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Pearls and Pitfalls in
HEAD AND NECK AND
NEUROIMAGING
Variants and
Other Difficult
Diagnoses

Nafi Aygun
Associate Professor of Radiology and Director of the Neuroradiology
Fellowship Program, Johns Hopkins University, Baltimore, MD, USA

Gaurang Shah
Associate Professor of Radiology, University of Michigan Health
System, Ann Arbor, MI, USA

Dheeraj Gandhi
Professor of Radiology, Neurology and Neurosurgery at the
University of Maryland School of Medicine, Baltimore, MD, USA
University Printing House, Cambridge cb2 8bs, United Kingdom

Published in the United States of America by Cambridge University Press, New York

Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the pursuit of
education, learning and research at the highest international levels of excellence.

www.cambridge.org
Information on this title: www.cambridge.org/9781107026643
© Cambridge University Press 2013
This publication is in copyright. Subject to statutory exception
and to the provisions of relevant collective licensing agreements,
no reproduction of any part may take place without the written
permission of Cambridge University Press.
First published 2013
Printed in Spain by Grafos SA, Arte sobre papel
A catalog record for this publication is available from the British Library
Library of Congress Cataloging in Publication data
Aygun, Nafi.
Pearls and pitfalls in head and neck and neuroimaging / Nafi Aygun, Gaurang Shah,
Dheeraj Gandhi.
p. ; cm.
Includes bibliographical references.
ISBN 978-1-107-02664-3 (Hardback)
I. Shah, Gaurang. II. Gandhi, Dheeraj. III. Title.
[DNLM: 1. Neuroimaging–methods. 2. Central Nervous System Diseases–diagnosis.
3. Diagnosis, Differential. 4. Otorhinolaryngologic Diseases–diagnosis. WL 141.5.N47]
RC349.D52
616.80 04754–dc23 2013010572
ISBN 978-1-107-02664-3 Hardback
Cambridge University Press has no responsibility for the persistence or accuracy of
URLs for external or third-party internet websites referred to in this publication,
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.
..........................................................................................................................

Every effort has been made in preparing this book to provide accurate and
up-to-date information which is in accord with accepted standards and
practice at the time of publication. Although case histories are drawn from
actual cases, every effort has been made to disguise the identities of the
individuals involved. Nevertheless, the authors, editors and publishers can
make no warranties that the information contained herein is totally free
from error, not least because clinical standards are constantly changing
through research and regulation. The authors, editors and publishers
therefore disclaim all liability for direct or consequential damages resulting
from the use of material contained in this book. Readers are strongly
advised to pay careful attention to information provided by the manufacturer
of any drugs or equipment that they plan to use.
To my parents, Vrindavan and Vinu Shah, for their love and support;
my wife Kinnari, for taking the journey with me; and my sons Sharvil and Sahil,
for bringing joy into our lives.

Gaurang Shah

To Bobby, my best friend and life partner and for Shreya and Diya,
my beautiful daughters and the love of my life.

Dheeraj Gandhi
Contents
Preface ix

Section 1 Cerebrovascular diseases Section 4 Infectious diseases

Case 1 Dense basilar artery sign 1 Case 36 Brain abscess 191
Case 2 Global anoxic brain injury 4 Case 37 Neurocysticercosis 194
Case 3 Acute infarction 8 Case 38 Tuberculosis 198
Case 4 Vertebral artery dissection 10 Case 39 Creutzfeldt–Jakob disease 207
Case 5 Subacute infarct 13 Case 40 Herpes encephalitis 210
Case 6 Subarachnoid hemorrhage 17
Case 7 Intracranial aneurysms 21
Case 8 Giant aneurysms 23
Section 5 Metabolic and neurodegenerative
Case 9 Acute intracerebral hematoma 26 conditions
Case 10 Cerebral amyloid angiopathy 30 Case 41 Wernicke’s encephalopathy 213
Case 11 Primary CNS vasculitis 34 Case 42 Hypertrophic olivary degeneration 217
Case 12 Reversible cerebral vasoconstriction Case 43 Adrenoleukodystrophy 219
syndrome 37
Case 13 Moyamoya disease/syndrome 40
Case 14 Cortical venous thrombosis 43 Section 6 Trauma
Case 15 Developmental venous anomalies 46
Case 44 Mild traumatic brain injury 224
Case 16 Dural arteriovenous fistula 49
Case 45 Isodense subdural hematoma 227
Case 17 Cavernous malformation 52

Section 7 Miscellaneous
Section 2 Demyelinating and inflammatory
Case 46 Posterior reversible encephalopathy syndrome 229
diseases Case 47 Late-onset adult hydrocephalus secondary to
Case 18 Tumefactive demyelinating lesion 55 aqueductal stenosis 232
Case 19 Acute disseminated encephalomyelitis 58 Case 48 Intracranial hypotension 234
Case 20 Progressive multifocal Case 49 Idiopathic intracranial hypertension 238
leukoencephalopathy 62 Case 50 Rathke’s cleft cyst 240
Case 21 Osmotic myelinolysis 65
Case 22 Neurosarcoidosis 72
Section 8 Artifacts and anatomic variations
Case 51 FLAIR sulcal hyperintensity secondary to general
Section 3 Tumors anesthesia 245
Case 23 Posterior fossa masses in children 80 Case 52 Virchow–Robin spaces 250
Case 24 Low-grade glioma 92 Case 53 Arachnoid granulations 255
Case 25 Diffuse intrinsic pontine glioma 105 Case 54 Benign external hydrocephalus 257
Case 26 Pseudoprogression of GBM 109 Case 55 Pitfalls in CTA 260
Case 27 Pseudoresponse in treatment of GBM 112 Case 56 Asymmetric pneumatization of the anterior
Case 28 Low-grade oligodendroglioma 114 clinoid process 264
Case 29 Primary CNS lymphoma 116
Case 30 Pineal region tumors 125
Case 31 Intraventricular masses 140
Section 9 Skull base
Case 32 Colloid cyst 153 Case 57 Fibrous dysplasia of skull base 267
Case 33 Primary intraosseous meningioma 161 Case 58 Sphenoid bone pseudolesion 271
Case 34 Suprasellar meningioma 171 Case 59 Clival lesions 276
Case 35 Pituitary macroadenoma 180 Case 60 Perineural spread 282

