Tài liệu 2015 top 3 differentials in neuroradiology

Top 3 Differentials in Neuroradiology A Case Review William T. O'Brien Sr. lrhieme lrhieme Top 3 Differentials in Neuroradiology A Case Review William T. O'Brien Sr., DO Program Director, Diagnostic Radiology Residency David Grant USAF Medical Center Travis Air Force Base, California Former Chairman, Department of Radiology Wilford Hall USAF Ambulatory Surgical Center Joint Base San Antonio-Lackland, Texas Associate Clinical Professor Department of Radiology University of california, Davis School of Medicine Sacramento, California Thieme New York •Stuttgart • Delhi• Rio de Janeiro Executive Editor: William Lamsback Important note: Medicine is an ever-changing science under­ Managing Editor: J. Owen Zurhellen IV going continuai development. Research and clinical experience Assistant Managing Editor: Heather Allen are continually expanding our knowledge, in particular our International Production Director: Andreas Schabert knowledge of proper treatment and drug therapy. 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If errors in this ISBN 978-1-60406-724-8 (e-book) work are found after publication, errata will be posted at www. 1. Title. II. Title: Top three differentials in neuroradiology. [DNLM: 1. thieme.com on the product description page. Neuro- Sorne of the product names, patents, and registered radiography-Case Reports. 3. Central Nervous System-radiogra­ designs referred to in this book are in fact registered trade­ phy-Case Diagnosis, Differential-Case Reports. 2. Reports. 4. Central Nervous System Diseases­ radiography-Case Reports. WL 141.5.N47] marks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the RC71.5 appearance of a name without designation as proprietary is 616.07'5-dc23 2014026028 © 2015 Thieme Medical Publishers, Inc. not to be construed as a representation by the publisher that it is in the public domain. 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This applies in preparation of microfilms, and electronic data processing and storage. The views expressed in this material are those of the author, and do not reflect the official policy or position of the United Also available as an e-book: States Govemment, the Department of Defense, or the Depart­ eISBN 978-1-60406-724-8 ment of the Air Force. Dedicated in memory of Robert L Meals, DO 12 March 1928-9 June 2005 © Susan Schary 2005 For decades, Dr. Meals inspired thousands of students while serving as Academic Chairman of the Department of Radiology, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania. Dr. Meals was more than an instructor; he was a mentor and a true friend. To those who chose to pursue a career in radiology, he will always be a legend. He is sorely missed but will never be forgotten. Contents Foreworcl by Richard E. Latchaw Preface Aclmowledgments vii viii ix Section 1. Brain Subsection la. Congenital and Developmental Subsection lb. Attenuation and Signal Abnormality 2 44 Subsection le. Masses and Masslike Lesions 110 Subsection Id. Vasculature and Cerebrospinal Fluid Spaces 186 Section IL Head and Neck vi Subsection Ha. calvarium and Skull Base 260 Subsection IIb. Temporal Bone 296 Subsection IIe. Sinonasal 330 Subsection IId. Maxillofacial 362 Subsection IIe. Neck (induding spaces) 382 Subsection Hf. Orbits 444 Section ID. Spine 484 Index of Differential Diagnoses, by Case 607 Index of Key Findi� 612 Foreword Unique/ derive from multiple diagnostic categories. For some appear­ ances, he even indudes some uncommon but potentially lbat is the best word to describe Top 3 DijJerentials in important considerations ("Additional Diagnostic Considera­ Neuroradiology by William T. O'Brien-unique in its approach tions"), thus providing more than just three possibilities for to the clinical practiœ of neuro-imaging, and unique in its cases with more nonspecific findings. He finishes each case approach to education in this rapidly expanding subspecialty. with dinical and imaging "Pearls," which provide quick dif­ The traditional clinical practiœ of a neurologist, neuro­ ferentiating features. He also provides some selected refer - surgeon, orthopedic surgeon-any physician ordering a ences for more in-depth reading on the topic. neuro-imaging examination-is to evaluate the patient's his­ Sorne imaging appearances within each section are unique, tory in conjunction with signs and symptoms, corne ta a without differential diagnoses and not having a Top 3; they probable conclusion, and then request an imaging study to are called "Aunt Minnies." Dr. O'Brien considers a number of confirm or deny that clinical conclusion. The clinical practice of a radiologist initially requires the these to be fundamental to the knowledge base of the student, sa they are presented at the end of each section. Each has an recognition of a combination of findings on an imaging study extensive