specialized MRA examination, which visualizes the intracranial arteries. The intracranial veins and dural sinuses can be removed by appropriate saturation bands. Similarly, if it is desired to specifically visualize the intracranial venous structures, one can remove the arterial structures by using saturation maps, which produces an MRV. The accompanying figures give demonstrations of these five methods of visualizing the intracranial arteries, veins, and dural venous sinuses (Figs. 1.13–1.17).

Fig. 1.13 Catheter angiography of intracranial arteries; typical catheter angiograms of the intracranial circulation. Angiograms are of the posterior circulation in (a–c) and of the anterior circulation in (d, e). (a) Early arterial phase of an anterior–posterior projection image from an injection of the left vertebral artery. (b) Late arterial phase of an anterior-projection image from an injection of the left vertebral artery and (c) lateral projection from an injection of the left vertebral artery. (d) Anterior–posterior projection image of the head from an injection of the left internal carotid artery in the neck, and (e) lateral projection image of the head from an injection of the left internal carotid artery


19

Fig. 1.14 Computed tomography angiography (CTA) of intracranial arteries. (a) Axial source (0.8 mm) single slice from the original data acquisition. (b) Fused axial 3 mm thick slices. (c) Coronal 10 mm thick slices. (d) Anterior 3D surface reconstructions of the entire data set. (e) Superior view of same data set. The major labeled arteries are labeled by the conventions in Figs. 1.6 and 1.8

Fig. 1.15 CTA of the veins and sinuses. Images were produced from CTA source images acquired in the later (more venous) phase. (a) Sagittal reconstruction of the image data at 25 mm-slice thickness. (b) Coronal 10 mm-thick reconstruction at the level of the internal cerebral veins and superior sagittal sinus. (c) Coronal reconstruction more posteriorly through the level of the transverse sinuses

20


Fig. 1.16 Magnetic resonance angiography (MRA) of the intracranial arteries. (a) Axial source images. (b) MIP reconstruction in the anterior–posterior direction. (c) Lateral MIP reconstruction as viewed from the side (MIP stands for maximum intensity projection – a technique for generating images similar to traditional catheter angiograms from axial source images.)

Fig. 1.17 MRV of the intracranial veins and sinuses. This technique is slightly different from the routine intracranial MRA in that the images are usually obtained in the coronal plane. (a) Coronal source images. (b) MIP reconstruction in the anterior–posterior direction. (c) MIP reconstruction in the lateral view

The Cerebral Hemispheres The Lobes of the Cerebral Hemispheres The cerebral hemispheres are organized into lobes (Fig. 1.18). The developmental embryology behind the lobes is far beyond the scope of this book, but, at a descriptive level, the traditional lobes of the hemispheres are the frontal, parietal, temporal, and occipital lobes – each taking its name from the bones that overlie them. However, some texts will also discuss the insular region as a unique portion of the brain, a portion that is not visible from the surface. Certain functions of the central nervous system localize within each lobe of the brain; those gross localizations of specific functions will be discussed in our anatomic survey [9–11].

The Cerebral Hemispheres

21

Fig. 1.18 Lobes of the brain and functional localizations. Lateral (in (a)) and medial (in (b)) views of the brain show the frontal, parietal, temporal, and occipital lobes. Superimposed on these regions are the important functional regions of the brain related to motor activity, sensory activity, hearing, speech, vision, and memory

The brain consists of two paired cerebral hemispheres, each a mirror image of the opposing side. Each consists of four lobes and the insular region and each has, with one important exception, fairly rigidly defined margins. The exception occurs on the lateral posterior surface of the hemisphere where the posterior temporal, parietal, and lateral occipital lobes all join. Each frontal lobe occupies the most anterior portion of the intracranial compartment and is the largest lobe of the cerebrum in humans. When viewed from the side or top of the brain, the rear margin of the frontal lobe is a major sulcus called the central sulcus. The central sulcus runs from the midportion of the Sylvian fissure (the large infolding in the lateral surface of the brain which separates the frontal lobe above from the temporal lobe below) up over the lateral aspect of the brain to near the midline. The most posteriorly located gyrus in front of the central sulcus is termed the precentral gyrus, which has the important function of being the motor cortex (the area in which motor movement is initiated). On the medial surface of the brain, the frontal lobe extends all the way back to the counterpart of the central sulcus called the angular sulcus. This defines the rear of the frontal lobe and the front of the parietal lobe. The temporal lobe, best viewed from the lateral side of the brain, composes that portion of the cortex that is below the Sylvian fissure. The front of the temporal lobe is rounded and lies in the middle cranial fossa (Fig. 1.6). The rear of the temporal lobe, where it merges into the parietal and the occipital regions, is less well defined. Important functions localized to the temporal lobe include speech on the lateral surface; regions important for memory, including a structure called the hippocampus, are located on the medial surface. The occipital lobe is the most posterior portion of the cortex. It is demarcated anteriorly on the medial surface by the parietal occipital fissure that separates the occipital lobe from the parietal lobe. On the lateral surface of the brain, the point at which the occipital lobe joins the temporal lobe inferiorly and the parietal lobe more superiorly is less well defined. The important function that localizes in the occipital lobe is vision, as the primary visual cortex (also called the calcarine cortex) is located primarily on the medial surface. The parietal lobe is demarcated on the medial aspect of the cerebral hemispheres by the parietal occipital sulcus posteriorly and by the angular sulcus anteriorly. On the lateral surface of the hemispheres the central sulcus forms the anterior margin of the parietal lobe. The more posterior and more inferior edges where the parietal lobe merges into the occipital lobe and temporal lobe, respectively, are less well defined. The most anterior gyrus of the parietal lobe, as it sits behind the central

22


sulcus on the lateral surface of the brain, is termed the postcentral gyrus and is concerned with the sensation of touch, referred to as the somato-sensory cortex. The last major cortical region is the insula or insular cortex. This portion of cortex forms the upper (from the inferior frontal lobe) and lower (from the upper temporal lobe) boundaries of the Sylvian fissure. At the deepest portion of the Sylvian fissure is additional cortex – contiguous with both the frontal and temporal lobes – that lies just lateral to the basal ganglia. None of this cortex is visible from a lateral view of the brain, but is best seen as a “T” shape on its side on coronal sections – in essence, it is cortex buried within the Sylvian fissure. In addition to the localization of function mentioned above on each of the lobes, the general concept of eloquent vs. noneloquent brain should be addressed. Eloquent brain is that which is closely tied to a specific, measurable neurologic function, such as speech, hearing, vision or motor, or sensory control of a specific part of the body. Lesions in each of these areas will cause an easily defined clinical deficit. These areas of the brain collectively make up only a small percentage of the cortical surface. Much larger areas of brain are devoted to secondary or higher-order associative functions. For example, the primary visual cortex in the calcarine area allows one to see, but the interpretation of vision and the correlation with other things such as memory occur in secondary and tertiary-associated visual areas. A lesion in one of these areas can be more clinically subtle than a lesion in one of the primary or more eloquent areas of brain. These gross localizations of the brain, as well as indicated areas of important function, are shown in Fig. 1.18.

The Cortical Gray Matter Within any lobe of the brain, the more detailed (i.e., microscopic) anatomy of the cerebral hemispheres shows that they are composed most superficially of a layer of cortex, or gray matter. This gray matter represents a majority of the neuronal cell bodies of the cerebral hemispheres with the exception of those seen in the deeper nuclei, discussed below. A neuron is the major interactive, computational component of the central nervous system. Functionally, a neuron consists of a central cell body which contains the nucleus of the cell, an array of processes (called dendrites) that extend out from the cell body and receive input from other cells, and an axon which transmits electrical impulses to other neurons. The axon is surrounded by a sheath of myelin, which enhances nerve conduction speed and is produced and maintained by nonneuronal cells called oligodendrocytes. These oligodendrocytes are one cell type of many included in the classification of glia – a classification which also includes astrocytes and microglial cells. The astrocytes are felt to produce and maintain the cytochemical supporting architecture of the brain – both normally and postinjury. Microglial cells are thought to participate in the removal of dead cellular material. A diagram of these cell types is shown in Fig. 1.19 [12, 13].

