NEURORADIOLOGY REVIEW SERIES

Head and Neck: Skull Base Imaging

Patricia A. Hudgins, MD There are a myriad of head and neck pathologies that extend from the extracranial to
Kristen L. Baugnon, MD the intracranial compartment, traversing the skull base, and knowledge of the imaging
appearance of this pathology is critical to practicing neurosurgeons. This article reviews
Department of Radiology and Imaging some of the important inflammatory or acquired head and neck pathology along the skull

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Sciences, Emory University School of
Medicine, Atlanta, Georgia
base, 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 evaluate
Correspondence: these processes, as well as the differentiating imaging findings on computed tomography
Patricia A. Hudgins, MD, and magnetic resonance imaging.
Professor of Radiology and Imaging
Sciences, KEY WORDS: Cerebrospinal fluid, Contrast-enhanced computed tomography, Gadolinium contrast, Idiopathic
Emory University School of Medicine, intracranial hypertension, Magnetic resonance imaging, Perineural tumor, Skull base
1364 Clifton Rd,
Atlanta, GA 30322. Neurosurgery 82:255–267, 2018 DOI:10.1093/neuros/nyx492 www.neurosurgery-online.com
E-mail: phudgin@emory.edu

Received, November 20, 2016.

T
Accepted, September 7, 2017. he close proximity of the extracranial
Published Online, October 10, 2017. head and neck (HN) to the intracranial
compartment makes knowledge of HN
Copyright 
C 2017 by the
anatomy and disease processes critical for the
Congress of Neurological Surgeons
neurosurgeon. In some locations, for example,
the cribriform plate, only a millimeter of bone or
less separates the nasal cavity from the extradural
space. In this review, we present important HN
lesions, essential anatomy, and stress imaging
findings that help differentiate benign from
malignant or aggressive disease processes.
For virtually all complicated sinus or skull
base lesions, both computed tomography (CT)
and magnetic resonance imaging (MRI) are
indicated. A noncontrast sinus or skull base CT,
which covers the mastoids, temporal bone, and
entire skull base, is recommended, and intra-
venous contrast is not usually necessary as the
MRI will provide soft tissue detail. For lesions
that are completely intraosseous, the mass may
only be appreciated on MRI (Figure 1). CT
is superior to MRI for subtle cortical bone
changes, 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 and
neck; ICA, internal carotid artery; IIH, idiopathic
intracranial hypertension; MRI, magnetic resonance
imaging; PNT, perineural tumor; SI, signal intensity
be done with iodinated contrast. In this era of
limiting ionizing radiation, there is no reason to
do CT both without and with contrast, and the
contrast-enhanced CT (CECT) will be all that is
necessary.
Adequate history prior to MRI is essential to
plan the correct study. In our practice, we have
over a dozen different MR protocols for HN
lesions that may have an osseous or intracranial
component. For skull base lesions, MR technique
should always include T1-W images without
contrast or fat saturation (FS) in order to
show marrow replacement by edema or tumor.
Referring physicians, including neurosurgeons,
frequently emphasize perceived need for Gd on
all brain MRI, but in fact Gd may obscure lesions
if 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 of
being able to demonstrate the complex skull base
anatomy in multiple planes. CT demonstrates
the bony anatomy best, while MRI has superior
soft tissue resolution.
The skull base is made of the paired frontal
and temporal bones, as well as the ethmoid and
occipital bones, and these bones form the floors
of the anterior, middle, and posterior cranial
fossa. The thin and complex anterior cranial
fossa separates the frontal and ethmoid sinuses
and orbits from the inferior frontal lobes and