discussion regarding pathophysiology and charac­ within the stated clinical context This is followed by the teristic imaging appearances, along with selected referenœs, iterative comparison of these findings to examples from similar to that found with the cases having Top 3 differential diagnostic categories, including masses, demyelinating dis­ possibilities. eases, ischemia, infection, degenerative disease, etc. This How did Dr. O'Brien validate his Top 3 choices with so iterative proœss may be mental or actually require compari­ many varied appearances in diverse clinical contexts? By son with published examples. The result is a differential doing extensive research as to the most common diagnoses diagnosis that may vary in specificity and depth. One might for a given finding; by consulting with many radiologists who list the top three possible diagnoses, or one could list the most subspecialize in neuroradiology, head and neck radiology, likelywith that which is the most dangerous and thus must be and excluded, along with one that would be easy to exclude with that tend to be favorites in general and subspecialty board more studies. examinations. spinal radiology; and by incorporating entities How dowe traditionally educate a reader of neuro-imaging How will this book change how we practice and teach studies7 We usually ensure that the novice reader has seen neuro-imaging? lt is vital that neuro-imagers have ingrained examples from the various diagnostic categories with which in their brain the basic categories of neuropathology, so that we deal, and has leamed how diseases within each category they can be sure that they caver ail potential disease catego­ differ from those in other categories. The organization of our ries when confronted with an unknown case. However, books and our teaching sessions is typically based upon such O'Brien's approach can easily be superimposed on that basic categories: Neoplasms, Congenital Disease, Infections, etc. knowledge of disease organization. lt is fast, accurate, and However, what happens when the imager is confronted removes the potential that the reader will be slowed down, with an "unknown," a finding that does not fit easily into trying to ensure that ail categories are covered. This approach one of the categories to which he or she has become so provides a way to be "complete" in developing differential accustomed? Unfortunately, even though the imager has diagnoses rapidly and accurately. leamed the appearances of the majority of entities within 1 found reading this book to be a joy. One can approach it by a given category of disease, the finding does not tell the playing the student, viewing each image as an unknown, imager to which category it belongs! So, the imager must determining what the most prominent finding is, and then now search the categorically based textbooks for a "look giving one's own Top 3. Frankly, this is a book not just for the alike," which is very time-consuming and may not even be resident or fellow, but one that will give any academic faculty successful. member a positive learning experienœ, just like the one that Dr. O'Brien's approach ta both the clinical practice and the 1 hadl education of neuro-imaging is quite unique amongst the textbooks 1 have seen over many years as a neuroradiologist He has divided this book into three sections: Brain, Head and Richard E. Latchaw, MD Neck, and Spine. Within each section, he conœntrates on the Professor of Radiology most apparent imaging finding(s) within the presenting clin­ Neuroradiology Section ical context, and gives the "Top 3" potential diagnoses for that University of California, Davis Medical Center appearance (that "gamut"), including entities that may well Sacramento, California vii Preface It is a distinct pleasure to present Top 3 Differentials in would not be considered in the Top 3 for the particular version of the original "Top 3" book, Top 3 Differentials in gamut. Instead, the primary aim of the book is to generate Radiology, had been an aspiration of mine since its publica­ and have an understanding of a reasonable list of gamut­ tion in 201O. This subspedalty version is primarily designed based differentials rather than to obtain the "correct" for senior radiology residents, neuroradiology fellows, and answer. staff radiologists preparing for the neuroradiology portion As with the earlier Top 3 Differentials in Radiology, it is of initial and recertification board examinations; however, it important to realize that the differentials and discussions are may also prove useful for dinicians and surgeons who based on the key finding or gamut and not necessarily the routinely utilize neuroimaging. illustrative cases that are shown This is by design, because 1 This book is organized into three main sections: brain, felt it would be more high-yield to base the differentials and head