Pearls and Pitfalls in head and neck and neuroimaging PDF
Preview Pearls and Pitfalls in head and neck and neuroimaging
Pearls and Pitfalls in HEAD AND NECK AND NEUROIMAGING Variants and Other Difficult Diagnoses Nafi Aygun AssociateProfessorofRadiologyandDirectoroftheNeuroradiology FellowshipProgram,JohnsHopkinsUniversity,Baltimore,MD,USA Gaurang Shah AssociateProfessorofRadiology,UniversityofMichiganHealth System,AnnArbor,MI,USA Dheeraj Gandhi ProfessorofRadiology,NeurologyandNeurosurgeryatthe UniversityofMarylandSchoolofMedicine,Baltimore,MD,USA UniversityPrintingHouse,Cambridgecb28bs,UnitedKingdom PublishedintheUnitedStatesofAmericabyCambridgeUniversityPress,NewYork CambridgeUniversityPressispartoftheUniversityofCambridge. ItfurtherstheUniversity’smissionbydisseminatingknowledgeinthepursuitof education,learningandresearchatthehighestinternationallevelsofexcellence. www.cambridge.org Informationonthistitle:www.cambridge.org/9781107026643 ©CambridgeUniversityPress2013 Thispublicationisincopyright.Subjecttostatutoryexception andtotheprovisionsofrelevantcollectivelicensingagreements, noreproductionofanypartmaytakeplacewithoutthewritten permissionofCambridgeUniversityPress. Firstpublished2013 PrintedinSpainbyGrafosSA,Artesobrepapel AcatalogrecordforthispublicationisavailablefromtheBritishLibrary LibraryofCongressCataloginginPublicationdata Aygun,Nafi. Pearlsandpitfallsinheadandneckandneuroimaging/NafiAygun,GaurangShah, DheerajGandhi. p.;cm. Includesbibliographicalreferences. ISBN978-1-107-02664-3(Hardback) I. Shah,Gaurang. II. Gandhi,Dheeraj. III. Title. [DNLM:1. Neuroimaging–methods. 2. CentralNervousSystemDiseases–diagnosis. 3. Diagnosis,Differential. 4. OtorhinolaryngologicDiseases–diagnosis. WL141.5.N47] RC349.D52 616.8004754–dc23 2013010572 ISBN978-1-107-02664-3Hardback CambridgeUniversityPresshasnoresponsibilityforthepersistenceoraccuracyof URLsforexternalorthird-partyinternetwebsitesreferredtointhispublication, anddoesnotguaranteethatanycontentonsuchwebsitesis,orwillremain, accurateorappropriate. .......................................................................................................................... Everyefforthasbeenmadeinpreparingthisbooktoprovideaccurateand up-to-dateinformationwhichisinaccordwithacceptedstandardsand practiceatthetimeofpublication.Althoughcasehistoriesaredrawnfrom actualcases,everyefforthasbeenmadetodisguisetheidentitiesofthe individualsinvolved.Nevertheless,theauthors,editorsandpublisherscan makenowarrantiesthattheinformationcontainedhereinistotallyfree fromerror,notleastbecauseclinicalstandardsareconstantlychanging throughresearchandregulation.Theauthors,editorsandpublishers thereforedisclaimallliabilityfordirectorconsequentialdamagesresulting fromtheuseofmaterialcontainedinthisbook.Readersarestrongly advisedtopaycarefulattentiontoinformationprovidedbythemanufacturer ofanydrugsorequipmentthattheyplantouse. To myparents, Vrindavan andVinu Shah,for their love and support; mywifeKinnari,fortakingthejourneywithme;andmysonsSharvilandSahil, for bringing joy into ourlives. GaurangShah To Bobby, mybest friend and life partnerand for Shreyaand Diya, mybeautiful daughters and thelove of my life. Dheeraj Gandhi Contents Preface ix Section 1 Cerebrovascular diseases Section 4 Infectious diseases Case 1 Densebasilar artery sign 1 Case 36 Brain abscess 191 Case 2 Global anoxic brain injury 4 Case 37 Neurocysticercosis 194 Case 3 Acuteinfarction 8 Case 38 Tuberculosis 198 Case 4 Vertebral artery dissection 10 Case 39 Creutzfeldt–Jakobdisease 207 Case 5 Subacute infarct 13 Case 40 Herpes encephalitis 210 Case 6 Subarachnoid hemorrhage 17 Case 7 Intracranialaneurysms 21 Section 5 Metabolic and neurodegenerative Case 8 Giant aneurysms 23 conditions Case 9 Acuteintracerebral hematoma 26 Case 10 Cerebral amyloidangiopathy 30 Case 41 Wernicke’s encephalopathy 213 Case 11 Primary CNS vasculitis 34 Case 