Differential Diagnosis in Computed Tomography E-Book

Francis A. Burgener

• Herausgeber: Thieme
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1688

Veröffentlichungsjahr: 2011

Beschreibung

<p><fontcolor="red"><strong><em>The new Burgener: Improve your interpretation skills with this bestselling comprehensive reference to interpreting abnormal CT findings</em></strong></font></p><p><em>Differential Diagnosis in Computed Tomography, 2nd edition</em>, is an invaluable reference aid in the evaluation of CT images to help confidently gain a general diagnostic impression and a reasonable differential diagnosis. In contrast to disease-oriented radiology texts, this book is organized by CT findings, enabling the reader to quickly match the appropriate differential diagnosis to CT results.</p><p><strong>Special features of the second edition:</strong></p><ul><li>Continuation of the successful Burgener concept: Comprehensive tables describe the imaging patterns of the various diseases that may present on CT, along with other characteristically associated imaging findings and pertinent physiopathologic, pathologic, and clinical data <li>Over 2,000 detailed, high-quality images demonstrating a wide range of common and uncommon CT findings <li>Chapters organized according to anatomic regions, from the brain to the pelvis and the musculoskeletal system, with new chapters on meningeal and calvarian lesions and on trauma <li>Updated and revised sections reflecting the latest advances in CT technology and indications, including accurate staging of intra-articular and spinal fractures and evaluation of vascular diseases <li>Extensive index systematically cross-references diseases and CT findings for optimal access to information</li></ul><p>Recognizing the central role that CT plays in the field of modern medical imaging, this book is essential for physicians who want to strengthen their diagnostic acumen and CT interpretation skills: radiologists in practice; residents preparing for board exams; and any other physician charged with understanding and interpreting CT images.</p>

Leseprobe

Differential Diagnosis in Computed Tomography

2nd edition

Francis A. Burgener, MD

Professor of RadiologyUniversity of Rochester Medical CenterRochester, New York, USA

Christopher Herzog, MD, MBA

Department of RadiologyRotkreuzklinikumMunich, Germany

Steven P. Meyers, MD, PhD

Professor of Radiology and NeurosurgeryUniversity of Rochester Medical CenterRochester, New York, USA

Wolfgang Zaunbauer, MD

Institute of RadiologyKantonsspital St. GallenSt. Gallen, Switzerland

In collaboration with:

Grégory Dieudonné, MD

Scott A. Mooney, MD

Richard T. White, DO

2146 illustrations

This edition includes texts and illustrations from Martti Kormano, MD, who authored Chapters 1, 2, 10, 18, 19, 20, 21, 22, 23, 24, 25, and 26 of the first edition.

ThiemeStuttgart • New York

Library of Congress Cataloging-in-Publication Data

Burgener, Francis A., author.

Differential diagnosis in computed tomography / Francis A. Burgener, Professor of Radiology, University of Rochester Medical Center, Rochester, New York, Steven P. Meyers, MD, PhD, Professor of Radiology/Imaging Sciences, Neurosurgery Radiology, Residency Program Director, Director of the Fellowship in Magnetic Resonance Imaging, University of Rochester School of Medicine and Dentistry, Rochester, New York, Christopher Herzog, Rotkreuzklinikum, Radiologisches Institut, Munich, Germany, Wolfgang Zaunbauer, Institute for Radiology, Kantonsspital St. Gallen, St. Gallen, Switzerland. -- Second Edition.

   p. ; cm.

 Includes bibliographical references and index.

 ISBN 978-3-13-102542-5 (hardback)

 1. Tomography. 2. Diagnosis, Differential. I. Meyers, Steven P., author. II. Herzog, Christopher, author. III. Zaunbauer, Wolfgang, author. IV. Title.

 [DNLM: 1. Tomography, X-Ray Computed. 2. Diagnosis, Differential. WN 206]

 RC78.7.T6B87 2011

 616.07 572--dc22

 2010053779

 616.07 54--dc22

                     2010052679

© 2012 Georg Thieme Verlag,Rüdigerstrasse 14, 70469 Stuttgart, Germanyhttp://www.thieme.deThieme New York, 333 Seventh Avenue,New York, NY 10001, USAhttp://www.thieme.com

Cover design: Thieme Publishing GroupTypesetting by Maryland Composition, Maryland, USA

Printed by Everbest Printing Co Ltd., China

ISBN 978 3 13 102542 5                1 2 3 4 5 6

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Contributors

Francis A. Burgener, MDProfessor of RadiologyUniversity of Rochester Medical CenterRochester, New York, USA

Christopher Herzog, MD, MBAInstitute of RadiologyRotkreuzklinikumMunich, Germany

Steven P. Meyers, MD, PhDProfessor of Radiology and NeurosurgeryUniversity of Rochester Medical CenterRochester, New York, USA

Wolfgang Zaunbauer, MDInstitute of RadiologyKantonsspital St. GallenSt. Gallen, Switzerland

In collaboration with:

Grégory Dieudonné, MDAssistant Professor of RadiologyUniversity of Rochester Medical CenterRochester, New York, USA—Contributed Chapter 29

Scott A. Mooney, MDClinical Assistant Professor of RadiologyUniversity of Rochester Medical CenterRochester, New York, USA—Contributed illustrations to Chapters 11, 12, 13, 14, 15, 27, 28, and 29

Richard T. White, DOProfessor of RadiologyUniversity of Rochester Medical CenterRochester, New York, USA—Contributed illustrations to Chapters 27, 28, and 29

Preface

Dr. Martti Kormano was my coauthor for the textbook Differential Diagnosis in Conventional Radiology, including all subsequent editions, as well as for the first edition of Differential Diagnosis in Computed Tomography. It was a great pleasure for me to work with him on these endeavors over two decades. Unfortunately for me, Dr. Kormano has since retired from his position as Chairman of the Diagnostic Radiology Department of the University Hospital in Turku, Finland, and because of personal commitments could not find the time and energy to be involved in the updating of this text. Because I am devoting my professional time exclusively to musculoskeletal radiology, I not only had to find new coauthors for Dr. Kormano’s section of the text, but I also needed help for my original chapters outside of my area of main interest. I was fortunate to find three colleagues to completely revise Dr. Kormano’s section of the original text and update some of my chapters. I believe Drs. Christopher Herzog, Steven P. Meyers, and Wolfgang Zaunbauer performed an outstanding job.

In the 15 years since the publication of the first edition, the scope of CT imaging has grown and assumed a much greater role in the field of medical imaging. Most of this growth is not related to the discovery of new disease processes but, rather, it is related to the development and refinement of CT technology. The greatly improved hardware and software in CT allows high- quality reconstruction images in various 2D and 3D planes, as well as dynamic examinations such as CT angiography and perfusion studies. These advancements result in many new indications for CT examinations such as the accurate staging of intra-articular and spinal fractures or the evaluation of vascular diseases. To account for this development, new sections have been added to every chapter and three new chapters (3, 4, and 15) have been included in this edition—resulting in a substantial increase in both text and illustrations. Furthermore, illustrations from the first edition have been updated with high-quality images.

CT has gained worldwide acceptance and, in addition to many new indications, has also replaced conventional radiographic techniques in many areas. CT is no longer the exclusive domain of the radiologist, but is also practiced and/or interpreted by a large number of clinicians and surgeons. With each examination, one is confronted with CT findings that require interpretation in order to arrive at a general diagnostic impression and a reasonable differential diagnosis. To assist the physician in attaining this goal, this book is based on CT findings rather than being disease-oriented like most other textbooks in radiology. Because many diseases present on CT in a variety of manifestations, some overlap in the text is unavoidable. To minimize repetition, the differential diagnosis of a CT finding is presented in tabular form whenever feasible. Most tables not only list the various diseases that may present on CT in a specific pattern, but also describe in succinct form other characteristically associated imaging findings and pertinent clinical data. The text is complemented by many CT images and drawings to visually demonstrate the image features under discussion.

I hope this revised and expanded second edition will be as well received as the original text, which was translated into eight languages. The concept of an imaging pattern approach in tabular form rather than a disease-oriented text was introduced by Dr. Kormano and myself in 1985 with the first edition of Differential Diagnosis in Conventional Radiology and has since been adopted by many authors. I take this as a compliment—after all, imitation is the sincerest form of flattery.

This book is meant for radiologists and physicians with some experience in the interpretation of CT examinations who wish to strengthen their diagnostic acumen. It is a comprehensive outline of CT findings and will be particularly useful to radiology residents preparing for their specialist examination. Any physician involved in the interpretation of CT examination should find this book helpful in direct proportion to his or her curiosity. It is my hope that the second edition of Differential Diagnosis in Computed Tomography will be as interesting as its predecessor to medical students, residents, radiologists, and physicians involved in the interpretation of CT images.

