Head and Neck: Skull Base Imaging

Head and Neck: Skull Base Imaging

Patricia A Hudgins, MD, Kristen L Baugnon, MD

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NEURORADIOLOGY REVIEW SERIES

Head and Neck: Skull Base Imaging

Patricia A. Hudgins, MD

Kristen L. Baugnon, MD

Department of Radiology and ImagingSciences, Emory University School ofMedicine, Atlanta, Georgia

Correspondence:Patricia A. Hudgins, MD,Professor of Radiology and ImagingSciences,Emory University School of Medicine,1364 Clifton Rd,Atlanta, GA 30322.E-mail: [email protected]

Received, November 20, 2016.Accepted, September 7, 2017.Published Online, October 10, 2017.

Copyright C© 2017 by theCongress of Neurological Surgeons

There are a myriad of head and neck pathologies that extend from the extracranial tothe intracranial compartment, traversing the skull base, and knowledge of the imagingappearance of this pathology is critical to practicing neurosurgeons. This article reviewssome of the important inflammatory or acquired head and neck pathology along the skullbase, neoplastic skull base lesions, and the intracranial extension of head and neck malig-nancy. Focus will be on the relevant anatomy, appropriate imaging protocols to evaluatethese processes, as well as the differentiating imaging findings on computed tomographyand magnetic resonance imaging.

KEY WORDS: Cerebrospinal fluid, Contrast-enhanced computed tomography, Gadolinium contrast, Idiopathicintracranial hypertension, Magnetic resonance imaging, Perineural tumor, Skull base

Neurosurgery 82:255–267, 2018 DOI:10.1093/neuros/nyx492 www.neurosurgery-online.com

T he close proximity of the extracranialhead and neck (HN) to the intracranialcompartment makes knowledge of HN

anatomy and disease processes critical for theneurosurgeon. In some locations, for example,the cribriform plate, only a millimeter of bone orless separates the nasal cavity from the extraduralspace. In this review, we present important HNlesions, essential anatomy, and stress imagingfindings that help differentiate benign frommalignant or aggressive disease processes.For virtually all complicated sinus or skull

base lesions, both computed tomography (CT)and magnetic resonance imaging (MRI) areindicated. A noncontrast sinus or skull base CT,which covers the mastoids, temporal bone, andentire skull base, is recommended, and intra-venous contrast is not usually necessary as theMRI will provide soft tissue detail. For lesionsthat are completely intraosseous, the mass mayonly be appreciated on MRI (Figure 1). CTis superior to MRI for subtle cortical bonechanges, but marrow processes are best charac-terized with non-Gadolinium (Gd) contrast-enhanced T1 MRI. If there is a contraindi-cation to MRI, the sinus/skull base CT should

ABBREVIATIONS: CECT, contrast-enhanced CT;CSF, cerebrospinal fluid;CT, computed tomography;FS, fat saturation; Gd, gadolinium; HN, head andneck; ICA, internal carotid artery; IIH, idiopathicintracranial hypertension;MRI,magnetic resonanceimaging; PNT, perineural tumor; SI, signal intensity

be done with iodinated contrast. In this era oflimiting ionizing radiation, there is no reason todo CT both without and with contrast, and thecontrast-enhanced CT (CECT) will be all that isnecessary.Adequate history prior to MRI is essential to

plan the correct study. In our practice, we haveover a dozen different MR protocols for HNlesions that may have an osseous or intracranialcomponent. For skull base lesions,MR techniqueshould always include T1-W images withoutcontrast or fat saturation (FS) in order toshow marrow replacement by edema or tumor.Referring physicians, including neurosurgeons,frequently emphasize perceived need for Gd onall brainMRI, but in fact Gdmay obscure lesionsif the correct technique is not done. Communi-cation between the neuroradiologist and neuro-surgeon has a positive impact on patient care.

SKULL BASE ANATOMY

Modern imaging has the unique advantage ofbeing able to demonstrate the complex skull baseanatomy in multiple planes. CT demonstratesthe bony anatomy best, while MRI has superiorsoft tissue resolution.The skull base is made of the paired frontal

and temporal bones, as well as the ethmoid andoccipital bones, and these bones form the floorsof the anterior, middle, and posterior cranialfossa. The thin and complex anterior cranialfossa separates the frontal and ethmoid sinusesand orbits from the inferior frontal lobes and

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HUDGINS AND BAUGNON

FIGURE 1. Seventy-year-old male with a history of osseous sarcoma and multiple bone metastases, now with new headache. A, Axial bone algorithm CT shows normalcentral skull base. Soft tissue in both sphenoid chambers appears benign with no bone erosion. B, Sagittal reformation from axial data set shows normal clivus. Floorof sella turcica appears intact. Sphenoid sinus soft tissue has no malignant characteristics. C, MRI was obtained same day as CT. On this T1-weighted sagittal image,there is complete replacement of the superior two-third of the clivus (arrow), erosion of the sella floor (arrowhead), and intracranial extradural extra-osseous tumor inthe retroclival location (short arrow). These findings were not seen on the bone window CT. D, Axial T1-weighted image shows normal SI in petrous bones (arrows)but replacement of marrow in clivus.