42 Hypertrophicolivarydegeneration 217 Case 12 Reversiblecerebral vasoconstriction Case 43 Adrenoleukodystrophy 219 syndrome 37 Case 13 Moyamoya disease/syndrome 40 Section 6 Trauma Case 14 Cortical venous thrombosis 43 Case 15 Developmental venous anomalies 46 Case 44 Mild traumatic brain injury 224 Case 16 Dural arteriovenous fistula 49 Case 45 Isodense subdural hematoma 227 Case 17 Cavernousmalformation 52 Section 7 Miscellaneous Section 2 Demyelinating and inflammatory diseases Case 46 Posteriorreversible encephalopathy syndrome 229 Case 47 Late-onsetadult hydrocephalussecondary to Case 18 Tumefactive demyelinating lesion 55 aqueductalstenosis 232 Case 19 Acute disseminated encephalomyelitis 58 Case 48 Intracranial hypotension 234 Case 20 Progressivemultifocal Case 49 Idiopathic intracranial hypertension 238 leukoencephalopathy 62 Case 50 Rathke’s cleft cyst 240 Case 21 Osmotic myelinolysis 65 Case 22 Neurosarcoidosis 72 Section 8 Artifacts and anatomic variations Case 51 FLAIR sulcal hyperintensity secondary togeneral Section 3 Tumors anesthesia 245 Case 52 Virchow–Robin spaces 250 Case 23 Posteriorfossa masses in children 80 Case 53 Arachnoid granulations 255 Case 24 Low-gradeglioma 92 Case 54 Benign external hydrocephalus 257 Case 25 Diffuse intrinsic pontine glioma 105 Case 55 Pitfalls in CTA 260 Case 26 Pseudoprogression of GBM 109 Case 56 Asymmetric pneumatization of the anterior Case 27 Pseudoresponse in treatment of GBM 112 clinoid process 264 Case 28 Low-gradeoligodendroglioma 114 Case 29 Primary CNS lymphoma 116 Case 30 Pineal region tumors 125 Section 9 Skull base Case 31 Intraventricular masses 140 Case 32 Colloid cyst 153 Case 57 Fibrous dysplasiaof skull base 267 Case 33 Primary intraosseousmeningioma 161 Case 58 Sphenoid bonepseudolesion 271 Case 34 Suprasellar meningioma 171 Case 59 Clivallesions 276 Case 35 Pituitary macroadenoma 180 Case 60 Perineuralspread 282 vii Contents Section 10 Temporal bone Section 16 Vessels Case 61 Cochleardysplasia 285 Case 84 Carotid artery dissection 381 Case 62 Labyrinthitis ossificans 289 Case 85 Traumaticarterial injury 384 Case 63 Superior semicircular canal dehiscence 292 Case 64 Fluid entrapment in the petrous apex cells 294 Section 17 Spinal column Case 65 Acquired cholesteatoma 299 Case 66 Malignantotitis externa 304 Case 86 Craniovertebral junction injuries 387 Case 67 Temporal bone fractures 307 Case 87 Odontoid fractures 390 Case 88 Vertebral compression fractures 398 Section 11 Paranasal sinuses Case 89 Sacral insufficiency fracture 401 Case 90 Paget’s diseaseof the spine 405 Case 68 Allergic fungal sinusitis 310 Case 91 Renal osteodystrophy 409 Case 69 Invasive fungalsinusitis 316 Case 92 Calcific tendinitisof the longus colli 414 Case 70 Spontaneous CSF leaks and sphenoid cephaloceles 324 Section 18 Intervertebral discs Case 71 Juvenile nasal angiofibroma 328 Case 93 T2hyperintense disc herniation 419 Section 12 Orbits Case 94 Disc herniation andcord compression 424 Case 95 Postoperativedisc herniation versus postsurgical Case 72 Idiopathic orbitalpseudotumor 331 scarring 427 Case 73 Optic neuritis 336 Case 96 Degenerativeendplate alterations 430 Section 13 Salivary glands Section 19 Spinal canal contents Case 74 Intraparotid lymph nodes 342 Case 97 Spinal dysraphism 434 Case 75 Benign mixed tumor 344 Case 98 Tethered spinal cord 445 Case 76 Firstbranchial cleft cyst 350 Case 99 ChiariI malformation 449 Case 100 Spinal vascular malformations 455 Case 101 Cord compression 458 Section 14 Neck Case 102 Demyelinating/inflammatory spinal cord lesion 466 Case 77 Nasopharyngeal cysts 354 Case 103 Subacute combineddegeneration 469 Case 78 Cystic nodal metastasis 357 Case 104 Intradural cyst 471 Case 79 Low-flow vascular malformations 360 Case 105 Spinal CSF leaks 475 Case 80 Parapharyngeal masses 364 Case 106 Leptomeningeal drop metastases 478 Section 15 Thyroid and