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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 normal
central skull base. Soft tissue in both sphenoid chambers appears benign with no bone erosion. B, Sagittal reformation from axial data set shows normal clivus. Floor
of 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 in
the 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 frontal
sinus, the lateral border the orbital roof (or orbital plate of
the frontal bone), and the medial border formed by the thin
cribriform plates, lateral lamella, and ethmoid roof (or fovea
ethmoidalis). The lesser wing of the sphenoid bone, with the
clinoid process, tuberculum sella, and planum sphenoidale, form
the 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 internal
carotid artery (ICA). The skull base divides the intracranial struc-
tures from not only the sphenoid sinuses, but also the extracranial
soft 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, and
the superior petrous ridge of the temporal bone demarcate the
junction of the central and posterior skull base. The posterior
skull base is made up by the posterior temporal and occipital
bones, and contains the foramina for cranial nerves VII to XII,
the jugular vein and ICA, and the largest foramen of the skull
base, the foramen magnum.
INFLAMMATORY/ACQUIRED SKULL BASE
PATHOLOGY
Mucoceles
When 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, whether
it is the frontal, ethmoid, or sphenoid sinus, or at the petrous
apex, increases and the sinus expands. An expanded, completely
opacified cell is a mucocele. The obstruction to the sinus ostium
may 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 setting
include careful assessment of the sinus ostium to determine the
cause of the obstruction, and assessment of the sinus or cell walls
to 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 the
mucocele or the thinned wall usually has a smooth interface with
the dura or periorbital fat. This characteristic lack of a feathery
interface implies that the process may be intracranial or intraor-
bital, but is extradural and extraconal, without dural or intraconal
extension.
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.2
Mucoceles that are relatively new are isointense on all sequences
to cerebrospinal fluid (CSF). Mucoceles with decreasing water
concentration vary from high signal on T1 and hyperintense
signal on T2 (Figure 3) to high signal on T1-weighted images
and markedly decreased SI on T2 images. In fact, the intensity
on T2 can be so low that the cell appears air filled and not
opacified. There is usually thin smooth enhancement of the
mucoperiosteum lining the mucocele.
Intracranial Complications of Sinusitis, Mastoiditis, and
Facial Infections
Local 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 abscess
can develop, which may be in close proximity to the infected
sinus or mastoid or even remote, as the infection can extend
hematogenously. The initial imaging should be a skull base and

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FIGURE 2. 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 probably
completely 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 destruction
of 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 (longer
arrow). B, Coronal T1 MR image shows the mass is well circumscribed and homogeneously high SI. There is a smooth interface with the brain suggesting
the dura is intact. Note lateral displacement of the left medial rectus muscle (long arrow) and superior oblique muscle (arrowhead). The mucocele contents
are proteinaceous, and therefore high SI on T1 MR without contrast. C, Coronal T2 MR with FS shows intact dura laterally as line between mucocele and
brain (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 smooth
interface 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, and
brain abscess (Figure 4). MRI with Gd shows thickened and
enhancing leptomeninges, and ependymal enhancement when
there is ventriculitis. The classic appearance of a brain abscess
is a ring-enhancing mass, with a rim of low SI on T2-weighted
images.3 Diffusion-weighted imaging is particularly helpful, as
empyemas 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 intracranial
abscess. A, Axial CECT shows a peripherally enhancing left frontal intra-axial mass (arrows) with surrounding vasogenic edema (short arrows). Note opacified frontal
sinus. B, Bone algorithm CT confirms opacified frontal sinus, but the posterior wall is intact (arrows). The infection can extend from the sinus intracranially presumably
through venous channels, without destroying the posterior wall. C, Axial T2-W FS image shows boggy edema in the left forehead and the completely opacified frontal
sinus, 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-W
Gd-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 diffusion
image 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 frontal
lobe, a limitation of diffusion imaging at any bone–brain interface.