olfactory bulbs, and is formed by the frontal and ethmoid bones,with the anterior border being the posterior table of the frontalsinus, the lateral border the orbital roof (or orbital plate ofthe frontal bone), and the medial border formed by the thincribriform plates, lateral lamella, and ethmoid roof (or foveaethmoidalis). The lesser wing of the sphenoid bone, with theclinoid process, tuberculum sella, and planum sphenoidale, formthe posterior border, dividing the anterior and central skull base.The central skull base contains the sella turcica, skull base

foramina and cranial nerves II through VI, and the internalcarotid artery (ICA). The skull base divides the intracranial struc-tures from not only the sphenoid sinuses, but also the extracranialsoft tissues deep to the skull base inferiorly, including the masti-cator, parotid, parapharyngeal, and pharyngeal mucosal spaces.The basi sphenoid portion of the clivus, the dorsum sella, andthe superior petrous ridge of the temporal bone demarcate thejunction of the central and posterior skull base. The posteriorskull base is made up by the posterior temporal and occipitalbones, and contains the foramina for cranial nerves VII to XII,the jugular vein and ICA, and the largest foramen of the skullbase, the foramen magnum.

INFLAMMATORY/ACQUIRED SKULL BASEPATHOLOGY

MucocelesWhen a pneumatized air cell is obstructed, mucous accumu-

lates and the cell walls gradually become thinned, deossified,and ultimately resorbed. The overall volume of the cell, whetherit is the frontal, ethmoid, or sphenoid sinus, or at the petrousapex, increases and the sinus expands. An expanded, completelyopacified cell is a mucocele. The obstruction to the sinus ostiummay be benign, such as fibrous dysplasia, or malignant, as in a

sinonasal squamous cell carcinoma.1 Mucoceles, when infected,are termed pyoceles. The goals of CT or MRI in this settinginclude careful assessment of the sinus ostium to determine thecause of the obstruction, and assessment of the sinus or cell wallsto detect intraorbital or intracranial extension.CT may show marked bony thinning, and in fact the osseous

wall may appear dehiscent (Figure 2). The content of themucocele or the thinned wall usually has a smooth interface withthe dura or periorbital fat. This characteristic lack of a featheryinterface implies that the process may be intracranial or intraor-bital, but is extradural and extraconal, without dural or intraconalextension.Signal intensity (SI) within the mucocele on MRI is variable

depending on how long the sinus or cell has been obstructed,and the relative water vs protein concentration of the contents.2Mucoceles that are relatively new are isointense on all sequencesto cerebrospinal fluid (CSF). Mucoceles with decreasing waterconcentration vary from high signal on T1 and hyperintensesignal on T2 (Figure 3) to high signal on T1-weighted imagesand markedly decreased SI on T2 images. In fact, the intensityon T2 can be so low that the cell appears air filled and notopacified. There is usually thin smooth enhancement of themucoperiosteum lining the mucocele.

Intracranial Complications of Sinusitis, Mastoiditis, andFacial InfectionsLocal complications of bacterial sinusitis, mastoiditis, and

less commonly severe facial infections include osteomyelitis,epidural abscess, subdural empyema, meningitis, ventriculitis,and cerebritis. Ultimately, a discrete intra-axial brain abscesscan develop, which may be in close proximity to the infectedsinus or mastoid or even remote, as the infection can extendhematogenously. The initial imaging should be a skull base and

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CT ANDMRI OF THE SKULL BASE

FIGURE2. Adult male with chronic sinusitis and headaches. Right frontal sinus mucocele.A, Axial noncon-trast CT shows a well-circumscribed extra-axial right frontal mass that is homogeneously mucoid density.B, Bone algorithm axial image shows the walls of the mucocele (arrows) are thin, deossified, and probablycompletely dehiscent. Note opacified left frontal sinus, without expansion or dehiscence of the walls.

FIGURE 3. Fifty-year-old male with left proptosis and headache. Left frontoethmoid mucocele. A, Coronal bone algorithm CT shows complete destructionof the left ethmoid roof, and lamina papyrecea, by a soft tissue mass. On the right, note the normal cribriform plate (small arrow) and ethmoid roof (longerarrow). B, Coronal T1 MR image shows the mass is well circumscribed and homogeneously high SI. There is a smooth interface with the brain suggestingthe dura is intact. Note lateral displacement of the left medial rectus muscle (long arrow) and superior oblique muscle (arrowhead). The mucocele contentsare proteinaceous, and therefore high SI on T1 MR without contrast. C, Coronal T2 MR with FS shows intact dura laterally as line between mucocele andbrain (arrow) is present. More medially the dura is thinned and possibly dehiscent, as the black line is not preserved (small arrow). There is still a smoothinterface with the gyrus rectus, and no vasogenic frontal lobe edema.

sinus or temporal bone CT, and if an MR examination is antici-pated, a CECT is not necessary.Imaging findings are both extra and intra-axial, and include

meningeal enhancement, cortical edema from cerebritis, andbrain abscess (Figure 4). MRI with Gd shows thickened and

enhancing leptomeninges, and ependymal enhancement whenthere is ventriculitis. The classic appearance of a brain abscessis a ring-enhancing mass, with a rim of low SI on T2-weightedimages.3 Diffusion-weighted imaging is particularly helpful, asempyemas and pyogenic brain abscesses have restricted diffusion