parathyroid Index 486 Case 81 Third branchial apparatusanomaly 370 Case 82 Parathyroid adenoma 372 Case 83 String sign 378 viii Preface “Ateacherisonewhomakeshimselfprogressivelyunnecessary.” Eachchapterisconcise,yetgivesacomprehensiveoverviewof –ThomasCarruthers the subject matter. Weunderstandthattimeispreciousandthereforewantedto Itiswithagreatsenseofpridethatweintroduceourendeavor createaresourcethatispreciseandtrustworthy.Itisourhope entitled Pearls and Pitfalls in Head and Neck and Neuro- thatthistreatiseiseasytofollow,unpretentious,andhelpful. imaging.Wehopethatthisbookwillbefuntoreadandfoster WewouldliketothankalltheCambridgeUniversityPress the understanding of difficult diagnoses and common pitfalls staff who helped us tremendously every step of the way. In in Neuroimaging. particular,weexpressourgratitudetoNishaDoshiandBeata We have different backgrounds and sub-specialty Neuro- imaging expertise, but have one thing in common – the love Mako. Gaurang would also like to express his gratitude to Suresh Mukherji, Mark Shiroishi, Sanjay Jain, Prasan Rao, and passion for teaching the residents and fellows. This has JayantNarangandMohammadArabiforsharingtheirimages resultedinaccumulationof thousandsof teachingfiles inour and wisdom. respective libraries. Years spent with the trainees in the read- Our sincere thanks to the clinicians working with us for ingroominwonderfulacademicinstitutionshavegivenusan providing ever so important clinical feedback and learning understanding of diagnoses that are commonly missed and thatcomeswithit.Lastbutnottheleast,wethankourfamilies imagingfindingsthat are likelyto be misinterpreted. for their unconditional support and patience during the Whileanumberofexcellentbooksexistonthesubjectand writingof this project. practiceof Neuroradiology, a book like thisis unique. It aims We hope that the readers will enjoy reading this book. tocoverthelacunaethatcommonlyexistintheknowledgeof We are open to any suggestions or criticism that the readers Neuroimaging and gives clarity to diagnoses that are difficult may have for its improvement and look forward to hearing to make withcertainty. from you. After deciding to proceed with this project, the three of us brainstormed and came up with 106 topics that we wanted to cover. These topics were divided into 19 sections. Nafi, Gaurang, and Dheeraj ix 1 E S A Dense basilar artery sign C Imaging description diffusely hyperdense vessels that can potentially mimic the dense artery sign. Partial volume averaging, vessel tortuosity, Intravascular clot can be seen on unenhanced CT as a focal orectesiamayalsomakeaportionofthevesselappeardenser hyperattenuation and may be the only sign of acute ischemia thantheotherparts.Mostofthesepossibilitiescanbeelimin- (Fig. 1.1). A thrombosed vessel has a higher CT attenuation atedbyusingthinnerslicesandcomparingthevesselsegment valuethananormalvessel,becauseclotcontainsmoreprotein inquestiontoothervesselsofsimilarsizeonthesameCT[4]. andlessserumthanbloodduetothedepositionoffibrinogen Ofcourse,itiscrucialtohaveappropriateclinicalcorrelation. and other clotting proteins and extraction of serum during Contrast-enhanced CT/CTA or MRI/MRA can be used as a the process of thrombus formation. When CT shows a focal problem solver in ambiguous cases. It should be also kept in hyperattenuation in the middle cerebral artery (MCA) this mind that the sensitivity of the dense vessel sign is relatively is known as the dense MCA sign. This provides not only a low. In other words, absence of dense artery sign does not diagnosis of MCA territory infarct but also some prognostic excludevessel occlusion or brain infarct. information,becausestrokepatientswhodemonstrateadense MCA sign on their initial CT do relatively poorly compared to those who do not have this sign (Fig 1.2) [1]. Clot in the Teaching points basilar artery is not as common as MCA