vii
 Contents

Section 10 Temporal bone Section 16 Vessels

Case 61 Cochlear dysplasia 285 Case 84 Carotid artery dissection 381
Case 62 Labyrinthitis ossificans 289 Case 85 Traumatic arterial injury 384
Case 63 Superior semicircular canal dehiscence 292
Case 64 Fluid entrapment in the petrous apex cells 294
Case 65 Acquired cholesteatoma 299 Section 17 Spinal column
Case 66 Malignant otitis externa 304 Case 86 Craniovertebral junction injuries 387
Case 67 Temporal bone fractures 307 Case 87 Odontoid fractures 390
Case 88 Vertebral compression fractures 398
Case 89 Sacral insufficiency fracture 401
Section 11 Paranasal sinuses Case 90 Paget’s disease of the spine 405
Case 68 Allergic fungal sinusitis 310 Case 91 Renal osteodystrophy 409
Case 69 Invasive fungal sinusitis 316 Case 92 Calcific tendinitis of the longus colli 414
Case 70 Spontaneous CSF leaks and sphenoid
cephaloceles 324
Case 71 Juvenile nasal angiofibroma 328 Section 18 Intervertebral discs
Case 93 T2 hyperintense disc herniation 419
Case 94 Disc herniation and cord compression 424
Section 12 Orbits Case 95 Postoperative disc herniation versus postsurgical
Case 72 Idiopathic orbital pseudotumor 331 scarring 427
Case 73 Optic neuritis 336 Case 96 Degenerative endplate alterations 430

Section 13 Salivary glands Section 19 Spinal canal contents

Case 74 Intraparotid lymph nodes 342 Case 97 Spinal dysraphism 434
Case 75 Benign mixed tumor 344 Case 98 Tethered spinal cord 445
Case 76 First branchial cleft cyst 350 Case 99 Chiari I malformation 449
Case 100 Spinal vascular malformations 455
Case 101 Cord compression 458
Section 14 Neck Case 102 Demyelinating/inflammatory spinal
Case 77 Nasopharyngeal cysts 354 cord lesion 466
Case 78 Cystic nodal metastasis 357 Case 103 Subacute combined degeneration 469
Case 79 Low-flow vascular malformations 360 Case 104 Intradural cyst 471
Case 80 Parapharyngeal masses 364 Case 105 Spinal CSF leaks 475
Case 106 Leptomeningeal drop metastases 478

Section 15 Thyroid and parathyroid Index 486

Case 81 Third branchial apparatus anomaly 370
Case 82 Parathyroid adenoma 372
Case 83 String sign 378

viii
Preface
“A teacher is one who makes himself progressively unnecessary.” Each chapter is concise, yet gives a comprehensive overview of
– Thomas Carruthers the subject matter.
It is with a great sense of pride that we introduce our endeavor We understand that time is precious and therefore wanted to
entitled Pearls and Pitfalls in Head and Neck and Neuro- create a resource that is precise and trustworthy. It is our hope
imaging. We hope that this book will be fun to read and foster that this treatise is easy to follow, unpretentious, and helpful.
the understanding of difficult diagnoses and common pitfalls We would like to thank all the Cambridge University Press
in Neuroimaging. staff who helped us tremendously every step of the way. In
We have different backgrounds and sub-specialty Neuro- particular, we express our gratitude to Nisha Doshi and Beata
imaging expertise, but have one thing in common – the love Mako. Gaurang would also like to express his gratitude to
and passion for teaching the residents and fellows. This has Suresh Mukherji, Mark Shiroishi, Sanjay Jain, Prasan Rao,
resulted in accumulation of thousands of teaching files in our Jayant Narang and Mohammad Arabi for sharing their images
respective libraries. Years spent with the trainees in the read- and wisdom.
ing room in wonderful academic institutions have given us an Our sincere thanks to the clinicians working with us for
understanding of diagnoses that are commonly missed and providing ever so important clinical feedback and learning
imaging findings that are likely to be misinterpreted. that comes with it. Last but not the least, we thank our families
While a number of excellent books exist on the subject and for their unconditional support and patience during the
practice of Neuroradiology, a book like this is unique. It aims writing of this project.
to cover the lacunae that commonly exist in the knowledge of We hope that the readers will enjoy reading this book.
Neuroimaging and gives clarity to diagnoses that are difficult We are open to any suggestions or criticism that the readers
to make with certainty. may have for its improvement and look forward to hearing
After deciding to proceed with this project, the three from you.
of us brainstormed and came up with 106 topics that we
wanted to cover. These topics were divided into 19 sections. Nafi, Gaurang, and Dheeraj

ix
CASE
1 Dense basilar artery sign
Imaging description diffusely hyperdense vessels that can potentially mimic the
dense artery sign. Partial volume averaging, vessel tortuosity,
Intravascular clot can be seen on unenhanced CT as a focal
or ectesia may also make a portion of the vessel appear denser
hyperattenuation and may be the only sign of acute ischemia
than the other parts. Most of these possibilities can be elimin-
(Fig. 1.1). A thrombosed vessel has a higher CT attenuation
ated by using thinner slices and comparing the vessel segment
value than a normal vessel, because clot contains more protein
in question to other vessels of similar size on the same CT [4].
and less serum than blood due to the deposition of fibrinogen
Of course, it is crucial to have appropriate clinical correlation.
and other clotting proteins and extraction of serum during
Contrast-enhanced CT/CTA or MRI/MRA can be used as a
the process of thrombus formation. When CT shows a focal
problem solver in ambiguous cases. It should be also kept in
hyperattenuation in the middle cerebral artery (MCA) this
mind that the sensitivity of the dense vessel sign is relatively
is known as the dense MCA sign. This provides not only a
low. In other words, absence of dense artery sign does not
diagnosis of MCA territory infarct but also some prognostic
exclude vessel occlusion or brain infarct.
information, because stroke patients who demonstrate a dense
MCA sign on their initial CT do relatively poorly compared
to those who do not have this sign (Fig 1.2) [1]. Clot in the Teaching points
basilar artery is not as common as MCA thrombus, but The dense basilar artery sign indicates basilar artery throm-
the same principles that lead to the dense MCA sign apply to bosis, basilar artery territory infarcts, and a poor outcome. In
basilar artery thrombosis (Fig. 1.1) [2]. Similarly, thrombosis the appropriate clinical setting, the specificity of this finding
of the other intracranial vessels, including the veins and dural is high although sensitivity is only moderate. Using thinner
sinuses, can be diagnosed on the basis of dense clot present slices, comparing the density of the vessel in question to that
within the vessel (Figs. 1.3, 1.4). of other vessels of similar size, helps to differentiate intralum-
inal clot from mimickers such as atherosclerosis, hemocon-
Importance centration, and vessel tortuosity. To confirm the presence of
Unenhanced CT is the first imaging study performed in most vessel occlusion, contrast-enhanced CT may be employed as
acute neurologic presentations. Diagnosing a vascular occlu- a quick problem solving tool, although CTA, MRI/MRA, and
sion early has great prognostic significance. Early initiation of sometimes digital subtraction angiography (DSA) are neces-
treatment is the most important factor in achieving improved sary to better characterize the extent of vessel occlusion,
outcomes in the setting of basilar occlusion [3]. collateral vessels, and infarcted areas.

Typical clinical scenario

MCA territory infarcts are relatively easy to diagnose clinic- references
ally, as patients present with focal neurologic deficits and 1. Zorzon M, Masè G, Pozzi-Mucelli F, et al. Increased density in the
consciousness is usually not altered. Basilar artery territory middle cerebral artery by nonenhanced computed tomography:
infarcts, on the other hand, may lack localizing features and prognostic value in acute cerebral infarction. Eur Neurol 1993; 33: 256–9.
are associated with varying degrees of alteration in conscious- 2. Goldmakher GV, Camargo EC, Furie KL, et al. Hyperdense basilar
ness that require a broader clinical differential diagnosis than artery sign on unenhanced CT predicts thrombus and outcome in acute
anterior circulation infarcts. posterior circulation stroke. Stroke 2009; 40: 134–9.
3. Eckert B, Kucinski T, Pfeiffer G, Groden C, Zeumer H. Endovascular
Differential diagnosis therapy of acute vertebrobasilar occlusion: early treatment onset as the
Increased attenuation in a vessel can result from increased most important factor. Cerebrovasc Dis 2002; 14: 42–50.
attenuation of the blood or the vessel wall in addition to 4. Gadda D, Vannucchi L, Niccolai F, et al. Multidetector computed
intraluminal clot formation. Atherosclerosis results in focally tomography of the head in acute stroke: predictive value of different
increased attenuation in vessel wall that can mimic thrombus. patterns of the dense artery sign revealed by maximum intensity
Increased hematocrit due to hemoconcentration or systemic projection reformations for location and extent of the infarcted area.
disorders such as chronic obstructive lung diseases may cause Eur Radiol 2005; 15: 2387–95.

1
 SECTION 1 Cerebrovascular diseases

A B C

Figure 1.1 Acute basilar artery thrombosis. (A, B) Axial unenhanced CT images show increased attenuation in the basilar artery (arrows) as
compared to the left middle cerebral artery (short arrow), indicating basilar artery thrombosis, in this patient with acute deterioration of
neurologic status and alertness. (C) Axial image from a CTA performed shortly after shows lack of contrast filling of the basilar artery (arrow)
compared to the carotids.

Figure 1.2 Axial CT images show increased

attenuation associated with the left MCA
and its branches (arrows) compatible with
thrombosis. Decreased gray/white
differentiation in the left insular ribbon and
putamen (short arrow) is compatible with
acute infarct.

2
 Dense basilar artery sign CASE 1

Figure 1.3 Axial CT shows a marked hyperattenuation in the

right transverse sinus, which was confirmed to represent acute
thrombosis.

Figure 1.4 Axial CT shows thrombosis of the straight sinus

(arrow) and the vein of Galen (short arrow) with associated
hypoattenuation in the bilateral thalami.

3
 CASE 2 Global anoxic brain injury
Imaging description Typical clinical scenario
Anoxic–ischemic injury to the brain as a result of cardiore- Patients are typically comatose following cardiorespiratory
spiratory insufficiency, such as seen in cardiac arrest, respira- arrest, prolonged hypotensive episode, asphyxia, drowning, etc.
tory arrest, prolonged hypotension, and asphyxia, is difficult to
diagnose because of the subtlety and symmetry of abnormal- Differential diagnosis
ities seen on MRI and CT scans. These scans are frequently In the proper clinical setting there is no differential diagnosis.
misinterpreted, particularly when radiologists are not aware In strict radiological terms the differential diagnosis is between
of the clinical circumstances. CT scans show diffuse decrease a normal scan and a severely abnormal scan, as missing this
in gray/white differentiation and mild edema in the early injury will result in generation of a normal MRI or CT report.
stages. On MRI, diffuse increase in the cortical signal is seen One important clue is the difference in attenuation/signal of
on FLAIR/T2-weighted images as well as diffusion-weighted the supratentorial brain and cerebellum. Because the supraten-
images (DWI) in most cases (Figs. 2.1, 2.2), although different torial structures are preferentially affected there is usually a
patterns are occasionally encountered, including signal stark difference between cerebellum and brain. When only the
changes in the deep gray matter structures only, in both gray deep gray matter is involved (Fig. 2.4) the differential diagnosis
and white matter, and in the white matter only [1]. may include Creutzfeldt–Jakob disease (CJD) and metabolic
The underlying pathophysiologic processes leading to toxic injury, although the clinical features should be helpful in
differences in pattern are not clearly understood, although differentiating these. Only white matter involvement may be
essentially all types of global anoxic–ischemic injury portend confused with leukoencephalopathies radiologically (Fig. 2.5).
a very poor prognosis. DWI sequence is the most sensitive
imaging modality. DWI shows a much increased contrast Teaching points
difference between the diffusely abnormal cortex and rela-
tively preserved white matter, creating a more “eye-pleasing” Global hypoxic injury results in symmetric and subtle
appearance compared to a normal DWI scan, which shows changes on MRI and CT scans that are easily missed. Radi-
only a mild difference between gray and white matter ologists should be familiar with the normal contrast present
(Fig. 2.3). However, there are differences in the normal con- between the gray and white matter on their DWI sequences
trast present between the cortex and white matter in different and look for changes in that contrast in comatose patients.
MRI scanners and different DWI sequences, and radiologists
should become familiar with the normal appearance of the
DWI images in their practice settings. High-b-value DWI references
may increase sensitivity [2]. 1. Kim E, Sohn CH, Chang KH, Chang HW, Lee DH. Patterns of
accentuated grey-white differentiation on diffusion-weighted imaging or
Importance the apparent diffusion coefficient maps in comatose survivors after global
Anoxic–ischemic injury, particularly when it is severe, often brain injury. Clin Radiol 2011; 66: 440–8.
results in brain death, which has enormous implications 2. Tha KK, Terae S, Yamamoto T, et al. Early detection of global cerebral
for cessation of life support, family counseling, and organ anoxia: improved accuracy by high-b-value diffusion-weighted imaging
harvesting. with long echo time. AJNR Am J Neuroradiol 2005; 26: 1487–97.

