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Full download Neuroradiology: Spectrum and Evolution of Disease 1st Edition Edition Juan Small file pdf all chapter on 2024
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Neuroradiology: Spectrum and
Evolution of Disease
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Neuroradiology: Spectrum and
Evolution of Disease
JUAN E. SMALL, MD, MSc
Section Chief, Neuroradiology
Lahey Hospital and Medical Center
Burlington, Massachusetts
DANIEL L. NOUJAIM, MD
Neuroradiologist
Department of Radiology
Beaumont Hospital
Dearborn, Michigan
HILLARY R. KELLY, MD
Radiologist
Massachusetts Eye and Ear Infirmary
Neuroradiologist
Massachusetts General Hospital
Assistant Professor of Radiology
Harvard Medical School
Boston, Massachusetts
PAMELA W. SCHAEFER, MD
Associate Director of Neuroradiology
Clinical Director of MRI
Massachusetts General Hospital
Associate Professor of Radiology
Harvard University
Boston, Massachusetts
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Ste 1800
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No part of this publication may be reproduced or transmitted in any form or by any means, electronic
or mechanical, including photocopying, recording, or any information storage and retrieval system,
without permission in writing from the publisher. Details on how to seek permission, further
information about the Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website:
www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described herein. In
using such information or methods they should be mindful of their own safety and the safety of
others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of practitioners, relying on their own
experience and knowledge of their patients, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.
Printed in China
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To Kirstin, Nathan, and Sean. You are the light, the
joy, and the love in my life.
—Juan E. Small
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Contributors
vi
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Contributors vii
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Preface
One of the few guarantees in life is that things will change. Disease disease on a static visual database. These gaps lead to a partial
is dynamic. The human body’s interaction with disease is adaptive. and inadequate conceptualization of disease. It follows that when
Our management of disease results in alterations. Therefore, it is a disease presentation varies from what we have seen before, we
important to consider that our most utilized imaging modalities are naturally confused. Doesn’t it make sense to learn about a
take only a snapshot of the current state of a disease process. As disease process not as a static entity with a classic appearance, but
such, they provide us with a static depiction of a disease entity. instead as a dynamic process which evolves? This book is meant
Inevitably, there will be gaps when we base our understanding of to bridge the gaps.
viii
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Acknowledgments
The editors would like to gratefully acknowledge the wonderful at Amirsys including Laura C. Wissler, MA, for her beautiful and
team at Elsevier including Robin Carter and Russell Gabbedy inspired illustrations, as well as Richard Coombs, MS, and Lane
(Content Strategists), Ann R. Anderson (Content Development R. Bennion, MS (contributing illustrators). Lastly, the completion
Specialist), Mandy Mincher (Production Manager), and Ryan Cook of this book would not have been possible without the help of
(Designer) for their help, support, and guidance throughout the Carol Spencer, the Medical Library Director at Lahey Hospital
making of this book. It has been a privilege and a pleasure to and Medical Center.
work with you. In addition, we are indebted to the talented team
ix
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SECTION I Brain 1
Figure 1.1. Five stages of parenchymal hematoma evolution on magnetic resonance imaging. One can easily remember the T1 and T2
characteristics of an evolving hematoma by memorizing this figure. Start from the center of the figure and move according to the direction of the
arrows to remember the signal characteristics of the five distinct phases of hematoma evolution.
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CHAPTER 1 Brain Parenchymal Hematoma Evolution 3
T1 T2 GRE
1
36 hours
1 month
Figure 1.2. Parenchymal hemorrhage at 36 hours and at 1 month after initial presentation. At 36 hours (acute phase), T2 signal is low and T1
signal remains intermediate consistent with intracellular deoxyhemoglobin. There is diffuse hypointensity on the gradient echo (GRE) image due to
the paramagnetic effects of deoxyhemoglobin. At 1 month (end of late subacute phase), central T1 and T2 hyperintensity is consistent with
extracellular methemoglobin, while peripheral T1 and T2 low signal is consistent with hemosiderin. The rim is hypointense on the GRE image due
to the superparamagnetic effects of hemosiderin. The hematoma is smaller due to retraction.