Francis A. Burgener, MD

Acknowledgments

It is impossible to thank individually all those who helped to prepare the second edition of this textbook. I wish to acknowledge the staff of our publisher, in particular, Dr. Clifford Bergman as well as Stephan Konnry and Annie Hollins, both of whom were more recently assigned by Thieme to this project to deal with, among other things, my old fashioned style relying primarily on paper, pencils, hard copies, and the telephone. Their hard work, dedication, and attention to detail for this edition are greatly appreciated. Furthermore, I am also indebted to Heidi Grauel for her editorial assistance and efficient handling of the page proofs.

I also wish to express our gratitude to the many radiologists who made this illustrative collection of computed tomography images available. Special thanks go to Drs. Allen Bernstein, Gary Hollenberg, Johnny Monu, Peter Rosella, Gwy Suk Seo, David Shrier, Charlene Varnis, Brian Webber, Eric Weinberg, and Andrea Zynda; all staff members of the University of Rochester Imaging Sciences Department; Drs. Thomas Vogl and Volkmar Jacobi, both of the Johann Wolfgang Goethe University Clinic, Frankfurt; and Drs. Tobias Hertle (Dresden), Sebastian Leschka (Zürich), Christoph Ozdoba (Bern), Reinhand Schöpf (Landeck), Nikolai Stahr (Winterthur), Björn Stinn (Zürich), and Alexander Von Hessling (Zürich).

I greatly appreciate the invaluable contribution by Dr. Patrick J. Fultz, Professor of Radiology at the University of Rochester Medical Center, who authored the original Chapter 29 of this text and graciously let us use this material in the new edition.

I wish to thank Margaret Kowaluk, Sarah Peangatelli, and Katherine Tower of the Imaging Sciences graphic services section at the University of Rochester Medical Center for their outstanding work in preparing the illustrations. The instructive new drawings were superbly executed by either Katherine Tower or Dr. Anna Zaunbauer-Womelsdorf, the daughter of one of the coauthors of this text. Their work is greatly appreciated.

Excellent secretarial support for this project was provided by Colleen Cottrell and Jill Derby for which I wish to express many thanks. The general secretarial assistance of Shirley Cappiello is also greatly appreciated. Last, but not least, I am most grateful to Alyce Norder who left the University and me after 30 years for the richness of the industry and subsequent partial retirement. She is, besides Jill Derby, the only person capable of deciphering my longhand and, as in the past, did a superb job in typing, editing, and proofreading the manuscript of the new edition of this text in her spare time, for which I am deeply grateful.

Finally, I appreciate the support of our families who have forfeited precious family time for the preparation of this text. Therefore, in appreciation of both their understanding and support, my coauthors and I dedicate this book to our wives Therese Burgener, Christine Herzog, Barbara Weber, and Isabella Zaunbauer.

Francis A. Burgener, MD

Contents

Contributors

Preface

Acknowledgments

Contents

List of Tables

I Intracranial Lesions

1 Brain and Extra-axial Lesions

Steven P. Meyers

2 Ventricles and Cisterns

Steven P. Meyers

3 Lesions Involving the Meninges and Skull

Steven P. Meyers

4 Vascular Lesions

Steven P. Meyers

II Head and Neck

5 Skull Base and Temporal Bone

Wolfgang Zaunbauer and Francis A. Burgener

6 Orbit and Globe

Wolfgang Zaunbauer and Francis A. Burgener

7 Nasal Cavity and Paranasal Sinuses

Wolfgang Zaunbauer and Francis A. Burgener

8 Suprahyoid Neck

Wolfgang Zaunbauer and Francis A. Burgener

9 Infrahyoid Neck

Wolfgang Zaunbauer and Francis A. Burgener

III Spine

10 Computed Tomography of Spinal Abnormalities

Steven P. Meyers

IV Musculoskeletal System

11 Soft Tissue Disease

Francis A. Burgener

12 Joint Disease

Francis A. Burgener

13 Generalized Bone Disease

Francis A. Burgener

14 Localized Bone Disease

Francis A. Burgener

15 Trauma and Fractures

Francis A. Burgener

V Thorax

16 Lungs

Christopher Herzog and Francis A. Burgener

17 Pleura, Chest Wall, and Diaphragm

Christopher Herzog and Francis A. Burgener

18 Heart and Mediastinum

Christopher Herzog

VI Abdomen and Pelvis

19 Liver

Christopher Herzog

20 Biliary System

Christopher Herzog

21 Spleen

Christopher Herzog

22 Pancreas

Christopher Herzog

23 Abdominal Wall

Christopher Herzog

24 Gastrointestinal Tract

Christopher Herzog

25 Peritoneum and Mesentery

Christopher Herzog

26 Retroperitoneum

Christopher Herzog

27 Kidneys

Francis A. Burgener

28 Adrenal Glands

Francis A. Burgener

29 Pelvis

Grégory Dieudonné and Francis A. Burgener

References

Index

List of Tables

I Intracranial Lesions

1 Brain and Extra-axial Lesions

Table 1.1 Congenital malformations of the brain

Table 1.2 Supratentorial intra-axial mass lesions

Table 1.3 Supratentorial extra-axial lesions

Table 1.4 Intra-axial lesions in the posterior cranial fossa (infratentorial)

Table 1.5 Extra-axial lesions in the posterior cranial fossa (infratentorial)

Table 1.6 Cystic, cystlike, and cyst-containing intracranial lesions

Table 1.7 Abnormalities and lesions of the basal ganglia

Table 1.8 Multiple or diffuse lesions involving white matter

Table 1.9 Intracranial hemorrhage

Table 1.10 Intracranial calcifications

2 Ventricles and Cisterns

Table 2.1 Lateral ventricles: common mass lesions

Table 2.2 Common lesions in the third ventricle

Table 2.3 Lesions in the fourth ventricle

Table 2.4 Excessively small ventricles

Table 2.5 Dilated ventricles

Table 2.6 Abnormal or altered configurations of the ventricles

Table 2.7 Intraventricular mass lesions

3 Lesions Involving the Meninges and Skull

Table 3.1 Abnormalities involving the meninges

Table 3.2 Lesions involving the skull

4 Vascular Lesions

Table 4.1 Congenital/developmental vascular anomalies/variants

Table 4.2 Acquired vascular disease

II Head and Neck

5 Skull Base and Temporal Bone

Table 5.1 Skull base apertures and their content

Table 5.2 Skull base lesions

Table 5.3 Temporal bone: diseases of the external auditory canal

Table 5.4 Temporal bone: diseases of the middle ear and mastoid

Table 5.5 Temporal bone: diseases of the inner ear and internal auditory canal

Table 5.6 Temporal bone: lesions of the petrous apex

Table 5.7 Temporal bone: jugular foramen lesions

6 Orbit and Globe

Table 6.1 Ocular lesions

Table 6.2 Optic nerve-sheath complex lesions

Table 6.3 Extraocular conal and intraconal lesions

Table 6.4 Extraocular extraconal lesions

7 Nasal Cavity and Paranasal Sinuses

Table 7.1 Lesions in the nasal cavity and paranasal sinuses

8 Suprahyoid Neck 296

Table 8.1 Pharyngeal mucosal space lesions

Table 8.2 Parapharyngeal space lesions

Table 8.3 Masticator space lesions

Table 8.4 Parotid space lesions

Table 8.5 Suprahyoid carotid space lesions

Table 8.6 Suprahyoid retropharyngeal space lesions

Table 8.7 Suprahyoid perivertebral space lesions

Table 8.8 Lesions of the mucosal area of the oral cavity

Table 8.9 Submandibular space lesions

Table 8.10 Sublingual space lesions

Table 8.11 Lesions of the buccal space

9 Infrahyoid Neck

Table 9.1 Visceral space lesions

Table 9.2 Laryngeal lesions

Table 9.3 Thyroid gland lesions

Table 9.4 Infrahyoid carotid space lesions

Table 9.5 Posterior cervical space lesions

Table 9.6 Infrahyoid retropharyngeal space lesions

Table 9.7 Infrahyoid perivertebral space lesions

Table 9.8 Anterior cervical space lesions

III Spine

10 Computed Tomography of Spinal Abnormalities

Table 10.1 Spine: Congenital and developmental abnormalities

Table 10.2 Solitary osseous lesions involving the spine

Table 10.3 Multifocal lesions involving the spine

Table 10.4 Spine: Extradural lesions

Table 10.5 Spine: Traumatic lesions

Table 10.6 Intradural extramedullary lesions

Table 10.7 Spine: Intradural intramedullary lesions

IV Musculoskeletal System

11 Soft Tissue Disease

Table 11.1 Fat-containing lesions

Table 11.2 Cystic soft tissue lesions

Table 11.3 Soft tissue calcifications

Table 11.4 Para-articular soft tissue calcifications

Table 11.5 Soft tissue ossification (heterotopic bone formation) 474

Table 11.6 Soft tissue gas 474

Table 11.7 Soft tissue lesions

12 Joint Disease This chapter does not include tables.

13 Generalized Bone Disease

Table 13.1 Widespread or diffuse osteosclerosis

Table 13.2 Generalized osteopenia

Table 13.3 Regional or localized osteoporosis

14 Local Bone Disease 500

Table 14.1 Bone lesions with fluid levels

Table 14.2 Localized bone lesions

15 Trauma and Fractures

Table 15.1 Dynamic classification of pelvic injuries (modified from Tile)