4
 Global anoxic brain injury CASE 2

Figure 2.1 Axial FLAIR and DWI images show diffusely and symmetrically increased signal in the cortex and deep gray matter structures
compatible with global anoxic injury. The patient had a cardiac arrest and was declared brain-dead shortly after the MRI.

Figure 2.2 Axial CT images show diffuse loss of gray/white differentiation throughout the supratentorial brain compatible with global anoxic
injury. Note the attenuation of the cerebellum, which appears prominent relative to diffusely decreased attenuation of the brain. This is the
“white cerebellum sign.” Similar differences are observed on MRI, in particular in DWI images.

5
 SECTION 1 Cerebrovascular diseases

Figure 2.3 Axial DWI images of a patient

with global anoxic injury (left) and of a
normal individual (right) highlight the
abnormality more clearly.

Figure 2.4 A less common pattern of global anoxic injury. Axial FLAIR and DWI images show preferential involvement of the deep gray matter
with preservation of the cortex except in the perirolandic area.

6
 Global anoxic brain injury CASE 2

Figure 2.5 A much rarer form of global

anoxic injury. White matter is involved and
the cortex is spared, although quantitative
apparent diffusion coefficient (ADC)
evaluation showed some cortical
abnormality as well.

7
 CASE 3 Acute infarction
Imaging description investigators have used cerebral blood flow (CBF)–CBV
mismatch or mean transit time (MTT)–CBV mismatch to
CT has an unparalleled track record in the detection of
assess the penumbral tissue on CTP, although the latter maps
intracranial hemorrhage and therefore is the first imaging study
may be optimal (Fig. 3.3). However, CT has disadvantages
obtained in this setting. In addition to excluding intracranial
of radiation exposure and, in institutions lacking 256- or
hemorrhage, CT may help demonstrate early signs of acute
320-slice CTs, entire brain coverage is not possible. Post-
ischemic stroke (AIS), such as insular ribbon sign, hyperdense
processing is relatively more cumbersome, and thresholds vary
cerebral artery sign, sulcal effacement, and development
based on post-processing techniques.
of acute parenchymal low attenuation (Fig. 3.1). Patients
who have advanced signs of infarction involving more than Importance
one-third of the middle cerebral artery (MCA) territory are
Radiologists must be familiar with early signs of stroke on
generally excluded from intravenous tissue plasminogen acti-
CT as well as assessment of perfusion abnormalities in the
vator (tPA) therapy because of a higher risk for hemorrhagic
setting of stroke.
conversion.
Advanced imaging as a triage tool for selecting patients
for intravenous (IV) or intra-arterial (IA) stroke therapies Typical clinical scenario
beyond 3 hours is a focus of evaluation of many ongoing Stroke is characterized by a sudden, acute neurologic deficit
clinical trials [1]. Central to the idea of advanced imaging is that is referable to the involved vascular territory. Common
to obtain a precise measure of the area of ischemic core versus presentations include hemiparesis, facial droop, aphasia,
ischemic but still viable tissue that is at risk for infarction in and loss of consciousness, although a myriad of possible com-
the absence of early recanalization (penumbra). It can be binations of neurologic signs and symptoms are possible.
argued that patients can only benefit from recanalization if
there is a relatively modest area of already infarcted tissue and Differential diagnosis
significant (ideally >20% of area of core infarction) ischemic With proper clinical correlation, imaging diagnosis of stroke
tissue that can be potentially salvaged. is easily accomplished, especially on MRI. However, one must
Ideally, imaging would provide an assessment (or confirm- be alert to the possibility that there are numerous causes
ation) of occlusion of a major cerebral artery, a precise measure of restricted diffusion on DWI studies that need to be differ-
of the area of irreversible infarction, and assessment of the entiated from acute stroke. Common causes of diffusion
surrounding perfusion abnormality. MRI, using diffusion- abnormalities other than stroke include encephalitis, trau-
weighted imaging (DWI), has become the gold standard to matic lesions, acute demyelination, brain abscess, and highly
demonstrate the area of irreversible infarction. This tissue cellular neoplasms.
demonstrates high signal on DWI images and corresponding
reduction in apparent diffusion coefficient (ADC) values.
Salvageable penumbra can be operationally defined as a
Teaching points
mismatch between the perfusion MR volume and the DW Revascularization may be futile if there is no significant
MR volume, where the perfusion MR volume indicates presum- salvageable penumbral tissue (DWI–PWI mismatch). More-
ably ischemic, hypoperfused penumbral tissue and the DW MR over, such recanalization is potentially harmful, since it
volume represents irreversibly ischemic infarct core (Fig. 3.2). would restore blood flow to an already infarcted area.
CT imaging has its proponents, and they rely on a combin-
ation of CT angiography (CTA) (to demonstrate the vascular
occlusion/cut-off) and CT perfusion (CTP). The area of irre- references
versible infarction on CTP should demonstrate decrease in 1. Köhrmann M, Schellinger PD. Acute stroke triage to intravenous
cerebral blood volume (CBV), and it can serve as a surrogate thrombolysis and other therapies with advanced CT or MR imaging:
for DWI imaging. Similar to DWI–PWI mismatch, pro MR imaging. Radiology 2009; 251: 627–33.

8
 Acute infarction CASE 3

Figure 3.1 (A) Hyperdense middle cerebral artery

(MCA) sign in a patient with acute left hemiparesis
(arrow). (B) In another patient with acute stroke, the
insular ribbon sign is noted (arrow). Additionally, the
right-sided sulci are effaced and there is early
parenchymal hypoattenuation, in comparison with
the normal left side.

Figure 3.2 Utility of MRI as a trial tool for IA thrombolysis. (A) DWI, (B) PWI (MTT map), and (C) 3D time-of-flight (TOF) MRA are
demonstrated in a patient with acute right MCA occlusion. Note a very small ischemic core on DWI, relatively large PWI defect, and occlusion
of right M1 segment (arrow). This was successfully recanalized with IA thrombolysis, and neurologic deficits markedly improved.

Figure 3.3 MCA ischemia of 90 minutes duration.

(A) CBV map reveals an essentially completely
infarcted right MCA and PCA territory.
(B) A “penumbra” map. The purple area corresponds
to CBV reduction and yellow areas highlight
“penumbral tissue (MTT–CBV).” It would be futile to
intervene in this patient because of lack of salvageable
tissue.

9
 CASE 4 Vertebral artery dissection
Imaging description Importance
Vertebral artery dissections (VADs) result from intimal injury, VADs are an important cause of stroke in the posterior circu-
laceration of the arterial wall, or spontaneous hemorrhage lation, particularly in young patients. Imaging signs are gener-
of the vasa vasorum causing a subintimal or intramural hema- ally more subtle than in CAD because of the smaller size of
toma. Spontaneous dissections are presumably related to an vertebral arteries.
inherent arteriopathy due to genetic factors and connective
tissue disorders such as Ehlers–Danlos syndrome type IV, Typical clinical scenario
Marfan syndrome, and fibromuscular dysplasia. Traumatic VADs are often associated with posterior neck pain and brainstem
and iatrogenic dissections are predominantly due to blunt/ or cerebellar ischemia. Ischemia from VADs is most frequently
penetrating injuries, chiropractic manipulation, or catheter observed in the distribution of the affected posterior inferior
angiography. cerebellar artery and commonly presents with lateral medullary
The imaging findings of VAD are similar to carotid artery (Wallenberg) syndrome. Nearly 10% of vertebral artery dissec-
dissection (CAD, see Case 84) with characteristic MR imaging tions extend intracranially, with the potential to form dissecting
findings of wall thickening or hematoma, crescentric high aneurysms, thereby presenting with subarachnoid hemorrhage.
signal in subacute phase, and narrowing of the flow void
(Fig. 4.1). In some cases, however, the lumen many be Differential diagnosis
enlarged due to development of dissecting aneurysm. MRA Proximal VADs need to be distinguished from atherosclerotic
and CTA are both utilized in the diagnosis of VAD, although steno-occlusive disease. One should remember that VAD gen-
CTA may be superior in identifying subtle signs of VAD erally occurs slightly distal to the origin of the vertebral artery,
(Fig. 4.2) such as small dissection flaps and dissecting aneur- and the origin is relatively spared. In contrast, atherosclerotic
ysms [1]. Lum et al. have described a “suboccipital rind sign” disease has a predilection for the vertebral artery origin.
in VADs that involve the V3 segment [2]. They argue that
in some cases of V3 dissections, the only imaging abnormality Teaching points
is the vertebral artery wall thickening, and the lumen appears
normal in caliber. The junction of the V1 and V2 segments is the most common
The V1 and V3 segments of the vertebral artery at the location of VAD. Proximal VADs typically spare the origin
points of entry (C6–C7) and exit (C1–C2 loops) from the of the vertebral artery. Intradural extension of distal VADs
foramen transversarium are common locations for VADs is a feared complication, with associated risk of SAH. The
(Fig. 4.3). The V1 segment dissections are most common. intradural VA is more susceptible to rupture than the extra-
Ischemic findings are common in VADs and generally dural VA because it has a much thinner adventitia layer.
embolic in nature. Embolic infarcts from VADs are most
frequently observed in the distribution of the affected poster-
ior inferior cerebellar artery although other presentations references
include basilar artery thrombosis or ischemia in the posterior 1. Vertinsky AT, Schwartz NE, Fishbein NJ, et al. Comparison of
cerebral artery. multidetector CT angiography and MR imaging of cervical artery
The distal, V3 segment dissections can migrate intracrani- dissection. AJNR Am J Neuroradiol 2008; 29: 1753–60.
ally and result in dissecting aneurysms and subarachnoid 2. Lum C, Chakraborty S, Schlossmacher M, et al. Vertebral artery
hemorrhage (SAH) (Fig. 4.4). SAH is a particularly feared dissection with a normal-appearing lumen at multisection CT
complication of distal V3 dissections since this complication angiography: the importance of identifying wall hematoma. AJNR Am
carries a high risk of morbidity and mortality. J Neuroradiol 2009; 30: 787–92.

10
 Vertebral artery dissection CASE 4

Figure 4.1 (A) MRA source image and (B) susceptibility-weighted image (SWI) in a patient with right-sided lateral medullary syndrome.
The source image shows narrowing of the vertebral artery (arrow). There is a small intramural hematoma that is well appreciated on SWI as
a rim of hypointensity (arrow).

Figure 4.2 (A) Contrast-enhanced MRA

and (B) CTA reconstructions in a patient
with MVA. The MRA reveals possible
dissection of right vertebral artery but it is
difficult to be certain that this is not an
artifact (arrow). CTA is complementary and
clearly shows severe narrowing of the right
vertebral artery. CTA also additionally
demonstrates a small left vertebral artery
dissection.

11
 SECTION 1 Cerebrovascular diseases

Figure 4.3 VAD involving the V1 segment, where the vertebral artery enters the foramen transversarium
(arrow). Note that the vertebral origin is spared, differentiating it from atherosclerotic disease.

Figure 4.4 Subarachnoid hemorrhage from dissection of the right vertebral artery. Non-contrast CT images reveal extensive subarachnoid
hemorrhage. The DSA image is a lateral view of the right vertebral artery. Note the focal narrowing of vertebral artery and an associated small
dissecting aneurysm (arrow).