and neck, and spine imaging; and further divided into discussions on the overall gamut/key finding rather than the subsections based upon anatomie region or pattern of imag­ illustrative case presented. Having an understanding of ing abnormality. Each section begins with a series of gamut-based differentials will allow one to subsequently unknown differential-based cases and ends with "Roentgen tailor the Iist of differentials for any case that is shown within dassics," which are cases with imaging findings character­ the gamut, whereas basing the differentials on the selected istic of a single diagnosis. images would be more limited in terms of future utility. On the first page of each case, readers are presented with Given the vast, evolving field of neuroimaging, this book is images from an unknown case, along with a clinicat history not meant to be a comprehensive reference book; rather, it is and an image legend. The images are meant to illustrate a meant to serve as a high-yield review for board preparation, key imaging finding, which is the basis for the subsequent as well as a quick reference for clinical practice. With these case discussion. The second page Iists the key imaging intentions in mind, the selection and ordering of differentials finding, from which a list of differentials is broken down for each gamut were based upon a combination of the most into the Top 3, along with "additional diagnostic considera­ likely diagnoses to be enrountered in a board setting, as well tions." The discussion section of each case provides a brief as clinical practice. Sorne "additional diagnostic considera­ review of important imaging and clinical manifestations for tions" were selected over others (which may actually be more all entities on the list of differentials, making this a high­ rommon) in order to provide the opportunity to discuss as yield reference for board preparation. lmaging pearls are many diagnostic entities as possible throughout the book. provided at the end of each case to allow for a quick review viii fact, many illustrative cases have a final diagnosis that Neuroradiology: A Case Review. Developing a neuroradiology 1 sinœrely hope that you find this Top 3 case-based of key points. The final diagnosis is provided for each case; approach enjoyable and useful, and I wish you all the best however, it is by no means the focus of this review book. In in your future endeavors. Acknowledgments This book would not have been possible without the contri­ image legend for each case in which they were involved. 1 butions of numerous colleagues and mentors. First and cannot possibly thank them enough for their significant foremost, 1 am forever indebted ta the faculty of David Grant contributions ta this book. Although there are far tao USAFMedicalCenter, the UniversityofCalifornia-Davis, and many ta name individually, 1 would like to espedally thank Oakland Children's Hospital, where 1 completed my radiol­ Paul M. Sherman, MD, who not only authored portions of ogy residency training, as well as the University of Cincin­ the neuroimaging sections in the original "Top 3" book, but nati and Cincinnati Children's Hospital Medical Center, also served as my neuroradiology mentor during residency where 1 completed my neuroradiology fellowships. The and bas been one of my neuroradiology partners in San dedicated staff at these institutions afforded me their Antonio for the past 4 years. time and expertise during my years of training and have Lastly, 1 would like to thank my family for their continu­ had a profound impact on my career. Their influence is what ous love and support, as well as the sacrifices they inspires me to remain in academics in the hopes of having a made during completion of this project. 1 have been similar impact on the next generation of radiologists. Severa! colleagues contributed to the content of this book blessed with a wonderful wife, Annie; two sons, Patrick and Liam; and a daughter, Shannon. Annie and 1 have been through images and case material, some of which was together for nearly two decades, and we could not be more induded in the original "Top 3" book, Top 3 Di.fferentials proud of our three incredible children. I am grateful in Radiology. Their contributions have greatly enhanced the beyond words for the joy that they bring into my life final manu script. The contributors are listed at the end of the each and every day. ix Brain Case 1 Fig. 1 .1 Axial T2 (a) and Tl (b) images demonstrate a "figure 8" appearance of the brain with a thickened cortex and absence of the normal gyral and sulcal pattern. The inner surface of the cortex has an irregular "cobblestone" appearance. Diffuse abnormal signal intensity is identified throughout the brain parenchyma. Susceptibility artifact from a shunt catheter is noted overlying the right occipital and posterior temporal lobes. • Clinical