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FIGURE 4. Adult patient with several weeks of sinusitis, now with severe headache, seizures, and altered mental status. Bacterial frontal sinusitis with intracranialabscess. A, Axial CECT shows a peripherally enhancing left frontal intra-axial mass (arrows) with surrounding vasogenic edema (short arrows). Note opacified frontalsinus.B, Bone algorithm CT confirms opacified frontal sinus, but the posterior wall is intact (arrows). The infection can extend from the sinus intracranially presumablythrough venous channels, without destroying the posterior wall. C, Axial T2-W FS image shows boggy edema in the left forehead and the completely opacified frontalsinus, filled with hyperintense debris and pus. The abscess has a low SI rim (arrows), a characteristic appearance for brain abscess on T2 images. D, Axial T1-WGd-enhanced image shows the peripheral enhancement of the abscess capsule, the central debris and pus, and surrounding vasogenic edema. There is diffuse thin non-nodular dural enhancement (arrows) of the entire left cerebral hemisphere, likely a combination of meningeal edema and possibly subdural pus. E, On this diffusionimage notice the markedly restricted diffusion in the abscess (arrows), a characteristic of brain abscess. There is artifact at the posterior frontal sinus wall and the frontallobe, a limitation of diffusion imaging at any bone–brain interface.

(Figure 4E). Advanced imaging techniques, such as perfusionimaging and diffusion tensor imaging,4 have been described butare usually not necessary as the clinical presentation is generallyunequivocal.Venous thrombosis, either cortical vein or major sinus, is a

potential serious complication of bacterial sinusitis or mastoiditis.Expansion of the venous sinus with loss of flow and a fillingdefect are common imaging findings on both CECT and MRI.5Cavernous sinus thrombosis is suspected when the lateral duralwall is displaced or convex laterally, the sinus contents are hetero-geneous from filling defects, and there is often narrowing orspasm of the ICA (Figure 5)6-8. Because sinus thrombosis isoften catastrophic, with cerebral edema, hemorrhage, and infarc-

tions as potential complications, early suspicion and imagingis stressed.9 Treatment, in addition to appropriate antibiotics,includes surgical drainage of the involved sinus or mastoidcomplex. Use of thrombolytics and even mechanical clot removalare controversial. Because venous thrombosis and especiallycavernous sinus thrombosis are rare, prospective comparisons oftreatment are not available.Skull base osteomyelitis is suspected in a diabetic patient with

headache and poorly controlled glucose. The process may beginin the external auditory canal, and is often a Pseudomonas species.A “routine” brain MRI may be normal early in the disease. TheMRI technique in this setting is critical, as noncontrast T1 imagesin all planes without FS are essential, and Gd images without


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FIGURE 5. Adult patient, immune deficient following treatment for leukemia, now has new neurological deficits with limited ocular motility on right.Right cavernous sinus septic thrombosis from invasive fungal sphenoid sinusitis. A, This T1-W axial image shows opacification of the posterior ethmoids andsphenoid chambers bilaterally. There is normal high SI marrow in the right petrous bone (white arrow), but loss of normal SI on the left (black arrow) fromosteomyelitis of the central skull base. B, T2-W axial image shows normal fluid in left Meckels cave (white arrow), and relatively concave lateral cavernoussinus dural wall (white arrowheads). On the right, there is debris and pus filling Meckel’s cave (black arrow) resulting in lack of normal CSF SI. The distancebetween the lateral wall of the right ICA (black line) is wider compared to the left, and the dural wall is displaced laterally (black arrowheads). Finally,notice the asymmetry between the cavernous ICA flow voids, an ominous sign of involvement of the right ICA by the angioinvasive fungus. C, This T1-WGd-enhanced axial image confirms the right cavernous sinus thrombosis with heterogeneous sinus enhancement due to thrombophlebitis (arrow), lateral duralwall displacement (arrowheads), and enhancement of the ICA walls (thin arrows).

FIGURE 6. Adult patient with poorly controlled diabetes, glucose at admission was over 400. Patient reports several weeks of unusual headaches, retro-orbital ache,new left-side hearing loss, and thick secretions from his left external auditory canal. A, Sagittal T1-W image is the initial sequence obtained in most brain MRI studies.This image, initially interpreted as normal, in fact shows edema in the occipital portion of the clivus (arrow) and thickening of the posterior nasopharyngeal wall(arrowheads). B, T1-W axial image is not always part of “routine” brain MRI, but in this patient skull base infection was suspected. The normal marrow SI in theoccipital bone is replaced with low SI edema and infection (white arrows). There is diffuse edema in the nasopharyngeal soft tissues, especially on the left (arrowheads).The edema involves the Eustacian tube, resulting in left mastoid opacification (black arrows). C, T1-W axial Gd-enhanced image without FS technique, same levelas B. There is diffuse skull base marrow enhancement, completely obscuring the osteomyelitis. Without the precontrast image, this could inadvertently be interpreted as“normal.” D, CT-guided biopsy for culture shows the transfacial needle in place for aspiration of the infected nasopharyngeal tissues. The needle was then advanced,with frequent CT imaging for correct trajectory, in order to biopsy the occipital bone.

adequate FS techniques even obscure the osteomyelitis (Figure 6).CT image-guided biopsy or aspiration, best before antibioticsare started, can access the infection through the face or condylarnotch of the mandible, confirming the infection, acquire samplefor culture, and exclude a skull base malignancy.

