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Contents I
MEDICAL RADIOLOGY
Diagnostic Imaging
Softcover Edition
Editors:
A. L. Baert, Leuven
K. Sartor, Heidelberg
Contents III
M. Forsting (Ed.)
Intracranial
Vascular
Malformations and
Aneurysms
From Diagnostic Work-Up to Endovascular Therapy
With Contributions by
C. Cognard · A. Dörfl er · M. Forsting · W. Küker · L. Pierot · L. Spelle · I. Szikora
I. Wanke
Foreword by
K. Sartor
With 157 Figures in 587 Separate Illustrations, 16 in Color and 9 Tables
123
IV Contents
Michael Forsting, MD
Professor of Neuroradiology
Institute of Diagnostic and Interventional Radiology
Department of Neuroradiology
University of Essen
Hufelandstrasse 55
45122 Essen
Germany
Medical Radiology · Diagnostic Imaging and Radiation Oncology
Series Editors: A. L. Baert · L. W. Brady · H.-P. Heilmann · M. Molls · K. Sartor
Continuation of Handbuch der medizinischen Radiologie
Encyclopedia of Medical Radiology
ISBN 3-540-26250-4 Springer-Verlag Berlin Heidelberg New York
ISBN 978 3-540-26250-3 Springer-Verlag Berlin Heidelberg New York
Library of Congress Cataloging-in-Publication Data
Intracranial vascular malformations and aneurysms : from diagnostic work-up to
endovascular therapy / M. Forsting (ed.) ; with contributions by C. Cognard ... [et al.] ;
foreword by K. Sartor.
p. ; cm. -- (Medical radiology)
Includes bibliographical references and index.
ISBN 354042430X (hardcover; alk. paper) ISBN 3540262504 (softcover; alk. paper)
1. Intracranial aneurysms. 2. Subarachnoid hemorrhage. 3. Diagnostic Imaging. I.
Forsting, M. (Michael), 1960- II. Cognard, C. (Christophe) III. Series.
[DNLM: 1. Intracranial Arteriovenous Malformations--diagnosis. 2. Diagnostic
Imaging. 3. Intracranial Aneurysms--diagnosis. 4. Intracranial Aneurysm--therapy. 5.
Intracranial Arteriovenous Malformations--therapy. WL 355 I615 2003]
RD594.2 .I586 2003
616.1’33--dc21 2002075766
This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recitations, broadcasting, reproduction on microfi lm or
in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the
provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always
be obtained from Springer-Verlag. Violations are liable for prosecution under the German Copyright Law.
Springer-Verlag is part of Springer Science+Business Media
http//www.springeronline.com
© Springer-Verlag Berlin Heidelberg 2004, 2006
Printed in Germany
The use of general descriptive names, trademarks, etc. in this publication does not imply, even in the absence of a specifi c
statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.
Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained
in this book. In every case the user must check such information by consulting the relevant literature.
Cover-Design and Typesetting: Verlagsservice Teichmann, 69256 Mauer
Printed on acid-free paper - 21/3151xq – 5 4 3 2 1
Contents V
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Foreword
The radiology of vascular malformations and aneurysms is intimately related to the
evolution of magnetic resonance (MR) imaging, digital subtraction angiography (DSA)
and catheter-based endovascular therapy. Prior to the advent of MR imaging radiologists knew little of so-called venous angiomas (today: developmental venous anomalies), cavernous hemangiomas (cavernomas) or capillary teleangiectasias, as most of
these angiodysplasias could not be diagnosed reliably by computed tomography (CT)
or invasive angiography, let alone the earlier encephalographic techniques with positive
or negative contrast. But only after MR imaging at fi eld strengths of 1 T or higher had
become standard did it become clear how common these aberrations of vascular development actually are, in particular cavernomas and developmental venous anomalies.
This surprised even the pathologists and again required the radiologists to learn more
about these anomalies and abnormalities, such as their pathogenesis, histopathology,
epidemiology, genetics, and natural history, including their propensity to bleed. It also
required them to be able to differentiate these angiodysplastic lesions from non-vascular
lesions of potentially graver signifi cance.
Advanced knowledge regarding vascular malformations and aneurysms is now there,
but the interested radiologist is still forced to gather it from multiple sources, mostly
original articles in journals, treatises on specifi c topics, and other publications of a more
or less limited scope. This is why Michael Forsting, a neuroradiological “all-rounder”
with a strong bent towards and considerable experience in minimally invasive endovascular therapy of intracranial vascular abnormalities, has put great effort into producing
a book that condenses the existing information in one handy volume. In doing so he has
been helped by members of his department at University of Essen as well as by friends
and colleagues from leading neuroradiologic institutes in several European countries.
What came out of this joint effort is a well-organized, beautifully illustrated monograph that leaves little to be desired: Whenever one is in need of concise, comprehensive clinical, diagnostic and (endovascular-) therapeutic information on intracranial
vascular malformations and aneurysms – here it is. The book, rich in important facts,
numbers and details, impresses perhaps most by its didactic structure and overall style.
For this reason, I believe, it will quickly fi nd a large readership among radiologists and
neuroclinicians alike. Possibly quite a number of copies will end up on the desks of clinical pathologists who sometimes do envy us for the possibility to visualize and diagnose
most brain lesions in vivo rather than in tabula.
Heidelberg Klaus Sartor
Contents VII
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Preface
Why a book about the diagnostic imaging and endovascular therapy of vascular malformations? There is a simple answer: This is a fascinating part of neuroradiology, it has
many interdisciplinary aspects and it has become a large fi eld of my and our professional
life. The book should have been ready at least one year earlier, but there was always
something new that had to be included. Still, I am sure, each reader will miss something
he or she has just heard at a meeting or read in the current issue of a journal. On the
other hand, there is already a wealth of established basic knowledge about diagnostic
imaging and endovascular therapy that will not change fast and justifi es writing a book
instead of a review paper.
There are a lot of basics one should know about vascular malformations of the brain,
and during our daily practice my colleagues and I see a lot of images and patients that
do not have a proper diagnosis or have had a lengthy odyssey before fi nding an expert.
We all hope that our book will fi nd readers who are willing to go into this important
aspect of radiology and will enable them to care for their patients in a professional way.
And it is not only written for interventional neuroradiologists: it should be of interest
for everybody working in “neuro-disciplines”.
Although we belong to the younger generation of European neuroradiologists – we
know that age is a moving target, but never mind – we chose not to write a modern
book with colored “memory boxes” or other such aids, but an old-fashioned textbook.
It is something to read at leisure – perhaps on a pleasant evening with a glass of red
wine beside you - and memory will be supported by some redundancies and repetitions.
Anyone in a hurry can run through the book just looking at the many images.
We invite all readers to help us improve the next edition. If something is good, let us
know! More importantly, if something is not good or even wrong, please give us a call or
send us an e-mail!
It was tough work, but fi nally we enjoyed it. We owe a debt of thanks to Ursula Davis
of Springer-Verlag, who continuously pushed us to fi nalize it, always friendly and always
stimulating.
Last but not least, a lot of people contributed substantially to this book without writing a chapter by themselves. They include my academic teachers Hermann Zeumer
(Hamburg), Armin Thron (Aachen) and Klaus Sartor (Heidelberg), who gave the fi rst
impulse to write this book. I would like to thank them for supporting me during my
whole professional career and for numerous stimulating discussions on vascular problems of the brain.
Essen Michael Forsting
Contents IX
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Contents
1 Developmental Venous Anomalies
M. Forsting and I. Wanke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.1 Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.2 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2
1.3 Diagnostic Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
1.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
2 Cavernomas and Capillary Telangiectasias
W. Kü k e r and M. Forsting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
2.1 Cavernomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
2.2 Capillary Telangiectasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
3 Pial Arteriovenous Malformations
C. Cognard, L. Spelle, and L. Pierot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
3.2 Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
3.3 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
3.4 Diagnostic Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
3.5 Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
4 Dural Arteriovenous Malformations
I. Szikora . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
4.1 Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
4.2 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
4.3 Diagnostic Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120
4.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126
5 Intracranial Aneurysms
I. Wanke, A. Dörfl er and M. Forsting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143
5.1 Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
5.2 Clinical Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152
5.3 Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162
5.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 249
List of Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
Developmental Venous Anomalies 1
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1 Developmental Venous Anomalies
M. Forsting and I. Wanke
CONTENTS
1.1 Pathology 1
1.2 Clinical Presentation 2
1.3 Imaging 9
1.4 Therapy 11
References 12
In a typical neurovascular working day, developmental venous anomalies (DVAs) are causing a lot of confusion. In part, this confusion is related to the term
“venous angioma”, which is used in many institutions as a synonym for DVA! But, “venous angioma” is
clearly a misnomer, because the term “angioma” usually suggests a severe disease with a substantial risk
of bleeding. In contrast, DVAs must be considered as
unusual, but nonpathological, venous drainage and
an embryologically determined variant of venous
drainage. On the other hand: DVAs are considered
to be the most common form of cerebral vascular
malformations, occurring in up to 4% of the population (Garner et al. 1991; Ostertun and Solymosi
1993; Truw it 1992). This high incidence is a good
reason to familiarize oneself with these lesions and
keep abreast of new fi ndings in this area.
In my experience, another factor contributing to
the DVA-related confusion is that many radiologists
and clinicians just see abnormal vessels on magnetic
resonance imaging (MRI) scans, immediately tell the
patient something about a vascular malformation,
and refer the patient for neurosurgical extirpation
of the lesion.
To avoid too much irritation, specifi cally within
the group of referring doctors, the term “venous
angioma” should be avoided and DVA should be
used. However, if you are reporting about a DVA, it is
usually necessary to explain what this is. And this is a
good reason to read the upcoming chapter.
M. Forsting, MD, PhD; I. Wanke, MD
Institute of Diagnostic and Interventional Radiology,
Department of Neuroradiology, University of Essen,
Hufelandstrasse 55, 45147 Essen, Germany
1.1
Pathology
The pathogenesis of a DVA is still unknown. Saito
and Kobayashi et al. (1981) hypothesized that an
intrauterine event during formation of the medullary veins or tributaries induces the formation of collateral venous drainage pathways. This hypothesis is
supported by the absence of normal draining veins in
the region of the large draining collector vein.
Another assumption is that an in-utero acquired
venous occlusion maintains the intrinsic venous
anastomoses within the white matter. The DVA then
expresses an early collateral adaptation, but develops on a preexisting venous system that has been
transformed. However, the majority of DVAs are not
associated with any sort of neural tissue damage or
dysfunction. Lasjaunias (1997) commented on this
theory that it can hardly be imagined that a signifi cant venous disorder (such as thrombosis) at an early
stage of development would not be associated with
some tissue abnormality. Furthermore, the fact that
DVAs do not exist in the diencephalon, brain stem, or
spinal cord and are only encountered where tectum
derivates exist, excludes DVAs from the group of
pathological malformations (Lasjaunias 1997).
The association of venous malformations with
other vascular malformations gave further room for
speculation. Mullan et al. (1996) hypothesized that
true arteriovenous (AV) malformations may be fi stulized venous malformations and that both vascular
anomalies may be related to a developmental failure
of the cortical venous system. However, these are nice
theories, but do not have any impact on diagnostic
work-up or patient management, nor are they supported by any study. Kilic et al. (2000) looked for
expression of structural proteins and angiogenic factors in cerebrovascular anomalies. Whereas AVM and
cavernomas had expression of vascular endothelial
growth factor, DVAs did not express any of the studied growth factors and mainly consisted of structural
proteins of angiogenically mature tissue. This fi nding strongly supports the idea of a simple variation of
2
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M. Forsting and I. Wanke
the venous drainage instead of being a true vascular
malformation.
In contrast, the relationship of DVAs with cavernous hemangiomas has been well documented
(Abe et al. 1990; Comey et al. 1997; Goulao et al.
1990; Rigamonti and Spetzler 1988; Wi l ms et al.
1994). There are also reports about de novo formation of cavernous hemangiomas in the vicinity of
DVAs (Ciricillo et al. 1994). The close relationship
of mixed malformations may be related to venous
hypertension within the regional microenvironment
with erythrocyte diapedesis and angiogenic growth
factor release (Cirillo et al. 1994; Robinson et al.
1995). Another interesting fi nding is that in families
affected with cavernomas – an autosomal dominant
inheritance has been established in these families
– none of the patients described to date with the
combination of cavernoma and DVA has a positive
familial history, nor has any genotypic classifi cation
been found. However, we have to accept the coincidence between DVAs and cavernomas, but have to
admit that we do not have any substantial hypothesis
what the pathogenetic origin of this coincidence is.
The histologic examination does not reveal any
vessel abnormality. The vessel wall is completely
normal in DVAs. The anomaly in DVAs is the course
of the draining vein. There is no arterial component in
this entity. Intervening brain tissue is present between
the veins compromising the lesion, and this brain
tissue is usually normal without evidence of hemosiderin staining or gliosis. On MRI, there is sometimes a
high T2-signal visible around the draining vein. However, this should not be interpreted as gliosis, but can
be explained by dilated perivascular and cerebrospinal
fl uid (CSF)-containing space (see Fig. 1.4).
Developmental venous anomalies represent the
most common vascular variant, accounting for 63%
of intracranial vascular malformations in one large
autopsy study, with an overall incidence of 2%–4%
(Sarwar and McCormick 1978). The lesion consists
of a tuft of abnormally enlarged medullary venous
channels that are radially arranged around, and drain
into a central venous trunk. The common trunk drains
intracerebrally into the deep or superfi cial venous
system (Lasjaunias 1997). It is important to bear in
mind that the vein’s course is not normal; however,
it does drain normal functioning brain tissue. This
should be of particular interest when surgery has to be
performed around the draining vein, e.g., if the DVA is
associated with a cavernoma. In these patients, it is of
the utmost importance to preserve the draining vein
and to remove only the cavernoma (see Fig. 1.7).
1.2
Clinical Presentation
Hemodynamically, DVAs represent low-fl ow, lowresistance lesions that are less likely to bleed. Garner
et al. (1991) calculated the hemorrhage rate to be
0.22% per year; McLaughlin et al. (1998) found
a symptomatic hemorrhage rate of 0.34% per year.
This range of hemorrhage risk is within the range we
expect from cavernous hemangiomas alone. Based
on these data and on hemodynamics, one might
already conclude that hemorrhages in the presence
of a DVA are not related to the DVA itself, but in
nearly all patients related to an associated cavernous
angioma! My opinion is that the risk of hemorrhage
a b
Fig. 1.1. a Axial nonen-
hanced computed tomography scan reveals a hyperdense dot within the right
frontal lobe representing
the transcerebral draining collector vein. b The
contrast-enhanced scan
with a 4-mm slice thickness
[explaining the decreased
signal-to-noise ratio compared to (a)] shows the
marked enhancement of the
vein and confi rms the diagnosis of a developmental
venous anomaly
Developmental Venous Anomalies 3
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a b
Fig. 1.2a, b. Axial (a) and sagittal (b) contrast-enhanced T1-weighted magnetic resonance imaging with a typical right fron-
tal developmental venous anomaly. Conspicuous on both views is the transcerebral draining vein. A second look reveals the
“Medusa head”, small venules radially arranged around and draining into the transcerebral collector vein
in a pure DVA is around zero! I did not fi nd a single
case report with a well documented intracerebral
hemorrhage (ICH) due to a pure DVA. However, this
is not evidence-based, just a simple clinical impression gained over the years. In all cases mentioning a
pure DVA as the cause of an ICH, imaging was not
optimal and did not rule out the more common constellation with an associated cavernoma.
The coincidence of DVAs and cavernomas, however, is evidence-based and therefore has to be taken
into consideration whenever facing a cavernoma or
a DVA. Up to one third of DVAs are associated with
cavernomas (see Figs. 6–9).
a
Fig. 1.3a, b. Axial
contrast-enhanced
T1-weighted magnetic
resonance imaging
with a developmental venous anomaly
located in the left
cerebellar hemisphere.
Again, the transparenchymal draining
vein is the most striking sign. On (b), the
Medusa head is clearly
visible. There is no
need for an additional
digital subtraction
angiography
A major problem of most studies reporting hemorrhages due to a DVA is how they ruled out an associated cavernoma. It is clearly not enough just to perform
T2-weighted images in patients with DVAs. All these
patients need an imaging work-up with T2*-weighted
MRI sequences to exclude or to visualize associated
cavernomas with the highest sensitivity.
Beside the risk and discussion of hemorrhagic
complications, DVAs have been associated with vague
neurological symptoms, such as nonspecifi c headaches and dizziness, or with more specifi c symptoms
and/or signs like seizures (McLaughlin et al. 1998).
However, having in mind the association of caver-
b
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