Presentation An infant boy with seizures, weakness, and failure to meet developmental milestones ( � Fig. 1.1 ) 2 Case 1 • Key lmaging Finding Agyria • Top 3 Differential Diagnoses • JYpe 1 lissencephaly. Type 1 or dassic lissencephaly is a con­ syndrome, Fukuyama congenital muscular dystrophy, and to genital neuronal migration disorder that results in a smooth a lesser degree, musde-eye-brain disease. Patients present appearance of the brain secondary to absence of the normal early in Iife with severe muscular weakness, eye abnormali­ gyral and sulcal pattern. There may be diffuse involvement ties, developmental delay or mental retardation, and compli­ (agyria) or focal involvement (pachygyria) of the cerebral cor­ cations of assodated brain malformations. Patients with tex. Diffuse involvement results in a "figure 8" appearance of Walker-Warburg often have characteristic findings, includ­ the brain with vertically oriented Sylvian fissures and absence ing occipital cephaloceles, cerebellar and brain stem hypo­ of the normal gyral and sulcal pattern. On pathologie evalua­ plasia, and kinking of the brain stem with a dassic "striking tion, there is a thickened, smooth four-layer cortex with a thin cobra" appearance on sagittal sequences. Hydrocephalus is ribbon of subcortical band heterotopia, rather than a normal present in the vast majority of cases. 1 lissencephaly may be associated with cytomegalovirus (CMV) infection, Miller-Dieker syndrome, and cerebellar hypoplasia. With CMV infection, periventricu­ • Band heterotopia. Gray matter heterotopia refers ta collec­ lar and intraparenchymal calcifications are noted. Patients rons migrate from the ependymal surface of the lateral ventri­ six-layer cortex. Type tions of disorganized neurons in abnormal locations. It results from premature arrest of normal neuronal migration. Neu­ with Miller-Dieker syndrome demonstrate midline septal des to the peripheral cortex, and then undergo organization calcifications, microcephaly, and characteristic dysmorphie into a normal six-layer cortex. If arrest occurs at any point during migration, heterotopias occur. Heterotopia may be facial features. • JYpe 2 lissencephaly. Type 2 or cobblestone lissencephaly is dassified as nodular (most common), which most often characterized by overmigration of neurons, severe dis­ occurs along the margins of the lateral ventricles, or band, organization of the gray matter, underdevelopment of gyri which is located within the subcortical or deep white matter. and sulci, and diffuse white matter hypomyelination. The When diffuse and subcortical in location, band heterotopia disorganized gray matter results in an irregular, "cobble­ may mimic lissencephaly. Patients typically present with stone" appearance of the cortex. There is an association with seizures, developmental delay, and spasticity. congenital muscular dystrophies, induding Walker-Warburg • Additional Differential Diagnoses • Prematurity. Prier ta -26 weeks gestation, the fetal brain nor­ • appearance at term. Therefore, lissencephaly should not be mally appears Iissencephalic due ta Jack of gyral and sulcal diagnosed until after 26 weeks gestation. When uncertain, a development. After 26 weeks gestation, the gyral and sulcal follow-up examination may be helpful to evaluate for interval pattern gradually gyral and sulcal formation. progresses until its relatively normal Diagnosis 1}'pe 2 cobblestone lissencephaly in a patient with Walker­ Warburg syndrome y' Pearls • The premature infant brain normally appears lissencephalic prier ta 26 weeks gestation. • Llssencephaly is a neuronal migration disorder with absence of normal gyri/sulci and a thickened cortex. 1 lissencephaly is smooth and may be associated CMV, Miller-Dieker, and cerebellar hypoplasia. • Type with • Type 2 lissencephaly has a "cobblestone" appearance and is associated with congenital muscular dystrophies. Suggested Readings Barlmvich AJ, Chuang SH, Norman D. MR of neuronal migration anomalies. AmJ Roentgenol 1988; 150: 179-187 Ghai S, Fong KW, Thi A, Chitayat D, Pantazi S, Blaser S. Prenatal US and MR imaging findings of lissenœphaly: review offetal œrebral sulcal devclopment Radio­ graphies 2006; 26; 389-405 3 Brain Case 2 Fig. 2.1 Axial Tl image demonstrates abnormal cortical thickening and absence of the normal gyri and sulci within the right occipital lobe. Abnormal cortical and subcortical signal intensity is noted involving the right occipital and temporal lobes. • Clinical Presentation A 2-day-old boy with seizures and spasms (� Fig. 2.1 ) 4 Case 2 • Key lmaging Finding Cortical malformation • Top 3 Differential Diagnoses • Pachygyria. Pachygyria is an incomplete or focal form of lissenœphaly. As with lissencephaly, there is both abnormal neuronal migration and failure to form the normal six-layer cortex. Instead, a four-layer cortex is most commonly seen