Table 15.2 Acetabular fracture classification of Letournel and Judet

Table 15.3 Classification of posterior hip dislocations (Thompson and Epstein) 562

Table 15.4 Classification of femoral head fractures associated with posterior hip dislocations (modified from Pipkin)

Table 15.5 Stability assessment of cervical spine injuries

Table 15.6 Column involvement of thoracolumbar spine fractures

Table 15.7 Differential diagnosis of loose intra-articular bodies

Table 15.8 Stress fractures

V Thorax 591

16 Lungs 592

Table 16.1 Diffuse lung disease

Table 16.2 Focal lung lesions

17 Pleura, Chest Wall, and Diaphragm This chapter does not include tables.

18 Heart and Mediastinum

Table 18.1 Mediastinal and hilar lesions

Table 18.2 Mediastinal vessels

Table 18.3 Heart

Table 18.4 Thoracic calcifications

VI Abdomen and Pelvis

19 Liver

Table 19.1 Focal liver lesion

Table 19.2 Diffuse liver disease

20 Biliary System

Table 20.1 Differential diagnosis of diseases of the biliary system

21 Spleen

Table 21.1 Differential diagnosis of diseases of the spleen

22 Pancreas

Table 22.1 Abnormal pancreas

23 Abdominal Wall

Table 23.1 Abnormalities of the abdominal wall

24 Gastrointestinal Tract

Table 24.1 Abnormal stomach 742

Table 24.2 Abnormal small intestine

Table 24.3 Abnormal colon

25 Peritoneum and Mesentery

Table 25.1 Peritoneal, mesenteric, and omental collections and masses

26 Retroperitoneum

Table 26.1 Retroperitoneal abnormalities

27 Kidneys

Table 27.1 Bosniak classification of cystic renal lesions

Table 27.2 Focal renal lesions

Table 27.3 Focal lesions in the perinephric space

28 Adrenal Glands

Table 28.1 Focal or diffuse adrenal enlargement

29 Pelvis 814

Table 29.1 Pelvic gastrointestinal lesions

Table 29.2 Reproductive system lesions

Table 29.3 Bladder lesions

Table 29.4 Pelvic peritoneal and extraperitoneal lesions

I Intracranial Lesions

Chapter 1 Brain and Extra-axial Lesions

Chapter 2 Ventricles and Cisterns

Chapter 3 Lesions Involving the Meninges and Skull

Chapter 4 Vascular Lesions

1 Brain and Extra-axial Lesions

Steven P. Meyers

Computed tomography (CT) can provide rapid multiplanar imaging of the brain, meninges, and skull. The use of dynamic rapid data acquisition combined with bolus injection of iodinated contrast agents allows for assessment of blood perfusion rates of normal and abnormal brain tissue, as well as the generation of high-resolution CT arteriograms and venograms. CT has proven to be a powerful imaging modality in the evaluation of (1) neoplasms of the central nervous system, meninges, calvarium, and skull base; (2) traumatic lesions; (3) intracranial hemorrhage; (4) ischemia and infarction, particularly using CT perfusion studies; (5) infectious and noninfectious diseases; and (6) metabolic disorders.

The appearance of brain tissue depends on the milliampere second (mAs) and kilovolts peak (kVp) used, as well as the age of the patient imaged. Myelination of the brain begins in the fifth fetal month and progresses rapidly during the first 2 years of life. The degree of myelination affects the appearance of the brain parenchyma on CT. In adults, the cerebral cortex has intermediate attenuation that is slightly higher relative to normal white matter. For infants younger than 6 months, differentiation of white matter relative to gray matter is limited secondary to the immature myelination of brain tissue. Myelination proceeds in a predictable and characteristic pattern with regard to locations and timing. These changes are more optimally seen with magnetic resonance imaging (MRI) than with CT.

Various pathologic processes can affect the attenuation properties of the involved tissue or organ. For example, intraparenchymal hemorrhage can have variable appearances in the brain depending on the age of the hematoma, oxidation states of the iron in hemoglobin, hematocrit, protein concentration, clot formation and retraction, location, and size. Oxyhemoglobin in a hyperacute blood clot has ferrous iron. After a few hours during the acute phase of the hematoma, the oxyhemoglobin loses its oxygen to form deoxyhemoglobin. Deoxyhemoglobin also has ferrous iron, although it has unpaired electrons. Later in the early subacute phase of the hematoma, deoxyhemoglobin becomes oxidized to the ferric state, methemoglobin. Initially, red blood cells in the clot are intact. In the late subacute phase, breakdown of the membranes of the red blood cells results in extracellular methemoglobin. In the chronic phase, methemoglobin becomes further oxidized and broken down by macrophages into hemosiderin.

The CT features of subdural hematomas are variable, although the appearances can progress in patterns similar to intraparenchymal hematomas. Acute subdural hematomas often have low-intermediate attenuation.

Other lesions that can result in zones of low attenuation are dermoids (intact or ruptured), teratomas, lipomas, and cystic structures with low protein concentration or cholesterol.

Nonhemorrhagic pathologic processes tend to decrease the attenuation of the involved tissues. Such processes include ischemia, infarction, inflammation, infection, demyelination, dysmyelination, metabolic or toxic encephalopathy, trauma, neoplasms, gliosis, radiation injury, and encephalomalacic changes. Exceptions to this phenomenon include neoplasms with high nuclear to cytoplasmic ratios (e.g., medulloblastomas and small cell lymphomas), fluid collections with high protein or mineral concentrations (e.g., colloid cysts and craniopharyngiomas), and lesions with fine or clumplike calcifications (e.g., ependymomas, meningiomas, and metabolic disorders such as hypoparathyroidism and Fahr disease).

Of the various human body tissues, the brain is the least tolerant of ischemia. A lack of sufficient blood flow to the brain for approximately 5 seconds results in loss of consciousness and for several minutes can result in irreversible cerebral ischemia and infarction. For normal brain function, cerebral blood flow (CBF) must be maintained at a constant rate to deliver oxygen and glucose as well as to remove CO2 and metabolic waste products. Maintenance of CBF is critical for neuronal function. With arterial occlusion, the loss of normal neuronal electrical activity occurs within seconds after arterial occlusion. Cellular death is dependent on the duration and magnitude of ischemia, the metabolic vulnerability of specific anatomical sites, and the oxygen content of blood. CT is important in the detection of cerebral infarction and for the presence of associated hemorrhage, which may preclude the use of thrombolytic therapy. Another clinical application of CT for stroke is a technique referred to as CT perfusion, which utilizes rapid infusion of intravenous (IV) iodinated contrast, and will be discussed at the end of this section.

Areas where there is a breakdown of the blood–brain barrier from pathologic disorders can be evaluated with iodine-based IV contrast agents. Leakage of these agents through the blood–brain barrier results in contrast enhancement localized to the involved pathologic regions. Contrast-enhanced CT images are an important portion of most imaging examinations of the head. In addition to pathologically altered intracranial tissues, contrast-enhancement can be normally seen in veins, the choroid plexus, the pituitary gland, and pineal gland. For this book, the attenuation of the various entities will be described as low, intermediate, high, or mixed and whether there is contrast enhancement or not.

Intracranial lesions are typically classified as being extra- or intra-axial. Extra-axial lesions arise from the skull, meninges, or tissues other than the brain parenchyma. They are characterized as being within epidural, subdural, or subarachnoid spaces or compartments. Lesions involving the meninges can be further categorized as involving the dura mater (e.g., with benign postoperative dural fibrosis) or involving the leptomeninges (pia and arachnoid). Abnormalities of the meninges are often best seen after the IV administration of contrast material. Dural enhancement usually has a linear configuration, whereas pathology involving the leptomeninges appears as enhancement within the sulci and basilar cisterns. Enhancement of the leptomeninges is usually related to significant pathology, such as neoplastic or inflammatory diseases.