Osseous Defects and CSF LeaksAcquired skull base defects are more common than congenital

defects and cephaloceles, and the most common causes inthe adult are endoscopic surgical procedures, trauma, andthe increasing incidence of obesity and idiopathic intracranial


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FIGURE 7. Obese adult woman with symptoms of idiopathic intracranial hypertension, and B2-transferrin positive rhinorrhea. Patients with IIH often have diffuseinner table and sinus roof thinning and dehiscence, and therefore more than one potential site for leak. This is an indication for cisternography. A, Axial bone windowalgorithm CT shows an enlarged geniculate ganglion on right (arrow), typical for dilatation of the cranial nerve (CN) VII CSF space, a geniculate ganglion meningocele.These are common in IIH and usually asymptomatic with respect to the facial nerve. B, Axial bone window CT cisternogram. There is diffuse CSF opacification fromthe intrathecal iodinated contrast following the LP. The small right facial nerve meningocele fills with contrast (white arrow) but no fluid has pooled in the middleear or mastoids. Note the fluid level in the sphenoid sinus with high-density contrast in the dependent portion (black arrow). The bone windows should be carefullyscrutinized to discover the site of the leak. C, Coronal CT cisternogram, same patient, confirms the sphenoid sinus CSF leak: a bone defect at the right lateral sphenoidsinus roof, an opacified cell, and pooling of iodinated high-density contrast extending from the subarachnoid space into the sinus (arrow).D, On this CT cisternogram,3 of the classic findings of CSF leak are present: a bone defect on the posterior frontal sinus wall, an opacified cell, and a track of iodinated high-density contrastextending from the frontal subarachnoid space into the sinus (arrow).

hypertension (IIH). Depending on the risk factor or pre-existingcondition, the location of the leak varies.The first step in working up a patient with clear rhinorrhea or

otorrhea suspected to be CSF is B2 transferrin test of the fluid.A small vial or even a red top tube can be sent home with thepatient, if they are not leaking at the time of the outpatient visit,and the fluid can be collected at home and refrigerated until thepatient can transfer the fluid to a lab. If B2 transferrin is detectedin the rhinorrhea or otorrhea, there is a leak.High-resolution noncontrast sinus and skull base CT is the

initial recommended imaging examination for the patient withsuspected CSF leak. The thin axial images, usually 0.625 mm, arethen used to generate coronal and sagittal reformations. A bonedefect with an opacified cell and nasal cavity below the defectare findings that predict a leak (Figure 7). If the B2 transferrinis positive, and there is only 1 osseous defect, in our experiencea cisternogram is not necessary. If there is more than 1 osseousdefect, a CT cisternogram may be helpful to determine whichsite is leaking CSF. MRI is often recommended to determine thecontents of the soft tissue within the nasal cavity or sinus cell, todistinguish between a cephalocele and meningoencephalocele.The CT cisternogram is best performed when the patient

is actively leaking or can exacerbate the leak with provocativemaneuvers such as head hanging or Valsalva. A noncontrast skullbase/sinus CT in the supine position is performed prior to thecisternogram. With this, pre-existing sinus fluid levels can be

seen, and osteoneogenesis or sinus wall sclerosis, which mightsimulate high-density contrast in the sinus, can be established asa baseline. The patient is then taken to the fluoroscopy suite, andintrathecal contrast is placed, with confirmation of cranial flow ofcontrast. The patient returns to CT, where a prone coronal CT isobtained. The advantage of the prone CT is that increased intra-abdominal pressure may exacerbate the leak, and in the proneposition, contrast may be seen extending through the defect, withpooling in the sinus cavity. However, patient breathing artifactmakes multiplanar reformations from the prone data set subop-timal. Therefore, in our practice, we repeat the CT once more, inthe supine position, and high-resolution reformations, includingin any necessary oblique plane, are obtained by the radiologist forsurgical planning. The precontrast and postcontrast images canthen be compared side to side to best determine the site of theleak.A thorough CSF leak work-up, including cisternography,

includes 4 separate skull base CT scans. It is critical that the lowestdose CT techniques are used to minimize patient exposure. In ouropinion, the risk benefit of the radiation dose weighed against thecomplications of CSF leak should be considered before any CTcisternogram is requested and performed.MRI has several roles in skull base defects. Coronal and

sagittal images, perpendicular to the skull base, best show osseousanatomy. In the adult, high SI on T1 within the bones is normal.In young adults, SI may be intermediate, but with aging there is


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a gradual increase in SI on T1 images. Lower SI on T1 images ischaracteristic for metastases, direct invasion by HNmalignancies,or skull base osteomyelitis. T1 images and bone algorithm CTtogether best show skull base thinning or discrete defects, and canhelp plan surgical repair by determining the size of the defect,and whether there is a cephalomeningocele. Thin-section T2images, also perpendicular to the skull base, add specificity, as theydetermine the contents of a meningocele and whether dura, brainparenchyma, or vessels fill the cephalocele.10 T2-W images canalso demonstrate tethering and traction gliosis, when present, inthe adjacent brain parenchyma. Although gadolinium sequencesare usually requested by referring surgeons, they usually add littleto the work-up. Enhancement of the dura at the defect or even inthe cephalocele does not necessarily imply infection.MR cisternography with intrathecal Gd contrast is reserved for

cases with small osseous defects, more than 1 defect and potentialfor more than 1 leak site, or leaks that are difficult to confirm, andshould only be considered when conventional imaging techniquesfail to confirm or localize a leak. The use of intrathecal gadoliniumagents is off-label in the US, as it is neurotoxic in higher doses, butinternationally there is extensive experience with MR cisternog-raphy.11,12 Less than 1 mL of Gd-DTPA (Magnevist; Schering,Berlin, Germany) is diluted in 5 cc of patient’s CSF or sterilepreservative-free saline, and placed in the subarachnoid space viaa lumbar puncture. Multiplanar postcontrast FS T1 images areobtained within an hour (Figure 8). If initial images are negativefor a leak, MRI can be repeated up to 24 h later if a delayed leakis suspected (Figure 9).13In summary, in our experience, cisternography is rarely

necessary, as skull base and sinus CT are usually adequate to detecta defect in a patient with a positive B2-transferrin test, or a historyof meningitis. Cisternography is reserved for those instances whenthere is more than 1 potential site of leak, and is not recommendedif a leak is suspected in the absence of otorrhea or rhinorrhea, asthe examination will likely be negative.

IIH and Skull Base DefectsThe association between obesity, IIH, and skull base changes

has only recently been recognized. Generalized skull basethinning, deossification, and osseous dural defects, with orwithout meningoencephaloceles, are common in the femalepatient with elevated body mass index.14-17 When the defect isat the roof of an air space, the chronic increased intracranialpressure gradually leads to “sag” of the sinus or mastoid roof, anda frank defect with egress of CSF can result. In our experience,the incidence of meningitis, perhaps the most serious compli-cation of a skull base defect, is low, probably because the highpressure maintains CSF flow from intracranial to the sinus cell.In one series of patients with CSF leak and IIH, the overall risk ofmeningitis was 10%.18 Additionally, in our experience, once thepatient is leaking, their intracranial pressure typically normalizes,and they do not often have the more typical symptoms of highpressure headaches and papilledema, in spite of other imaging

FIGURE 8. MR cisternogram with intrathecal Magnevist Gd contrast.Normal study with no documented leak. This is a coronal relatively T1-WMRimage with FS in a patient with suspected CSF leak. CSF mixed with 0.5 mLof Magnevist was placed via a lumbar puncture into the subarachnoid space,the patient was tilted head down in both the prone and supine positions toallow cranial flow of the contrast. One hour after the LP, the MR was obtainedat 1 mm slice thickness. Note high SI in the suprasellar and Sylvian cisterns.There is more contrast within the left lateral ventricle (arrow), and asymmetricventricular filling is a normal finding. If there was a sphenoid sinus leak, thehigh SI contrast would accumulate within the sinus.

findings suspicious for chronically elevated intracranial pressure,such as a large empty sella, and multiple skull base defects andmeningoceles. Endonasal endoscopic repair of the anterior skullbase osseous defect is the preferred treatment for small lesions,but a holistic approach to the obese patient with weight loss,bariatric surgery, acetazolamide, and possibly CSF diversion willlikely result in fewer recurrences of the leak.19-21 After transsphe-noidal surgery, the obese patient has a greater risk for CSF leak.22

SKULL BASE NEOPLASMSBenign skull base neoplasms in the adult are usually invasive

pituitary macroadenoma, osseous meningioma, nerve sheathtumors, and paragangliomas.Malignancies of the skull base, both primary to the skull

base and osseous in origin, include chordoma, chondrosarcoma,multiple myeloma, metastases, and lymphoma. Chordoma andchondrosarcoma are often so characteristic in appearance onT2-weighted MRI that a specific diagnosis can be given.23The main role of imaging is to determine the extent of theneoplasm, whether there is intracranial disease, cranial nerveinvolvement, tumor around the vertebral or basilar artery, or


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FIGURE 9. Adult patient with prior history of endoscopic sinus surgery on left side only, now with rhinorrhea that was positive for B2-transferrin. A,CT coronal reformation from axial data set, bone algorithm, shows resection of left middle turbinate from prior endoscopic sinus surgery. The normal rightcribriform plate (arrow) is relatively low lying and possibly dehiscent. Soft tissue (arrowheads) in left superior nasal cavity obscures left cribriform plate.Cribriform plates, normally perforated to allow afferent olfactory fibers from middle turbinate to cross into olfactory groove, are common location for CSFfistula following sinus surgery. B, Coronal T2-weighted MR image shows high SI in a left ethmoid air cell (arrowhead), and at the base of the cribriformplates eccentric to the right (short black arrow). Note normal CSF in the left olfactory recess (long arrow), but complete absence of CSF on the right side(white arrow). It is impossible on the T2 image to differentiate benign fluid in the ethmoid sinus or nasal cavity roof from CSF. C, This is a coronal, FSimage, with dark CSF, relatively T1-weighted, obtained 60 min following intrathecal placement of 0.5 mL of Magnevist. Note the high signal collection inthe right superior nasal cavity (arrow). This is CSF that has collected in the right nasal cavity roof. This leak was proved endoscopically, and repaired via atransnasal approach.