White Matter of the Cerebral Hemispheres The white matter in the cerebral hemispheres is located deep to the cortex and functionally can be thought of as the wiring that connects cortex to cortex and to other structures. Many white matter tracts originate in one portion of the cortex and extend to other portions of the cortex, or to deep nuclei, the brainstem or all the way down to the spinal cord. At that point, the white matter fiber tracks (axons) join and synapse with additional nerve cell nuclei (a collection of neuron cell bodies) and pass out of the spinal cord and the spinal canal as peripheral nerves to supply both motor and sensory function to the remainder of the body. Usually not just one, but several synapses can occur between a cortical neuron and the final termination of a string of connected neurons that end in bodily tissue.


23

Fig. 1.19 Cellular elements of the brain (neurons, oligodendrocytes, astrocytes, microglia). This diagram demonstrates a simplification of the complex network of neurons and their supporting elements. A single neuron has been highlighted. Note its extensive dendritic processes connecting with other neurons, as well as its single long axon which can connect locally or distally to additional neurons

Deep Gray Matter Nuclei of the Cerebral Hemispheres The deep nuclei of the cerebral hemispheres are paired structures, symmetric about the midline, with the most important and radiologically visible ones being the caudate and the lentiform nucleus (composed of the globus pallidus and the putamen). Many images will also include the thalamus as part of the “deep gray matter,” although, unlike the aforementioned structures, it is of different embryologic origin. Regardless of their developmental origin, all of these structures are composed predominantly of gray matter [14, 15]. The blood supply to the basal ganglia region does not arise solely from branches of the main supratentorial vessels. Instead, portions of the basal ganglia are fed directly from the M1 segment of the MCA, from vessels arising off of the basilar tip and from the P1 segments of the PCA. The caudate is a gray matter structure with a curved, comet shape. The largest portion is the head of the caudate, located anteriorly and nestled in the postero-lateral aspect of the anterior end of the lateral ventricle. The body of the caudate tapers considerably as it extends upwards and posteriorly over the body of the lateral ventricle, ending near the rear of the lateral ventricle. The lentiform nucleus consists of a lateral putamen and medial globus pallidus, which, together, are in the shape of a very fat, broad-based lens. The apex of the lens, which points medially, is the globus pallidus,

24


Fig. 1.20 Deep nuclei of cerebral hemispheres. This oblique view shows the relationship of the deep nuclei of the cerebral hemispheres to the midline, the ventricles, and the cortical surface. On either side of midline, the claustrum, caudate, amygdala, putamen, and globus pallidus together are the deep nuclei of the hemispheres. The thalamus is an additional grey matter structure on either side of the third ventricle but, unlike the deep nuclei, it is not of hemispheric origin

the broader lateral aspect is the putamen. The internal capsule sits around the medial apex of the lentiform nucleus and resembles a “V” in axial cross-section, with the apex of the V situated medially. This is a white matter structure containing a large number of long tracts, some of which ascend toward the cortex and some of which descend from the cortex to the more inferior parts of the brain and spinal cord. The thalamus is composed of many nuclei and sits medially to the posterior limb of the internal capsule. Many of the thalamic nuclei are important way-stations for most of the primary sense functions, such as vision and hearing. These structures are demonstrated in Fig. 1.20.

Imaging Appearance of the Normal Cerebral Hemispheres The imaging appearance of the cerebral hemispheres presented here will follow closely the description of the lobes of the cerebral hemispheres as well as the line drawings in Figs. 1.6 and 1.18. As shown in Figs. 1.21–1.23, the lobes of the brain are well demonstrated on CT in the axial, sagittal and coronal planes. Similarly, these same lobes are well seen on MR in these same three planes, as shown in Figs. 1.24–1.26, and on US in Figs. 1.27 and 1.28. Normal brain is characterized by the ability to clearly see the cortex as having a distinctly different appearance from the underlying white matter on CT and on most pulse sequences in MR. The normal brain is also symmetric with respect to the midline. Deep grey matter structures of the cerebral hemispheres, such as the basal ganglia described below, are also easily discernible from their surrounding white matter. Another attribute of “normal” brain is having an appropriate amount of brain parenchyma for the patient’s age. On a series of CT scans at different ages, Fig. 1.29 shows the normal amount of brain parenchyma that might be expected. As can be seen, as the patient ages the relative amount of brain parenchyma (both white matter and grey matter) decreases. This loss becomes even mildly noticeable only in the third and fourth decades of life, but then becomes increasingly prominent as one gets into the septuagenarian and octogenarian years. If a patient has more loss of brain parenchyma than is age appropriate, then one should consider the possibility of a global process affecting the brain. In addition to the brain having an age appropriate amount of total mass, the amount of gray and white matter also changes with age. Often, the amount of brain parenchyma lost with time is most visible in the


25

Fig. 1.21 Multislice CT of normal cerebrum, source axial images. (a) Near the top of the brain, (b) at the top of the lateral ventricles, (c) at the mid portion of the third ventricle, and (d) at the mid portion of the temporal lobe. The major structures are indicated by the following legends: frontal lobe (fr), occipital lobe (occ), parietal lobe (par), temporal lobe (temp), Sylvian fissure (syl), falx cerebri (falx), lateral ventricle (lv), third ventricle (III), and fourth ventricle (IV)

white matter around the ventricles. Consequently, it is normal for the ventricles to show an increase in size with aging to compensate for this normal, gradual loss of periventricular white matter. Normal changes of white matter density (on CT) and the signal intensity of white matter (on MR) occur with age. These changes are primarily related to the fact that a newborn brain has very little myelin around axons and the fact that the newborn brain contains comparatively more water within the tissue than the adult brain. Together, these findings show that in the young child the white matter density in absolute CT number is lower relative to gray matter than it is in the adult. On MR scanning, aging leads to signal changes consistent with myelination that appears over time in the developing brain. The newborn brain shows very little myelination and this is evidenced by the lack of dark signal in the white matter structures on T2-weighting. The normal structures gradually acquire myelination and an associated decrease in signal intensity on T2, which approaches the adult pattern by approximately 2 years of age (Fig. 1.30). On US, the normal cerebral hemispheres have symmetry, visible distinction of grey matter from white matter and ventricular size and position as seen on MR and CT. Due to constraints of scanning geometry,

26


Fig. 1.22 Multislice CT of normal cerebrum. The axial source images have been reformatted into the coronal plane: (a) through the frontal lobes, (b) through the anterior horn of the lateral ventricle and the anterior portion of the temporal lobes, (c) at the top of the brainstem, and (d) through the occipital lobes and cerebellum (legends as in Fig. 1.21)

Fig. 1.23 Multislice CT of normal cerebrum. The axial source images have been reformatted into the sagittal plane: (a) through the midline and (b) laterally through the Sylvian fissure and temporal lobe (legends as in Fig. 1.21)

Cerebellum

27

Fig. 1.24 MR of the normal cerebrum. Axial T2-weighted images: (a) through the inferior, anterior aspect of the temporal lobes, (b) through the midportion of the temporal lobe and inferior portion of the frontal lobes, (c) through portions of the frontal, parietal, and occipital lobes, and (d) superiorly placed axial image through the frontal and parietal lobes (legends as in Fig. 1.21)

it is difficult to angle the US transducer through the anterior fontanelle sufficiently to see the very lateral aspect of the skull. Visualizing structures in the posterior fossa using US can also be difficult.