Intra-axial lesions are located in the brain parenchyma or brainstem. Differential diagnoses of extra-axial and intra-axial masslike lesions are presented in Tables 1.2,1.3,1.4,and1.5. Intra-axial masslike lesions are presented according to location: supra- versus infratentorial. Infratentorial neoplasms are more common in children and adolescents than adults. During childhood, intra-axial tumors such as astrocytomas, medulloblastomas, ependymomas, and brainstem gliomas are the most common neoplasms. In adults; metastatic lesions and hemangioblastomas are the most common intra-axial infratentorial tumors, and acoustic schwannomas and meningiomas are common extra-axial infratentorial neoplasms. Infratentorial lesions are discussed in Tables 1.4and1.5.

Multidetector CT is an excellent imaging modality for evaluation of the skull base, orbits, nasopharynx, oropharynx, and floor of the mouth because of its multiplanar imaging capabilities and high spatial resolution. CT is a useful method for imaging the location and extent of osseous lesions at the skull base, such as metastatic tumors, myelomas, chordomas, and chondrosarcomas.

CT can be used for the evaluation of congenital and developmental anomalies of the brain, such as semilobar holoprosencephaly, septo-optic dysplasia, schizencephaly, gray matter heterotopia, cortical dysplasia, unilateral megalencephaly, and Dandy-Walker malformation.

Diseases of white matter are classified into two major groups, dysmyelinating and demyelinating diseases. Dysmyelinating diseases, also known as leukodystrophies, are a group of disorders resulting from enzyme deficiencies that cause abnormal formation and metabolism of myelin. Demyelinating diseases are a group of disorders in which myelin is degraded or destroyed after it has formed in a normal fashion.

Abnormalities involving the lateral, third, and fourth ventricles, as well as the cerebral aqueduct, are well seen with CT because of the difference of attenuation between the brain parenchyma and cerebrospinal fluid (CSF). The production of CSF occurs in the choroid plexus within the ventricles. CSF circulates from the lateral ventricles through the foramina of Monro into the third ventricle. The third ventricle communicates with the fourth ventricle via the cerebral aqueduct. CSF from the fourth ventricle enters into the subarachnoid space through the foramina of Luschka and Magendie. Mass lesions along the CSF pathway can result in obstructive hydrocephalus with dilation of the ventricles proximal to the blockage.

Some asymmetry of the lateral ventricles can be seen normally. Altered morphology of the ventricles can result from various congenital anomalies (e.g., holoprosencephaly, septo-optic dysplasia, unilateral hemimegalencephaly, gray matter heterotopia, and Dandy-Walker malformation), as well as from distortion from intra- or extra-axial mass lesions.

The sizes of sulci can vary depending on multiple variables, such as age, congenital malformations, vascular abnormalities (e.g., cerebral infarcts, Sturge-Weber syndrome, and arteriovenous malformations [AVMs]), intra- or extra-axial mass lesions, hydrocephalus, and inflammatory diseases. Sulci should have CSF attenuation within them. The presence of contrast enhancement within the sulci and basilar cisterns is usually associated with pathology, such as inflammatory or neoplastic disease. Acute subarachnoid hemorrhage is typically seen as amorphous zones with high attenuation within the sulci and cisterns near the site of bleeding.

CT angiography (CTA) is a powerful imaging modality for evaluating normal and abnormal blood vessels. CTA has proven to be clinically useful in the evaluation of intracranial arteries, veins, and dural venous sinuses. Pathologic processes involving intra cranial blood vessels, such as aneurysms, AVMs, arterial occlusions, and dural venous sinus thrombosis, can be seen with CTA.

CT perfusion is a relatively new technique using dynamic IV infusion of contrast to measure CBF, cerebral blood volume (CBV), and mean transit time (MTT) of contrast enhancement to selected volumes of interest in the brain. CT perfusion has major clinical use in the evaluation of cerebral infarcts and adjacent zones of decreased perfusion (penumbra and oligemic areas) at risk for progression to infarction. Maintenance of CBF is critical for neuronal function. With arterial occlusion, loss of normal neuronal electrical activity occurs within seconds after arterial occlusion. Cellular death is dependent on the duration and magnitude of ischemia, the metabolic vulnerability of specific anatomical sites, and the oxygen content of blood. Normal CBF ranges from 50 to 60 mL/100 g/min. When the CBF is reduced to 15 to 20 mL/100 g/min for several hours (mild to moderate hypoxia), spontaneous and evoked neuronal electrical activity decreases significantly secondary to ischemia, although it can be reversed with reperfusion with CBF > 50 mL/100 g/min. With severe hypoxia/anoxia resulting from CBF < 10 mL/100 g/min, cellular membrane depolarization and ischemia leading to brain infarction may occur in several minutes.

When thrombotic or embolic arterial occlusions occur, CBF in the involved brain tissue is usually heterogeneous, with a central core showing the greatest reductions in CBF causing irreversible cell damage and infarction and a surrounding zone (referred to as the salvageable penumbra) that may have moderate reduction in CBF resulting in ischemia that may be reversible with reperfusion. The penumbra typically shows loss of neuronal electrical activity without immediate anoxic depolarization, as well as loss of autoregulation. If reperfusion does not occur, the penumbra will progress to infarction. An oligemic zone of mildly reduced CBF may also be seen surrounding the penumbra, which is less vulnerable to infarction than the penumbra. Thrombolytic medication can be useful and beneficial when it results in timely reperfusion to the penumbra and oligemic zones. Estimating the sizes of the penumbra and oligemic zones can be done in the acute setting with dynamic contrast-enhanced CT. CT perfusion with iodinated contrast delivered as an IV bolus can use the linear relationship between contrast concentration and attenuation to directly calculate and quantify CBF, CBV, and MTT for sites of ischemia and infarction in the brain prior to thrombolytic treatment (Fig. 1.1).

Fig. 1.1a–g Cerebral artery embolus. Coronal (a) and axial (b) computed tomography angiogram (CTA) images show an embolus occluding nearly all blood flow through the M1 segment of the right middle cerebral artery. Cerebral blood flow (CBF) (c), cerebral blood volume (CBV) (d), and mean transit time (MTT) (e) are displayed qualitatively using a color scale. Locations for regions of interest are shown in (f), with respective quantitative values for CBF, CBV, and MTT in (g) showing sites of core infarction and penumbra and oligemic zones.

Table 1.1 Congenital malformations of the brain

Lesions

CT Findings

Comments

Disorders of diverticulation (formation of cerebral hemispheres and ventricles)

Holoprosencephaly

Alobar: Large monoventricle with posterior midline cyst, lack of hemisphere formation with absence of falx, corpus callosum, and septum pellucidum. Fused thalami. Can be associated with facial anomalies (facial clefts, arrhinia, hypotelorism, and cyclops).

Fig. 1.2

Semilobar: Monoventricle with partial formation of interhemispheric fissure, occipital and temporal horns, and partially fused thalami. Absent corpus callosum and septum pellucidum. Associated with mild craniofacial anomalies.

Fig. 1.3a, b

Lobar: Near complete formation of interhemispheric fissure and ventricles. Fused inferior portions of frontal lobes, dysgenesis of corpus callosum with formation of posterior portion without anterior portion, malformed frontal horns of lateral ventricles, absence of septum pellucidum, separate thalami, and neuronal migration disorders.

Fig. 1.4a, b

Syntelencephaly (middle interhemispheric variant): Partial formation of interhemispheric fissure in the anterior and occipital regions with fusion of the portions of the upper frontal and/or parietal lobes. Genu and splenium of the corpus callosum can be observed with a focal defect in the body.

Holoprosencephaly: Spectrum of diverticulation disorders that occur during weeks 4 to 6 of gestation characterized by absent or partial cleavage and differentiation of the embryonic cerebrum (prosencephalon) into hemispheres and lobes. Causes include maternal diabetes, fetal genetic abnormalities such as trisomy 16 (Patau syndrome), and trisomy 18 (Edwards syndrome). Familial holoprosencephaly: mutations of HPE1 on chromosome 21q22.3, HPE2 on 2p21, HPE3 on 7q36, HPE4 on 18p, and HPE5 on 13q32. Clinical manifestations depend on the severity of the malformation and include early death, seizures, mental retardation, facial dysmorphism, and developmental delay. Patients with syntelencephaly often have mild to moderate cognitive dysfunction, spasticity, and mild visual impairment.