circumferential tumor around the ICA.24 When an endonasalapproach is considered for biopsy or resection, a noncon-trast CT of the skull base including the nasal cavity, sinuses,and sphenoid sinus is acquired to plan the surgical approach.Advanced imaging techniques such asMR and CT perfusion havebeen promoted to predict response to radio/chemotherapy, butin the author’s experience are early in development and clinicalapplication.25Ecchordosis physaliphora is a small benign retroclival mass of

notochordal origin found in 2% of the population. The mass isusually asymptomatic and found incidentally on headCT or brainMRI. There is often a stalk between the clivus and the mass,it is hyperintense on T2, and does not enhance (Figure 10).26Chordoma is located centrally, involves the clivus and specificallythe spheno-occipital synchondrosis, and is markedly hyperintenseon T2-weighted images. This tumor is usually well circumscribedbut with lytic bone destruction. There is variable enhancementon both CECT and MRI with gadolinium contrast (Figure 11).Enhancement pattern and size are imaging characteristics usedto differentiate the incidental ecchordosis from clival chordoma.Encasement of the vertebral, basilar, or ICA can occur. There are2 histopathologic subtypes, but imaging cannot differentiate theclassic chordoma from the chondroid chordoma. The transnasalendoscopic approach is commonly used for resection, but mostresections are subtotal.27-29

If a patient with a suspected ecchordosis develops pain or newcranial nerve palsy, a chordoma is likely. Repeat MRI is recom-

mended to determine if the mass has increased in size. In ourexperience, this has occurred on 1 occasion, when a small lesionwas thought to be ecchordosis but the patient returned with severeheadache and new cranial nerve (CN) VI palsy. In retrospect, theecchordosis was a small chordoma.A T2 hyperintense mass within the skull base, off-midline, is

usually a chondrosarcoma. The petro-occipital fissure is the mostcommon site of origin. The chondrosarcoma usually enhancesto a variable degree. Imaging characteristics are similar to thechordoma, including lytic appearance with or without bonedestruction and demineralization, T2 hyperintensity, and variableenhancement, and differ only in lateral location of skull base.An invasive macroadenoma is probable when the pituitary

gland is replaced by tumor atMRI, and the sella floor is destroyed.Nerve sheath tumors such as neurofibroma or schwannoma areusually at a cranial nerve foramen or inseparable from a cranialnerve. Skull base meningiomas, on the other hand, almost alwayshave an intracranial extra-axial component even when the massis predominantly intraosseous, and is not isolated in locationto a skull base foramen (Figure 12). When they are locatedat a foramen, they can mimic a nerve sheath tumor; however,characteristic features ofmeningiomas include an enhancing duraltail, as well as calcification and hyperostosis in the adjacentbone. In our experience, there is often extracranial extensionof schwannoma, meningioma, and paraganglioma, and theextracranial portion is often overlooked by the interpreting radiol-ogist and neurosurgeon.


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FIGURE 10. Adult male underwent MRI for transient ischemic event, now asymptomatic. No history of malignancy. Benign and clinically incidentalecchordosis physaliphora. A, T1 sagittal image shows abnormal low SI osseous lesion (arrow) in the mid clivus. B, T2 axial image shows the intraosseouslesion is midline, with a speckled appearance (arrows). C, Axial bone window from a CT angiogram performed as part of a stroke work-up shows a smallspicule of bone (black arrow) extending from the lesion (white arrow) into the prepontine cistern in close proximity to the basilar artery (arrowhead). Withoutthe MRI, the CT would have been called normal.

FIGURE 11. Thirty-five-year-old woman with headaches and CN VI palsy on left. Central skull base chordoma. A, Axial bone CT shows complex destructive centralskull base mass composed of mixed soft tissue and bone fragments. B, T1 sagittal MR image shows a heterogeneous mass predominantly in sphenoidal portion of clivus.Note sella and pituitary gland are spared (arrowheads) making invasive macroadenoma unlikely. The intracranial extra-axial “thumbing” of the pons (arrows) ischaracteristic of chordoma. C, T2 hyperintense central skull base destructive mass is typical for chordoma. There is a smooth interface where the tumor distorts thepons (arrows), suggesting that the mass is still extra-axial. D, There is only minimal enhancement within the tumor. Note the mass is in the skull base with extensionanterior into retropharyngeal space (arrows) and posterior into posterior fossa (black arrowheads), a pattern that usually implies the tumor started in the bony skull.The nasopharyngeal mucosa over the mass is intact (white arrowheads). Basilar artery (white arrow) is patent but dorsally displaced.

Paragangliomas or glomus tumors within or near the skull basehave characteristic imaging appearances. The mass can occur inthe jugular foramen (glomus jugulare paraganglioma), the middleear cavity, (glomus tympanicum paraganglioma), along the facialnerve (glomus faciale), or on the extracranial surface of the skullbase, in the carotid sheath (a glomus vagale paraganglioma). Thesetumors are variable in size, have irregular skull base erosion, anda characteristic T2 SI and heterogeneous enhancement patterncalled “salt and pepper” (Figure 13).