Cerebellum The cerebellum consists of two small, laterally located hemispheres and a single midline structure (the vermis); all are located in the posterior fossa, which lies below the tentorium cerebelli. The cerebellum also sits behind the brainstem, which runs from top to bottom in the anterior midline of

28


Fig. 1.25 MR of the normal cerebrum. Coronal T2-weighted images: (a) through the midportion of the frontal lobes and the anterior tips of the temporal lobes, (b) slightly posterior to (a), (c) at the level of the brainstem, and (d) through the parietal and temporal lobes and the posterior fossa (legends as in Fig. 1.21)

the posterior fossa and also behind the fourth ventricle (Fig. 1.6). Organizationally, the cerebellar hemispheres are similar to the cerebral hemispheres, with cortex or gray matter on the surface, white matter below the cortex and, most deep and central within the cerebellar hemispheres, deep nuclei composed of gray matter near the fourth ventricle (Fig. 1.31). These three components function in a similar manner to the cerebrum, with a majority of the neurons being present in the cortex, the white matter representing the interconnecting axon bundles and the deep nuclei having additional specific neurologic functions [16–18].

Fig. 1.26 MR of the normal cerebrum. Sagittal T1-weighted images: (a) through the midline and (b) laterally through the Sylvian fissure and temporal lobe (legends as in Fig. 1.21)

Fig. 1.27 Ultrasound (US) of the normal cerebrum. Coronal images through the anterior fontanelle: (a) frontal lobes, (b) anterior aspect of the temporal lobes and anterior horn of lateral ventricle, (c) brainstem, and (d) oblique axial/ coronal image through body of lateral ventricle (legends as in Fig. 1.21)

Fig. 1.28 US of the normal cerebrum. Sagittal images through the anterior fontanelle: (a) through the midline and (b) laterally through the Sylvian fissure and temporal lobe (legends as in Fig. 1.21)

Fig. 1.29 CT of normal brain at different ages. A simple axial image that includes the frontal horns of the lateral ventricles, the temporal lobes, and the occipital lobes of the brain is demonstrated in (a) at 9 day old, (b) at 5 years of age, (c) at 45 years of age, and (d) at 75 years of age. Note the general slow loss of brain substance with increasing prominence of the sulci, the Sylvian fissures, and the size of the ventricles

Fig. 1.30 MR of normal brain at two different ages. At 1 month of age: (a) A sagittal T1 and (b) an axial T2 image; and at 4 years of age: (c) a sagittal T1, and (d) an axial T2 image. On the T1-weighted images in the 1 month old (in (a)), grey matter is whiter than white matter, while on the T2-weighted images (in (b)) white matter is brighter than grey matter. By 4 years of age (the changes normally occur by 2 years old), white matter is now brighter on T1-weighted images (in (c)), and grey matter is brighter on T2-weighted images (in (d))

Fig. 1.31 Cerebellar hemispheres and vermis. Line drawing demonstrating the major components of the cerebellum

32


Gray Matter of the Cerebellar Hemispheres All of the neurons within the cerebellum are located in either the cerebellar cortex or the deep nuclei. As in the cerebral hemispheres, the cerebellar cortex is infolded, though in the cerebellum the gyri are called folia. Also, as in the cerebrum, the prominence of the sulci between the folia increases with advancing age. Whereas the primary functions of the majority of neurons in the cerebral gray matter are concerned with motion, sensation, thought, vision, hearing, etc., the correlation between specific anatomic locations in the cerebellum and a specific action is less precise. Rather, the cerebellum should be thought of as a kinesthetic memory device which coordinates complex actions and serves as the source of muscle or motion memory for complex activities. Damage to the cerebellum most obviously produces incoordination of motor movement. Extensive edema or any other space-occupying lesion (such as a tumor mass or large clot from hemorrhage) in the inferiorly located cerebellar tonsil – an important structure of the cerebellum – can cause it to herniate downward through the foramen magnum and cause death. This structure is also low-lying in some congenital abnormalities, such as Chiari malformations.

Deep Cerebellar White Matter Continuing the cerebral hemispheric analogy, the deep white matter in the cerebellum serves to interconnect the cerebellar cortex, the deep nuclei, and the remaining portions of the central nervous system. Diseases involving white matter can involve any of the white matter within the cerebral hemispheres, the cerebellum or the brainstem, and spinal cord.

Imaging Appearance of the Cerebellar Hemispheres In general, the cerebellum is imaged in the axial plane on CT and in the axial, sagittal, and coronal planes on MR imaging. As in the cerebral hemispheres, on MR most pulse sequences show adequate differentiation of gray and white matter such that the cerebellar cortex is easily discernible from the deeper white matter structures. The normal appearance of the cerebellum on MR is shown in Fig. 1.32; the normal appearance of both the cerebellum and the brainstem on CT is shown in Fig. 1.33 and on US in Fig. 1.34.

Brainstem The brainstem is divided into three regions – the midbrain, pons, and medulla (Fig. 1.35). The brainstem is anterior to the cerebellum and extends from the base of the cerebral hemispheres inferiorly, down to the start of the cervical spinal cord at the level of the foramen magnum, the large, central bony opening in the floor of the rear of the skull. The brainstem is a key component of the connectivity of the central nervous system as well as the site of many important clusters of neurons or nuclei. Numerous white matter pathways pass through the brainstem, connecting the brain cortices, the basal ganglia, and the cerebellum to one another and to the spinal cord and, thence, to the remainder of the body. The nuclei located with the substance of the brainstem control the function of the majority of the cranial nerves (twelve pairs of nerves that arise symmetrically from the brain and brainstem and are responsible for many functions, including the senses of vision, hearing, and taste; and motor and sensation to portions of the head, neck, and body), as well as participate in the

Brainstem

33

Fig. 1.32 Routine MR images of the cerebellum. In (a) axial T2 image at level of mid medulla through the inferior portion of the cerebellar hemispheres, (b) axial T2 image at the midpons through midportion of the cerebellar hemispheres, (c) axial T2 image at the midbrain through the upper portion of the hemispheres, and (d) coronal T2 image through the midportion of the cerebellar hemispheres

coordination of various specific functions of the nervous system. A detailed discussion of these cranial nerves and other brainstem nuclei is not appropriate for this text; however, it is correct to state that lesions within the brainstem can be very discrete in their functional impairment since specific nuclei have clearly defined neurologic functions. The brainstem components, from superior to inferior, are the midbrain, the pons, and the medulla [19–21]. The midbrain has a short, approximately 1 cm vertical dimension; the pons has a vertical dimension of several centimeters and the medulla likewise. The pons has the largest cross-sectional area and, when viewed from the side, the belly of the pons extends anteriorly farther than the midbrain and medulla. The belly of the pons consists of large, white matter tracts, extending bilaterally in a postero-lateral direction and sweeping back into the cerebellum on either side. The lowest portion of the brainstem, the medulla, connects the pons above to the cervical spinal cord at the level of the skull base (the cervicomedullary junction). With the exception of the first and second cranial nerves, all cranial nerves arise from the brainstem, with the third cranial nerve being the most superior, and progressing inferiorly, successively pass through the fourth, fifth, sixth, and so on, eventually to the twelfth cranial nerve (Fig. 1.35). Thus, the brainstem consists of both white matter tracts connecting the various brain regions and grey matter nuclei.

Fig. 1.33 Axial CT scan at level of cerebral peduncles (a), midbrain and upper parts of cerebellum (b), mid pons (c), and medulla (d)

Fig. 1.34 Routine US mages of the cerebellum and brainstem. Typical coronal image (a), midline sagittal in (b) & (d), oblique sagittal in (c)

Ventricles

35

Fig. 1.35 Brainstem. View of the brainstem in relation to the cerebral hemispheres above and the cerebellum posteriorly. The levels of the brainstem include the upper midbrain, which connects to the cerebral peduncles that connect to the cerebral hemispheres, the middle rounded pons, and the inferiorly located medulla. The brainstem connects to the cerebellum by three pairs of cerebellar peduncles

The Imaging Appearance of the Normal Brain Stem The brainstem is normally imaged with axial CT images and with sagittal, axial, and coronal MR images. While the internal structure of the brainstem is composed of numerous white matter tracts as well as an additional, fairly large number of gray matter nuclei, this often appears homogenous in signal whether on CT or MR. At the superior aspect of the brainstem, the red nuclei (which is a large, medially located nucleus within the midbrain) is easily discernible on most MR pulse sequences. The points of connection between the brainstem and the cerebellum, the brainstem and the cerebral hemispheres, and the brainstem and the cervical spinal cord are areas of smooth transition. No sharp demarcation is evident between these adjacent structures, as the white matter tracts smoothly tie these various components of the central nervous system to one another (Figs. 1.33 [CT], 1.34 [US], and 1.36 [MR]).

Ventricles The Ventricles – Normal Shape, Size, and Position The normal shape of the lateral ventricles (the large, fluid-filled cavities within each cerebral hemisphere), when viewed from above, is two “C”s positioned back-to-back, with an additional extension (or horn) of the ventricle extending back into the occipital pole. The confluence of this occipital horn with the rear of the “C” on each side is known as the atrium of the lateral ventricle. One can think of the atrium as the point of confluence of the body, occipital horn, and temporal horn. From the atrium, the temporal horn extends laterally and anteriorly from the atrium into the core of the

36


Fig. 1.36 MR images of the brainstem. In (a) sagittal T1 image through the midline, (b) axial T2 image at the level of the cerebral peduncles, (c) axial T2 image at the junction of the cerebral peduncles and midbrain, (d) axial T2 image at the mid pons, (e) axial T2 image at the ponto-medullary junction, (f ) axial T2 image at the medulla, (g) coronal T2 image showing the belly of the pons and the medulla, and (h) coronal T2 image through the cerebral peduncles

Ventricles

37

Fig. 1.37 Ventricles. Oblique view of the ventricles demonstrating the paired “C”-shaped ventricles that have an extension going posteriorly as the occipital horn. These paired lateral ventricles communicate on either side via the foramen of Monro with the midline third ventricle. The midline third ventricle then communicates via the Aqueduct of Sylvius with the fourth ventricle, which then communicates through the single midline foramen of Magendie and the paired lateral foramina of Luschka with the subarachnoid space

temporal lobe. Similarly, the body of the ventricle extends forward and medially with the right- and left-sided structures abutting in the midline. At the anterior extent of the body of the ventricle, the anterior horn diverges laterally and the foramen of Monro opens downward into the anterior aspect of the third ventricle. The third ventricle is a thin, midline structure bounded laterally by the thalami and located immediately below the corpus callosum, the large white matter tract running from sideto-side. The cerebral aqueduct, or Aqueduct of Sylvius, connects the rear of the third ventricle to the midline fourth ventricle, which lies immediately behind the brainstem and in front of the cerebellum (Fig. 1.37) [22, 23].

The Nonventricular CSF Spaces (Cisterns) Cerebrospinal fluid is present not only within the ventricular system where it is produced, but also overlies the outside surface of the cerebral hemispheres, brainstem, and cerebellum. In the subarachnoid space, where the arachnoid does not closely follow the contours of the brain, cisterns – focal, enlarged pools of CSF – form [24, 25]. A number of these cisterns have specific names. For example, where the pituitary gland sits at the inferior central base of the brain, the large CSF collection in the midline above the pituitary fossa is called the suprasellar cistern; above the cerebellum in the midline is the superior cerebellar cistern; anterior to the pons is the prepontine cistern; and below the cerebellum inferiorly in the midline is the cisterna magna. Additional off-midline CSF spaces, primarily in the posterior fossa, include the ambient wing and quadrigeminal cistern at the level of the midbrain and the cerebellar pontine angle cistern, which is on either side of the medulla near the internal auditory canal (Fig. 1.38 extraventricular CSF spaces). These CSF-containing spaces also extend inferiorly to bathe the spinal cord all the way down to the level of the sacrum, with the large collection of CSF in the lower back or lumbar region referred to as the lumbar cistern.

38


Fig. 1.38 Nonventricular CSF spaces (cisterns). Cerebrospinal fluid is present not only within the ventricular system, but overlying the outside surface of the cerebral hemispheres, brainstem, and cerebellum. Named cisterns that are present in the midline include the suprasellar cistern, the superior cerebellar cistern, the prepontine cistern, and the cisterna magna. Additional off-midline CSF spaces, primarily in the posterior fossa, include the ambient wing and quadrigeminal cistern at the level of the midbrain and the cerebellar pontine angle cistern which is on either side of the medulla near the internal auditory canal

CSF Dynamics In the normal adult, several hundred milliliters of CSF are continuously produced as an ultrafiltrate of the serum component of blood by the formative organ, the choroid plexus. This specialized structure is located within the lateral, third, and fourth ventricles. There is bulk flow of CSF out of the lateral ventricles on each side, through their respective foramen of Monro and into the anterior third ventricle. CSF then flows from the rear of the third ventricle downward through the cerebral aqueduct into the fourth ventricle. The fourth ventricle has single midline (the foramen of Magendie) and paired lateral (the foramina of Luschka) openings that allow exit of CSF inferiorly into the subarachnoid space at the base of the posterior fossa. Once CSF exits the ventricular system, it bathes both the brain and the spinal cord in the subarachnoid space. After the CSF circulates through the ventricular system and the subarachnoid space, it is eventually returned to the systemic circulation via structures called arachnoid granulations, which protrude into the superior sagittal sinus. Clinical Note: The size of the ventricles can be increased either because they are being dilated by too much spinal fluid within a normal-sized ventricular system or because the ventricles have dilated in response to a loss of brain tissue [26]. In the first case, too much spinal fluid may be present in the ventricles due to overproduction of spinal fluid, blockage of normal flow of spinal fluid in its attempt to move through the ventricular system, or impaired absorption of spinal fluid once it is outside the ventricular system. In the latter cases, the ventricles expand in response to a loss of brain tissue and, in effect, the ventricles are expanding to fill the “vacuum” created by the loss of brain parenchyma.

Ventricles

39

Overproduction of spinal fluid most commonly occurs in the case of tumors of the choroid plexus. These tumors are usually choroid plexus papillomas (benign tumors of the choroid plexus), but in less than 5% of cases they may be malignant choroid plexus carcinomas. This overproduction of spinal fluid results in the dilatation of the ventricles. Blockage of the ventricular system at any level produces dilatation of the ventricles upstream from the blockage. For example, blockage of a level of the foramen of Monroe will cause dilatation of the lateral ventricle. A blockage of the lateral ventricle at the atrial region will cause dilatation of the temporal horn. A mass that occludes the rear of the third ventricle or the aqueduct will cause enlargement of both lateral ventricles and the third ventricle. A blockage at the level of the normal foramina that allows exit from the fourth ventricle (Magendie and Luschka) will cause dilatation of all of the ventricles. This last could be accomplished, for example, by an adhesive process from a prior infection at the skull base. A similar response to prior infection can block the arachnoid granulations near the superior sagittal sinus and cause impaired resorption of cerebrospinal fluid, leading to diffuse enlargement of all of the ventricles. Not only can the ventricles enlarge from overproduction of CSF or from blockage of flow, they can also enlarge secondary to marked parenchymal loss. For example, a global anoxic event that does not cause a discrete infarct of brain, but rather a diffuse loss of brain parenchyma, often

Fig. 1.39 Imaging of the ventricles and extraventricular CSF spaces by MR, with axial T2-weighted images: (a) at the top of the lateral ventricle, (b) at the midthird ventricle, (c) at the level of the suprasellar cistern, and (d) at the midpons and cerebellar pontine angle cisterns

40


presents with abnormally enlarged ventricles for the patient’s age. Alternatively, the ventricles may enlarge as a result of the loss of grey matter and white matter associated with aging.