Septo-optic dysplasia (de Morsier syndrome)

Dysgenesis/hypoplasia or agenesis of septum pellucidum, optic nerve hypoplasia, and squared frontal horns; association with schizencephaly in 50% of patients. Optic canals are often small. May be associated with schizencephaly and gray matter heterotopia.

Patients can have nystagmus, decreased visual acuity, and hypothalamic-pituitary disorders (decreased thyroid stimulating hormone and/or growth hormone). Clinical exam shows small optic discs. May be sporadic from in utero insults or from abnormal genetic expression from mutations (HESX1 gene on chromo-some 3p21.1–3p21.2) during formation of the basal prosencephalon. Some findings overlap those of mild lobar holoprosencephaly.

Arrhinia/arrhinencephaly

Fig. 1.5a–d

Absence of olfactory lobes and sulci. Other anomalies may be seen involving the corpus callosum, hypothalamus, and pituitary gland.

Arrhinia refers to the absence of nose formation; arrhinencephaly refers to the congenital absence of the olfactory lobes. Typically associated with other congenital craniofacial anomalies such as cleft palate/lip, hypertelorism, and hypoplasia of the nasal cavity. Considered to result from insult in utero or genetic mutation.

Neuronal migration disorders

Lissencephaly (agyria or “smooth brain”)

Fig. 1.6a, b

Absent or incomplete formation of gyri and sulci with shallow sylvian fissures and “figure 8” appearance of brain on axial images, abnormally thick cortex, and gray matter heterotopia with smooth gray-white matter interface.

Severe disorder of neuronal migration (occurs during weeks 7–16 of gestation) with absent or incomplete formation of gyri, sulci, and sylvian fissures. Typically in association with microcephaly (defined as head circumference 3 standard deviations below normal). Associated with severe mental retardation, developmental delay, seizures, and early death. Other associated CNS anomalies are dysgenesis of the corpus callosum, microcephaly, hypoplastic thalami, and cephaloceles. Associated with mutations at LIS gene at 17p13.3, chromosome 17 (Miller-Dieker syndrome); DCX gene at Xq22.3-q23; and RELN gene at 7q22.

Pachygyria (nonlissencephalic cortical dysplasia)

Thick gyri with shallow sulci involving all or portions of the brain. Thickened cortex with relatively smooth gray-white interface may have areas of low attenuation in the white matter (gliosis).

Severe disorder of neuronal migration with etiologies similar to lissencephaly. Clinical findings related to degree of extent of this malformation.

Gray matter heterotopia

Laminar heterotopia appears as a band or bands of gray matter attenuation within the cerebral white matter.

Fig. 1.7a, b

Nodular heterotopia appears as one or more nodules of gray matter attenuation along the ventricles or within the cerebral white matter.

Fig. 1.8

Fig. 1.9a, b

Focal subcortical heterotopia can be seen as irregular nodular or multinodular masslike zones with gray matter attenuation in subcortical regions.

Fig. 1.9

Disorder of neuronal migration (weeks 7–22 of gestation) in which a collection or layer of neurons is located between the ventricles and cerebral cortex. Can have a bandlike (laminar) or nodular appearance isodense to gray matter; may be unilateral or bilateral. Associated with seizures and schizencephaly.

Schizencephaly (split brain)

Fig. 1.10a, b

Uni- or bilateral clefts in the brain extending from the ventricle to cortical surface lined by gray matter heterotopia, which may be polymicrogyric. The clefts may be narrow (closed lips) or wide (open lips).

Association with seizures, blindness, retardation, and other CNS anomalies (septo-optic dysplasia, etc.). Clinical manifestations related to severity of malformation. Ischemia or insult to portion or germinal matrix before hemisphere formation.

Unilateral hemimegalencephaly

Fig. 1.11

Nodular or multinodular region of gray matter heterotopia involving all or part of a cerebral hemisphere with associated enlargement of the ipsilateral lateral ventricle and hemisphere.

Neuronal migration disorder associated with hamartomatous overgrowth of a portion of or the whole hemisphere.

Dysgenesis of the corpus callosum

Fig. 1.12 a, b

Fig. 1.13a, b

Spectrum of abnormalities ranging from complete to partial absence of the corpus callosum. Widely separated and parallel orientations of frontal horns and bodies of the lateral ventricles, high position of the third ventricle in relation to the interhemispheric fissure, and colpocephaly. Associated with interhemispheric cysts, lipomas, and anomalies such as Chiari II malformation, gray matter heterotopia, Dandy-Walker malformation, holoprosencephaly, azygous anterior cerebral artery, and cephaloceles.

Failure or incomplete formation of corpus callosum (7–18 wk of gestation). Axons that normally cross from one hemisphere to the other are aligned parallel along the medial walls of lateral ventricles (bundles of Probst).

Malformations in cerebral cortical development

Polymicrogyria

Fig. 1.14a–c

Multiple small gyri occur unilaterally (40%), bilaterally (60%), and often in the region of the sylvian fissures. On CT, the small gyri may appear as zones of thickened cortex.

Malformation in late stages of neuronal migration resulting in abnormal neuronal organization of the brain cortex. Sites involved lack a normal six-layered cerebral cortex associated with abnormal sulcation.

Focal cortical dysplasia

Fig. 1.15

Nodular superficial zone with gray matter attenuation.

Malformation in late stages of neuronal migration resulting in a focal region of abnormal neuronal organization of the brain cortex. Can be associated with seizures.

Neural tube closure disorders

Chiari I malformation

Fig. 1.16

Cerebellar tonsils extend > 5 mm below the foramen magnum in adults, 6 mm in children younger than 10 y. Syringohydromyelia in 20% to 40% of cases, hydrocephalus in 25%, basilar impression in 25%. Less common association: Klippel-Feil syndrome and atlanto-occipital assimilation.

Cerebellar tonsillar ectopia. Most common anomaly of CNS. Not associated with myelomeningocele.

Chiari II malformation (Arnold-Chiari)

Fig. 1.17

Small posterior cranial fossa with gaping foramen magnum through which there is an inferiorly positioned vermis associated with a cervicomedullary kink. Beaked dorsal margin of the tectal plate. Myelomeningoceles in all patients. Hydrocephalus and syringomyelia common. Dilated lateral ventricles posteriorly (colpocephaly).

Complex anomaly involving the cerebrum, cerebellum, brainstem, spinal cord, ventricles, skull, and dura. Failure of fetal neural folds to close properly, resulting in altered development affecting multiple sites of the CNS.

Chiari III malformation

Features of Chiari II plus lower occipital or high cervical encephalocele.

Rare anomaly associated with high mortality.

Cephaloceles (meningoceles or meningoencephaloceles)

Fig. 1.18a, b

Fig. 1.19a, b

Fig. 1.20

Defect in skull through which there is either herniation of meninges and CSF (meningocele) or meninges, CSF, and brain tissue (meningoencephaloceles).

Congenital malformation involving lack of separation of neuroectoderm from surface ectoderm with resultant localized failure of bone formation. Occipital location most common in Western hemisphere, frontoethmoidal location most common site in Southeast Asians. Other sites include parietal and sphenoid bones. Cephaloceles can also result from trauma or surgery.

Cerebellar hypoplasia

Chiari II with vanishing cerebellum

Intracranial findings of Chiari II with complete or near complete absence of the cerebellum.

Myeloceles in Chiari II malformations may rarely be associated with in utero destruction of the fetal cerebellum.

Hypoplasia of cerebellar hemisphere

Hypoplasia or absence of a cerebellar hemisphere.

In utero insult causing loss of formative cerebellar cells from ischemia or apoptosis.

Dandy-Walker malformation

Fig. 1.21a, b

Vermian aplasia or severe hypoplasia, communication of fourth ventricle with retrocerebellar cyst, hypoplasia of cerebellar hemispheres, enlarged posterior fossa, and high position of tentorium and transverse venous sinuses. Hydrocephalus common. Associated with other anomalies, such as dysgenesis of the corpus callosum, gray matter heterotopia, schizencephaly, holoprosencephaly, and cephaloceles.

Abnormal formation of the roof of the fourth ventricle with absent or near incomplete formation of the cerebellar vermis.

Vermian hypoplasia (also referred to as “Dandy-Walker variant”)

Mild vermian hypoplasia with communication of posteroinferior portion of the fourth ventricle with cisterna magna. No associated enlargement of the posterior cranial fossa.

Occasionally associated with hydrocephalus, dysgenesis of the corpus callosum, gray matter heterotopia, and other anomalies.

Cerebellar dysplastic malformations

Joubert syndrome

Small dysplastic vermis with midline cleft between apposing cerebellar hemispheres, “molar tooth” axial appearance from small midbrain, and thickened superior cerebellar peduncles.