pathologicaliy. Imaging findings are characterized by short, broad gyri with a lack of sulcation in the involved segments. Symptoms depend upon the extent and location of parenchy­ mal involvement. Patients may present with seizures, devel­ opmental delay, mental retardation, and/or spasticity. • Polymicrogyria. Polymicrogyria is a neuronal migration abnormality characterized by abnormal distribution of neu­ rons along the cortical surface. Multiple, small gyri replace the normal organized gyral and sulcal pattern. It is thought to result from laminar necrosis of neurons after they reach the cortical surface. It is commonly seen in association with cyto­ megalovirus (CMV) infection. Para-Sylvian locations are com­ monly involved. The polymicrogyria pattern is best depicted on magnetic resonanœ imaging (MRI). Abnormal signal is commonly seen in the subjacent white matter. dinically, patients present with seizures, developmental delay, mental • atous overgrowth of ail or a portion of one cerebral hemi­ sphere with associated neuronal migration abnormalities of varying severity. It is thought to occur as a result of an insult during neuronal migration. The ipsilateral hemisphere and ventricle are enlarged. Affected gyri are thickened and may show a primitive lissenœpahlic appearanœ with shallow or absent sulci. There is often abnormal attenuation (computed tomography) and signal intensity (MRI) within the subjacent white matter. Calcifications are not uncommon. dinically, the patient may present with seizures, developmental delay, mental retardation, and/or hemiplegia. Syndromes associated with hemimegalencephaly include neurofibromatosis type 1, Klippel-Trenaunay-Weber syndrome, tuberous sderosis, and Proteus syndrome. Additional Differential Diagnoses • Subcortical band heterotopia. Gray matter heterotopia refers to collections of disorganized neurons in abnormal locations due to premature arrest of normal migration. Neurons migrate from the ependymal surface of the lateral ventricles to the peripheral cortex, and then undergo orga­ pial surface to the ventricle. The defts are typically para­ Sylvian in location and lined by polymicrogyric gray matter. In Type I (dosed-lip) schizenœphaiy, the gray matter Iinings are apposed with a small ventricular dimple of cerebrospinal fluid (CSF) extending into the deft. Type II (open-lip) schizen­ nization into a normal six-layer cortex. If arrest occurs at any point during migration, heterotopias occur. Heteroto­ œphaly consists of a large CSF-filled space between the gray matter linings. Schizenœphaly may be bilateral and asso­ dated with septooptic dysplasia. dinical manifestations depend upon the severity of the lesion. Patients with type I are often almost normal in terms of development, but may have seizures and hemiparesis. Type II patients usually dem­ pia may be classified as nodular, which most often occurs along the margins of the lateral ventricles, or band-type, which occurs within the subcortical or deep white matter. Patients typically present with seizures, developmental delay, and spasticity. • Schizencephaly. Schizencephaly is a congenital malformation characterized by gray matter-lined clefts extending from the • retardation, and, occasionally, hemiparesis. Polymicrogyria may be associated with various syndromes, including Aicardi (callosal anomalies, infantile spasms, and retinal lesions) and Zellweger (cerebrohepatorenal) syndromes. • Hemimegalencephaly. Hemimegalencephaly is a hamartom­ onstrate mental retardation, seizures, hypotonia, spasticity, inability to walk or speak, and blindness. Diagnosis Pachygyria � Pearls • Pachygyria is a form of focal lissencephaly with a thickened, four-layer cortex (instead of the normal six layers). • With polymicrogyria, small gyri replace the normal, orga­ nized gyral pattern; it is associated with CMV. • Heterotopia (nodular or band) refers to collections of disor­ ganized neurons in abnormal locations. Suggested Readings Barlwvich AJ, Clmang SH, Norman D. MR of neuIOllill migration anomalies. AmJ Roentgenol 1988; 150: 179-187 Broumandi DD. Haywanl UM, Benzian]M, Gonzalez 1, Nelson MD. Best cases from the AFIP: hemimegalenœphaly. Radiographies 2004; 24: 843-848 Hayashi N, Tsutswrù Y, Barlcvvich AJ. Morphological features and associated anoma­ lies of schizencephaly in the dinkal population: detailed analysis of MR images. Neuroradiology 2002; 44: 418-427 5 Brain Case 3 Fig. 3.1 Axial fluid-attenuated inversion recovery (FLAIR) MR image demonstrates asymmetry of the cerebral hemispheres with the right smaller than the left and associated prominence of the sulci on the right. An enlarged medullary vein is seen along the anterior margin of the right lateral ventride. Hazy, periatrial white matter signal intensity corresponds to regions of terminal myelination. • Clinical Presentation A 2-year-old girl with developmental delay (� Fig. 