Imaging Appearance of the Normal Ventricles, CSF Spaces, and CSF Dynamics The CSF-containing spaces of the brain will appear on CT scans as areas of low (dark) density, with CT numbers close to that of water. This allows CT scanning to very adequately show both the ventricles and the extraaxial CSF collections. Similarly, the CSF spaces are well demonstrated on MR scanning, though the appearance of the spinal fluid will vary significantly with the pulse sequence chosen. On a T1-weighted pulsed sequence, for example, CSF will appear black. On a T2-weighted sequence, the CSF will appear very white within the image. Finally, on a FLAIR sequence, which can be thought of as a T2-weighted sequence that has additional magnetic and radiofrequency pulses, all of the free water in CSF spaces becomes black. Consequently, on both the T1-weighted sequence and on a FLAIR sequence, the spinal fluid will appear black, and on a T2-weighted sequence spinal fluid will be white. The major ventricular structures, as well as the extraaxial CSF spaces, are shown on CT, MR, and US in Figs. 1.21–1.28, 1.32–1.34, 1.36, and 1.39.

References 1. Barkovich AJ. Pediatric Neuroimaging, 2005, Lippincott, Philadelphia, pp 252–253. 2. van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet 2007;369(9558):306–318. 3. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart, pp 253–282 (Section 5.4 Arteries of the Brain). 4. Snell RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 17. The Blood Supply of the Brain and Spinal Cord, pp 473–479. 5. Krabbe-Hartkamp MJ, van der Grond J, de Leeuw F-E, et al. Circle of Willis: morphologic variation on threedimensional time-of-flight MR angiograms. Radiology 1998;207:103–111. 6. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart, pp 283–285 (Section 5.5 Veins of the Brain). 7. Snell RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 17. The Blood Supply of the Brain and Spinal Cord, pp 479–480. 8. Grossman RI, Yousem DM. Neuroradiology: The Requisites, 2003, Mosby, Philadelphia, pp 217–220. 9. Kiernan J. Barr’s The Human Nervous System – An Anatomical Viewpoint, 2009, Lippincott, Philadelphia – Chapter 13. Topology of the Cerebral Hemispheres pp 211–218 and Chapter 15 Functional Localization in the Cerebral Cortex, pp 227–244. 10. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart, pp 307–324 (Section 5.7.5 Telencephalon). 11. Snell RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 7. Cerebrum pp 247–280 and Chapter 8 The Structure and Functional Localization of the Cerebral Cortex, pp 286–301. 12. Kiernan J. Barr’s The Human Nervous System – An Anatomical Viewpoint, 2009, Lippincott, Philadelphia – Chapter 14. Histology of the Cerebral Cortex, pp 219–226. 13. Snell RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 8. The Structure and Functional Localization of the Cerebral Cortex, pp 281–286. 14. Kiernan J. Barr’s The Human Nervous System – An Anatomical Viewpoint, 2009, Lippincott, Philadelphia – Chapter 12. Corpus Striatum, pp 199–210. 15. Snell RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 7 Cerebrum, pp 260–261. 16. Kiernan J. Barr’s The Human Nervous System – An Anatomical Viewpoint, 2009, Lippincott, Philadelphia – Chapter 10 Cerebellum, pp 157–172.

References

41

17. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart, pp 303–304 (Section 5.7.3 Cerebellum). 18. Snell RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia Chapter 6, pp 225–245 (The cerebellum and its connections). 19. Kiernan J. Barr’s The Human Nervous System – An Anatomical Viewpoint, 2009, Lippincott, Philadelphia – Chapter 6. Brainstem: External Anatomy, pp 79–86 and Chapter 7 Brainstem: Nuclei and Tracts, pp 87–112. 20. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart pp 288–303 (Sections 5.7.1 Pons and Medulla and 5.7.2 Midbrain). 21. Snell RS. Clinical Neuroanatomy for Medical Students, 2001 Lippincott, Chapter 5, pp 189–224 (The Brainstem). 22. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart, pp 239–253 (Section 5.3 Cerebrospinal Fluid Containing Spaces). 23. Snell, RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 16: The ventricular system, the cerebrospinal fluid and the blood brain and blood cerebrospinal fluid barriers, pp 443–456. 24. Kretschmann H-J, Weinrich W. Cranial Neuroimaging and Clinical Neuroanatomy: Atlas of MR Imaging and Computed Tomography, 2004, 3rd Edition, Thieme, Stuttgart Chapter 16: The ventricular system, the cerebrospinal fluid and the blood brain and blood cerebrospinal fluid barriers, pp 456, 457. 25. Snell, RS. Clinical Neuroanatomy for Medical Students, 2001, Lippincott, Philadelphia – Chapter 16: The ventricular system, the cerebrospinal fluid and the blood brain and blood cerebrospinal fluid barriers, pp 443–456. 26. Osborn AG, Blaser SI, Salzman KL, et al. Diagnostic Imaging – Brain, 2004, Amerisys, Salt Lake City II:1:12–27.

Chapter 2

The General Appearance of Edema and Hemorrhage on CT, MR and US (Including a General Introduction to CT, MR and US Scanning)

Abstract This chapter begins with a discussion of the terminology and hardware of computed tomographic (CT), magnetic resonance (MR), and ultrasound (US) imaging. This includes an introduction to CT numbers and very basic MR image formation, sequence types, and sequence usages. The remainder of the chapter is an introduction to edema and hemorrhage. The two basic types of edema are cytotoxic and vasogenic. The appearance of these types of edema is presented on CT, MR, and US. The general imaging of hemorrhage – without following in detail the evolution of these findings with time – and the various spaces in which it occurs in the brain are discussed and demonstrated on CT, MR, and ultrasound. Keywords Computed tomography (CT) • Magnetic resonance (MR) • Ultrasound (US) • Edema • Cytotoxic edema • Vasogenic edema • Hemorrhage

Introduction This chapter will build on the anatomy and imaging findings of normal brain detailed in Chap. 1. Knowing the normal appearance of brain is mandatory to make an intelligent assessment of the changes in brain as a result of injury. In this chapter, we begin with a brief introduction on the basics of computed tomography (CT), then magnetic resonance (MR) and finally, ultrasound (US) imaging of the brain. Second, we will discuss the general topic of edema and how it appears on each of the three imaging modalities. Finally, in a broad sense, we will introduce hemorrhage and its imaging appearance. In all cases in this chapter, we will not discuss in detail the manner in which the basic findings change considerably over time. That detailed discussion, including the most complicated topic of all – the changing appearance of hemorrhage over time on MR scanning – is reserved for Chap. 4.