Malformation with hypoplasia of vermis, dysplasia and heterotopia of cerebellar nuclei, lack of decussation of superior cerebellar peduncles, and near complete absence of medullary pyramids. Clinical: ataxia, mental retardation, and abnormal eye movements.

Rhombencephalosynapsis

Dysmorphic cerebellum with no apparent separation of cerebellar hemispheres, aplasia, or severe hypoplasia of vermis.

Malformation with fusion of cerebellar hemispheres, dentate nuclei, and superior cerebellar peduncles; absent or hypoplastic vermis. Clinical: truncal ataxia, cerebral palsy, mental retardation, and seizures.

Lhermitte-Duclos disease

Fig. 1.22a, b

Poorly defined zone of low and intermediate attenuation with laminated appearance and localized mass effect located in the cerebellum. No enhancement.

Uncommon cerebellar dysplasia with gross thickening of cerebellar folia and disorganized cellular structure.

Fig. 1.2 Alobar holoprosencephaly. Axial image after ventricular shunting shows the absence of interhemispheric fissure and the lack of cerebral and cerebellar lobe formation.

Fig. 1.3a, b Semilobar holoprosencephaly. Axial images show fusion of the anterior portion of the brain with the presence of only the posterior portion of the interhemispheric fissure.

Fig. 1.4a, b Lobar holoprosencephaly. Axial images show fusion of the inferior portions of the frontal lobes. The other portions of the frontal lobes are separated, as are the parietal and occipital lobes.

Fig. 1.5a–d Arrhinia. Oblique coronal (a,b), parasagittal (c), and axial (d) images show the lack of formation of the nasal bones and severe hypoplasia of the nasal cavity.

Fig. 1.6a, b Lissencephaly. Axial images show the complete lack of gyral formation.

Fig. 1.7a, b Gray matter heterotopia, band type. Axial CT (a) image shows a band of intermediate attenuation representing the gray matter heterotopia, which is well seen on the axial proton density-weighted magnetic resonance image (MRI) (arrows) (b).

Fig. 1.8 Gray matter heterotopia, nodular ependymal type. Axial image shows nodular zones with gray matter attenuation along the margins of the lateral ventricles.

Fig. 1.9a, b Gray matter heterotopia, subcortical masslike type. Axial CT image (a) shows a masslike zone with gray matter attenuation involving the anterior left frontal lobe, as seen on the axial T2-weighted MRI (b).

Fig. 1.10a, b Schizencephaly, open lip type. Axial CT (a) and T2-weighted (b) images show large zones of communication between the lateral ventricles and subarachnoid space that are lined with gray matter.

Fig. 1.11 Unilateral hemimegalencephaly. Axial image shows enlargement of the left cerebral hemisphere with abnormally thickened cerebral cortex and gyri.

Fig. 1.12a, b Dysgenesis of the corpus callosum. Axial images show the absence of the corpus callosum with widely separated lateral ventricles.

Fig. 1.13a, b Lipoma of the corpus callosum. Axial (a) and sagittal (b) images show a lipoma with calcifications involving the anterior portion of the corpus callosum (arrow).

Fig. 1.14a–c Polymicrogyria. Axial CT images (a,b) and axial T2-weighted MRI (c) show numerous small gyri.

Fig. 1.15 Cortical dysplasia. Axial image shows abnormal cortical thickening involving the right frontal and parietal lobes (arrow).

Fig. 1.16 Chiari I malformation. Sagittal image shows extension of the cerebellar tonsils below the foramen magnum to the level of the posterior arch of C1.

Fig. 1.17 Chiari II malformation. Sagittal image shows extension of the cerebellum through the foramen magnum, as well as a malformed fourth ventricle, dysgenesis of the corpus callosum, and a ventricular shunt catheter.

Fig. 1.18a, b Parietal-occipital meningoencephalocele. Sagittal (a) and axial (b) images show a bone defect through which brain and meninges extend superficially.

Fig. 1.19a, b Frontal meningoencephalocele. Axial (a) and coronal (b) images show a bone defect through which brain and meninges extend superficially.

Fig. 1.20 Ethmoid meningocele. Coronal image shows a bone defect at the right cribriform plate with inferior extension of the dura.

Fig. 1.21a, b Dandy-Walker malformation. Axial CT image (a) and sagittal T1-weighted MRI (b) show absence of the vermis and hypoplasia of the cerebellar hemispheres.

Fig. 1.22a, b Lhermitte-Duclos disease. Axial T1-weighted MRI (a) and axial postcontrast CT image (b) show a nonenhancing lesion in the left cerebellar hemisphere (arrow).

Table 1.2 Supratentorial intra-axial mass lesions

Lesions

CT Findings

Comments

Congenital

Gray matter heterotopia

Laminar heterotopia appears as a band or bands of gray matter attenuation within the cerebral white matter (seeFig. 1.7,p. 8).

Nodular heterotopia appears as one or more nodules of gray matter attenuation along the ventricles (seeFig. 1.8,p. 8) or within the cerebral white matter (seeFig. 1.9,p. 9).

Focal subcortical heterotopia can be seen as irregular nodular or multinodular masslike zones with gray matter attenuation in subcortical regions (seeFig. 1.9,p. 9).

Disorder of neuronal migration (weeks 7–22 of gestation) in which a collection or layer of neurons is located between the ventricles and cerebral cortex. Can have a bandlike (laminar) or nodular appearance isodense to gray matter; may be unilateral or bilateral. Associated with seizures and schizencephaly.

Unilateral hemimegalencephaly

Fig. 1.11,p. 9

Nodular or multinodular region of gray matter heterotopia involving all or part of a cerebral hemisphere with associated enlargement of the ipsilateral lateral ventricle and hemisphere.

Neuronal migration disorder associated with hamartomatous overgrowth of a portion of or the whole hemisphere.

Neoplastic astrocytoma

Low-grade astrocytoma: Focal or diffuse mass lesion usually located in white matter with low to intermediate attenuation, with or without mild contrast enhancement. Minimal associated mass effect.

Fig. 1.23

Juvenile pilocytic astrocytoma subtype: Solid/cystic focal lesion with low to intermediate attenuation, usually with prominent contrast enhancement. Lesions located in the cerebellum, hypothalamus, adjacent to third or fourth ventricles, and brainstem.

Fig. 1.24

Gliomatosis cerebri: Infiltrative lesion with poorly defined margins with mass effect located in the white matter, with low to intermediate attenuation. Usually no contrast enhancement until late in disease. Anaplastic astrocytoma: Often irregularly marginated lesion located in white matter with low to intermediate attenuation, with or without contrast enhancement.

Fig. 1.25a, b

Low-grade astrocytoma: Often occurs in children and adults (20–40 y). Tumors comprised of well-differentiated astrocytes. Association with neurofibromatosis type 1, 10-y survival; may become malignant. Juvenile pilocytic astrocytoma subtype: Common in children; usually favorable prognosis if totally resected.

Gliomatosis cerebri: Diffusely infiltrating astrocytoma with relative preservation of underlying brain architecture. Imaging appearance may be more prognostic than histologic grade; ~2-y survival.

Anaplastic astrocytoma: Intermediate between low-grade astrocytoma and glioblastoma multiforme; ~2-y survival.

Glioblastoma multiforme

Fig. 1.26

Irregularly marginated mass lesion with necrosis or cyst, mixed low and intermediate attenuation, with or without hemorrhage, prominent heterogeneous contrast enhancement, peripheral edema; can cross the corpus callosum.

Most common primary central nervous system (CNS) tumor in adults, highly malignant neoplasms with necrosis and vascular proliferation, usually in patients older than 50 y; extent of lesion underestimated by CT; survival < 1 y.

Giant cell astrocytoma/tuberous sclerosis

Fig. 1.27

Circumscribed lesion located near the foramen of Monro with mixed low to intermediate attenuation, with or without cysts and/or calcifications, and heterogeneous contrast enhancement.

Subependymal hamartoma near the foramen of Monro; occurs in 15% of patients younger than 20 y with tuberous sclerosis. Slow-growing lesions can progressively cause obstruction of CSF flow through the foramen of Monro; long-term survival usual if resected.

Pleomorphic xanthoastrocytoma

Circumscribed supratentorial lesion involving the cerebral cortex and white matter, low to intermediate attenuation, with or without cyst (s), heterogeneous contrast enhancement, with or without enhancing mural nodule associated with cyst.

Rare type of astrocytoma occurring in young adults and children; associated with seizure history.

Oligodendroglioma

Fig. 1.28a, b

Circumscribed lesion with mixed low to intermediate attenuation, sites of clumplike calcification, and heterogeneous contrast enhancement; involves white matter and cerebral cortex; can cause chronic erosion of the inner table of the calvarium.