Figure 1.3. By convention, the most mature form of hemoglobin present defines the stage of hematoma evolution. The five stages of hemorrhage
depicted in Fig. 1.1 are seen in the bottom row of Fig. 1.3. Each stage depicts the most mature form of hemoglobin present in the hematoma.
They are not meant to imply homogeneity. The top row depicts intermediate stages of hematoma evolution between each step. In the
intermediate stages, the most mature form of hemorrhage is seen at the periphery.
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4 PART I Parenchymal Hemorrhage and Trauma
T1 T2 GRE
25 days
6 months
Figure 1.4. Parenchymal hemorrhage 25 days and 6 months after initial presentation. At 25 days (between early subacute to late subacute
phase), there is a T1 hyperintense rim and central hypointensity consistent with methemoglobin surrounding deoxyhemoglobin. T2 signal intensity
has evolved more rapidly, with near complete T2 hyperintensity, consistent with extracellular methemoglobin throughout the hematoma. At 6
months (between late subacute and chronic phases), hypointensity surrounds the encephalomalacic collapsing cavity on both T1 and T2 images
consistent with hemosiderin as the most mature form of hemoglobin. The hematoma is much smaller due to retraction.
GRE T2 T1 C+ CT
A B C D
Figure 1.5. Chronic collapsed posthemorrhagic cavity. Axial magnetic resonance images (A–C) and computed tomography (CT) image (D) of the
brain demonstrate hemosiderin within a thin collapsed T2 and T1 hypointense posthemorrhagic cavity barely visible on the CT image. GRE,
Gradient echo.
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CHAPTER 1 Brain Parenchymal Hematoma Evolution 5
A B C
D E F
Figure 1.6. Sources of confusion—superimposed blood products of differing ages and hemorrhagic fluid levels. A patient on anticoagulation with
a prior left frontal parenchymal hematoma and known subacute left frontal hemorrhagic cavity presents after an acute exacerbation. Coronal (A)
and axial (B and C) computed tomography images at the time of the acute exacerbation demonstrate a hypodense left frontal hemorrhagic cavity
with peripheral areas of hyperdense acute hemorrhage (arrows). There are also foci of acute subarachnoid hemorrhage (arrowheads). Axial T2 (D),
axial T1 (E), and axial gradient echo (F) magnetic resonance imaging (MRI) images of the brain performed on the same day demonstrate a
hemorrhagic fluid level within the subacute hemorrhagic cavity. Without the presence of an appropriate history, and considering the presence of
multiple confounding factors, it would be difficult to predict the age of this hemorrhage based on the MRI signal characteristics alone.
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2 Subdural Hemorrhage and Posttraumatic Hygroma
Lindsay A.N. Duy, Juan E. Small
Bone
Periosteal dura
Meningeal dura
Border cells
Arachnoid barrier
Subarachnoid space
Pia mater
Brain
Figure 2.1. A subdural hematoma is a crescent-shaped extraaxial collection of blood within the innermost layer of the dura, as depicted in red at
the bottom of the illustration. A magnified view of the meningeal layers between the inner table of the skull and the cerebral cortex is presented in
the top of the illustration. The dura consists of several different layers of adherent cells. The innermost layer is the dural border cell layer. It is
within this layer that subdural hematomas form.
6
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CHAPTER 2 Subdural Hemorrhage and Posttraumatic Hygroma 7
2
MV
MA
PA
SS
DP
BV
Figure 2.2. Dural vasculature. Both dural arteries and veins exist
along the superior and inferior aspects of the dura. Although
superficial meningeal arteries (MA) and veins (MV) are superficially
located, a rich dural venous plexus (DP) likely involved in cerebrospinal Figure 2.3. Acute subdural hematoma. A coronal image, performed
fluid resorption is located within the inner portion of the dura. This after an acute fall several hours prior, demonstrates left tentorial,
dural plexus is most dense parasagittally. BV, Bridging vein; PA, parafalcine, and right hemispheric hyperdense acute subdural
penetrating arteriole extending to inner dural plexus; SS, superior hematomas (red arrows).
sagittal sinus. (Modified from Mack J, Squier W, Eastman JT.
Anatomy and development of the meninges: implications for subdural
collections and CSF circulation. Pediatr Radiol. 2009;39:200–210.)
other words, many portions of these subdural collections are not
simply “blood” or “hematoma.” It should be now readily apparent
The fact that SDHs form within the innermost layer of the why the imaging characteristics of these collections generally do
dura is of crucial importance for a conceptual understanding of not conform to the magnetic resonance imaging (MRI) stages
the different types of subdural collections. This is because there of hematoma evolution so firmly established for parenchymal
is a rich venous plexus within this layer (Fig. 2.2). The small hematomas (Fig. 2.7).
caliber of these vascular structures is beyond the resolution of Both SDHs and subdural hygromas can be either acute or
our current imaging. Although there is still much that is unknown chronic. SDHs are classified into acute, subacute, or chronic
about its function, this venous plexus is thought to play a role categories, depending on the amount of time elapsed since the
in cerebrospinal fluid (CSF) resorption into the venous system. time of injury. As previously noted, this determination is classically
based on the density of the collection. At its most basic, the CT
density of a simple SDH depends on the time interval between
SUBDURAL HEMATOMA EVOLUTION: OVERVIEW the bleeding episode and imaging (Fig. 2.8).
At its most basic, there are two types of traumatic subdural col- Unfortunately, no uniformity exists as to the terminology and
lections: SDH and subdural hygroma. An acute SDH represents determination of these categories. For instance, categorization
acute blood products with or without clot formation. On CT of an acute SDH may be considered for a collection less than a
imaging, an acute SDH often presents as a hyperdense subdural week old, the subacute category reserved for collections ranging
collection (Fig. 2.3). in age from 1 to 3 weeks, and the chronic category reserved for
A subdural hygroma is the accumulation of clear or xanthochro- a collection older than 3 weeks. A prerequisite for dating by this
mic CSF within the subdural space. An acute subdural hygroma method is knowledge of the exact time of onset, which is frequently
results from the acute accumulation of CSF within the dural border absent in routine clinical practice. Alternatively, acute SDH may
cell layer. This can result from an acute tear in both the arachnoid be defined by blood products that are still clotted, subacute SDH
and the dural border cell layer, resulting in communication of reserved for collections in which the clot has lysed (generally
these two spaces. Alternatively, this can also result from the acute 2 days to several days), and chronic SDH for collections older
impairment of CSF resorption (as often seen in the setting of than 3 weeks. This method also leads to difficulties because the
subarachnoid hemorrhage), affecting the intradural venous plexus degree of clot formation can vary markedly, based on our previ-
along the inner layer of the dura. On CT imaging, an acute subdural ous discussion. Lastly, various patterns of subdural hemorrhage
hygroma exists when a CSF isodense or nearly isodense subdural may be seen other than simply a collection of uniform density
collection accumulates acutely (Fig. 2.4). (Fig. 2.9).
Of course, the presence of a subdural hygroma and an SDH Perhaps the most important differentiating feature between
is not mutually exclusive. Varying degrees and combinations of acute and chronic SDHs is the formation of neomembranes
clotted blood, unclotted blood, bloody CSF, and clear CSF can encapsulating the hemorrhage. Intracranial reparative processes
therefore be present within an acute subdural collection (Fig. 2.5). begin immediately after the acute separation of the dural border
These varying degrees and combinations of clot, blood, and cell layer and formation of an SDH. There is proliferation of the
bloody CSF are what lead to the marked heterogeneity of patient dural border cell layer shortly after injury, fibroblast appearance
imaging presentations (Fig. 2.6). within a day, formation of an outer membrane within a week,
The variable concentrations of either blood or CSF within a and formation of an inner membrane in approximately 3 weeks
specific area of the acute subdural collection lead to different fluid (Fig. 2.10).
properties and therefore different fluid behavior as time elapses. In Text continued on p 12
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8 PART I Parenchymal Hemorrhage and Trauma
A B C
Figure 2.4. Acute subdural hygroma. Axial computed tomography image conducted shortly after a motor vehicle accident (A) demonstrates
hyperdense subarachnoid hemorrhage within the right sylvian fissure (white arrow). One day later (B), a hypodense collection consistent with an
acute subdural hygroma is seen overlying the right frontal lobe (gray arrow). Complete resolution of the collection is evident 1 month later (C).
DURA
CLOT
BRAIN
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CHAPTER 2 Subdural Hemorrhage and Posttraumatic Hygroma 9
A B
C D
Figure 2.7. Variable concentrations of blood and cerebrospinal fluid (CSF) in a subdural collection lead to differentiating imaging features of
subdural hematoma and subdural CSF. Axial noncontrast computed tomography (CT) image of the brain (A) demonstrates right hemispheric and
parafalcine subdural collections (orange arrows). Comparing coronal noncontrast CT (B) to coronal post contrast T1 (C) and coronal T2 magnetic
resonance (D) images of the brain demonstrates to better advantage the differences between various portions of the right hemispheric subdural
collection. In particular, on the coronal T2 image, the differences between the normal left-sided subarachnoid space (blue arrow), right-sided
subdural hematoma (red arrow), right-sided subdural clot (orange arrow), and subdural CSF (yellow arrow) are readily evident.
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10 PART I Parenchymal Hemorrhage and Trauma
A B C
Figure 2.8. Classic descriptions of acute, subacute, and chronic subdural hematoma density. A left tentorial hyperdense subdural hematoma is
evident on an axial computed tomography image a few hours after head trauma (A, white arrow). At 2.5 weeks, heterogeneously isodense blood
products are evident (B, white arrow). By 4 weeks, the hematoma is entirely hypodense as compared with the brain parenchyma (C, white arrow).
A B C
Figure 2.9. Different patterns of subdural density may be seen. An acute homogeneously hyperdense subdural hematoma (A, arrow) easily lends
itself to a word description of its density. Other patterns of hemorrhage, including heterogeneous (B, arrow) and layering (C, arrow) collections, do
not as easily conform to simply hyperdense, isodense, or hypodense categories. Estimating age based on density is therefore more challenging
for complex collections.
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CHAPTER 2 Subdural Hemorrhage and Posttraumatic Hygroma 11
OM
CSDH
DURA
OM
DURA
A B
IM
IM
IM
BRAIN
C D
Figure 2.10. Neomembranes encapsulate a chronic subdural hematoma. Operative photographs during craniotomy for chronic subdural
hematoma evacuation demonstrate an outer membrane (OM) immediately under the reflected dura (A). After partial removal of the OM, the
chronic subdural hematoma (CSDH) can be seen as heterogeneous old blood products (B). After removal of the chronic blood products, the inner
membrane (IM) is evident (C). Only after incision of the IM can the brain be seen (D). (Courtesy Dr. Khalid Al-Kharazi.)
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immédiat du village. — Une herborisation dans le lit de l’Oued El-
Kantara, et à la base de la Montagne-de-sel (Djebel Mélah), nous
présente la plupart des espèces sociales caractéristiques de la
région saharienne, entre autres les Limoniastrum Guyonianum,
Statice pruinosa, Linaria fruticosa, Sonchus quercifolius, etc.
Liste des plantes observées près d’El-Outaïa dans le lit de l’Oued El-Kantara et à
la base de la Montagne-de-sel.