CT Scanning: The Absolute Basics In any discussion of the pathology within the central nervous system (CNS – the brain and spinal cord), one should have an understanding of the basic underlying principles of the modality that is used to image the brain, in addition to an anatomic understanding of the brain. Therefore, at this point, we will provide an overview of the basic principles of CT scanning and, more specifically, those principles that are directly applicable to imaging the CNS [1]. Once one understands CT


43

44

2 The General Appearance of Edema and Hemorrhage

technology, we can move beyond that into the specific findings on CT that occur in the setting of injury. Abnormalities are recognized in one of two ways: either anatomy is distorted (i.e., something there that shouldn’t be, or something not there that should be) and/or an alteration occurs in the normal CT numbers of the tissue. CT numbers, as we shall see, are an essential component of the information provided by a CT scan. A CT scanner consists of the basic components of a patient table (on which the patient to be scanned lies); the scanner gantry (which contains the rotating portion that holds the X-ray tube generator and detector array) and a computer system (for performing the necessary calculations to go from measurements to a viewable image) (Fig. 2.1). The patient lies supine on the movable scanner table as the portion of the body to be scanned passes through the middle of the opening in the gantry. During the scan, the X-ray tube continually generates X-rays, which pass sequentially through the patient and then on to an array of detectors. The computer begins with the detector-made measurements of the radiation that is “left over” after passing through the patient and calculates what the tissues in the body must have looked like to have produced the observed measurements. The term “density” is often used to describe the distribution of matter that must have been present to partially absorb the X-ray beam and produce the measured residual beam at the detectors. However, a more technically accurate description is that the scanner computes the amount of radiation absorption that occurs at each scanned point in the body. Fortunately, a close correlation exists between the density of a tissue and its ability to stop X-ray photons. For our purposes we will, therefore, use the shorter term “density,” rather than the technically more accurate (but much more cumbersome) phrase, “relative ability to absorb X-ray photons,” for the remainder of this book. When the CT scanner computer finishes its calculations for a single image, the result is a crosssectional image of the brain in which white represents structures that are more dense and dark represents structures that are less dense. The CT image can be thought of as a density map, showing the relative propensity of different portions of the image to absorb the X-rays that the CT scanner beam sends through the patient. Within the scanner, it is the job of the computer to reconstruct and calculate the density distribution which must have existed to produce the measured absorptions, and

Fig. 2.1 CT scanner. A typical CT scanner. The table on which the patient lies, is at the front of the scanner. The table then moves into the central bore of the CT scanner. Within the scanner gantry is a rotating ring with both the X-ray tube and the detector array

MR Scanning: The Absolute Basics

45

Table 2.1 CT numbers Air –1000 Fat –100 to –50 Water 0 Most tissues 20–40 Hemorrhage 50%), “It is likely that this event happened at that time and caused this appearance.” Finally, if a pattern of injury is present, one should note whether it is descriptive of an acute, subacute, or a chronic appearance. This is important, as the injury pattern does not fix the time of injury if it is a chronic injury pattern (past the period when dynamic dating is of use); it only confirms that an injury did occur. It does say that the injury could have happened at a specific previous time, but it does not necessarily say that it did happen at a specific previous time.

Chapter 9

The Root Causes of Uncertainty in Dating Neurologic Events Based on Imaging Findings

Abstract The final chapter discusses the possible causes of uncertainty in the dating of a neurologic event based on imaging findings – variations in interpretation from expert to expert and variations in the manner that consensus findings are interpreted by different experts, multiple different imaging findings that localize to different points in time, and imaging findings that do not appear to correlate with the clinical picture. Keywords Uncertainty • Chronic dating • Pattern dating

Introduction We have now discussed in some great detail the normal brain and the changes in the brain of edema or hemorrhage in response to injury as they appear on CT, MR, and US. We have discussed the evolution of these findings on computed tomography (CT) and magnetic resonance (MR) with time ranges for the occurrence of the changes. We have further discussed what this progression of findings allows one to say on the basis of imaging studies acquired at discrete points in time following the inciting event. What we have not discussed up to this point is why there is any uncertainty in dating neurologic events or, put another way, why two different medical experts could look at the same set of images and come up with different interpretations either on the presence or absence of injury at all, and on the time when the injury occurred. Reasons for this uncertainty in dating form a short list of possible causes. These are the following: 1. The interpretation of the available images varies from expert to expert, with disagreement as to whether certain findings are present or not. 2. Image findings are acknowledged to be present by all observers; however, the interpretation of the findings varies from expert to expert. 3. Multiple findings are present for which the neuroradiological dating methods we have discussed produce conflicting time periods as to the probable occurrence of the injury. 4. The radiographic findings and time periods deduced from the images are at odds with the clinical picture. Each of these four main causes of uncertainty in dating neurologic events is now discussed.


119

120

9 The Root Causes of Uncertainty in Dating Neurologic Events

The Interpretation of the Available Images Varies from Expert to Expert, with Disagreement as to Whether Certain Findings Are Present or Not The first root cause of uncertainty in dating neurologic events is the uncertainty that arises from the presence or absence of subtle findings. For example, the patient may have undergone a clinical event, which possibly could have produced an anoxic or ischemic injury. Subsequent CT or MR examinations may be interpreted by one observer as being normal and by a second observer as showing subtle signs of early ischemia. The assumption, therefore, made by the two different interpreters based on the images would be, in the first case that the images support no evidence of ischemic or anoxic injury and, in the second case that the images are consistent with an early and/or a mild degree of anoxic or ischemic injury. This example presumes that the controversial findings are subtle, such that there can be a valid difference of opinion between two equally qualified experts as to whether the findings are present or not. This situation is distinctly different from the following situation in which the area of disagreement is not on the findings (often in these cases, the presence of an abnormality and/or injury is obvious to all observers) but in the meaning and implication of the findings.

Image Findings Are Acknowledged to be Present by All Observers; However, the Interpretation of the Findings Varies from Expert to Expert This cause of uncertainty in dating neurologic events based on radiological findings is explained by the fact that the interpretation of scans is an art and not a science. The first reason mentioned for disagreement between experts concerns the situation in which the imaging findings are subtle, and their mere presence is open to debate. However, in this case, the issue is not what the findings are, but rather what they mean. For example, presume that a patient has had a definite hypoxic-ischemic event and the region of affected brain undergoes a period of swelling which is maximal at 3–5 days. Consider a single scan, obtained 3 days after the acute event (for example, Figs. 4.1d or 4.2e from Chap. 4), reviewed by two different experts, each unaware of when the scan was performed after the acute event. The first expert looks at the scan, notes some edema is present, but not as much as would represent maximal swelling. This expert assesses the sharpness of the edge of the infarction and the amount of decreased density within the infarct compared to adjacent uninfarcted brain and concludes that the scan must have been obtained before the period of maximal swelling – i.e., on day 2 or 3. The second observer views the same exact set of images and also assesses the sharpness of the margin and density of the infarct and also concludes that there is submaximal swelling. However, this radiologist feels that the images were obtained after the period of maximal swelling – i.e., on day 6 or 8. That is the manner by which two experts look at the same images, note the same findings, but come to two different conclusions as to what the images say about the age of the infarction. Similarly, different impressions of the images as they relate to the size of the hemorrhage, the density of the hemorrhage on CT, and the maturation of the hemorrhage in the time sequence as assessed by MR may contribute to a discrepancy between two observers when assessing the same images. Two observers may also be in complete agreement as to the presence of the findings and describe to a high degree of concordance the identical injury, loss of brain, abnormal signal, presence of blood of a certain density (on CT) or signal (on MR) and still disagree on the points that those findings fix along a timeline of events. In other words, no matter how elegant and convincing one’s guidelines and time points are, other experts’ time points for identical findings may differ by degree from one’s own.

Conclusion

121

Multiple Findings are Present for Which the Neuroradiological Dating Methods We Have Discussed Produce Conflicting Time Periods as to the Probable Occurrence of the Injury This cause of disparity relates to the fact that some patients will present with more than one potentially “datable” lesion. When the principles of dating are applied to multiple lesions, not all of the lesions will “date” to the same time in some patients. For example, the patient may have multiple infarcts which, by the dating characteristics, seem to have occurred at different times; or the patient may have an infarct and a hemorrhage which, by dating methodology, do not appear to have occurred at the same time. Any of these cases presents a dilemma which must be solved for the expert’s own opinions to be consistent. The expert is presented, really, with only one of two options. On the one hand, the expert may decide that the dating of the two separate processes is correct. This means that the two (or more) events did not occur at the same time. Alternatively, after rereviewing the available examinations, the expert may decide that the initial dating of one or both of the events may have been incorrect. The initial assessment may have used time windows that were too narrow. Could the beginning and end points for the possible injury in each case be widened to the extent that the two events were possibly concurrent? That is an assessment that an expert must make. If, based on all the available imaging material available, that determination cannot be made, then the first option is the most likely explanation for the findings.

Radiographic Findings Which Are at Odds with the Clinical Picture This is, perhaps, the most difficult and perplexing situation that can confront an expert. In this setting, the imaging studies point to a certain time window, but the time window when the injury should have – even must have – occurred is not in accordance with the clinical setting. This circumstance is an expansion of the preceding situation. As in that setting, the expert has a limited number of options. One’s first option is to consider that the radiologic dating and the clinical dating point to and describe two separate events. This would be the case when another potentially injurious event occurred, separate from the one thought to have occurred by the dating method. It may be that either the radiologic event or the alleged clinical event was “silent” and only one of the two events produced real clinical symptoms. Alternatively, as in the previous case, it may be that the dating was in error. So again, a reassessment must be made of the imaging findings and the time windows they imply to see if it might be possible that a revision of the radiologic time window endpoints could include the date implicated by the clinical history.

Conclusion This chapter has highlighted the most common causes for discrepancies between experts in their evaluation of radiological images. An understanding of these dynamics is important, as the members of the expert community seek to use the principles described within this book to skillfully, expertly, and ethically serve the patients and families who are affected by these neurologic situations.

Index

A Anterior cerebral artery (ACA), 11 Anterior inferior cerebellar artery (AICA), 11 Apparent diffusion coefficient (ADC) map, 72 B Basal ganglia infraction, 97–98 Blood-brain barrier (BBB), 60 Brain anatomical planes, 3–4 anatomical view, 9–10 blood supply arterial vessels, 10–14 imaging method, 16–20 venous vessels, 14–16 brainstem components, 32 CT images, 34 MR images, 36 nuclei function, 32–33 regions, 32–34 US images, 34 cerebellum components function, 28 cortex, gray matter, 32 CT images, 34 deep cerebellar white matter, 32 MR images, 33 structure, 27–28, 32 US images, 32, 34 cerebral hemispheres CT, different ages, 22, 24–25, 28, 30 CT imaging, 24–26 deep gray matter nuclei, 23–24 gray matter, 22, 23 lobes, 20–22 MR imaging, 24, 27–29 US imaging, 24, 29–30 white matter, 22 image orientation, 3 tissue layers arachnoid membrane, 6–8

cortex, outersurface, 8 dura, 5, 6, 7 epidural space, 5–6, 53 graphical representation of, 5 imaging, 8–9 pia, 8 scalp, 4 skull, 4–5, 6 subarachnoid space, 7–8, 37 subdural space, 6–7, 53 ventricle brainstem images, 36–39, 40 cerebellum, 33–34, 40 cerebrum images, 25–30, 39, 40 cisterns, CSF spaces, 37–38 CSF dynamics, 38–40 shape, size and position, 35, 37 Brainstem components, 32 CT images, 34 MR images, 36 nuclei function, 32–33 regions, 32–34 US images, 34 C Cerebellum components function, 28 cortex, gray matter, 32 CT images, 32, 34 deep cerebellar white matter, 32 MR images, 32, 33 structure, 27–28, 32 US images, 32, 34 Cerebral hemispheres CT and MR imaging, 24–29 deep gray matter nuclei, 23–24 gray matter, 22, 23 lobes, 20–22 white matter, 22 Chronic injury pattern dating edema and infarction (see also Parenchymal injury, chronic dating) computed tomography, 111

123

124 Chronic injury pattern dating (cont.) magnetic resonance, 112 pediatric patient, HIE, 112 hemorrhage (see also Hemorrhage) middle-aged patient, 113–114 older infarction, 114–115 subdural hematoma, 113 Chronic pattern dating, 118 Chronic subdural hematoma, 113 Computed tomography (CT), 43–45 brainstem, 34, 35 cerebellum, 32, 34 cerebral hemispheres, 24–26 chronic injury pattern dating, 111 chronic subdural hematoma, 113 components, 44 contrast, role BBB disruption, 65–66 bolus, 61, 62 for causative pathology, 65–67 enhancing tissues, 64 vascular filling percentage, brain, 60 central nervous imaging system, 59 dating process, 67 enhancement clinical importance, 67 cranial vault, 64 CT contrast, 60 dura and choroid plexus, 64 MR contrast, 62 MR scanning dose and pulse sequence choice, 62 effects vs. flow void effects, 62–63 T1-and T2-weighted images, 62 principles, 60 administration of, 60 for CT, 59, 60 intact blood-brain barrier, 60 for MR, 60 density, 44 dynamic dating edema, 70, 104 hemorrhage, 75–76, 77, 78, 79, 104–105 dynamic dating, medical-legal setting, 103–105 edema (see also Edema) acute and subacute phase, 70 acute infarction, 70–71 chronic infraction, 70 general appearance, 51–52 hyperacute phase, 70 geographic infarction, 92–93 global anoxia, 94 global atrophy, 94–95 hemorrhage axial image, 76–79 patients hematocrit, 75 time evolution, 76 time period, dating, 69, 70

Index numbers, 45 x-ray beam absorbtion, 44 Computed tomography angiography (CTA), 16, 17, 19 Cytotoxic edema, 48. See also Edema D Diffuse axonal injury, 75 Diffusion-weighted imaging (DWI), 46, 50, 71–72 Dynamic dating, medical-legal setting computed tomography edema, 70, 104 hemorrhage, 75–76, 77, 78, 79, 104–105 CT with MR, 107–109 image interpretation, 118 magnetic resonance edema, 71–72, 73, 105–106 hemorrhage, 76–85, 106–107 E Edema change over time, CT acute and subacute phase, 70 acute infarction, 70–71 chronic infraction, 70 hyperacute phase, 70 change over time, MR acute infarctions, 72–73 acute phase, 72 diffusion-weighted sequence, 71–72 hyperacute, 71–72 parenchymal enhancement, 72 subacute and chronic phase, 72 change over time, US, 85–86 CT scanning, 51–52, 70–71 cytotoxic, 48 definition, 48 dynamic changes, 70–73 dynamic dating, CT and MR, 103–104, 105–106 effect on bilateral basal ganglia infarctions, 49, 50, 51 intracranial structure, 49–50 ventricles, 50–51 loss of G-W matter differentiation, 48–50 mass effect, 50–51 MR scanning, 49–51, 52 US scanning abnormallity, 51, 52 silhouetting of the sulci, 53 vasogenic, 48 ventricle size reduction, 50 F Fluid-attenuated inversion-recovery (FLAIR) sequence, 40, 46, 71–72

Index

125

H Hemorrhage change over time, CT axial image, 76–79 patients hematocrit, 75 time evolution, 76 time period, dating, 69–70 change over time, MR blood-breakdown product, 76–77 FLAIR imaging, 82–85 gradient echo imaging, 82–85 hemoglobin, 76 hydration state, clot, 77–78 signal changes, 78 time evolution, 78, 80 T1-weighted images, 80–84 T2-weighted images, 80–84 change over time, US, 85–86 chronic injury pattern dating, 113–115 CT scanning, 54–55 dynamic dating, CT, 103, 104–105 intraparenchymal hemorrhages CT scan, 55 MR scan, 56 intraventricular hemorrhages, images, 57 location epidural hematoma, 53, 74 intraparenchymal hemorrhage, 53, 74–75 intraventricular hemorrhage, 53, 75 subarachnoid hemorrhage, 53, 54, 74 subdural hematoma, 53, 54, 74 magnetic resonance, 106–107 MR scanning, 55 occurrence, 53 subarachnoid hemorrhage CT scan, 53 MR scan, 54 US scanning, 55–56 Hypoxic-ischemic encephalopathy (HIE), 95–96, 112

M Magnetic resonance (MR) brainstem, 35, 36 cerebellum, 32, 33 cerebral hemispheres, 24, 27–29 chronic geographic infarction, 93 chronic injury pattern dating, 112 components, 45–46 contrast, role dose and pulse sequence choice, 62 effects vs. flow void effects, 62–63 T1-and T2-weighted images, 62 dynamic dating edema, 105–106 hemorrhage, 106–107 dynamic dating, medical-legal setting, 105–107 edema (see also Edema) acute infarctions, 72–73 acute phase, 72 diffusion-weighted sequence, 71–72 general appearance, 52 hyperacute, 71–72 parenchymal enhancement, 70, 72 subacute and chronic phase, 72 factors, 45–46 global anoxia, 94, 95 global atrophy, 94–95, 96 hemorrhage blood-breakdown product, 76–77 chemical changes, hemoglobin, 76–78 FLAIR imaging, 82–85 gradient echo imaging, 82–85 hydration state, clot, 77–78 signal changes, 78 time evolution, 78, 80 T1-weighted images, 80–84 T2-weighted images, 80–84 injury, central sulcus region, 95–96, 98 pulse weightings, 46 weighted image, 46 Magnetic resonance angiography (MRA), 16, 18 Magnetic resonance venography (MRV), 16, 18 Middle cerebral artery (MCA), 11

I Image interpretation principle chronic pattern, certain timings, 118 dynamic period, 2-week, 117 imaging criteria, precise timings, 118 non classic pattern, past 2 weeks, 118 uncertainty causes acknowledged, all observer, 120 varies, expert to expert, 120 Internal carotid arteries (ICA), 10–11 Ischemia region, variations duration, 91 metabolic activity, 92 perfusion, 90–91 severity of insult, 91

P Parasagittal infarction, 99 Parenchymal injury, chronic dating characteristic, 89–90 factors affecting, ischemia duration, 91 metabolic activity, 92 regional variations, perfusion, 90–91 severity of insult, 91 pattern basal ganglia, 97–98 geographic infarct, 92–93 global anoxia, 94 global atrophy, 94–95 neonatal HIE, 95–96, 112

G Gradient echo imaging, 48, 85

126 Parenchymal injury, chronic dating (cont.) parasagittal injury, 99 perirolandic region, 98, 99 PVL/white matter loss, 96–97 principle, 89–90 Posterior cerebral artery (PCA), 11–12 Posterior inferior cerebellar artery (PICA), 11 S Shear injury, 74 Superior cerebellar artery (SCA), 11 T T1-weighted images, 45–46, 81 T2-weighted images, 45–46, 81–83 U Ultrasound (US) scanning cerebellum, 32, 34 cerebral hemispheres, 24, 29–30 change over time, edema and hemorrhage, 85–86

Index edema, 51, 52 (see also Edema) hemorrhage, 55–57 PVL/white matter loss, 96–97 sonar image, tissues, 47 Uncertainty causes, image findings interpretation acknowledged, all observer, 120 varies, expert to expert, 120 multiple findings, 121 radiologic dating, 121 V Vasogenic edema, 48. See also Edema Ventricle brainstem images, 36–39, 40 cerebellum, 33–34, 40 cerebrum images, 25–30, 39, 40 cisterns, CSF spaces, 37–38 CSF dynamics, 38–40 shape, size and position, 35, 37 W White matter loss, 96–97

Dating Neurological Injury: A Forensic Guide for Radiologists, Other Expert Medical Witnesses, and Attorneys

Forensic Pathology for Police, Death Investigators, Attorneys, and Forensic Scientists

Applying Statistics in the Courtroom: A New Approach for Attorneys and Expert Witnesses

Applying statistics in the courtroom: a new approach for attorneys and expert witnesses

The Forensic Evaluation of Traumatic Brain Injury: A Handbook for Clinicians and Attorneys

The MMPI, MMPI-2 & MMPI-A in Court: A Practical Guide for Expert Witnesses and Attorneys

The Forensic Evaluation of Traumatic Brain Injury: A Handbook for Clinicians and Attorneys

Forensic Pathology for Police, Death Investigators, Attorneys, and Forensic Scientists

Dating and Other Dangers

Dating and Other Dangers

Culture Competence in Forensic Mental Health: A Guide for Psychiatrists, Psychologists, and Attorneys

MRI Physics for Radiologists: A Visual Approach

Expert witnesses: criminologists in the courtroom

A Guide to Sports and Injury Management

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys 2nd edition (Forensic Science and Medicine)

Brain Injury and Returning to Employment: A Guide for Practitioners

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys

Forensic Ethics and the Expert Witness

Physeal Injury Other Than Fracture

Injury Prevention for Young Children: A Research Guide (Bibliographies and Indexes in Medical Studies)

Forensic Computing. A Practioners Guide

Biostatistics for Radiologists: Planning, Performing, and Writing a Radiologic Study

Biostatistics for Radiologists: Planning, Performing, and Writing a Radiologic Study

The Good Dating Guide: The Do's and Don'ts of Dating

Mastering Forensic Psychiatric Practice: Advanced Strategies for the Expert Witness

Treating Self-Injury: A Practical Guide

Dating For Dummies

Dating Neurological Injury: A Forensic Guide for Radiologists, Other Expert Medical Witnesses, and Attorneys

Forensic Pathology for Police, Death Investigators, Attorneys, and Forensic Scientists

Applying Statistics in the Courtroom: A New Approach for Attorneys and Expert Witnesses

Applying statistics in the courtroom: a new approach for attorneys and expert witnesses

The Forensic Evaluation of Traumatic Brain Injury: A Handbook for Clinicians and Attorneys

The MMPI, MMPI-2 & MMPI-A in Court: A Practical Guide for Expert Witnesses and Attorneys

The Forensic Evaluation of Traumatic Brain Injury: A Handbook for Clinicians and Attorneys

Forensic Pathology for Police, Death Investigators, Attorneys, and Forensic Scientists

Dating and Other Dangers

Dating and Other Dangers

Culture Competence in Forensic Mental Health: A Guide for Psychiatrists, Psychologists, and Attorneys

MRI Physics for Radiologists: A Visual Approach

Expert witnesses: criminologists in the courtroom

A Guide to Sports and Injury Management

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys 2nd edition (Forensic Science and Medicine)

Brain Injury and Returning to Employment: A Guide for Practitioners

Criminal Poisoning: Investigational Guide for Law Enforcement, Toxicologists, Forensic Scientists, and Attorneys

Forensic Ethics and the Expert Witness

Physeal Injury Other Than Fracture

Injury Prevention for Young Children: A Research Guide (Bibliographies and Indexes in Medical Studies)

Forensic Computing. A Practioners Guide

Biostatistics for Radiologists: Planning, Performing, and Writing a Radiologic Study

Biostatistics for Radiologists: Planning, Performing, and Writing a Radiologic Study

The Good Dating Guide: The Do's and Don'ts of Dating

Mastering Forensic Psychiatric Practice: Advanced Strategies for the Expert Witness

Treating Self-Injury: A Practical Guide

Dating For Dummies

Recommend Documents