INTRACRANIAL EXTENSION OF HNMALIGNANCY

In the American Joint Commission on Cancer Seventhedition,30 the term “nonsurgical” does not appear, but insteadtumors may be staged as T4a or b if there is intracranialextension. Intracranial extension of HN tumors, especiallyintradural invasion, carries a poor prognosis.31 The developmentof new surgical techniques, especially endoscopic resection via the


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FIGURE 12. Adult male with tinnitus on right. Skull base meningioma. A, Axial T1 MR image shows abnormal low SI in right clivus (white arrows),similar soft tissue around the ICA (white arrowheads), and 2 low SI lesions at the expected location of the right distal sigmoid sinus (short black line) andjugular foramen (long black line). B, Gd-enhanced axial T1 MR image with FS, at same level as A, shows enhancement in the intraosseous meningioma,making it less conspicuous than on non-Gd enhanced image. Soft tissue around right ICA is meningioma in carotid sheath, causing narrowing and distortionof the ICA. Note heterogeneous enhancement in distal sigmoid venous sinus (short arrow) from slow flow and thrombosis as a result of the meningioma (longarrow) in the jugular foramen. C, Gd-enhanced coronal T1 MR with FS shows heterogeneous enhancement in distal right sigmoid venous sinus (short blackarrows) from slow flow and thrombosis as a result of the meningioma (long black arrows) in the jugular foramen. Note intracranial extra-axial meningioma(white arrows).

FIGURE 13. Adult woman with skull base headache, right vocal cord paralysis, and tinnitus. Glomus jugulare paraganglioma on right. A, Axial bonewindow CT shows classic irregular osseous erosion from right glomus jugulare paraganglioma (arrows). Note normal left jugular foramen (arrowheads). B,Axial T2 MR image with FS shows classic heterogeneous SI in right jugular foramen paraganglioma (arrows), described as “salt and pepper.” The low SIfoci likely represent flow voids from intratumoral vessels or fibrosis. C, Axial Gd-enhanced T1 image with FS shows characteristic robust enhancement in theglomus jugulare. Tumor surrounds the right ICA (arrowheads).

transsphenoidal or even transorbital approach, has been appliedto virtually all HN tumors with intracranial extension.32-34 BothCT and MRI are generally needed to stage and plan surgicalor radiation therapy for advanced HN tumors with skull baseand intracranial extension.35 When MRI is to be obtained, the

CT can be performed without contrast, at submillimeter sliceincrements through the skull base and sinuses to allow recon-structions in axial, sagittal, and coronal planes. MRI shouldbe carefully performed, and it is critical that a “routine” brainMRI not be ordered. A dedicated skull base MRI begins with


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FIGURE14. Adult male with nasal obstruction, chronic “sinusitis,” left proptosis and fixed globe.Malignantsinonasal squamous cell carcinoma with orbital and intracranial extension. A, Coronal FS T2 image showsrelatively low SI left maxillary sinus and nasal cavity mass. Malignant characteristics include destructionof left lamina papyrecea and nodular intraorbital extension (white arrows). There is cribriform plate andethmoid roof destruction (black short arrows), with tumor above the anterior skull base. B, Coronal FSGd-enhanced T1 coronal image shows normal thin line between tumor and brain (arrowheads), and loss ofthin black line between mass and skull base (arrows). This is a finding very suggestive of intradural extensionof the tumor.

thin-section precontrast T1 images in the 3 standard planes, asthey are most sensitive for bone invasion,36 and also includes FST2 and postcontrast imaging.Dural invasion by HN tumors determines both treatment and

prognosis. Thin linear continuous dural enhancement is likelydue to reactive changes in the dura and should not be usedto predict dural invasion.37 Imaging findings that best correlatewith dural invasion by the tumor are both dural enhancementand focal nodularity of the enhancing intracranial tumor, withsensitivity of 88%, specificity of 100%, and accuracy of 95%.37Dural enhancement of greater than 5 mm was 91% sensitive inpredicting invasion. Pial enhancement alone is less sensitive forpredicting dural invasion. A more recent study assessing duralinvasion suggested that when the MRI reported dural invasionthere was a 16% chance that it could still be normal.38 This studywas limited in that the reports from the MRI studies were used,and the images were not re-reviewed, a common error found inclinical journals that attempt to evaluate imaging sensitivity andspecificity. With such an approach, both the interpreting radiol-ogist and the modality are being assessed, not just the modality.A thin band of low SI between the intracranial tumor and theenhancing dura, on T1-enhanced images, has been reported toimply no dural invasion (Figure 14).39 To our knowledge, aprospective study of accuracy of high-resolution FS gadolinium-enhanced MRI has not been performed. Since even MRI cannot

with 100% accuracy predict dural invasion, we suggest that inequivocal cases, with only 5 mm of dural enhancement and nonodularity of the mass, surgery not be withheld based on MRfindings alone.Sinonasal tumors can gain intracranial access via direct invasion