thrombus, but The dense basilar artery sign indicates basilar artery throm- the same principles thatlead to the dense MCA sign apply to bosis,basilararteryterritoryinfarcts,andapooroutcome.In basilar artery thrombosis (Fig. 1.1) [2]. Similarly, thrombosis the appropriate clinical setting, the specificity of this finding oftheotherintracranialvessels,includingtheveinsanddural is high although sensitivity is only moderate. Using thinner sinuses, can be diagnosed on the basis of dense clot present slices,comparingthedensityofthevesselinquestiontothat withinthe vessel (Figs. 1.3,1.4). ofothervesselsofsimilarsize,helpstodifferentiateintralum- inal clot from mimickers such as atherosclerosis, hemocon- Importance centration, and vessel tortuosity.To confirm thepresenceof Unenhanced CTisthefirst imagingstudyperformedinmost vessel occlusion, contrast-enhancedCTmay beemployedas acute neurologic presentations. Diagnosing a vascular occlu- aquickproblemsolvingtool,althoughCTA,MRI/MRA,and sionearlyhasgreatprognosticsignificance.Earlyinitiationof sometimes digital subtraction angiography (DSA) are neces- treatmentisthemostimportantfactorinachievingimproved sary to better characterize the extent of vessel occlusion, outcomes in thesettingof basilar occlusion [3]. collateralvessels,andinfarctedareas. Typical clinical scenario MCA territory infarcts are relatively easy to diagnose clinic- references ally, as patients present with focal neurologic deficits and 1. ZorzonM,MasèG,Pozzi-MucelliF,etal.Increaseddensityinthe consciousness is usually not altered. Basilar artery territory middlecerebralarterybynonenhancedcomputedtomography: infarcts, on the other hand, may lack localizing features and prognosticvalueinacutecerebralinfarction.EurNeurol1993;33:256–9. areassociatedwithvaryingdegreesofalterationinconscious- 2. GoldmakherGV,CamargoEC,FurieKL,etal.Hyperdensebasilar ness that require a broader clinical differential diagnosis than arterysignonunenhancedCTpredictsthrombusandoutcomeinacute anterior circulation infarcts. posteriorcirculationstroke.Stroke2009;40:134–9. 3. EckertB,KucinskiT,PfeifferG,GrodenC,ZeumerH.Endovascular Differential diagnosis therapyofacutevertebrobasilarocclusion:earlytreatmentonsetasthe Increased attenuation in a vessel can result from increased mostimportantfactor.CerebrovascDis2002;14:42–50. attenuation of the blood or the vessel wall in addition to 4. GaddaD,VannucchiL,NiccolaiF,etal.Multidetectorcomputed intraluminal clot formation. Atherosclerosis results in focally tomographyoftheheadinacutestroke:predictivevalueofdifferent increasedattenuationinvesselwallthatcanmimicthrombus. patternsofthedensearterysignrevealedbymaximumintensity Increased hematocrit due to hemoconcentration or systemic projectionreformationsforlocationandextentoftheinfarctedarea. disorderssuchaschronicobstructivelungdiseases maycause EurRadiol2005;15:2387–95. 1 SECTION1 Cerebrovasculardiseases A B C Figure1.1 Acutebasilararterythrombosis.(A,B)AxialunenhancedCTimagesshowincreasedattenuationinthebasilarartery(arrows)as comparedtotheleftmiddlecerebralartery(shortarrow),indicatingbasilararterythrombosis,inthispatientwithacutedeteriorationof neurologicstatusandalertness.(C)AxialimagefromaCTAperformedshortlyaftershowslackofcontrastfillingofthebasilarartery(arrow) comparedtothecarotids. Figure1.2 AxialCTimagesshowincreased attenuationassociatedwiththeleftMCA anditsbranches(arrows)compatiblewith thrombosis.Decreasedgray/white differentiationintheleftinsularribbonand putamen(shortarrow)iscompatiblewith acuteinfarct. 2 Densebasilararterysign CASE1 Figure1.3 AxialCTshowsamarkedhyperattenuationinthe righttransversesinus,whichwasconfirmedtorepresentacute thrombosis. Figure1.4 AxialCTshowsthrombosisofthestraightsinus (arrow)andtheveinofGalen(shortarrow)withassociated hypoattenuationinthebilateralthalami. 3
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