3.1 ) 6 Case 3 • Key lmaging Finding Asymmetry of cerebral hemispheres • Top 3 Differential Diagnoses • Nonnal variant. Slight variation in size of an entire cerebral hemisphere, one or more lobes, or individual sulci is not uncommon, occurring in -10% of normal cases. Parenchymal morphology, attenuation, and signal intensity should other­ wise be normal and are useful discriminators from pathologie causes of parenchymal volume Joss. Patients are oft:en neuro­ logically and developmentally intact for age. volume Joss as a result of some form of insult Hypoxic-ischemic injury is the most common cause of enœphalomalacia, followed by trauma and infectious or inflammatory processes. Ischemic injury typically follows a vascular distribution. During the acute phase of injury, there is often focal edema and swelling. In the chronic stage, there is volume Joss with surrounding gliosis. In Iateral œrebral hemisphere. Venous drainage is diverted through enlarged medullary and subependymal veins. Hemiatrophy results, likely from venous hypertension. Magnetic resonanœ imaging (MRI) shows œrebral atrophy, abnormal leptomenin­ geal enhanœment, and increased enhanœment within a hyper­ trophied ipsilateral choroid plexus. The involved hemisphere may demonstrate abnormal signal, cortical enhanœment, and the setting of an asymmetric small œrebral hemisphere, a large cortical calcifications in a "tram trad<" configuration. • Encephalomalacia. Enœphalomalacia refers to parenchymal • • Additional Differential Diagnoses Dyke-Davidolf-Mason syndrome (DDMS). DDMS refers to compensatory enlargement of the ipsilateral calvarium, para­ nasal sinuses, and mastoid air cells secondary to underdevel­ opment or atrophy of the underlying œrebral hemisphere. The most common causes of ipsilateral cerebral atrophy include a large-territory ischemic insult at a young age or SWS. Symptoms are related to the causative process. • Hemimegalencephaly. Hemimegalencephaly is a hamartom­ atous overgrowth of all or a portion of one œrebral hemi­ sphere with associated neuronal migration abnormalities. lt is thought to result from an insult during neuronal migration. The ipsilateral hemisphere and ventride are enlarged. Affected gyri are thickened and may show a lissenœpahlic appearance with shallow or absent suld. There is oft:en abnor­ mal attenuation {computed tomography) and signal intensity (MRI) within the white matter of the ipsilateral hemisphere. • territory infarct (middle œrebral artery) is the most likely cause of enœphalomalacia. • Sturge-Weber syndrome (SWS; encephalotrigeminal angioma­ tosis). SWS is a sporadic phakomatosis thought to result from abnormal development of venous drainage. lt is characterized by a cutaneous port-wine stain (usually in the Vl distribution of the trigeminal nerve) and pial angiomatosis overlying the ipsi­ calcifications are not uncommon. Œnically, patients may present with seizures, developmental delay, mental retarda­ tion, and hemiplegia. Associated syndromes indude neuro­ fibromatosis type 1, Klippel-Trenaunay-Weber syndrome, tuberous sderosis, and Proteus syndrome. • Rasmussen encephalitis. Rasmussen enœphalitis is a rare, progressive, inflammatory neurological disorder of unknown origin. A viral or postviral autoimmune etiology bas been postulated. Patients present in childhood with persistent, relentless, focal motor seizures (epilepsia partialis continua), hemiplegia, and cognitive deficits. Early on, MRI demon­ strates abnormal edema and increased T2 signal within the involved hemisphere. Chronically, findings are more charac­ teristic with abnormal signal, asymmetric atrophy, and decreased perfusion and metabolism on the affected side. Treatment consists of functional hemispherectomy. Diagnosis Sturge-Weber syndrome � Pearls • Enœphalomalacia refers to parenchymal volume Joss from some form of insult; ischemia is most common. • Hemimegalencephaly is a hamartomatous overgrowth of all or part of one cerebral hemisphere. • SWS is characterized by seizures, cutaneous port-wine stain, and pial angiomatosis of the ipsilateral hemisphere. Suggested Readings Shapiro R, Galloway SJ, Shapiro MD. Minimal asyrnrnetryof the brain: a normal variant ArnJ RDentgenol 1986; 147: 753-756 Sener RN, Jinkins JR. MR of cranioœrebral herniatrophy. Œn Irnaging 1992; 16: 93-97 7 Brain Case 4 Fig. 4.1 Axial T2 (a) and fluid-attenuated inver­ sion recovery (FLAIR) (b) images of the brain demonstrate a hypoin­ tense subependymal nodular lesion within the frontal horn of the right lateral ventricle. The lesion is isointense to white matter on Tl sequences (c) and dem­ onstrates homogeneous enhancement (d). Wedge-shaped regions of cortical and sub­ cortical signal abnormal­ ity are also noted on the T2/FLAIR sequences (left hemisphere). (Courtesy of Paul M. Sherman, MD.) • Clinical Presentation An adolescent with seizures (� Fig. 4.1 ) 8