12
CASE
5 Subacute infarct
Imaging description infarcts may potentially present late because the visual field
cut caused by the infarct may not be noticed by the patient [2].
Brain infarcts in the subacute stage demonstrate enhancement
Likewise, patients with multiple small infarcts occasionally
and may mimic enhancing tumors or infectious processes
present late, as they may not have any significant neurologic
(Fig. 5.1). Enhancement of the infarcted brain parenchyma is
deficits. The non-specific symptoms they have, such as head-
different than “luxury perfusion,” which involves enhance-
ache, dizziness, drowsiness, and weakness, may be attributable
ment of the vessels around the infarct in the acute phase.
to other underlying conditions.
Infarcted tissue enhancement usually starts approximately
4–5 days after the insult and may increase in the following
week [1]. Edema associated with infarcts peaks around the
Differential diagnosis
fourth day and starts dissipating afterwards, although some Most infarcts have specific clinical and radiologic features and
level of swelling of the infarcted tissue is usually present for therefore require no differential diagnosis. The enhancing
approximately 2 weeks. Diffusion-weighted imaging (DWI) subacute infarcts can be recognized by their distinctive shape
signal increase (apparent diffusion coefficient [ADC] signal and location that conform to a vascular territory, most com-
decrease) is seen shortly after the infarct, peaks around the monly the PCA territory. A gyral pattern of enhancement is
second day and gradually diminishes afterwards, with ADC seen in subacute infarcts, with a greater degree of enhance-
normalization occurring around day 10. Brain MRI performed ment of the cortex compared to white matter (Fig. 5.2).
5–14 days after the infarct may show an enhancing lesion with Multiple small infarcts in the subacute phase may mimic
swelling and relative lack or absence of ADC signal decrease metastases or other enhancing lesions (Fig. 5.3). The distribu-
that might lead to an erroneous diagnosis. tion within a vascular territory or in the watershed zones is
helpful in differential diagnosis. Short-term follow-up imaging
Importance may be very helpful in problem cases, as evolving infarcts
show significant changes and often improve over a short
Enhancing mass-like lesions of the brain usually require exten-
interval, in contrast to mass lesions.
sive work-up that frequently involves invasive procedures
which may be harmful. Misdiagnosing an infarct leads not
only to unnecessary work-up but also to delay in identifying Teaching points
and treating the underlying cause of the infarct for secondary PCA territory infarcts and small embolic infarcts may come
stroke prevention. to clinical attention late and present with non-specific
symptoms. Subacute infarcts show parenchymal enhance-
Typical clinical scenario ment and mass effect on MRI, which when coupled with
Most infarcts, particularly of the anterior circulation, present lack of clinical suspicion and restricted diffusion mimic
with acute symptoms that are easily recognized by the patient masses, metastases, and other enhancing lesions.
and healthcare personnel. MRI performed at the early stages of
infarcts is very sensitive and specific for acute infarcts, and no
significant diagnostic difficulty is encountered in this phase. references
Infarcts that lack motor or sensory deficits, however, may 1. Elster AD. Magnetic resonance contrast enhancement in cerebral
be relatively asymptomatic or have symptoms that are non- infarction. Neuroimaging Clin N Am 1994; 4: 89–100.
specific, which may lead to delayed clinical presentations and 2. Finelli PF. Neuroimaging in acute posterior cerebral artery infarction.
delayed imaging. Posterior cerebral artery (PCA) territory Neurologist 2008; 14: 170–80.

13
 SECTION 1 Cerebrovascular diseases

A B

Figure 5.1 (A) Axial FLAIR and (B) post-contrast coronal T1-weighted images show a large area of abnormal signal and enhancement in
the left temporo-occipital region within the PCA territory with associated swelling. Accompanying DWI did not show significant signal
abnormality. This was the first imaging study performed on this patient with subacute infarct.

14
 Subacute infarct CASE 5

A B

Figure 5.2 (A) Axial FLAIR image shows an area of hyperintensity in

the left mesial occipital lobe with no significant mass effect or volume
loss. (B) DWI showed no signal increase, and a gyral pattern of
enhancement is seen on (C) post-contrast T1-weighted image. This
C
patient presented with a 7-day history of headache and drowsiness.

15
 SECTION 1 Cerebrovascular diseases

A B

Figure 5.3 (A) Axial FLAIR through the posterior fossa shows a
cortical signal abnormality in the left cerebellum with (B) normal ADC
map and (C) patchy enhancement on post-contrast T1-weighted
image in a patient with pancreatic cancer and no recent symptoms.
This was initially interpreted as possible metastasis but later
C
confirmed to be a subacute infarct.

16
CASE
6 Subarachnoid hemorrhage
Imaging description Importance
Acute hemorrhage in the subarachnoid space appears as areas Aneurysmal subarachnoid hemorrhage (SAH) is a medical emer-
of hyperdensity in the basal cisterns, cerebral sulci, and/or the gency with a very high rate of morbidity and mortality. Patients
ventricles. There are several imaging findings that can help should receive a prompt work-up and timely intervention to
locate the site of a ruptured aneurysm. The distribution of prevent the secondary mortality from aneurysm rebleeding.
blood in the subarachnoid space and thickness of a localized
clot can often help with such localization. Additionally, the Typical clinical scenario
presence of a parenchymal hematoma is one of the most Most patients experience a sudden, worst headache of their
significant predictors for evaluating the location of the rup- life. However, higher-grade patients may experience altered
tured aneurysm (Fig. 6.1). level of consciousness or focal neurological deficits, or become
CTA is increasingly gaining popularity as the procedure of comatose. Nearly 40–50% of patients may die within the first
choice for initial, and in a majority of cases definitive, evalu- week after the hemorrhage.
ation (Fig. 6.2). The advantages of CTA include its near-
uniform availability, safety profile, high spatial resolution, Differential diagnosis
and limited time required to perform the test. Additionally, Perimesencephalic hemorrhage may have an imaging appearance
it can be obtained at the same sitting when the patient gets that can be confused with aneurysmal SAH. A location centered
the non-contrast CT. CTA has the ability to demonstrate the around the anterior aspect of the midbrain, absence of large
precise relationship between bony structures of the skull and amounts of intraventricular blood, and potential extension to
the aneurysm. CTA may also help demonstrate other char- the posterior interhemispheric fissure are characteristic imaging
acteristics of the aneurysm that are less well studied on digital features of this condition (Fig. 6.3). There is lack of parenchymal
subtraction angiography (DSA) – for example, presence of hematoma and a 4-vessel angiogram is negative for aneurysm.
endoluminal thrombus as well as calcification of the aneur- One of the most common causes of false positive detection
ysm wall. Preoperative knowledge of these aneurysm charac- of aneurysm on CTA is infundibular dilatation at the origin
teristics significantly aids in therapeutic decisions. The of posterior communicating (Fig. 6.4) or anterior choroidal
reported overall sensitivity of CTA exceeds 90% when com- arteries [1]. The infundibulum is typically conical in shape,
pared with DSA in most recent publications [1]. However, if measures 3mm or smaller, and has a vessel that arises from its
there is any doubt regarding the findings on CTA, one should apex. Also, venous contamination may result in false positive
have a low threshold for recommending further evaluation diagnosis of aneurysm when venous structures abut the arter-
with a DSA. ial bifurcation (Fig. 6.5).
DSA still remains the gold-standard imaging study for
evaluation of intracranial aneurysms, with highest reported
sensitivity. The advantages include its very high spatial reso- Teaching points
lution and its ability to demonstrate small vessels and their CTA is gaining widespread popularity as the initial, and in
relationship with the neck of the aneurysm, as well as yielding many cases definitive, evaluation for aneurysmal SAH. How-
information for planning endovascular repair (Fig. 6.1). ever, potential possible pitfalls of CTA should be kept in mind.
However, it is not uniformly available and has an associated
risk of ischemic complications due to its invasive nature.
“Diagnostic” cerebral angiography is therefore being increas- references
ingly replaced by CTA, although it still retains its place as a 1. Marshall SA, Kathuria S, Nyquist P, Gandhi D. Noninvasive imaging
prelude to endovascular intervention and also as a definitive techniques in the diagnosis and management of aneurysmal subarachnoid
means of evaluation if initial CTA is negative. hemorrhage. Neurosurg Clin N Am 2010; 21: 305–23.

17
 SECTION 1 Cerebrovascular diseases

Figure 6.1 (A) CT reveals diffuse SAH and a left-sided gyrus rectus hematoma, predictive of ruptured anterior communicating artery (Acom)
aneurysm. (B) An irregular Acom aneurysm is confirmed (arrow) on DSA of right ICA. (C) The aneurysm was embolized at the same sitting.

Figure 6.2 (A) SAH with slightly thicker hematoma along the right MCA, suggesting the possibility of right MCA aneurysm. (B) CTA reveals a
right MCA (arrows) as well as a pericallosal aneurysm (short arrows). Right MCA aneurysm was the source of the SAH, confirmed at surgery.

18
 Subarachnoid hemorrhage CASE 6

Figure 6.3 A typical example of benign perimesencephalic hemorrhage on CT (arrow). The accompanying AP angiogram of left vertebral artery
is unremarkable for an aneurysm in the posterior fossa.

Figure 6.4 Sagittal MIP image reveals a possible aneurysm (arrow) along the communicating segment of the ICA, although it is difficult to
exclude an infundibulum. A DSA clearly demonstrates a small vessel (Pcom: double arrow) arising from the apex, confirming this to be an
infundibulum.

19
 SECTION 1 Cerebrovascular diseases

A B

Figure 6.5 Venous contamination can result in false positive appearance of an aneurysm. (A) In this patient with SAH, a basilar tip aneurysm
(arrow) was diagnosed on CTA, contaminated by venous filling. (B) The DSA shows the basilar tip to be unremarkable.

20
CASE
7 Intracranial aneurysms
Imaging description intracranial aneurysms. These include patients with polycystic
kidney disease, Marfan syndrome, coarctation of the aorta,
Intracranial saccular (berry) aneurysms are common intracra-
fibromuscular dysplasia, family history of intracranial aneur-
nial vascular lesions with an estimated prevalence in the gen-
ysms, and Ehlers–Danlos syndrome. These patients should
eral population ranging from 2% to 6% [1]. Digital subtraction
receive screening with a highly sensitive and specific
angiography (DSA) has the highest spatial resolution of all
technique.
vascular imaging studies and remains a gold-standard tech-
nique. However, while DSA is the most sensitive for such Differential diagnosis
detection and characterization of aneurysms, it is not practical
Infundibular dilatation at the vessel origins may simulate an
as a screening tool because of its invasive nature and a small
aneurysm on CTA or MRA (Fig. 7.3). The characteristic
risk of neurologic complications.
features of infundibula that separate these from aneurysms
The sensitivity of CTA has continued to increase, with
are their conical shape, diameter less than 3mm, and a vessel
some studies reporting it to be even comparable to that of
arising from the apex. Occasionally, a vessel loop may simulate
DSA [1]. Images are generally reconstructed in 2D maximum
an aneurysm on MIP projections. However, careful review of
intensity projection (MIP) or 3D volume rendering (VR)
source images or generation of multiplanar reconstruction
(Fig. 7.1). The sensitivity and specificity are reported to be
(MPR) images in different planes will generally resolve one
as high as 90%, but depend on the size of the aneurysm.
from the other. Occasionally, a venous structure in close
According to Villablanca et al., CTA has >90% sensitivity
proximity to the artery may simulate an aneurysm on CTA
for aneurysms of the middle cerebral artery, regardless of the
(see Fig. 6.5).
size of the aneurysm [2]. However, CTA may not clearly
identify small aneurysms in the area of the carotid siphon
and paraclinoid region. Teaching points
Magnetic resonance angiography (MRA) is an excellent Multi-slice CTA and MRA, especially at 3T strength, are
screening diagnostic method in asymptomatic patients with excellent techniques for the detection of intracranial aneur-
risk of harboring an intracranial aneurysm. The advantages ysms. MRA has a slight advantage, since there is lack of
include its non-invasive nature, the lack of radiation exposure, ionizing radiation and it can be obtained without the need
and the high sensitivity. Multiple overlapping thin-slice acqui- to inject contrast agent.
sition (MOTSA) combines the advantages of 2D and 3D time-
of-flight (TOF) techniques (Fig. 7.2) and is widely utilized for
the circle of Willis MRA. In a systematic review comparing references
MRA with DSA, MRA had a sensitivity of 87%, a specificity of 1. Pozzi-Mucelli F, Bruni S, Doddi M, et al. Detection of intracranial
95%, a positive predictive value of 97% per aneurysm [3]. aneurysms with 64 channel multidetector row computed tomography:
MRA is often a preferred screening technique for unruptured comparison with digital subtraction angiography. Eur J Radiol 2007; 64:
aneurysms. 15–26.
2. Villablanca JP, Hooshi P, Martin N et al. Three-dimensional helical
Importance
computerized tomography angiography in the diagnosis, characterization,
Rupture of intracranial aneurysm results in subarachnoid and management of middle cerebral artery aneurysms: comparison
hemorrhage, a condition with significant morbidity and mor- with conventional angiography and intraoperative findings. Journal of
tality. Therefore, the screening techniques used for detection Neurosurgery, 2002; 97: 1322–32.
of unruptured aneurysms should have very high sensitivity as 3. White PM, Wardlaw JM, Easton V. Can noninvasive imaging
well as specificity to be useful. accurately depict intracranial aneurysms? A systematic review. Radiology
2000; 217: 361–70.
Typical clinical scenario
There is no evidence to support screening the general popula-
tion for intracranial aneurysms. Nevertheless, specific patient
populations present an increased risk for formation of