through the nasal cavity, sinuses, or orbit.40 Another commonpattern for HN tumors to access the intracranial compartment isvia the cranial nerves. Nasopharyngeal carcinomamay also extendthrough the normal defect in the pharyngobasilar fascia where theICA gains intracranial access.41Perineural tumor (PNT) extension from a HN malignancy

should be suspected when there is a new cranial nerve palsy ina patient with a malignant skin, sinus, parotid gland, or skull basemass. Many times, patients with perineural spread of tumor canbe misdiagnosed with more benign conditions such as Bell’s palsyor trigeminal neuralgia.42 However, it is also important to notethat up to 30% to 45% of patients with significant perineuralspread can remain asymptomatic, with normal nerve functionon examination.43 Thus, it is important for the radiologist toscrutinize the entire course of the cranial nerves on the imagingwork-up and surveillance of these patients, and to be familiarwith the perineural pathways and imaging findings of PNTspread. However, in our experience, the imaging may be so subtlethat the findings are missed even by an experienced interpretingradiologist.


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FIGURE 15. Adult male with “Bell’s palsy” on left. Perineural spread of tumor from adenoid cystic carcinoma of the parotid gland. A, Axial T1 image shows value ofnoncontrast imaging. The poorly defined aggressive parotid mass (arrows) extends to the skull base, displacing the ICAmedially (arrowhead), and filling the stylomastoidforamen (white arrows) where CN VII exits the cranial vault. B, On this T1 image, slightly higher than A, there is tumor eroding and widening the stylomastoidforamen (arrows). C, T1 coronal image shows perineural adenoid cystic carcinoma extending through the left foramen ovale (white arrow) and into the cavernoussinus (arrowheads). On the right side, the normal CN V3 (black arrow) can be seen in the foramen ovale.D, Axial T1 FS image with Gd enhancement shows the leftcavernous sinus mass (small arrows), and tumor involving the cisternal CNV (long arrow). Gd-enhanced images are usually recommended when perineural tumor issuspected, but precontrast T1 images are also critical to show the widened foramen and enlarged nerve.

The most common cranial nerves involved with PNT spreadare branches of the trigeminal and facial nerves. Tumors ofthe face, sinuses, or skull base most often involve branches ofthe maxillary division of the trigeminal nerve (V2), extendingintracranially through foramen rotundum, whereas nasopha-ryngeal tumors, masticator space, or oral cavity tumors caninvolve the mandibular nerve (V3) and extend cranially throughforamen ovale. Parotid gland tumors often involve the facialnerve. However, there are also communications between the facialnerve and the trigeminal nerve, in which tumor can track fromone nerve to another, most commonly parotid tumors trackingalong the facial nerve, then involving the auriculotemporal nerve,a branch of V3.44 Tumors can also spread from the vidian canal(extending from V2 in the pterygopalatine fossa) to the greatersuperficial petrosal nerve to reach the geniculate ganglion of thefacial nerve. Most often, tumor extends in a retrograde fashiontoward the brain; however, anterograde extension along CNbranches also occurs.45

Contrast-enhanced MRI with FS is the most sensitive imagingmodality for detecting PNT spread. Dedicated skull base imagingprotocols are imperative, as these abnormalities will not be pickedup on a routine MRI of the brain, and multiplanar imaging,particularly in the coronal plane, is essential to fully evaluatethe skull base (Figure 15). Thin-section T1 precontrast imagesare important to detect enlargement and soft tissue along thecourse of the nerve, and within the foramina. However, the mostsensitive sequences are thin-section T1 fat-suppressed postcon-trast images, as fat-suppressed postcontrast images will increasethe conspicuity of both enlargement and abnormal enhancementwithin and along the nerves, suppressing the normal fat withinthe foramina and surrounding bone marrow. Thin-section imagesare necessary to distinguish between normal perineural vascularplexus enhancement and abnormal enhancement within the nerve

itself. CT findings of PNT spread include loss of the normal fatwithin the foramina and enlargement or widening of the foramen;however, these are often relatively late findings. Cranial extensionof PNT can lead to involvement of the cavernous sinus andGausserian ganglion in Meckels cave (in the setting of trigeminaldisease), and even extension to the cisternal segments of thenerves and brainstem. Secondary imaging features of PNT spreadinclude loss of end organ function, with denervation changes inthe muscles of mastication (in the setting of V3 motor divisiondisease), and facial muscles (in the setting of CN VII disease).Acute denervation changes in muscles can be confusing and showedema (increased signal on T2 images) and enhancement, andchronic changes include muscular fatty atrophy, with decreasedvolume and increased signal on T1 images.46

CONCLUSION

Osseous involvement and intracranial extension of HNpathology along the skull base is common, and knowledge of itsappearance on imaging is paramount for the practicing neuro-surgeon. For nearly every skull base pathology, skull base protocolMRI and thin-section CT are complementary in the evalu-ation. This review emphasizes the more common lesions, criticalanatomy, and an approach that describes skull base pathologyas primarily intraosseous and originating in bony skull base,extracranial, or HN in origin with secondary skull base invasion,or intracranial in origin with secondary skull base invasion.

DisclosureThe authors have no personal, financial, or institutional interest in any of the

drugs, materials, or devices described in this article.


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Head and Neck: Skull Base Imaging

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