Uncommon slow-growing gliomas with usually mixed histologic patterns (astrocytoma, etc.). Usually in adults older than 35 y; 85% supratentorial. If low grade, 75% 5-y survival; higher grade lesions have a worse prognosis.

Central neurocytoma

Circumscribed lesion located at the margin of the lateral ventricle or septum pellucidum with intraventricular protrusion, heterogeneous low and intermediate attenuation, with or without calcifications and/or small cysts, heterogeneous contrast enhancement.

Rare tumors that have neuronal differentiation; imaging appearance similar to intraventricular oligodendrogliomas. Occur in young adults. Benign slow-growing lesions.

Ganglioglioma, ganglioneuroma, gangliocytoma

Circumscribed tumor, usually supratentorial, often temporal or frontal lobes, low to intermediate attenuation, with or without cysts, with or without contrast enhancement.

Ganglioglioma (contains glial and neuronal elements), ganglioneuroma (contains only ganglion cells). Uncommon tumors; seen in young adults younger than 30 y. Seizure presentation, slow-growing neoplasms. Gangliocytoma (contains only neuronal elements and dysplastic brain tissue). Favorable prognosis if completely resected.

Ependymoma

Fig. 1.29

Circumscribed lobulated supratentorial lesion, often extraventricular, with or without cysts and/or calcifications, low to intermediate attenuation, variable contrast enhancement.

Occurs more commonly in children than adults, one third supratentorial, two-thirds infratentorial; 45% 5-y survival.

Pineal gland tumors

Fig. 1.30a, b

Tumors often have intermediate attenuation to intermediate to slightly high attenuation, with contrast enhancement, with or without central and/or peripheral calcifications. Malignant tumors are often larger than benign pineal lesions (pineocytoma), as well as heterogeneous attenuation and contrast enhancement pattern, with or without leptomeningeal tumor.

Pineal gland tumors account for 8% of intracranial tumors in children and 1% of tumors in adults; 40% of tumors are germinomas, followed by pineoblastomas and pineocytomas, teratomas, choriocarcinomas, endodermal sinus tumors, astrocytomas, and metastatic tumors.

Hamartoma/tuberous sclerosis

Fig. 1.31

Cortical-subcortical lesion with variable attenuation, calcifications in 50% of older children; contrast enhancement uncommon.

Subependymal hamartomas: Small nodules located along and projecting into the lateral ventricles; calcification and contrast enhancement common.

Cortical and subependymal hamartomas are nonmalignant lesions associated with tuberous sclerosis. Tuberous sclerosis is an autosomal dominant disorder associated with hamartomas in multiple organs.

Hypothalamic hamartoma

Fig. 1.32a–c

Sessile or pedunculated lesions at the tuber cinereum of the hypothalamus; often intermediate attenuation similar to gray matter; typically no contrast enhancement; rarely contain cystic and/or fatty portions.

Usually occur in children with isosexual precocious puberty (0–8 y) or seizures (gelastic or partial complex) in second decade; congenital/developmental heterotopia/hamartoma (nonneoplastic lesions).

Lipoma

Fig. 1.33

CT: Lipomas have low attenuation equal to fat elsewhere in the field of view.

MRI: Lipomas have signal isointense to subcutaneous fat on T1-weighted images (high signal) and on T2-weighted signals; signal suppression occurs with frequency-selective fat saturation techniques or with a short time to inversion recovery (STIR) method; typically no gadolinium contrast enhancement or peripheral edema. Lipomas can be nodular or curvilinear. Lipomas can occur in many locations, commonly the corpus callosum, cerebellopontine angle cistern, and tectal plate.

Benign fatty lesions resulting from congenital malformation often located in or near the midline; may contain calcifications and/or traversing blood vessels.

Primitive neuroectodermal tumor

Fig. 1.34a, b

Circumscribed or invasive lesions, low to intermediate attenuation; variable contrast enhancement, frequent dissemination into the leptomeninges.

Highly malignant tumors located in the cerebrum, pineal gland, and cerebellum that frequently disseminate along CSF pathways.

Dysembryoplastic neuroepithelial tumor

Fig. 1.35a, b

Circumscribed lesions involving the cerebral cortex and subcortical white matter, low to intermediate attenuation, with or without small cysts; usually no contrast enhancement.

Benign superficial lesions commonly located in the temporal or frontal lobes.

Lymphoma

Fig. 1.36

Primary CNS lymphoma: Focal or infiltrating lesion located in the basal ganglia, periventricular regions, or posterior fossa/brainstem; low to intermediate attenuation; with or without hemorrhage/necrosis in immunocompromised patients; usually show contrast enhancement. Diffuse leptomeningeal contrast enhancement is another pattern of intracranial lymphoma.

Primary CNS lymphoma more common than secondary, usually in adults older than 40 y. B-cell lymphoma is more common than T-cell lymphoma. Increasing incidence related to the number of immunocompromised patients in the population. CT imaging features of primary and secondary lymphoma of brain overlap. Intracranial lymphoma can involve the leptomeninges in secondary lymphoma > primary lymphoma.

Hemangioblastoma

Circumscribed tumors usually located in the cerebellum and/or brainstem; small contrast-enhancing nodule with or without cyst or larger lesion with prominent heterogeneous enhancement with or without contrast-enhancing vessels within the lesion or at the periphery, Occasionally lesions have evidence of recent or remote hemorrhage.

Rarely occurs in cerebral hemispheres; occurs in adolescents and young and middle-aged adults. Lesions are typically multiple in patients with von HippelLindau disease.

Metastases

Fig. 1.37a, b

Circumscribed spheroid lesions in the brain; can have various intra-axial locations, often at gray-white matter junctions; usually low to intermediate attenuation; with or without hemorrhage, calcifications, or cysts; variable contrast enhancement. Often associated with adjacent low attenuation from axonal edema.

Represent ~33% of intracranial tumors, usually from extracranial primary neoplasm in adults older than 40 y. Primary tumor source: lung > breast > gastrointestinal (GI) > genitourinary (GU) > melanoma.

Neurocutaneous melanosis

Extra- or intra-axial lesions usually < 3 cm in diameter with irregular margins in the leptomeninges or brain parenchyma/brainstem (anterior temporal lobes, cerebellum, thalami, and inferior frontal lobes).

CT: May show subtle hyperdensity secondary to increased melanin, with or without vermian hypoplasia, with or without arachnoid cysts, with or without Dandy-Walker malformation.

MRI: Zones with intermediate to slightly high signal on T1-weighted images secondary to increased melanin, with gadolinium contrast enhancement; with or without vermian hypoplasia, with or without arachnoid cysts, with or without Dandy-Walker malformation.

Neuroectodermal dysplasia with proliferation of melanocytes in leptomeninges associated with large and/or numerous cutaneous nevi. May change into CNS melanoma.

Inflammatory

Cerebritis

Fig. 1.38a–c

Poorly defined zone or focal area of decreased attenuation, minimal or no contrast enhancement; involves cerebral cortex and white matter for bacterial and fungal infections.

Focal infection/inflammation of brain tissue from bacteria or fungi, secondary to sinusitis, meningitis, surgery, hematogenous source (cardiac and other vascular shunts), and/or immunocompromised status. Can progress to abscess formation.

Pyogenic brain abscess

Fig. 1.39a, b

Circumscribed lesion with a central zone of low attenuation (with or without air-fluid level) surrounded by a thin rim of intermediate attenuation; peripheral poorly defined zone of decreased attenuation representing edema; ringlike contrast enhancement that is sometimes thicker laterally than medially.

Formation of brain abscess occurs 2 weeks after cerebritis with liquefaction and necrosis centrally surrounded by a capsule and peripheral edema. Can be multiple. Complication from meningitis and/or sinusitis, septicemia, trauma, surgery, or cardiac shunt.

Fungal brain abscess

Fig. 1.40

Findings can vary depending on organism; lesions occur in meninges and brain parenchyma; solid or cystic-appearing lesions with decreased attenuation, nodular or ring pattern of contrast enhancement, peripheral zone with decreased attenuation in brain lesions (edema).

Occur in immunocompromised or diabetic patients with resultant granulomas in meninges and brain parenchyma. Cryptococcus involves the basal meninges and extends along perivascular spaces into the basal ganglia; Aspergillus and Mucor spread via direct extension through the paranasal sinuses or hematogenously and invade blood vessels, resulting in hemorrhagic lesions and/or cerebral infarcts. Coccidioidomycosis usually involves the basal meninges.