21
 SECTION 1 Cerebrovascular diseases

A B

Figure 7.1 (A) CTA on 320 slice CT demonstrating excellent automated bone subtraction and a tiny, 2mm left anterior cerebral artery
aneurysm (arrow). (B) This aneurysm is confirmed on DSA (arrow).

Figure 7.2 3D MOTSA TOF MRA was performed as a screening

test in a 38-year-old female with polycystic kidney disease. Note a
5mm basilar tip aneurysm (arrow).

Figure 7.3 (A) Lower resolution of CTA and MRA

(compared to DSA) may result in false positive
diagnosis of aneurysm (arrow, in this case on CTA).
(B) DSA is able to display a conical shape of the
abnormality and small posterior communicating
artery arising from the apex of this lesion (arrow),
A B confirming this to be an infundibulum.

22
CASE
8 Giant aneurysms
Imaging description Importance
Giant intracranial aneurysms present unique challenges in Giant aneurysms are rare but very difficult lesions in terms of
diagnosis, characterization, and management. By definition, their characterization on imaging, as well as management.
aneurysms that exceed 25mm in greatest diameter are termed Care should be taken not to confuse these with other intracra-
giant aneurysms. Giant aneurysms may be either saccular or nial masses.
fusiform in morphology.
In terms of location, these lesions are most commonly Typical clinical scenario
identified in the extradural internal carotid artery (ICA), more Giant aneurysms most often present with symptoms of mass
specifically in the cavernous segment. Other locations that are effect on adjacent structures, although SAH may also be the
involved with some frequency include the middle cerebral initial presentation in some patients. Cavernous ICA aneur-
artery (MCA) and the vertebral-basilar system. CT is generally ysms may exert mass effect on the nerves coursing through the
the first imaging study obtained, especially in the patients cavernous sinus, resulting in compressive neuropathies of 3rd,
where the initial presentation is with subarachnoid hemor- 4th and/or 6th cranial nerves. Giant aneurysms may also result
rhage (SAH) or ischemic symptoms. Giant aneurysms are in ischemic symptoms, due to embolic phenomenon occurring
appreciated as round or oval masses that are slightly hyper- from intraluminal thrombus that these lesions frequently
dense compared to the gray matter (Fig. 8.1). Calcification is a harbor.
frequent occurrence and can be seen either in the periphery in
an “egg shell” fashion or scattered within the thrombosed Differential diagnosis
portion of the lumen. Administration of contrast allows the Differential considerations include other intracranial masses.
identification of the patent lumen of the aneurysm. For example, the aneurysms in the cavernous ICA frequently
Cerebral digital subtraction angiography (DSA) is frequently project into the pituitary sella and suprasellar cistern and
needed, and is helpful both in delineating the branch vessels may be misdiagnosed as hemorrhagic pituitary macroadeno-
and for planning therapy. However, as a sole imaging study, it mas. Clues to the correct recognition include demonstrating
is insufficient in precise characterization of these complex the continuity of the mass with the carotid artery, identifica-
aneurysms. Because it only demonstrates the patent lumen, it tion of a flow void, and pulsatility artifacts. Hemorrhagic
may sometimes grossly underestimate the size or the extent of primary neoplasms and large cavernous malformations can
the aneurysm (Fig. 8.2). DSA must always be complemented simulate giant aneurysm on account of blood products of
with cross-sectional studies for evaluating these complex lesions. varying ages (Fig. 8.4). However, these lesions are intra-
MRI is a very useful tool for the evaluation of giant aneur- axial, whereas giant aneurysms are located in the subarach-
ysms, but it can be confusing to interpret. Partially thrombosed noid space.
giant aneurysms appear as extra-axial masses that consist of
areas of mixed signal intensities representing clot of varying
ages [1]. An eccentric or central patent lumen may be seen as an
Teaching points
area of flow void (Figs. 8.1, 8.3). The pulsations of the aneurysm Giant aneurysms should always be entertained in the differ-
or vessel wall create unique ghosting artifacts on MR, propagat- ential diagnosis of large extra-axial masses, especially those
ing in the phase-encoding direction (Fig. 8.1). This artifact is that are hyperdense on CT and/or demonstrate blood prod-
quite helpful in making a specific diagnosis of giant aneurysm. ucts on MRI.
MRA is complementary to MRI in depicting the patent portion
of the lumen. A standard 3D MRA may occasionally be mis-
leading and fail to demonstrate the aneurysm if there is very references
slow flow in the sac of the aneurysm. Contrast-enhanced 3D 1. Atlas SW, Grossman RI, Goldberg HI, et al. Partially thrombosed giant
time-of-flight (TOF) MRA and dynamic contrast-enhanced intracranial aneurysms: correlation of MR and pathologic findings.
MRA may be able to provide better detail of the lumen. Radiology 1987; 162: 111–14.

23
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