(Figure 4E). Advanced imaging techniques, such as perfusion
imaging and diffusion tensor imaging,4 have been described but
are usually not necessary as the clinical presentation is generally
unequivocal.
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 filling
defect are common imaging findings on both CECT and MRI.5
Cavernous sinus thrombosis is suspected when the lateral dural
wall is displaced or convex laterally, the sinus contents are hetero-
geneous from filling defects, and there is often narrowing or
spasm of the ICA (Figure 5)6-8 . Because sinus thrombosis is
often catastrophic, with cerebral edema, hemorrhage, and infarc-
tions as potential complications, early suspicion and imaging
is stressed.9 Treatment, in addition to appropriate antibiotics,
includes surgical drainage of the involved sinus or mastoid
complex. Use of thrombolytics and even mechanical clot removal
are controversial. Because venous thrombosis and especially
cavernous sinus thrombosis are rare, prospective comparisons of
treatment are not available.
Skull base osteomyelitis is suspected in a diabetic patient with
headache and poorly controlled glucose. The process may begin
in the external auditory canal, and is often a Pseudomonas species.
A “routine” brain MRI may be normal early in the disease. The
MRI technique in this setting is critical, as noncontrast T1 images
in 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 and
sphenoid 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) from
osteomyelitis of the central skull base. B, T2-W axial image shows normal fluid in left Meckels cave (white arrow), and relatively concave lateral cavernous
sinus 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 distance
between 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-W
Gd-enhanced axial image confirms the right cavernous sinus thrombosis with heterogeneous sinus enhancement due to thrombophlebitis (arrow), lateral dural
wall 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 the
occipital 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 level
as 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 antibiotics
are started, can access the infection through the face or condylar
notch of the mandible, confirming the infection, acquire sample
for culture, and exclude a skull base malignancy.
Osseous Defects and CSF Leaks
Acquired skull base defects are more common than congenital
defects and cephaloceles, and the most common causes in
the adult are endoscopic surgical procedures, trauma, and
the 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 diffuse
inner 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 window
algorithm 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 from
the intrathecal iodinated contrast following the LP. The small right facial nerve meningocele fills with contrast (white arrow) but no fluid has pooled in the middle
ear 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 carefully
scrutinized 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 sphenoid
sinus 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 contrast
extending from the frontal subarachnoid space into the sinus (arrow).

hypertension (IIH). Depending on the risk factor or pre-existing
condition, 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 the
patient, if they are not leaking at the time of the outpatient visit,
and the fluid can be collected at home and refrigerated until the
patient can transfer the fluid to a lab. If B2 transferrin is detected
in 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 with
suspected CSF leak. The thin axial images, usually 0.625 mm, are
then used to generate coronal and sagittal reformations. A bone
defect with an opacified cell and nasal cavity below the defect
are findings that predict a leak (Figure 7). If the B2 transferrin
is positive, and there is only 1 osseous defect, in our experience
a cisternogram is not necessary. If there is more than 1 osseous
defect, a CT cisternogram may be helpful to determine which
site is leaking CSF. MRI is often recommended to determine the
contents of the soft tissue within the nasal cavity or sinus cell, to
distinguish between a cephalocele and meningoencephalocele.
The CT cisternogram is best performed when the patient
is actively leaking or can exacerbate the leak with provocative
maneuvers such as head hanging or Valsalva. A noncontrast skull
base/sinus CT in the supine position is performed prior to the
cisternogram. With this, pre-existing sinus fluid levels can be
seen, and osteoneogenesis or sinus wall sclerosis, which might
simulate high-density contrast in the sinus, can be established as
a baseline. The patient is then taken to the fluoroscopy suite, and
intrathecal contrast is placed, with confirmation of cranial flow of
contrast. The patient returns to CT, where a prone coronal CT is
obtained. The advantage of the prone CT is that increased intra-
abdominal pressure may exacerbate the leak, and in the prone
position, contrast may be seen extending through the defect, with
pooling in the sinus cavity. However, patient breathing artifact
makes multiplanar reformations from the prone data set subop-
timal. Therefore, in our practice, we repeat the CT once more, in
the supine position, and high-resolution reformations, including
in any necessary oblique plane, are obtained by the radiologist for
surgical planning. The precontrast and postcontrast images can
then be compared side to side to best determine the site of the
leak.
A thorough CSF leak work-up, including cisternography,
includes 4 separate skull base CT scans. It is critical that the lowest
dose CT techniques are used to minimize patient exposure. In our
opinion, the risk benefit of the radiation dose weighed against the
complications of CSF leak should be considered before any CT
cisternogram is requested and performed.
MRI has several roles in skull base defects. Coronal and
sagittal images, perpendicular to the skull base, best show osseous
anatomy. 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 is

characteristic for metastases, direct invasion by HN malignancies,
or skull base osteomyelitis. T1 images and bone algorithm CT
together best show skull base thinning or discrete defects, and can
help plan surgical repair by determining the size of the defect,
and whether there is a cephalomeningocele. Thin-section T2
images, also perpendicular to the skull base, add specificity, as they
determine the contents of a meningocele and whether dura, brain
parenchyma, or vessels fill the cephalocele.10 T2-W images can
also demonstrate tethering and traction gliosis, when present, in

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the adjacent brain parenchyma. Although gadolinium sequences
are usually requested by referring surgeons, they usually add little
to the work-up. Enhancement of the dura at the defect or even in
the 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 potential
for more than 1 leak site, or leaks that are difficult to confirm, and
should only be considered when conventional imaging techniques
fail to confirm or localize a leak. The use of intrathecal gadolinium
agents is off-label in the US, as it is neurotoxic in higher doses, but
internationally 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 sterile
preservative-free saline, and placed in the subarachnoid space via
a lumbar puncture. Multiplanar postcontrast FS T1 images are
obtained within an hour (Figure 8). If initial images are negative
for a leak, MRI can be repeated up to 24 h later if a delayed leak
is suspected (Figure 9).13
In summary, in our experience, cisternography is rarely
necessary, as skull base and sinus CT are usually adequate to detect
a defect in a patient with a positive B2-transferrin test, or a history
of meningitis. Cisternography is reserved for those instances when
there is more than 1 potential site of leak, and is not recommended
if a leak is suspected in the absence of otorrhea or rhinorrhea, as
the examination will likely be negative.
IIH and Skull Base Defects
The association between obesity, IIH, and skull base changes
has only recently been recognized. Generalized skull base
thinning, deossification, and osseous dural defects, with or
without meningoencephaloceles, are common in the female
patient with elevated body mass index.14-17 When the defect is
at the roof of an air space, the chronic increased intracranial
pressure gradually leads to “sag” of the sinus or mastoid roof, and
a 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 high
pressure maintains CSF flow from intracranial to the sinus cell.
In one series of patients with CSF leak and IIH, the overall risk of
meningitis was 10%.18 Additionally, in our experience, once the
patient is leaking, their intracranial pressure typically normalizes,
and they do not often have the more typical symptoms of high
pressure 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-W MR
image with FS in a patient with suspected CSF leak. CSF mixed with 0.5 mL
of Magnevist was placed via a lumbar puncture into the subarachnoid space,
the patient was tilted head down in both the prone and supine positions to
allow cranial flow of the contrast. One hour after the LP, the MR was obtained
at 1 mm slice thickness. Note high SI in the suprasellar and Sylvian cisterns.
There is more contrast within the left lateral ventricle (arrow), and asymmetric
ventricular filling is a normal finding. If there was a sphenoid sinus leak, the
high 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 and
meningoceles. Endonasal endoscopic repair of the anterior skull
base 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 will
likely 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 NEOPLASMS
Benign skull base neoplasms in the adult are usually invasive
pituitary macroadenoma, osseous meningioma, nerve sheath
tumors, 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 and
chondrosarcoma are often so characteristic in appearance on
T2-weighted MRI that a specific diagnosis can be given.23
The main role of imaging is to determine the extent of the
neoplasm, whether there is intracranial disease, cranial nerve
involvement, 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 right
cribriform 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 CSF
fistula 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 cribriform
plates 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, FS
image, with dark CSF, relatively T1-weighted, obtained 60 min following intrathecal placement of 0.5 mL of Magnevist. Note the high signal collection in
the 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 a
transnasal approach.

circumferential tumor around the ICA.24 When an endonasal
approach 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 as MR and CT perfusion have
been promoted to predict response to radio/chemotherapy, but
in the author’s experience are early in development and clinical
application.25
Ecchordosis physaliphora is a small benign retroclival mass of
notochordal origin found in 2% of the population. The mass is
usually asymptomatic and found incidentally on head CT or brain
MRI. There is often a stalk between the clivus and the mass,
it is hyperintense on T2, and does not enhance (Figure 10).26
Chordoma is located centrally, involves the clivus and specifically
the spheno-occipital synchondrosis, and is markedly hyperintense
on T2-weighted images. This tumor is usually well circumscribed
but with lytic bone destruction. There is variable enhancement
on both CECT and MRI with gadolinium contrast (Figure 11).
Enhancement pattern and size are imaging characteristics used
to differentiate the incidental ecchordosis from clival chordoma.
Encasement of the vertebral, basilar, or ICA can occur. There are
2 histopathologic subtypes, but imaging cannot differentiate the
classic chordoma from the chondroid chordoma. The transnasal
endoscopic approach is commonly used for resection, but most
resections are subtotal.27-29
If a patient with a suspected ecchordosis develops pain or new
cranial nerve palsy, a chordoma is likely. Repeat MRI is recom-
mended to determine if the mass has increased in size. In our
experience, this has occurred on 1 occasion, when a small lesion
was thought to be ecchordosis but the patient returned with severe
headache and new cranial nerve (CN) VI palsy. In retrospect, the
ecchordosis was a small chordoma.
A T2 hyperintense mass within the skull base, off-midline, is
usually a chondrosarcoma. The petro-occipital fissure is the most
common site of origin. The chondrosarcoma usually enhances
to a variable degree. Imaging characteristics are similar to the
chordoma, including lytic appearance with or without bone
destruction and demineralization, T2 hyperintensity, and variable
enhancement, and differ only in lateral location of skull base.
An invasive macroadenoma is probable when the pituitary
gland is replaced by tumor at MRI, and the sella floor is destroyed.
Nerve sheath tumors such as neurofibroma or schwannoma are
usually at a cranial nerve foramen or inseparable from a cranial
nerve. Skull base meningiomas, on the other hand, almost always
have an intracranial extra-axial component even when the mass
is predominantly intraosseous, and is not isolated in location
to a skull base foramen (Figure 12). When they are located
at a foramen, they can mimic a nerve sheath tumor; however,
characteristic features of meningiomas include an enhancing dural
tail, as well as calcification and hyperostosis in the adjacent
bone. In our experience, there is often extracranial extension
of schwannoma, meningioma, and paraganglioma, and the
extracranial 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 incidental
ecchordosis physaliphora. A, T1 sagittal image shows abnormal low SI osseous lesion (arrow) in the mid clivus. B, T2 axial image shows the intraosseous
lesion 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 small
spicule of bone (black arrow) extending from the lesion (white arrow) into the prepontine cistern in close proximity to the basilar artery (arrowhead). Without
the 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 central
skull 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) is
characteristic of chordoma. C, T2 hyperintense central skull base destructive mass is typical for chordoma. There is a smooth interface where the tumor distorts the
pons (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 extension
anterior 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 base
have characteristic imaging appearances. The mass can occur in
the jugular foramen (glomus jugulare paraganglioma), the middle
ear cavity, (glomus tympanicum paraganglioma), along the facial
nerve (glomus faciale), or on the extracranial surface of the skull
base, in the carotid sheath (a glomus vagale paraganglioma). These
tumors are variable in size, have irregular skull base erosion, and
a characteristic T2 SI and heterogeneous enhancement pattern
called “salt and pepper” (Figure 13).
INTRACRANIAL EXTENSION OF HN
MALIGNANCY
In the American Joint Commission on Cancer Seventh
edition,30 the term “nonsurgical” does not appear, but instead
tumors may be staged as T4a or b if there is intracranial
extension. Intracranial extension of HN tumors, especially
intradural invasion, carries a poor prognosis.31 The development
of 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) and
jugular 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 distortion
of the ICA. Note heterogeneous enhancement in distal sigmoid venous sinus (short arrow) from slow flow and thrombosis as a result of the meningioma (long
arrow) in the jugular foramen. C, Gd-enhanced coronal T1 MR with FS shows heterogeneous enhancement in distal right sigmoid venous sinus (short black
arrows) 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 bone
window 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 SI
foci likely represent flow voids from intratumoral vessels or fibrosis. C, Axial Gd-enhanced T1 image with FS shows characteristic robust enhancement in the
glomus jugulare. Tumor surrounds the right ICA (arrowheads).

transsphenoidal or even transorbital approach, has been applied
to virtually all HN tumors with intracranial extension.32-34 Both
CT and MRI are generally needed to stage and plan surgical
or radiation therapy for advanced HN tumors with skull base
and intracranial extension.35 When MRI is to be obtained, the
CT can be performed without contrast, at submillimeter slice
increments through the skull base and sinuses to allow recon-
structions in axial, sagittal, and coronal planes. MRI should
be carefully performed, and it is critical that a “routine” brain
MRI not be ordered. A dedicated skull base MRI begins with

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FIGURE 14. Adult male with nasal obstruction, chronic “sinusitis,” left proptosis and fixed globe. Malignant
sinonasal squamous cell carcinoma with orbital and intracranial extension. A, Coronal FS T2 image shows
relatively low SI left maxillary sinus and nasal cavity mass. Malignant characteristics include destruction
of left lamina papyrecea and nodular intraorbital extension (white arrows). There is cribriform plate and
ethmoid roof destruction (black short arrows), with tumor above the anterior skull base. B, Coronal FS
Gd-enhanced T1 coronal image shows normal thin line between tumor and brain (arrowheads), and loss of
thin black line between mass and skull base (arrows). This is a finding very suggestive of intradural extension
of the tumor.

thin-section precontrast T1 images in the 3 standard planes, as
they are most sensitive for bone invasion,36 and also includes FS
T2 and postcontrast imaging.
Dural invasion by HN tumors determines both treatment and
prognosis. Thin linear continuous dural enhancement is likely
due to reactive changes in the dura and should not be used
to predict dural invasion.37 Imaging findings that best correlate
with dural invasion by the tumor are both dural enhancement
and focal nodularity of the enhancing intracranial tumor, with
sensitivity of 88%, specificity of 100%, and accuracy of 95%.37
Dural enhancement of greater than 5 mm was 91% sensitive in
predicting invasion. Pial enhancement alone is less sensitive for
predicting dural invasion. A more recent study assessing dural
invasion suggested that when the MRI reported dural invasion
there was a 16% chance that it could still be normal.38 This study
was limited in that the reports from the MRI studies were used,
and the images were not re-reviewed, a common error found in
clinical journals that attempt to evaluate imaging sensitivity and
specificity. 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 the
enhancing dura, on T1-enhanced images, has been reported to
imply no dural invasion (Figure 14).39 To our knowledge, a
prospective 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 in
equivocal cases, with only 5 mm of dural enhancement and no
nodularity of the mass, surgery not be withheld based on MR
findings alone.
Sinonasal tumors can gain intracranial access via direct invasion
through the nasal cavity, sinuses, or orbit.40 Another common
pattern for HN tumors to access the intracranial compartment is
via the cranial nerves. Nasopharyngeal carcinoma may also extend
through the normal defect in the pharyngobasilar fascia where the
ICA gains intracranial access.41
Perineural tumor (PNT) extension from a HN malignancy
should be suspected when there is a new cranial nerve palsy in
a patient with a malignant skin, sinus, parotid gland, or skull base
mass. Many times, patients with perineural spread of tumor can
be misdiagnosed with more benign conditions such as Bell’s palsy
or trigeminal neuralgia.42 However, it is also important to note
that up to 30% to 45% of patients with significant perineural
spread can remain asymptomatic, with normal nerve function
on examination.43 Thus, it is important for the radiologist to
scrutinize the entire course of the cranial nerves on the imaging
work-up and surveillance of these patients, and to be familiar
with the perineural pathways and imaging findings of PNT
spread. However, in our experience, the imaging may be so subtle
that the findings are missed even by an experienced interpreting
radiologist.

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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 of
noncontrast imaging. The poorly defined aggressive parotid mass (arrows) extends to the skull base, displacing the ICA medially (arrowhead), and filling the stylomastoid
foramen (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 stylomastoid
foramen (arrows). C, T1 coronal image shows perineural adenoid cystic carcinoma extending through the left foramen ovale (white arrow) and into the cavernous
sinus (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 left
cavernous sinus mass (small arrows), and tumor involving the cisternal CNV (long arrow). Gd-enhanced images are usually recommended when perineural tumor is
suspected, but precontrast T1 images are also critical to show the widened foramen and enlarged nerve.

The most common cranial nerves involved with PNT spread
are branches of the trigeminal and facial nerves. Tumors of
the face, sinuses, or skull base most often involve branches of
the maxillary division of the trigeminal nerve (V2), extending
intracranially through foramen rotundum, whereas nasopha-
ryngeal tumors, masticator space, or oral cavity tumors can
involve the mandibular nerve (V3) and extend cranially through
foramen ovale. Parotid gland tumors often involve the facial
nerve. However, there are also communications between the facial
nerve and the trigeminal nerve, in which tumor can track from
one nerve to another, most commonly parotid tumors tracking
along 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 greater
superficial petrosal nerve to reach the geniculate ganglion of the
facial nerve. Most often, tumor extends in a retrograde fashion
toward the brain; however, anterograde extension along CN
branches also occurs.45
Contrast-enhanced MRI with FS is the most sensitive imaging
modality for detecting PNT spread. Dedicated skull base imaging
protocols are imperative, as these abnormalities will not be picked
up on a routine MRI of the brain, and multiplanar imaging,
particularly in the coronal plane, is essential to fully evaluate
the skull base (Figure 15). Thin-section T1 precontrast images
are important to detect enlargement and soft tissue along the
course of the nerve, and within the foramina. However, the most
sensitive sequences are thin-section T1 fat-suppressed postcon-
trast images, as fat-suppressed postcontrast images will increase
the conspicuity of both enlargement and abnormal enhancement
within and along the nerves, suppressing the normal fat within
the foramina and surrounding bone marrow. Thin-section images
are necessary to distinguish between normal perineural vascular
plexus enhancement and abnormal enhancement within the nerve
itself. CT findings of PNT spread include loss of the normal fat
within the foramina and enlargement or widening of the foramen;
however, these are often relatively late findings. Cranial extension
of PNT can lead to involvement of the cavernous sinus and
Gausserian ganglion in Meckels cave (in the setting of trigeminal
disease), and even extension to the cisternal segments of the
nerves and brainstem. Secondary imaging features of PNT spread
include loss of end organ function, with denervation changes in
the muscles of mastication (in the setting of V3 motor division
disease), and facial muscles (in the setting of CN VII disease).
Acute denervation changes in muscles can be confusing and show
edema (increased signal on T2 images) and enhancement, and
chronic changes include muscular fatty atrophy, with decreased
volume and increased signal on T1 images.46
CONCLUSION
Osseous involvement and intracranial extension of HN
pathology along the skull base is common, and knowledge of its
appearance on imaging is paramount for the practicing neuro-
surgeon. For nearly every skull base pathology, skull base protocol
MRI and thin-section CT are complementary in the evalu-
ation. This review emphasizes the more common lesions, critical
anatomy, and an approach that describes skull base pathology
as 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.
Disclosure
The authors have no personal, financial, or institutional interest in any of the
drugs, materials, or devices described in this article.

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