Encephalitis

Fig. 1.41

Poorly defined zone or zones of decreased attenuation, minimal or no contrast enhancement; involves the cerebral cortex and/or white matter; minimal localized mass effect. Herpes simplex typically involves the temporal lobes/limbic system with or without hemorrhage; cytomegalovirus (CMV) usually in periventricular/subependymal locations.

HIV often involves periatrial white matter.

Infection/inflammation of brain tissue from viruses, often seen in immunocompromised patients (e.g., herpes simplex, CMV, HIV, and progressive multifocal leukoencephalopathy) or immunocompetent patients (e.g., St. Louis encephalitis, eastern or western equine encephalitis, and Epstein-Barr virus).

Tuberculoma

Fig. 1.42

Intra-axial lesions in cerebral hemispheres, basal ganglia, and brainstem (adults) and cerebellum (children). Lesions can have decreased attenuation, central zone of low attenuation with a thin peripheral rim of intermediate attenuation; with solid or rim pattern of contrast enhancement; with or without calcification. Meningeal lesions: Nodular or cystic zones of basilar meningeal enhancement.

Occurs in immunocompromised patients and inhabitants of developing countries. Caseating intracranial granulomas via hematogenous dissemination; meninges > brain lesions.

Parasitic brain lesions

Toxoplasmosis

Fig. 1.43

Single or multiple solid and/or cystic-appearing lesions located in basal ganglia and/or corticomedullary junctions in cerebral hemispheres, low to intermediate attenuation; nodular or rim pattern of contrast enhancement; with or without mild peripheral low attenuation (edema). Chronic phase: calcified granulomas.

Most common opportunistic CNS infection in patients with AIDS; caused by ingestion of food contaminated with parasites (Toxoplasma gondii). Can be seen as a congenital or neonatal infection (TORCH syndrome: toxoplasmosis, other agents, rubella, cytomegalovirus, herpes simplex).

Cysticercosis

Fig. 1.44a, b

Single or multiple cystic-appearing lesions in brain or meninges; acute/subacute phase: Low to intermediate attenuation, rim with or without nodular pattern of contrast enhancement, with or without peripheral low attenuation (edema). Chronic phase: calcified granulomas.

Caused by ingestion of ova (Taenia solium) in contaminated food (undercooked pork); involves meninges > brain parenchyma > ventricles.

Hydatid cyst

Echinococcus granulosus: Single or rarely multiple cystic-appearing lesions with low attenuation surrounded by a thin wall; typically no contrast enhancement or peripheral edema unless superinfected; often located in vascular territory of the middle cerebral artery. Echinococcus multilocularis: Cystic (with or without multilocular) and/or solid lesions, central zone of intermediate attenuation surrounded by a slightly thickened rim, with contrast enhancement; peripheral zone of decreased attenuation (edema) and calcifications are common.

Caused by parasites E. granulosus (South America, Middle East, Australia, and New Zealand) and E. multilocularis (North America, Europe, Turkey, and China). CNS involvement in 2% of cases of hydatid infestation.

Inflammatory disorders

Radiation necrosis

Focal lesion with or without mass effect or poorly defined zone of low to intermediate attenuation, with or without contrast enhancement involving tissue (gray matter and/or white matter) in field of treatment.

Usually occurs from 4 to 6 months to 10 y after radiation treatment; may be difficult to distinguish from neoplasm. Positron emission tomography (PET) and magnetic resonance spectroscopy might be helpful for evaluation.

Demyelinating disease: multiple sclerosis, acute disseminated encephalomyelitis (ADEM)

Fig. 1.45a–c

Lesions located in cerebral or cerebellar white matter, brainstem, or basal ganglia; lesions usually have low to intermediate attenuation on CT. Zones of active demyelination may show contrast enhancement and mild localized swelling.

MRI: Zones of low to intermediate signal on T1-weighted images and high signal on fluid attenuation inversion recovery (FLAIR) and T2-weighted images; with or without gadolinium contrast enhancement. Contrast enhancement can be ringlike or nodular, usually in acute/early subacute phase of demyelination. Lesions rarely can have associated mass effect simulating neoplasms.

Multiple sclerosis is the most common acquired demyelinating disease usually affecting women (peak age 20–40 y). Other demyelinating diseases include acute disseminated encephalomyelitis/immune mediated demyelination after viral infection; toxins (exogenous from environmental exposure or ingestion of alcohol, solvents, etc., or endogenous from metabolic disorders, e.g., leukodystrophies and mitochondrial encephalopathies), radiation injury, trauma, and vascular disease.

Sarcoidosis

Poorly marginated intra-axial zone with low to intermediate attenuation; usually shows contrast enhancement with localized mass effect and peripheral edema. Often associated with contrast enhancement in the leptomeninges.

Multisystem noncaseating granulomatous disease of uncertain cause that can involve the CNS in 5% to 15% of cases. Associated with severe neurologic deficits if untreated.

Hemorrhage

Intracerebral hemorrhage/hematoma

Attenuation of the hematoma depends on its age, size, location, hematocrit, hemoglobin oxidation state, clot retraction, and extent of edema.

Hyperacute phase (4–6 h): Hemoglobin primarily as diamagnetic oxyhemoglobin (iron Fe2+ state). CT: High attenuation on CT.

MRI: Intermediate signal on T1-weighted images and slightly high signal on T2-weighted images.

Acute phase (12–48 h): Hemoglobin primarily as para-magnetic deoxyhemoglobin (iron, Fe2+ state). CT: High attenuation in acute clot directly related to hematocrit, hemoglobin concentration, and high protein concentration. Hematocrit in acute clot approaches 90%.

Fig. 1.46

Fig. 1.47

Fig. 1.48

Fig. 1.49,p. 27

MRI: Intermediate signal on T1-weighted images, low signal on T2-weighted images, surrounded by a peripheral zone of high T2 signal (edema).

Early subacute phase (> 2 d): Hemoglobin becomes oxidized to the iron Fe3+ state, methemoglobin, which is strongly paramagnetic. CT: High attenuation.

MRI: When methemoglobin is initially intracellular, the hematoma has high signal on T1-weighted images progressing from peripheral to central and low signal on T2-weighted images, surrounded by a zone of high T2 signal (edema). When methemoglobin eventually becomes primarily extra-cellular, the hematoma has high signal on T1-weighted images and high signal on T2-weighted images.

Late subacute phase (> 7 d to 6 wk): Intracerebral hematomas decrease 1.5 HU per day. Hematomas become isodense to hypodense; peripheral contrast enhancement from blood–brain barrier breakdown and vascularized capsule.

Chronic phase: Hemoglobin as extracellular methemoglobin is progressively degraded to hemosiderin.

CT: Chronic hematomas have low attenuation with localized encephalomalacia. Zones with high attenuation represent new sites of rebleeding.

MRI: Hematoma progresses from a lesion with high signal on T1- and T2-weighted images, with a peripheral rim of low signal on T2-weighted images (hemosiderin), to predominant hemosiderin composition and low signal on T2-weighted images.

Can result from trauma, ruptured aneurysms or vascular malformations, coagulopathy, hypertension, adverse drug reaction, amyloid angiopathy, hemorrhagic transformation of cerebral infarction, metastases, abscesses, and viral infections (herpes simplex, CMV).

Cerebral contusions

Fig. 1.47

CT: Appearance of contusions is initially one of focal hemorrhage involving the cerebral cortex and subcortical white matter. Contusions eventually appear as focal superficial encephalomalacia zones.

Contusions are superficial brain injuries involving the cerebral cortex and subcortical white matter that result from skull fracture and/or acceleration/deceleration trauma to the inner table of the skull. Often involve the anterior portions of the temporal and frontal lobes and inferior portions of the frontal lobes.

Metastases

Fig. 1.48a, b

The CT appearance of a hemorrhagic metastatic lesion is one of an intracerebral hematoma involving a portion or all of the neoplasm, usually associated with peripheral edema (decreased attenuation), often multiple; with contrast enhancement in nonhemorrhagic portions of lesions.

Metastatic intra-axial tumors associated with hemorrhage include bronchogenic carcinoma, renal cell carcinoma, melanoma, choriocarcinoma, and thyroid carcinoma. May be difficult to distinguish from hemorrhage related to other etiologies, such as vascular malformations and amyloid angiopathy.

Vascular

Arteriovenous malformation (AVM)

Lesions with irregular margins that can be located in the brain parenchyma (pia, dura, or both locations).

CT: AVMs contain multiple tortuous tubular vessels that have intermediate or slightly increased attenuation that shows contrast enhancement. Calcifications occur in 30% of cases. Computed tomography angiography (CTA) shows arteries, veins, and nidus of AVM even when there is an intra-axial hemorrhage.

Fig. 1.49a, b

MRI: