Core Radiology - Head & Neck Imaging

Paranasal sinuses, nasal cavity, � anterior skull base
Overview of the sinonasal tract and anterior skull base

Sinonasal histology and development
• The nasal cavity and paranasal sinuses are lined with Schneiderian epithelium, a ciliated
mucosa of ectodermal origin that propels contents along anatomic drainage pathways
toward the nasopharynx.
• The sinuses develop at different times in children. At birth, the maxillary and ethmoid
sinuses are present but hypoplastic. Only later does the sphenoid pneumatize,
followed by the frontal sinuses.
Sinonasal and anterior skull base anatomy
cribriform plate
fovea ethmoidalis
frontal recess
lamina papyracea
agger nasi cell infundibulum
hiatus semilunaris
uncinate process maxillary sinus ostium
middle meatus
middle turbinate
maxillary
sinus
frontal
sinus
ethmoid
air cells sphenoid
sinus
ethmoid
infundibulum
clivus
Neuro Head & Neck: 754

Sinonasal and anterior skull base anatomy (continued)
• The superior, middle, and inferior nasal turbinates/conchae are three paired bony
protuberances within the nasal cavity that form air passages inferior to each, called the
superior, middle, and inferior meatuses.
• The inferior meatus is the drainage site of the nasolacrimal duct.
• The ostiomeatal complex (OMC) or unit is the common pathway for the maxillary, frontal,
and anterior ethmoid sinuses to drain into the middle meatus. The OMC is a functional unit
comprising the maxillary sinus ostium, ethmoid infundibulum, uncinate process, ethmoid
bulla, hiatus semilunaris, and middle meatus.
• The frontal sinus drains via the frontal recess either into the ethmoid infundibulum or
directly into the middle meatus. Some authors include the frontal recess in the OMC.
• The maxillary sinus is the largest sinus and drains via the maxillary sinus ostium and
infundibulum, which if obstructed can cause isolated maxillary sinus disease.
• The ethmoid sinuses or air cells are divided into anterior and posterior air cells by the basal
lamella of the middle turbinate where it attaches to the lamina papyracea.
The lamina papyracea is the thin part of the ethmoid bone separating the ethmoid air cells from the orbit.
The ethmoid labyrinth is covered superiorly by the fovea ethmoidalis, an extension of the orbital part of
the frontal bone.
Between the orbital plates on either side are the cribriform plates, the horizontal portion of the ethmoid
bone that lies lower than the fovea ethmoidalis and supports the olfactory bulbs.
• The sphenoethmoidal recess is the common pathway for the sphenoid sinus and posterior
ethmoid air cells to drain into the superior meatus.
• The anterior skull base, which separates the anterior cranial fossa from the sinonasal tract
and orbits, is comprised of the orbital parts of the frontal bone, cribriform plates of the
ethmoid bone, and planum sphenoidale and lesser wings of the sphenoid bone.
Sinonasal anatomic variants
• The variable depth of the olfactory fossa, which is bounded by the vertical and horizontal
lamella of the cribriform plate, is important due to the risk of penetration at this site during
endoscopic sinus surgery.
• The agger nasi cell is an anteriormost ethmoid air cell located anterior to the frontal recess.
A large agger nasi cell may narrow the frontal recess.
• A supraorbital cell is an anterior ethmoid cell that extends superior to the orbit and anterior
ethmoidal notch, which carries the anterior ethmoid artery. The presence of supraorbital
pneumatization places the artery at greater intraoperative risk.
• A Haller (infraorbital) cell is an ethmoid air cell located along the medial orbital floor, which
may narrow the maxillary ostium if large or inflamed.
A right-side Haller cell on axial and coronal CT (arrows).

Sinonasal anatomic variants (continued)
• An Onodi (sphenoethmoidal) cell is a posteriormost ethmoid air cell that extends superior
and lateral to the sphenoid sinus. An Onodi cell should be recognized to avoid intraoperative
damage to the adjacent optic nerve.
Onodi cell on sagittal and coronal CT (arrows).

• Additional anatomic variants that are usually asymptomatic but can contribute to sinonasal
obstruction if large include nasal septal deviation, concha bullosa (pneumatized middle
turbinate), and paradoxical (inward) curvature of the middle turbinate.
Imaging of the sinuses
• CT is the primary modality for imaging the bony detail of the sinuses.
• Imaging is usually not appropriate for acute uncomplicated rhinosinusitis but is indicated
for suspected orbital or intracranial complications of acute rhinosinusitis, suspected acute
invasive fungal sinusitis, surgical planning for chronic or recurrent acute rhinosinusitis, or
suspected sinonasal mass.
• MRI is useful for its soft tissue contrast in evaluating suspected orbital or intracranial
complications of sinusitis or a sinonasal mass. While both may appear as sinus opacification
on CT, contrast enhancement on MRI clearly distinguishes mucosal lesions from obstructed
secretions.
• MRI of routine sinus disease is unreliable due to the varying signal intensities of sinus
contents: inspissated secretions that are clearly opacified sinus on CT can have low signal
that could be mistaken for normal aeration on MRI.
• The purpose of preoperative sinus CT is to identify anatomic variations (noted above) that
may lead to surgical complications if the surgeon is unaware and to provide intraoperative
navigation.
• Thinning or bony dehiscence (absence of bone) due to prior injury or chronic inflammation
should be identified, particularly at the cribriform plate (risk of entry into the anterior
cranial fossa), lamina papyracea (orbit), and sphenoid sinus walls (carotid canal and optic
nerve).

Inflammatory sinonasal disease
Rhinosinusitis
• Rhinosinusitis is inflammation of the paranasal sinuses and nasal mucosa. It is a clinical
diagnosis (based on symptoms such as purulent nasal drainage, nasal obstruction, facial
pressure, and hyposmia), with imaging reserved for suspected complications, surgical
planning, or suspected obstructing mass.
• Acute rhinosinusitis lasts <4 weeks. The most common cause is viral, followed by bacterial
infection. See below for separate discussion of fungal disease.
• Chronic rhinosinusitis lasts ≥12 consecutive weeks. Chronic sinusitis is probably related to
obstruction of sinonasal drainage pathways. The goal of functional endoscopic sinus surgery
(FESS) is to open/widen these pathways.
• Systemic risk factors for rhinosinusitis include:
Mucociliary clearance defects: e.g., cystic fibrosis, primary ciliary dyskinesia.
Immunodeficiencies: e.g., common variable immune deficiency, hypogammaglobulinemia.
Small vessel vasculitides: granulomatosis with polyangiitis (Wegener’s) especially when there is bony
erosion and septal perforation, and eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
especially when there is nasal polyposis.
• Odontogenic sinusitis is the most common cause of unilateral/isolated maxillary sinusitis.
The usual etiologies are a maxillary premolar or molar tooth with periapical abscess or, after
extraction, an oroantral fistula.
Coronal CT shows opacification

of the bilateral maxillary sinuses,
thought to present odontogenic
sinusitis, at least on the left. Note
dental caries (yellow arrow) involving
a left upper maxillary tooth and
associated periapical lucency (red
arrow) representing a periapical
abscess or granuloma.
• Sinus mucosal thickening is a common but nonspecific imaging finding. Acute sinusitis is
more likely to feature an air-fluid level and bubbles within the fluid. Sclerotic thickening
of sinus walls, due to prolonged mucoperiosteal inflammation, is characteristic of chronic
sinusitis.

Fungal rhinosinusitis
Allergic fungal sinusitis: Coronal (left image) and axial noncontrast CT shows marked pan-sinus disease with
curvilinear hyperattenuation in the affected sinuses (arrows). There is erosion of the ethmoid sinus walls.
Case courtesy Mary Beth Cunnane, MD, Massachusetts Eye and Ear Infirmary.
• Fungal sinus diseases are classified as noninvasive or invasive, based on extension to the
submucosa, vessels, and/or bone.
• Noninvasive fungal rhinosinusitis includes allergic fungal rhinosinusitis and fungal ball.
Affected patients are immunocompetent.
• Invasive fungal rhinosinusitis is divided into acute and chronic forms. The vast majority of
affected patients have diabetes mellitus or are immunocompromised (e.g., hematologic
malignancy, chemotherapy-related neutropenia, transplantation).
• Noninvasive and chronic invasive fungal rhinosinusitis are most commonly due to Aspergillus
and dematiaceous (brown-black) molds. Acute invasive fungal rhinosinusitis is most
commonly caused by aspergillosis or mucormycosis.
• Allergic fungal rhinosinusitis is the most common form of fungal sinusitis, representing
a subtype/variant of chronic rhinosinusitis with nasal polyposis caused by a localized
hypersensitivity reaction to fungi, typically in atopic individuals.
Imaging shows complete opacification of multiple sinuses with secretions that are hyperattenuating (CT)
and low T2 signal intensity (MRI) and cause expansile remodeling/pressure erosion of the sinus walls.
• Fungus balls are dense aggregates of (noninvasive) hyphae and (nonallergic) mucin separate
from the sinus mucosa.
Imaging shows opacification of a single sinus (usually maxillary) with an irregular mass that is
hyperattenuating (CT) and low T2 signal intensity (MRI), often with intralesional mineralization/
calcification. There may be bony erosion.
• Invasive fungal rhinosinusitis is a serious acute or chronic infection where fungal hyphae
invade mucosa, vessels, and/or other sinonasal tissues and cause necrosis.
The most common but nonspecific imaging finding of invasive fungal rhinosinusitis is severe unilateral
sinonasal opacification.
Later in the disease course, more specific imaging signs include extrasinus soft tissue infiltration into the
premaxillary and retroantral fat, intracranial or orbital involvement, and bony erosion.
Non-enhancement of a nasal turbinate on MRI (black turbinate sign) in an immunocompromised patient is
highly suggestive of necrosis in the setting of invasive fungal rhinosinusitis.

Complications of rhinosinusitis
Acute frontal sinusitis complicated by epidural and subdural empyemas: Axial post-contrast T1-weighted MRI
(left image) demonstrates left frontal epidural (yellow arrow) and subdural (red arrows) collections with rim
enhancement and associated restricted diffusion on DWI (right image), consistent with empyemas. There is
diffuse left frontal scalp subcutaneous edema representing cellulitis.
• Spread of infection to the orbit may cause preseptal or orbital cellulitis, orbital abscess,
subperiosteal abscess, or septic ophthalmic vein and cavernous sinus thrombosis.
• Spread of infection to the cranial cavity may cause meningitis, cerebritis, or suppurative
collections (epidural abscess, subdural empyema, or brain abscess). The frontal lobe is the
typical site of sinogenic brain abscess.
• Acute frontal sinusitis complicated by osteomyelitis and subgaleal/subperiosteal abscess is
known as Pott's puffy tumor.
Acute frontal sinusitis complicated by Pott's puffy tumor: Axial contrast-enhanced CT shows opacified frontal
sinuses and focal defect in the anterior sinus wall (green arrow) with overlying soft tissue swelling and a gas-
fluid collection (red arrows) in the frontal scalp, compatible with abscess (Pott's puffy tumor).
Sinonasal inflammatory polyps
• Sinonasal inflammatory polyps and nasal polyposis refer to multiple bilateral pedunculated
protrusions of mucosa, edematous stroma, and inflammatory infiltrate, most commonly
arising from the middle meatus and ethmoid region.
• In adults, a significant minority of cases of chronic rhinosinusitis are associated with nasal
polyposis, which together in turn is sometimes associated with asthma and sensitivity to
aspirin or other nonsteroidal anti-inflammatory drugs. This syndrome is known as aspirin/
NSAID-exacerbated respiratory disease or Samter’s triad.
• In children, the most common risk factor for chronic rhinosinusitis with nasal polyposis is
cystic fibrosis.

Paranasal sinus retention cyst
• Retention cysts are well-defined, rounded collections of mucous or serous fluid arising in
the sinus lining due to obstruction of small seromucinous glands. “Mucous retention cyst” is
often used generically to include both mucous and serous retention cysts.
• Retention cysts are usually asymptomatic but can obstruct sinus drainage pathways. They
are most commonly located in the maxillary sinus.
Mucocele
Mucocele of the frontal sinus:

Axial noncontrast CT shows an expanded, fluid-
filled right frontal sinus (arrow) with thinning of
the sinus walls. Incidentally, the left frontal sinus is
congenitally absent.
Case courtesy Mary Beth Cunnane, MD,
Massachusetts Eye and Ear Infirmary.
• A mucocele is an expanded, airless paranasal sinus filled with mucoid secretions due to
drainage obstruction.
• Mucoceles may be secondary to inflammatory sinus disease (most commonly) or tumor.
• Imaging shows complete opacification of a single sinus cavity with expansile remodeling and
thinning of the bony walls. The sinus contents tend to appear homogeneous on CT and MR;
however, the MR signal intensity is variable depending on the degree of dessication.
• Mucoceles are most common in the frontal sinus.
Silent sinus syndrome
• Silent sinus syndrome is an acquired condition of painless maxillary sinus atelectasis due to
chronic obstruction of the maxillary sinus ostium with resorption of the air.
• Imaging and physical examination show facial asymmetry due to unilateral maxillary sinus
volume loss, complete or partial opacification of the sinus, and enophthalmos.
Nasal septal perforation
• Nasal septal perforation usually involves the cartilaginous septum and is generally related to
ischemia or inflammation.
• The most common cause is iatrogenic/traumatic (e.g., septoplasty). Other causes include
cocaine, granulomatosis with polyangiitis (Wegener’s), and granulomatous infections.

Benign non-inflammatory sinonasal and anterior skull base lesions
Choanal polyp
Antrochoanal polyp: Coronal (left image) and axial noncontrast CT show a polypoid lesion (arrows) involving
the left maxillary sinus and nasopharynx, with erosion of the middle turbinate and medial wall of the maxillary
sinus.
• Choanal polyps are solitary pedunculated lesions that extend through the nasal cavity to the
posterior nasal aperture (choana), possibly prolapsing into the nasopharynx.
• The vast majority are antrochoanal polyps, which originate in the maxillary sinus (antrum)
and widen the maxillary ostia.
• Choanal polyps are histologically similar to inflammatory polyps but considered clinically
distinct. They mostly occur in children and young adults.
Sinonasal papilloma
Inverted papilloma: Axial noncontrast CT shows Inverted papilloma in a different patient: Axial
a polypoid lesion of the left maxillary sinus with contrast-enhanced T1-weighted MRI with fat
erosion of the medial wall of the maxillary sinus, the suppression shows a lobulated extra-axial mass
ethmoid air cells, and the turbinates. The sinus is (arrows) arising from the frontal sinus. The
not expanded. There is reactive bony sclerosis of the mass demonstrates characteristic cerebriform
lateral wall of the maxillary sinus (arrow). enhancement.
Case courtesy Mary Beth Cunnane, MD, Case courtesy Gregory Wrubel, MD, Brigham and
Massachusetts Eye and Ear Infirmary. Women’s Hospital.
• Sinonasal (Schneiderian) papillomas are benign polypoid neoplasms arising from the
Schneiderian epithelium.
• The most common histologic type of sinonasal papilloma is the inverted type, followed by
exophytic and oncocytic types.

Sinonasal papilloma (continued)
• Inverted and oncocytic papillomas have malignant potential, typically transforming to
squamous cell carcinoma, while exophytic papillomas do not.
• Inverted and oncocytic papillomas typically arise from paranasal sinuses or the lateral nasal
wall, while exophytic papillomas tend to arise from the nasal septum.
• Inverted papillomas classically show a convoluted cerebriform pattern on T2-weighted and
contrast-enhanced T1-weighted MR images (alternating curvilinear bands of high and low
signal intensity). At CT, bone erosion and remodeling are common, although the site of
attachment may demonstrate focal hyperostosis.
Juvenile nasopharyngeal angiofibroma (JNA)
Juvenile nasopharyngeal angiofibroma: Axial contrast-enhanced CT through the pterygopalatine fossa in soft
tissue (left image) and bone windows shows an avidly enhancing mass in the left nasopharynx, pterygopalatine
fossa, and sphenoid sinus, with characteristic widening (arrows) of the pterygopalatine fossa. There is resultant
anterior displacement of the posterior wall of the maxillary sinus relative to the left (dotted blue line).
Case courtesy Sanjay Prabhu, MD, Boston Children’s Hospital.
• Juvenile nasopharyngeal angiofibroma (JNA) is the most common benign neoplasm of the
nasopharynx and typically arises from the posterior aspect of the nasal cavity near the
sphenopalatine foramen.
• While benign, JNA may be locally aggressive and, due to its vascularity, presents a risk for
life-threatening bleeding.
• JNA almost always affects adolescent/young adult males, who present with epistaxis and/or
nasal obstruction.
• On imaging, JNA shows intense contrast enhancement with a salt-and-pepper appearance
on MRI due to vascular flow voids. The mass can extend into the pterygopalatine fossa,
expanding it and anteriorly bowing the posterior maxillary sinus wall (Holman-Miller/antral
sign).
• The most common arterial supply of JNA consists of distal internal maxillary artery branches.
Embolization is often performed to reduce lesion vascularity prior to resection.

Congenital nasal masses
• The most common pediatric midline nasal masses are anomalies of neuroectodermal
development at the frontonasal region including, in decreasing frequency, dermoid/
epidermoid cyst, encephalocele, and nasal glial heterotopia.
• Nasal dermoid/epidermoid cysts, usually associated with dermal sinus tracts, are
ectodermal inclusions that appear as a round cyst along the anterior nose from the tip up
to the crista galli. Dermoid cysts may have fat density/signal, while epidermoid cysts show
restricted diffusion.
Nasal dermoids: Sagittal T2-weighted MRI (left image) demonstrates a well-defined midline nasal lesion
(arrow) associated with a widened foramen cecum. Axial CT of a different patient (right image) shows a
similarly located lesion with internal fat density (arrow).
• Frontoethmoidal encephaloceles, also known as anterior or sincipital cephaloceles, refer
to herniations of meninges, CSF, and/or brain tissue through an anterior skull or skull base
defect. The protrusion can be located at the glabella (via the fonticulus nasofrontalis),
nasal cavity (via the foramen cecum), or medial orbit (via the lacrimal bone). MRI best
demonstrates the soft tissue mass contiguous with intracranial contents.
Encephalocele: Axial T2-weighted MRI shows focal

herniation of brain tissue through a small defect in
the left frontal calvarium (arrow).
• Nasal glial heterotopias, also known as nasal gliomas, are non-neoplastic masses of
dysplastic neuroglial tissue isolated to the nasal dorsum or nasal cavity. MRI shows a soft
tissue mass without connection to intracranial contents.
Nasal glioma:
Sagittal T1-weighted post-contrast MRI
demonstrates a non-enhancing, multilobulated
lesion at the dorsum of the nose (arrows) without
communication with the intracranial compartment.
This was a biopsy-proven nasal glioma.

Fibro-osseous lesions
• Fibro-osseous lesions in the craniofacial skeleton are a spectrum of pathologic ossifications
with variable amounts of fibroblastic stroma. While benign, they can cause symptoms
related to mass effect or facial deformity.
• Osteomas are the most common neoplasm in the paranasal sinuses, occurring as a polypoid
growth most frequently within the frontal sinus followed by ethmoid air cells. They are
mostly made of dense bone.
Gardner syndrome is the association of familial adenomatous polyposis with multiple skull osteomas and
soft tissue tumors such as desmoid.
• Craniofacial fibrous dysplasia is one of the most common sites of fibrous dysplasia
(along with femur, tibia, and ribs), wherein bone is replaced with disorganized fibrous
tissue. CT shows ill-defined regions of bony expansion with radiolucent ground glass,
sclerotic, or mixed density. MRI variably shows heterogeneous signal intensity and contrast
enhancement.
Fibrous dysplasia:
Axial CT through the face shows a well-circumscribed, expansile osseous lesion with ground glass matrix in
the right maxilla.
The distribution of fibrous dysplasia is classified as polyostotic (involving multiple bones) or monostotic
(involving a single bone only). Of note, craniofacial fibrous dysplasia is considered a monostotic site even
when multiple cranial bones are involved.
McCune-Albright syndrome is the association of polyostotic fibrous dysplasia with autonomous endocrine
hyperfunction and café-au-lait macules.
Mazabraud syndrome is the association of polyostotic fibrous dysplasia with intramuscular myxomas.
• Ossifying fibromas are benign bone neoplasms that most commonly occur in the mandible,
followed by maxilla. Imaging shows a solitary, well-defined, expansile lesion with variable
radiolucency/density.

Malignancies of the sinonasal tract and anterior skull base
Overview of sinonasal and anterior skull base malignancies
• The most common malignant neoplasm in the sinonasal tract is squamous cell carcinoma,
but this histology is not as overwhelming of a majority as in other mucosal sites of the upper
aerodigestive tract. There are a wide variety of other malignancies.
• Sinonasal epithelial cancers:
Squamous cell carcinoma (most common).
Adenoid cystic carcinoma.
Non-salivary-type adenocarcinoma.
Sinonasal undifferentiated carcinoma (SNUC).
Sinonasal neuroendocrine carcinoma (SNEC).
• Nonepithelial sinonasal cancers:
Lymphoma (most common). Extramedullary plasmacytoma.
Olfactory neuroblastoma. Sarcomas.
Mucosal melanoma.
• Most of the various sinonasal malignancies have nonspecific imaging appearances and it
is usually not possible to predict the histology with confidence. The role of imaging lies
in localizing the tumor and evaluating the extent of disease, which affects the optimal
treatment approach.
Sinonasal malignancies are usually aggressive masses that cause extensive bony destruction.
Internal contrast enhancement, though often heterogeneous, distinguishes neoplasms from inflammatory
lesions such as hypertrophic mucosa, polyps, or obstructed secretions/mucocele.
Owing to high cellularity, many of these malignancies have intermediate intensity (“evil gray”) on T2-
weighted images and more restricted diffusion.
• Important findings to describe include the presence of perineural tumor spread, crossing the
anterior skull base into the intracranial compartment, and extension into the orbit.
Perineural tumor spread appears as nerve thickening and enhancement, obliteration of perineural fat
pads, and/or enlargement of neural foramina/canals.
Intracranial involvement may appear as nodular dural thickening or vasogenic edema in the brain.
Orbital invasion most commonly occurs through the lamina papyracea, which is the weakest orbital wall.
Squamous cell carcinoma
• Squamous cell carcinoma is the most common sinonasal malignancy, most commonly
affecting the maxillary sinus.
• Major risk factors for sinonasal squamous cell carcinoma are smoking and human
papillomavirus (HPV) infection.
Adenoid cystic carcinoma
• Adenoid cystic carcinoma is the most common sinonasal tumor of minor salivary gland
origin, most commonly affecting the maxillary sinus.
• Adenoid cystic carcinomas have the highest risk of perineural spread. Those in the sinonasal
tract most commonly affect the maxillary division of the trigeminal nerve (CN V2).
Adenocarcinoma
• Sinonasal adenocarcinomas arise from surface epithelial glands, most commonly in the nasal
cavity and ethmoid air cells, and are divided into intestinal-type and nonintestinal-type.
• Intestinal-type adenocarcinoma is strongly associated with occupational wood dust
exposure.

Olfactory neuroblastoma (esthesioneuroblastoma)
Esthesioneuroblastoma with intracranial extension: Axial and coronal post-contrast T1-weighted MRI
demonstrate an avidly enhancing lobulated mass (arrows) extending from the right superior nasal cavity into
the anterior cranial fossa. Multiple cysts are noted at the tumor-brain interface.
• Olfactory neuroblastoma, previously known as esthesioneuroblastoma, is a malignant neural
crest-derived tumor that arises from olfactory epithelium in the superior nasal cavity.
• When the tumor extends intracranially, the presence of cysts at the margins of the
intracranial portion is highly suggestive of olfactory neuroblastoma.
Mucosal melanoma
• Mucosal melanoma refers to malignant melanoma that arises from mucosal epithelium,
which is uncommon compared to cutaneous melanoma.
• The head and neck, most commonly in the sinonasal tract, is the most common site.
• On MRI, internal high signal on T1-weighted images corresponding to melanin can be
suggestive of the diagnosis, but these tumors are frequently amelanotic.
Lymphoma
• The most common histology is diffuse large B-cell lymphoma, although in Asia and Latin
America, extranodal NK/T-cell lymphoma, nasal type, is more common.
• B-cell lymphomas predominate in the paranasal sinuses, while T-cell lymphomas
predominate in the nasal cavity.
Extramedullary plasmacytoma
• Solitary extramedullary plasmacytoma is a plasma cell malignancy presenting as an
extraosseous soft tissue mass; multiple myeloma is the systemic form.
• Extramedullary plasmacytoma usually affects the head and neck region, most commonly in
the sinonasal tract.
Rhabdomyosarcoma
• Rhabdomyosarcoma is the most common soft tissue malignancy in the head and neck in
children and the most common sinonasal sarcoma.
• Half of head and neck rhabdomyosarcomas occur in a so-called parameningeal site: nasal
cavity, nasopharynx, paranasal sinuses, infratemporal and pterygopalatine fossae, middle
ear, or mastoid. Parameningeal sites carry an unfavorable prognosis, while the orbits and
other non-parameningeal head and neck locations are considered favorable sites.

Orbits
Overview and anatomy of the orbits
Bony orbits and foramina
supraorbital foramen
optic canal
frontal bone
ethmoid bone
sphenoid lesser wing
sphenoid greater wing lacrimal bone
zygomatic bone nasal bone
superior orbital fissure nasal septum
inferior orbital fissure palatine bone
infraorbital foramen maxilla
• The orbit is a conical cavity formed by 7 bones: frontal, ethmoid, palatine, lacrimal, maxilla,
zygomatic, and sphenoid.
• The orbital roof is part of the anterior skull base.
• The orbital floor is the roof of the maxillary sinus.
• Medially, the orbit borders the ethmoid air cells (across the lamina papyracea). Laterally, the
orbit borders the temporal fossa (across the zygoma and greater wing of sphenoid).
• The orbital apex is the region around three bony openings (optic canal, superior orbital
fissure, and inferior orbital fissure) and the annulus of Zinn (common tendinous ring).
• The following structures pass through the optic canal:
Optic nerve. Ophthalmic artery.
• The following structures pass through the superior orbital fissure, which includes all of the
cranial nerves (CN) of the cavernous sinus except CN V2:
CN III (oculomotor nerve) innervates the superior, medial, and inferior recti, and inferior oblique muscles.
CN IV (trochlear nerve) innervates the superior oblique muscle (mnemonic: SO4).
CN V1 (ophthalmic division of trigeminal nerve) provides sensory innervation to the upper face.
CN VI (abducens nerve) innervates the lateral rectus muscle (mnemonic: LR6).
Superior ophthalmic vein drains into the cavernous sinus.
Superior branch of inferior ophthalmic vein drains into the superior ophthalmic vein or cavernous sinus.
• The following structures pass through the inferior orbital fissure, which includes several
branches of CN V2 (maxillary division of trigeminal nerve) after it passes from the cavernous
sinus through foramen rotundum and divides in the pterygopalatine fossa:
Zygomatic nerve (from CN V2) provides sensory innervation to the skin of the lateral cheek and temple.
Infraorbital nerve (from CN V2) provides sensory innervation to skin of the inferior eyelid, medial cheek,
upper lip, and lateral nose.
Inferior branch of inferior ophthalmic vein drains into the pterygoid venous plexus.

Compartments of the orbits
extraconal conal intraconal
Axial T2 anterior segment

(aqueous humor)
lens
posterior segment
(vitreous humor)
*optic nerve/sheath complex
lateral rectus muscle
medial rectus muscle
Coronal T1 superior oblique muscle
levator palpebrae superioris +

superior rectus complex
superior ophthalmic vein

* lateral rectus muscle
intraorbital fat
inferior rectus muscle
medial rectus muscle
• The orbital septum divides the orbit (postseptal space) from the periorbital soft tissues
(preseptal space). The septum is thin fibrous tissue that extends from the periosteum
(periorbital) of the orbital rims towards the tarsal plates of the eyelids.
• Classical teaching divides the orbit into four compartments: extraconal, conal, intraconal,
and ocular compartments. The first three are also known as the retrobulbar space.
• The extraconal compartment contains the lacrimal gland, some neurovascular structures,
and fat between the muscles and orbital periosteum. Lesions of the bony orbit and
extraorbital processes can encroach on the extraconal space.
• The conal compartment refers to an imaginary cone formed by the rectus muscles and
interconnecting connective tissue bands.
• The intraconal compartment contains the optic nerve-sheath complex (optic nerve,
surrounding CSF, and meninges), other neurovascular structures, and fat central to the
myofascial cone.
• The ocular compartment is the globe. Ocular lesions are not always included in discussion of
“orbital” lesions even though the orbital cavity contains the globe.
• In reality, fascial planes in the orbit are more complex and transcend the intraconal/
extraconal artificial boundaries.
Lacrimal apparatus
• The lacrimal apparatus consists of a secretory system and an excretory system.
• The lacrimal gland, lodged in the superotemporal angle of the orbit, consists of a palpebral
lobe and an orbital lobe (which is deeper and larger).
• Tears drain via the lacrimal canaliculi near the medial canthus into the lacrimal sac, lodged
in the lacrimal fossa at the inferomedial preseptal orbit.
• The lacrimal sac empties via the nasolacrimal duct into the nasal inferior meatus.
Orbital muscles
• Six extraocular muscles move the eye: four recti (superior, inferior, medial, lateral) and two
oblique (superior and inferior).
• The rectus muscles arise from the annulus of Zinn.
• The superior oblique muscle arises just superomedial to the annulus of Zinn. The tendon is
reflected at the trochlea, a fibrocartilaginous structure attached to the superior nasal aspect
of the frontal bone.
• The inferior oblique muscle arises from the medial corner of the orbital floor.
• The levator palpebrae superioris runs with the superior rectus in a muscle complex. The
levator muscle (innervated by CN III) and Müller’s (superior tarsal) muscle (innervated by
sympathetics) lift the upper eyelid.
Globe
• The globe has three layers: sclera, uvea, and retina.
• The sclera is continuous anteriorly with the cornea.
• The uvea is composed of the choroid, ciliary body, and iris.
• The retina forms most of the inner surface, extending from the optic disc posteriorly to the
ora serrata anteriorly.
• The lens separates the anterior and posterior segments of the globe.
• The iris separates the anterior and posterior chambers of the anterior segment, which
communicate via the pupil.
• The anterior segment is filled with aqueous humor, while the posterior segment is filled with
vitreous humor.
Optic nerve
• Although named CN II, the optic nerve is a part of the central nervous system: it is
surrounded by meninges, CSF, and myelin from oligodendroglia (rather than Schwann cells).
• The optic nerve is divided into 4 segments: intraocular (optic disc/papilla/nerve head),
intraorbital (the longest part), intracanalicular (within the optic canal), and intracranial
(within the middle cranial fossa).
• The two optic nerves converge at the optic chiasm in the suprasellar region.

Orbital and ocular infection
Overview of orbital infection
• The most common etiology of orbital infection is direct spread of infection from the
paranasal sinuses, especially bacterial rhinosinusitis involving ethmoid air cells. Other
etiologies of orbital infection are trauma, foreign body, odontogenic infection.
• Orbital infection includes a spectrum of entities ranging in severity from mild to vision- or
life-threatening.
Preseptal cellulitis
• Preseptal (periorbital) cellulitis involves the anterior soft tissues of the eyelids, superficial to
the orbital septum.
• Preseptal cellulitis is generally mild and much more common than orbital cellulitis.
• Patients present with eyelid swelling and erythema.
• Imaging shows subcutaneous fat stranding and swelling of the eyelids and face but normal
orbital fat.
Orbital cellulitis
Orbital cellulitis with epidural abscess: Axial contrast-enhanced CT through the orbits (left image) shows left
proptosis and both pre- and post-septal inflammatory change (red arrows), without a discrete fluid collection.
There is complete opacification of the left ethmoid sinus and opacification of the sphenoid sinus. CT through
the brain (right) demonstrates two locules of gas in the extra-axial space (yellow arrows) directly posterior to
the left frontal sinus, representing an epidural abscess.
• Orbital (postseptal) cellulitis involves the muscles and fat deep to the orbital septum.
• Orbital cellulitis is serious due to risk of complications such as abscess and intracranial
spread via the valveless ophthalmic veins.
• Patients present with not only eyelid swelling and erythema, but also painful
ophthalmoplegia, chemosis, and/or proptosis.
• Imaging shows orbital fat stranding, sometimes with extraocular muscle edema, proptosis,
or an intraconal or extraconal phlegmon (inflammatory soft tissue mass that has not yet
organized into an abscess).
Subperiosteal abscess
• Subperiosteal abscess is a suppurative collection involving the bony orbit under its
periosteum (periorbital). It can arise associated with or independent of orbital cellulitis.
• Imaging shows a convex rim-enhancing collection tracking along a bone surface, most
commonly the medial orbital wall in the setting of ethmoid sinusitis.
Orbital abscess
• Orbital abscess is an abscess located within the soft tissues of the orbit, due to consolidation
of orbital cellulitis or rupture of subperiosteal abscess.
• Imaging shows, as with abscesses elsewhere, a focal rim-enhancing collection.
Cavernous sinus thrombosis
• The cavernous sinus is the most common site of septic dural venous sinus thrombosis, due
to drainage of sites of medial facial, orbital, sinonasal, or dental infection.
• Patients present with headache, fever, proptosis, chemosis, and cranial nerve palsies (e.g.,
ophthalmoplegia).
• Imaging shows convex bulging of the lateral wall of the cavernous sinus and filling defects on
post-contrast images. Indirect signs include dilatation (and/or thrombosis) of the superior
ophthalmic vein.
Endophthalmitis/panophthalmitis
• Endophthalmitis refers to bacterial or, less commonly, fungal infection within the globe,
involving the vitreous and/or aqueous humors. Further extensive involvement of the ocular
wall and periocular orbital tissues is called panophthalmitis.
• Most cases are due to direct inoculation, such as by trauma, surgery, or corneal ulcer.
• Imaging shows thickening and enhancement of the ocular wall, periocular fat stranding, and
abnormal high density/signal of the vitreous.
Dacryoadenitis
• Dacryoadenitis refers to lacrimal gland inflammation, which can be due to acute viral or
bacterial infection. Other causes include idiopathic orbital inflammation, IgG4-related
disease, and granulomatous diseases, which are discussed in the next section, as well as
Sjögren syndrome.
• Dacryoadenitis appears as diffuse gland enlargement (unilateral or bilateral) that generally
molds to orbital structures but may displace the globe inferomedially.
Dacryocystitis
Axial (left image) and coronal noncontrast CT through the orbits shows a rim-enhancement cystic structure in
the left lacrimal fossa (yellow arrows) with surrounding soft tissue stranding, representing an enlarged lacrimal
sac in the setting of dacryocystitis. Note communication with the nasolacrimal duct (red arrow).
• Dacryocystitis refers to lacrimal sac inflammation typically secondary to nasolacrimal duct
obstruction and subsequent bacterial infection.
• In infants, dacryocystitis usually complicates congenital nasolacrimal duct obstruction
(dacryostenosis) or dacryocystocele. Obstruction can also be acquired in older adults.
• Dacryocystitis appears as a prominent rim-enhancing structure centered in the lacrimal
fossa near the medial canthus with adjacent preseptal fat stranding.

Orbital inflammatory disorders
Idiopathic orbital inflammation (pseudotumor)
• Idiopathic orbital inflammation, originally known as orbital pseudotumor, refers to an orbital
mass or structure enlargement related to a nonspecific inflammatory infiltrate of unknown
cause. It is diagnosed after excluding systemic autoinflammatory, infectious, and neoplastic
etiologies.
• Idiopathic orbital inflammation is the most common cause of a painful orbital mass in
adults. Pain helps distinguish this entity from mimics (e.g., lymphoma, thyroid eye disease).
• Most cases are unilateral and acute or subacute in onset.
• The main anatomic subtypes and their imaging findings are:
Idiopathic dacryoadenitis: diffuse lacrimal gland enlargement and enhancement.
Idiopathic orbital fat inflammation: fat stranding and/or ill-defined soft tissue involving several
structures.
Idiopathic orbital myositis: smooth enlargement of one or several extraocular muscles; most commonly
affects the lateral rectus muscle and also involves the anterior tendon (unlike thyroid eye disease).
• Less common subtypes and their imaging findings include:
Optic perineuritis: optic nerve sheath thickening and enhancement.
Tolosa-Hunt syndrome: cavernous sinus thickening and enhancement.
IgG4-related ophthalmic disease
• Immunoglobulin G4 (IgG4)-related disease is a multisystem fibro-inflammatory disorder. The
diagnosis requires histopathology or serology demonstrating IgG4 expression.
• The orbit is the most frequently involved site in the head and neck. In turn, the most
common site of IgG4-related ophthalmic disease is the lacrimal gland. Similar to idiopathic
orbital inflammation, other common sites of involvement include the extraocular muscles
and orbital fat.
• A distinguishing feature in some cases of IgG4-related ophthalmic disease is infiltration/
enlargement of the infraorbital nerve.
• The combination of lacrimal and major salivary gland involvement (parotid or
submandibular) was previously called Mikulicz syndrome, and now termed IgG4-related
chronic sclerosing dacryoadenitis and sialadenitis.
Granulomatous diseases
• Granulomatous inflammation in the orbit appears similar radiologically to idiopathic/
nonspecific inflammation but may be associated with a systemic disorder such as sarcoidosis
or granulomatosis with polyangiitis. These more commonly affect the globe (e.g., uveitis,
scleritis, conjunctivitis), but involvement of the extraocular orbit is better seen on imaging.
• Sarcoidosis of the extraocular orbit most often involves the lacrimal gland, but it may
also affect the optic nerve sheath, extraocular muscles, or orbital fat. Concurrent thoracic
manifestations of sarcoidosis point towards the diagnosis.
• Granulomatosis with polyangiitis can involve the orbit, with an infiltrative mass in the
orbital fat being the most common type, followed by dacryoadenitis and then extraocular
myositis, usually contiguous with sinonasal disease.

Thyroid-associated orbitopathy
Thyroid orbitopathy in a patient with Graves disease: Coronal (left image) and axial noncontrast CT through
the orbits shows bilateral exophthalmos, increased orbital fat, and enlargement of inferior and medial rectus
muscle bellies sparing the tendons (Coca-Cola bottle sign).
• Thyroid-associated orbitopathy, also known as Graves ophthalmopathy/orbitopathy or
simply thyroid eye disease, is an autoimmune disorder of the orbital soft tissues in patients
with thyroid disease. Although usually associated with Graves disease (the most common
cause of hyperthyroidism), it can also occur in patients with euthyroid or hypothyroid
autoimmune thyroiditis.
• The pathogenesis consists of inflammation involving the orbital muscles and fat,
overproduction of glycosaminoglycans (mostly hyaluronic acid) by fibroblasts, and
adipogenesis.
• Thyroid-associated orbitopathy is the most common cause of proptosis and extraocular
muscle enlargement. Imaging demonstrates proptosis with orbital fat expansion and mild
fat stranding early in the disease and, with extended disease activity, fusiform extraocular
muscle enlargement.
• Thyroid orbitopathy tends to be bilateral and spares the muscle tendons. The longitudinal
appearance of an enlarged muscle belly but a narrow anterior tendon is known as the Coca-
Cola bottle sign of thyroid orbitopathy.
• The inferior rectus muscle is most commonly affected first. The mnemonic I’M SLOw helps
remember the order of involvement of the extraocular muscles:
Inferior rectus g medial rectus g superior rectus g lateral rectus g obliques
• Atypical features such as isolated lateral rectus involvement, anterior tendon enlargement,
or unilaterality should prompt consideration of an alternative diagnosis, such as idiopathic
orbital inflammation or neoplasm.
• Severe muscle enlargement can crowd the orbital apex, resulting in dysthyroid optic
neuropathy that may require surgical decompression if not responsive to steroids.
Thyroid orbitopathy, fatty type: Coronal (left image)

and axial noncontrast CT through the orbits shows
bilateral exophthalmos and increased orbital fat.
The extraocular muscles do not appear abnormally
thickened.

Optic neuritis
Optic neuritis due to multiple sclerosis: Coronal fat suppressed T2-weighted MRI through the orbits (left
image) shows increased signal of the left optic nerve (arrow), with loss of clear distinction between the optic
nerve and the surrounding normal T2 hyperintense CSF. The right optic nerve appears normal. There was no
enhancement of the left optic nerve (not shown).
Axial FLAIR (right image) shows numerous foci of T2 prolongation within the periventricular white matter
(arrows), in a pattern consistent with multiple sclerosis.
• Optic neuritis refers to inflammation of the optic nerve.
• Causes of optic neuritis include:
Multiple sclerosis (MS) is the most common.
Aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (NMOSD).
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease.
Arteritic versus non-arteritic anterior ischemic optic neuropathy (AION versus NAION).
Viral infection.
Sarcoidosis.
Lupus.
Chronic relapsing inflammatory optic neuropathy (CRION).
• The patients are typically young adults who present with acute, painful, central visual loss.
In older patients, ischemic optic neuropathy is more likely than optic neuritis.
• Acutely, the optic nerve shows enlargement, T2 prolongation, and contrast enhancement.
Chronically, the optic nerve atrophies.
• Concurrent brain white matter lesions support the diagnosis of MS. Note, however, the optic
nerve is not one of the sites that can fulfill the McDonald criteria for dissemination in space.

Multicompartmental orbital masses
Lymphoma
Orbital lymphoma: Coronal (left) and axial noncontrast CT through the orbits shows left-sided proptosis and an
ill-defined, slightly hyperattenuating mass (arrows) in the left superior-lateral orbit. The mass conforms to the
shape of the globe, rather than deforming it. The left lacrimal gland is not separately identified.
• Orbital lymphoproliferative lesions are a spectrum ranging from benign reactive lymphoid
hyperplasia to lymphoma. Most of these are ocular adnexal lymphomas (involving the
support structures of the eye as opposed to intraocular lymphoma).
• Lymphoma is the most common primary orbital tumor in older adults, although it may also
be secondary to systemic disease.
• The most common histology of orbital lymphoma is low-grade extranodal marginal zone
B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma).
• Similar to the above inflammatory disorders, lymphoproliferative lesions can affect any
orbital structure as a mass or diffuse infiltration but are most commonly extraconal,
particularly involving the lacrimal gland.
• Both lymphoproliferative and inflammatory masses tend to mold to the globe and other
orbital structures. However, compared to idiopathic orbital inflammation, lymphomas have
lower ADC values on MRI and clinically are unlikely to present with orbital pain.
Plexiform neurofibroma
• Plexiform neurofibromas are the most common type of orbital neurofibroma and are almost
always associated with neurofibromatosis type 1 (NF1).
• Orbital plexiform neurofibromas typically involve trigeminal nerve branches, extending
from the periorbital/preseptal soft tissues of the eyelid to the deep orbit, infiltrating both
extraconal and intraconal compartments.
• On imaging, plexiform neurofibromas appear as infiltrative, serpentine masses with variable
contrast enhancement. Associated findings of NF1 may be seen on the orbital imaging study,
including sphenoid wing dysplasia, buphthalmos (enlarged globe), and optic nerve glioma.
Venolymphatic malformation (VLM)
• Orbital venolymphatic (combined venous-lymphatic) malformations (VLM), previously called
lymphangiomas, are congenital slow-flow vascular malformations that present in children
and grow with the patient.
• Orbital VLMs most commonly involve the extraconal compartment but may be found
anywhere in the orbit. A key diagnostic clue is transspatial location with the mass spanning
multiple compartments.
• On imaging, orbital VLM appears as a multilocular cystic mass, often with complex internal
contents and fluid-fluid levels from prior hemorrhage. Enhancement is variable, though
typically peripheral and septal.
Metastasis
Scirrhous breast cancer metastasis: Coronal (left image) and axial CT through the orbits demonstrates ill-
defined soft tissue in the left orbit (arrows), with loss of the normal definition of the optic nerve-sheath
complex, medial rectus, and inferior rectus. Despite the presence of the mass, there is no significant proptosis.
• Orbital metastases arrive hematogenously and can form a mass or diffuse infiltrate in any
compartment. Common sites are the choroid, bones, fat, and extraocular muscles.
• In adults, the primary tumors are typically carcinomas and most commonly from the breast.
Scirrhous breast cancer metastases characteristically can cause enophthalmos, whereas
other primaries cause proptosis.
• In young children, the most common source of metastases to the orbit is neuroblastoma. On
cross-sectional imaging, these appear as an extraconal mass centered in the orbital lateral
wall or roof with permeative bony destruction, calcifications, and aggressive periosteal
reaction.
Patients with orbital neuroblastoma metastases present with periorbital ecchymoses (raccoon eyes).
Iodine-123 MIBG scintigraphy is the preferred study to detect bone metastases of neuroblastoma.
Extraconal masses
Dermoid cyst
• Dermoid cysts are congenital ectodermal inclusion cysts made of keratinous and sebaceous
debris. In the extracranial head and neck, the orbital region is the most common site of
dermoids.
• Orbital dermoid cysts are the most common extraconal mass in children. They occur near
suture lines, most commonly in the superolateral quadrant at the zygomaticofrontal suture.
• Imaging shows a circumscribed, unilocular cyst with at most thin rim enhancement,
sometimes causing irregular bone scalloping. The internal contents can be heterogeneous
but a fatty component or fat-fluid level, when present, is characteristic.
Rhabdomyosarcoma
• Rhabdomyosarcoma is the most common extraocular orbital malignancy in children.
• Orbital rhabdomyosarcomas are predominantly the embryonal subtype, which tend to arise
in the superior orbital soft tissues.
• Most orbital rhabdomyosarcomas are extraconal in location, but up to half have intraconal
extension as well.
• Imaging shows a solitary, circumscribed, enhancing soft tissue mass.
• Isolated orbital involvement carries a favorable prognosis relative to parameningeal sites.
Bone invasion and extraorbital extension classifies the tumor as parameningeal.

Infantile hemangioma
• Infantile hemangiomas, previously known as
capillary hemangiomas, are the most common
neoplasms of the head and neck, including
orbits, in infants.
• Infantile hemangiomas are characterized
histologically by capillary-like vascular spaces
lined with GLUT1-expressing endothelium and
clinically by presenting weeks after birth (but
are not present at birth). The course features
proliferation during infancy followed by
spontaneous involution in childhood.
• Infantile hemangiomas can be superficial
(cutaneous “strawberry hemangioma”), deep
(subcutaneous), or combined. Most orbital/ Cavernous hemangioma: Axial T1-weighted post-
periorbital infantile hemangiomas are entirely contrast MRI through the orbits demonstrates
a well-circumscribed, intraconal ovoid mass
or largely extraconal, usually centered in the
(arrows) that demonstrates inhomogeneous,
anterior orbit or eyelid. patchy enhancement.
• Imaging shows a lobulated, intensely enhancing Case courtesy Mary Beth Cunnane, MD,
mass. Internal septations and flow voids on MRI Massachusetts Eye and Ear Infirmary.
are typical.
Peripheral nerve sheath tumors
• Schwannomas and localized neurofibromas are benign peripheral nerve sheath tumors with
indistinguishable imaging appearances when they occur in the orbit. Schwannoma is more
common.
• The most commonly affected nerves are the extraconal sensory branches of CN V1. However,
involvement of intraconal nerves is also possible.
• Nerve sheath tumors are solitary, circumscribed, ovoid masses that are hypointense
on T1-weighted images, hyperintense on T2-weighted images (sometimes with central
hypointensity, called the target sign), and contrast-enhancing.
Lacrimal gland tumors
• The most common lacrimal gland neoplasm is lymphoma.
• Like inflammatory disorders, lymphoma usually appears as diffuse gland enlargement that
molds to orbital structures like putty.
• The most common lacrimal epithelial neoplasm is pleomorphic adenoma (benign mixed
tumor), while the most common epithelial malignancy is adenoid cystic carcinoma.
• Epithelial lacrimal gland tumors are usually masses arising focally from the orbital lobe that
displace orbital structures like a marble (indenting the globe, distorting the extraocular
muscles, and remodeling or destroying orbital walls).
• Epithelial lacrimal gland tumors are unilateral. Bilateral involvement would be more typical
of systemic inflammatory or lymphoproliferative disorders.

Intraconal masses
Optic pathway glioma
Low-grade optic nerve glioma in a young adult:

Axial T1-weighted post-contrast fat suppressed (top
left image), axial T2-weighted fat suppressed (top
right image), and coronal T2-weighted fat suppressed
(bottom left image) MRI through the orbits
demonstrates fusiform, T2 hyperintense enlargement
of the distal right optic nerve (arrows) with no
appreciable enhancement of the lesion.
• Optic pathway gliomas, or simply optic gliomas, are the most common optic nerve tumors.
• Optic gliomas most commonly occur in children. They are the most common central
nervous system tumor in patients with neurofibromatosis type 1 (NF1), in whom bilateral
involvement is frequent.
• The most common histology is pilocytic astrocytoma, an indolent (WHO grade I) tumor with
excellent prognosis. Malignant (high-grade) gliomas can occur in adults.
• On imaging, low-grade optic gliomas appear as fusiform enlargement of the optic nerve with
variable contrast enhancement.

Optic nerve sheath meningioma
Optic nerve-sheath meningioma: Axial

post-contrast fat-sat T1-weighted image
demonstrates marked enhancement
surrounding the left optic nerve with a
tram-track appearance (arrows).
• Meningiomas are the most common tumors arising from the optic nerve sheath.
• Optic nerve meningiomas usually occur in adults with a female predilection and rarely in
children unless associated with neurofibromatosis type 2 (NF2).
• Patients present with slowly progressive visual impairment, classically with preservation of
the central visual field (peripheral constriction).
• On imaging, the nerve sheath appears circumferentially thickened, with uniform contrast
enhancement and often calcifications. The enhancing tumor surrounding the nonenhancing
optic nerve produces the tram-track sign on axial images and doughnut sign on coronal
images.
Cavernous venous malformation
• Venous malformations, previously known as cavernous hemangiomas, are encapsulated
slow-flow vascular malformations that are the most common orbital mass in adults.
• Orbital venous malformations can be located anywhere but are usually intraconal.
• MRI shows a well-defined mass that is isointense on T1-weighted images and hyperintense
on T2-weighted images, demonstrating patchy enhancement that slowly fills in.
Orbital venous varix
• Orbital varices are distended veins freely
connected to the normal circulation, arising
primarily as congenital malformations but
sometimes secondary to arteriovenous
malformations or fistulae.
• Orbital varices represent the most common
cause of spontaneous orbital hemorrhage
but patients usually present with intermittent
positional/stress proptosis.
• Orbital varices appear as ovoid or tubular,
intensely enhancing structures, often
intraconal but not always.
• Varices can be distinguished from other
vascular lesions in that they demonstrate
Delay-phase axial CT angiogram shows bilateral
dynamic distension with maneuvers that
orbital varices.
increase venous pressure such as the Valsalva
maneuver or prone positioning. Doppler
ultrasound demonstrates slow flow.
Ocular masses
Ocular metastases
• Metastases are the most common intraocular malignancies.
• The uvea, typically the choroid, is the most common ocular site for hematogenous
deposition of metastases due to its vascularity.
• The most common primary tumor types are carcinomas, such as breast and lung cancer.
• On imaging, metastases are typically irregular, enhancing masses broadly based on the
choroid.
Uveal melanoma
• Uveal melanoma is the most common primary intraocular malignancy in adults.
• Most cases arise from the choroid or ciliary body and are discovered incidentally on
fundoscopy.
• On imaging, uveal melanoma is usually a mushroom-shaped or biconvex mass based at the
uvea that shows intrinsic T1 hyperintensity and contrast enhancement.
• The most common site of metastasis is the liver.
Retinoblastoma
• Retinoblastoma is the most common primary intraocular malignancy in children.
• Patients usually present in the first few years of life with leukocoria (white pupillary reflex).
• Unilateral cases are usually sporadic,
due to somatic mutations in the
tumor suppressor gene Rb. Bilateral
retinoblastomas are due to heritable
germline mutations in the gene, but
family history is positive only in a
minority.
• On imaging, retinoblastoma appears
as an enhancing retinal mass in a
normal-sized globe. Calcifications are
characteristic.
• Trilateral retinoblastoma describes the
association of bilateral retinoblastoma
with pineoblastoma. The addition of
a suprasellar tumor is quadrilateral
retinoblastoma.
• Survivors of heritable retinoblastoma Retinoblastoma: Noncontrast axial CT through the orbits in
a 20-month old child demonstrates a normal-sized left orbit
treated with radiation have greater
with a coarse retinal calcification (arrow).
risk of a second malignancy many
Case courtesy Mary Beth Cunnane, MD, Massachusetts Eye
years later. The most common are
and Ear Infirmary.
osteosarcoma and leiomyosarcoma.

Pediatric ocular and optic nerve non-neoplastic disorders
Retinopathy of prematurity (ROP)
Retinopathy of prematurity: Noncontrast

axial CT through the orbits shows bilateral
microphthalmia with scattered orbital
calcifications (red arrows). Peripheral high
attenuation material in the right globe (yellow
arrow) represents prior vitreous hemorrhage.
• Retinopathy of prematurity (ROP) is a disorder of retinal neovascularity in preterm infants,

likely incited by hypoxia and hyperoxia. Complications include retinal/vitreous hemorrhage
and detachment.
• On imaging, both globes are small (microphthalmia) and often show increased attenuation
on CT due to prior hemorrhage or neovascularity.
Coats disease
• Coats disease is an idiopathic disorder characterized by retinal telangiectasias and exudates
that lead to retinal detachment.
• Patients with Coats disease are predominantly boys, slightly older than those affected by
retinoblastoma.
• The globe is normal in size but features proteinaceous subretinal fluid that does not
enhance.
Persistent hyperplastic primary vitreous (PHPV)
PHPV: Axial T1- (left image) and T2-weighted MRI through the orbits shows microphthalmia of the right globe
with diffuse T1 hyperintense signal in the vitreous. There is a triangular retrolental soft tissue with linear stalk
extending to the optic nerve head representing hyaloid remnant of the Cloquet canal (arrows).
• Persistent hyperplastic primary vitreous (PHPV) is persistent embryonic vasculature within
the vitreous that leads to hemorrhage, cataracts, and retinal detachment. Affected infants
are typically full term.
• On imaging, there is typically unilateral microphthalmia with increased attenuation/signal of
the vitreous body. Characteristically, there is the martini glass sign of a Y-shaped soft tissue
stalk along the hyaloid (Cloquet) canal of the posterior segment, extending from optic disc
to the lens.

Ocular coloboma
Axial contrast-enhanced CT shows a

large right posterior globe outpouching,
representing a coloboma.
• Colobomas are focal congenital defects (fissure, cleft, or outpouching) typically caused by
incomplete fusion of the embryonic choroidal/optic fissure, but the term can be applied to
defects in any structure in the eye and eyelid.
• Colobomas are associated with numerous syndromes including trisomies 13 and 18 and
CHARGE syndrome (coloboma, heart defects, atresia choanae, retarded growth and
development, genitourinary anomalies, and ear anomalies).
• On imaging, posterior colobomas appear as a focal bulge elongating the globe in the region
of the optic disc. They are often associated with microphthalmia and a retrobulbar cyst.
Septo-optic dysplasia
• Septo-optic dysplasia is part of the holoprosencephaly spectrum of malformations,
characterized by optic nerve hypoplasia, agenesis of the septum pellucidum, and often
hypothalamic-pituitary dysfunction.
• On imaging, the bilateral optic nerves and optic chiasm are small and the septum pellucidum
is absent. The posterior pituitary may be ectopically located.
• In septo-optic dysplasia plus, there is associated polymicrogyria and/or schizencephaly, a
full-thickness cleft in the cerebral hemisphere that creates a communication between the
ventricles and the extra-axial subarachnoid space.
Ocular trauma
Globe rupture and foreign body
• Globe rupture, or open-globe injury, is usually diagnosed on clinical examination but CT can
be helpful in unclear cases or to exclude orbital foreign bodies.
• CT features specific for globe rupture include flat tire sign of globe deformity (wall contour
irregularity and decreased globe volume), change in anterior chamber depth, intraocular
foreign body, or intraocular gas.
• Increased depth of the anterior chamber suggests posterior segment rupture, while
decreased depth suggests anterior segment rupture (e.g., corneal perforation).
• Nonacute mimics include globe outpouchings (coloboma, staphyloma), pthisis bulbi
(atrophic and calcified globe), focal ocular calcifications (optic nerve drusen, senile scleral
plaques), and scleral bands or intraocular gas/air placed to treat retinal detachment.

Ocular detachments and hemorrhage
• Retinal detachment that is complete/extensive takes a “V” configuration, convergent on the
optic disc and extending to the ora serrata. Vitreous, serous, or hemorrhagic fluid fills the
subretinal space (between retina and choroid).
Retinal detachment is most commonly related to retinal tears (rhegmatogenous), which can be traumatic
or, more often, spontaneous related to posterior vitreous detachment. Myopia is a major risk factor.
Non-rhegmatogenous causes consist of exudative effusion (e.g., infection, inflammation, neoplasm) or
traction related to neovascularization.
Retinal detachment: Axial noncontrast

CT shows increased attenuation in the
posterior left globe with a V-shaped
configuration.
• Choroidal detachment takes an hourglass configuration that diverges as it approaches the

optic disc so as to spare the posterior pole of the globe, can extend anteriorly beyond the
ora serrata, and can appose the retina at the convexities (kissing choroid sign). Serous or
hemorrhagic fluid fills the suprachoroidal space (between choroid and sclera).
The most common cause of choroidal detachment is ocular hypotony, which can be traumatic or, more
often, related to recent surgery. Other causes are inflammatory, neoplastic, or vascular.
Choroidal detachment in two different patients:

Axial noncontrast CT (left image) shows extensive hyperdense hemorrhage in the left globe, including
choroidal detachment with subchoroidal hemorrhage resulting in the kissing choroid sign (yellow arrow).
There is also contour abnormality at the posterior globe concerning for open globe injury (red arrow).
Axial contrast-enhanced CT (right image) demonstrates choroidal detachment of the left globe with
hypodense subchoroidal blood products in an hourglass configuration. This was thought to be secondary
to intraocular metastatic squamous cell carcinoma, as suggested by the nodular enhancement at the
posterior globe (blue arrow), which was confirmed on subsequent MRI.
• Vitreous hemorrhage appears as hyperattenuation of the posterior segment on CT.
Causes of vitreous hemorrhage include trauma (including abusive head trauma in young children),
spontaneous vitreous detachment and/or retinal tear, and conditions causing retinal neovascularity.
Terson syndrome is the association of vitreous hemorrhage (and/or retinal hemorrhage) secondary to
intracranial subarachnoid hemorrhage, likely related to elevated intracranial pressure.
Nonacute mimics include intraocular silicone oil used to treat retinal detachment.

Lens dislocation
• Rupture of the zonular fibers that attach the lens to the ciliary body can result in
displacement of the lens posteriorly or, less commonly, anteriorly.
• In partial dislocations, the lens appears angled into the vitreous humor. In complete
dislocations, the lens usually lies in the dependent portion of the vitreous.
• Trauma is the most common cause of lens dislocation. The most common nontraumatic
cause of lens dislocation (ectopia lentis) is Marfan syndrome.
Retrobulbar hemorrhage
• Retrobulbar hemorrhage is an accumulation of blood in the soft tissues behind the globe,
which is usually due to blunt orbital trauma.
• Traumatic retrobulbar hemorrhage is the most common cause of orbital compartment
syndrome, which is a clinical diagnosis of elevated intraorbital pressure that impairs ocular
perfusion. Soft tissue emphysema can also contribute to intraorbital pressure. Imaging may
show proptosis, tenting of the posterior globe, and straightening of the optic nerve.
Carotid-cavernous fistula
Left carotid-cavernous fistula: Axial CT angiogram shows arterial phase filling of an enlarged left superior
ophthalmic vein (left image, yellow arrow) and a distended left cavernous sinus (right image, red arrow).
• Carotid-cavernous fistulas are arteriovenous fistulas that connect the carotid tree to the
cavernous sinus.
• Direct/high-flow fistulas (involving the cavernous internal carotid artery) are most common,
usually due to trauma presenting acutely in young men. Indirect fistulas involve low-flow
shunts from meningeal branches of the internal or external carotid arteries, presenting
insidiously in postmenopausal women.
• Indirect clues on imaging are signs of orbital congestion like fat stranding, extraocular
muscle enlargement, and proptosis. CTA shows asymmetric enlargement and early contrast
enhancement of the cavernous sinus and superior ophthalmic vein.

Face
Facial fractures
Overview
• Complex facial fractures are best described with respect to a handful of regional fracture
patterns with attention to form and function rather than as a laundry list of bones or
buttresses involved.
• Displacement, fragmentation, bone loss, as well as region-specific anatomic considerations
are important descriptors that influence treatment strategy.
• A combination of multiplanar reformatted and 3D volume-rendered CT images are often
helpful for diagnosis and surgical planning.
• A panfacial fracture involves all thirds of the face: frontal bone, midface, and mandible.
frontal sinus fractures
naso-orbito-ethmoid
(NOE) fractures
nasoseptal fractures
zygomaticomaxillary
complex (ZMC) fractures
Le Fort fractures
mandibular fractures
Frontal sinus fractures

• The management of frontal sinus fractures depends on the sites involved (anterior table,
posterior table, and frontal recess), displacement, and comminution.
• Involvement of the posterior table (which occurs almost always in addition to anterior table
fracture) confers risk of CSF leak and intracranial infection.
• Disruption of the frontal recess (frontonasal duct) confers risk of frontal sinus mucocele/
mucopyocele development.
Orbital fractures
• Fractures of the orbital rims and/or walls are part of several midface fracture complexes
discussed separately below: naso-orbito-ethmoid, zygomaticomaxillary complex, and Le Fort
II and III.
• An orbital blowout fracture refers to a pure internal orbital fracture, which involves an
orbital wall but spares the orbital rim, that expands the orbital volume. The most common
types are orbital floor blowout, followed by medial orbital wall blowout.

Orbital fractures (continued)
• A trapdoor fracture is a special type of orbital floor blowout that usually occurs in children
where the inferiorly displaced fracture fragment recoils and entraps herniated orbital
soft tissue, which can cause restricted motility or necrosis of the inferior rectus muscle.
Entrapment is a clinical diagnosis.
• Large orbital blowouts (e.g., >2 cm2 defect area or >1.5 mL outward herniated volume)
predict the development of noticeable enophthalmos after the acute swelling subsides.
Naso-orbito-ethmoid fractures
• Naso-orbito-ethmoid (NOE) fractures involve the upper central midface, classically along 5
key edges: from the pyriform aperture across the lateral nasal wall, inferior orbital rim and
floor, medial orbital wall, frontomaxillary suture, and nasomaxillary suture.
• NOE fractures are classified by the morphology of the central fragment where the medial
canthal tendon inserts:
Type I: noncomminuted large central fragment.
Type II: comminuted central fragment not disrupting area of medial canthal tendon insertion.
Type III: comminuted central fragment disrupting area of medial canthal tendon insertion.
• Displaced NOE fractures can cause telecanthus (increased distance between the medial
corners of the eyes) and obstruction of nasolacrimal and frontal sinus drainage pathways.
Nasoseptal fractures
• Nasal fractures are the most common facial fractures. Isolated nasal fractures should be
distinguished from more serious naso-orbito-ethmoid fractures.
• Most commonly, lateral-oblique forces fracture the bony nasal pyramid (nasal bones and/or
frontal processes of the maxillae). Frontal forces additionally involve the anterior nasal spine
and/or cartilaginous or bony nasal septum.
• Associated septal hematoma can cause necrosis of the cartilage and subsequent saddle nose
deformity.
Le Fort fractures
Le Fort I Le Fort II Le Fort III
Fracture involves lateral margin Pyramidal fracture, involves Fractures involve the
of the pyriform (nasal) aperture the inferior orbital rim, along zygomatic arch, along with
with the orbital floor and the lateral and medial orbital
Allows free movement of the medial orbital wall. walls.
hard palate (floating palate).
Allows free movement of the Allows free movement of the
nose and hard palate (floating entire midface (craniofacial
maxilla). dissociation).

Le Fort fractures (continued)
• Le Fort midfacial fractures detach the involved maxillary occlusion-bearing segment (palate,
alveolus, and maxillary teeth) from the skull base (pterygomaxillary disjunction).
• All Le Fort fractures involve the pterygoid plates of the sphenoid bone and maxillary sinus
walls. Le Fort fractures are classified by the anterosuperior course of the fracture lines,
which can occur alone or in combination on each side of the face (see illustration above).
• Displaced Le Fort fractures at any level can result in malocclusion or midfacial deformity.
Associated palatal fractures are common and contribute to malocclusion.
• The non-occlusion-related components of the upper level Le Fort fractures can be treated
as combinations of naso-orbito-ethmoid, zygomaticomaxillary complex, and/or orbital
fractures. However, the reporting of Le Fort II and III fractures remains relevant as they
are included among the Denver screening criteria for blunt cerebrovascular injury, which
warrants CTA of the neck arteries and circle of Willis.
Zygomaticomaxillary complex fractures
zygomaticofrontal suture
zygomaticotemporal suture
zygomaticosphenoid suture
zygomaticomaxillary suture
• A complete zygomaticomaxillary complex (ZMC) fracture liberates a tetrapod fragment via

suture diastasis or fracture near the 4 articulations of the zygoma:
Zygomaticofrontal suture: along lateral orbital rim.
Zygomaticomaxillary buttress: from inferior orbital rim and floor through maxillary sinus walls.
Zygomaticotemporal suture: along zygomatic arch.
Zygomaticosphenoid suture: along lateral orbital wall.
• Also possible are incomplete fractures that involve an isolated limb of the ZMC, such as the
zygomatic arch, lateral orbital rim/wall, or inferior orbital rim.
• The appearance of the zygomaticosphenoid suture (e.g., displacement, angulation,
telescoping) is a sensitive landmark for evaluating overall ZMC alignment.
• Displacement or malalignment of ZMC fractures disrupt facial profile and width.
• Because the orbital floor is involved in classic ZMC fractures, they are sometimes called
orbitozygomatic fractures. As with other internal orbital fractures, ZMC fractures with
significant orbital volume expansion can cause late enophthalmos.

Mandibular fractures
• Mandibular fractures are the second most common facial fractures and lead to
malocclusion.
• Mandibular fractures are described by the anatomic segments involved: condylar process
(further divided into head, neck, and base), coronoid process, ramus and angle, body (from
third molar to canine), and parasymphysis/symphysis.
• Given its ring-like structure, mandibular fractures are more likely than not to occur at
multiple sites.
A guardsman fracture is the association of parasymphyseal and bilateral condylar fractures of the
mandible.
• Fractures that extend to the periodontal ligament space of an erupted tooth should be
specially noted as they are managed as open (contaminated) fractures.
• Displaced or complex mandibular fractures, particularly those involving the condyles, are
associated with increased risk of blunt vascular injury and therefore warrant a neck CTA.
Dentoalveolar trauma
• Tooth fractures are classified by involvement of the crown, root, or both. Crown fractures
are categorized by involved layers: enamel-only, enamel-dentin, or enamel-dentin-pulp.
• Partial axial displacement of a tooth may be directed out of or into its socket, known as
extrusive and intrusive luxation, respectively. Avulsion refers to complete displacement out
of the socket.
• Fractures of the alveolar process can spare the socket or involve the socket and allow
eccentric displacement of a tooth from its socket, which is called lateral luxation.

Salivary glands
Overview and anatomy of the salivary glands
Overview
• The major salivary glands are, in order of decreasing size, the parotid, submandibular, and
sublingual glands.
• There are also numerous unnamed minor salivary glands throughout the mucosa of the
head and neck, especially the palate.
• Neoplasms in smaller glands are more likely to be malignant, with the risk highest in
sublingual and minor salivary glands, followed by the submandibular gland, and least in the
parotid gland.
Parotid glands
• The parotid glands are divided by the facial nerve into superficial and deep lobes. Since the
facial nerve is not normally visible on imaging, radiologists use the retromandibular vein as
the demarcation.
• The deep lobe extends through the stylomandibular tunnel into the prestyloid
parapharyngeal space, discussed later in this chapter.
• The inferior projection of the superficial lobe overlying the angle of the mandible is called
the parotid tail.
• The parotid glands are the only salivary glands to contain internal lymph nodes, mostly
located in the superficial lobe along the retromandibular vein.
• Accessory parotid glands may be located along the parotid duct, which is also called Stensen
duct, superficial to the masseter muscle.
Submandibular gland
• The submandibular glands sit partly in the floor of the mouth (sublingual space) and mostly
in the neck (submandibular space). Each gland wraps around the posterior margin of the
mylohyoid muscle, which separates the floor of the mouth from the neck.
• The gland may remodel the adjacent inner surface of the angle of the mandible, causing a
normal variant depression called a Stafne bone cavity/cyst.
• The submandibular duct, which is also called Wharton duct, opens on the side of the
frenulum of the tongue.
Sublingual gland
• The sublingual glands sit at the anterior aspect of the floor of the mouth.
• Although normally confined to the sublingual space, the gland may herniate into the
submandibular space through a normal variant discontinuity in the mylohyoid muscle called
a mylohyoid boutonnière.
• The sublingual glands drain via numerous small ducts, collectively termed Rivinus ducts,
which may form a larger common duct, the Bartholin duct, that empties into the Wharton
duct.

Benign salivary neoplasm
Pleomorphic adenoma
Pleomorphic adenoma: Axial T2-weighted (top left

image), T1-weighted (top right image), and post-
contrast fat saturated T1-weighted (bottom left
image) MRI shows a T2 hyperintense, T1 hypointense,
enhancing circumscribed mass (arrows) in the anterior
aspect of the superficial left parotid.
• Pleomorphic adenoma, also called benign mixed tumor, is the most common salivary gland
tumor, accounting for 70% of all salivary tumors, and is most common in the parotid gland.
• The typical patient is a middle-aged female.
• MRI shows a well-defined mass with bosselated margins (small undulations), very high signal
intensity on T2-weighted images, and strong contrast enhancement. Large pleomorphic
adenomas can have heterogeneous signal.
• Although pleomorphic adenoma is benign, there is risk of malignant transformation. The
standard treatment for parotid pleomorphic adenoma is superficial parotidectomy.
Warthin tumor
• Warthin tumor, also called papillary cystadenoma lymphomatosum or adenolymphoma, is
the second most common benign parotid neoplasm.
• The typical patient is an elderly male. The vast majority are smokers.
• Imaging shows a well-defined but heterogeneous mass in the parotid gland with
weak contrast enhancement and, in a significant minority of cases, complicated cystic
components.
• Multifocality or bilaterality accounts for up to 20% of cases of Warthin tumors, making them
the most common multifocal or bilateral parotid neoplasms. They have a predilection for the
parotid tail region.
• Compared to pleomorphic adenoma, malignant transformation of Warthin tumor is rare.

Malignant parotid neoplasm
Mucoepidermoid carcinoma
• Mucoepidermoid carcinomas are the most common primary salivary gland malignancy,
especially in the parotid gland.
• Low-grade mucoepidermoid carcinoma typically appears as a well-defined, enhancing mass
that is hyperintense on T2-weighted images. This appearance is indistinguishable from
benign pleomorphic adenoma on MRI.
• High-grade mucoepidermoid carcinoma has infiltrative margins and lower signal on T2-
weighted images.
Adenoid cystic carcinoma
Adenoid cystic carcinoma with perineural spread:

Axial post-contrast T1-weighted MRI demonstrates
(top left image) a heterogeneously enhancing right
parotid mass involving the superficial and deep lobes
(yellow arrows).
Axial (top right image) and coronal (bottom left image)
post-contrast T1-weighted MRI through the skull base
shows asymmetric enlargement and enhancement
of the V3 division of the right trigeminal nerve and
associated enlargement of the right foramen ovale
(red arrows), consistent with perineural tumor spread.
• Adenoid cystic carcinomas are the most common primary malignancy of the submandibular,
sublingual, and minor salivary glands. They are also the second most common primary
parotid gland malignancy.
• Among head and neck malignancies, adenoid cystic carcinoma has the highest risk of
perineural spread, which portends a poor prognosis. However, the most common histology
of head and neck cancers to show perineural spread is squamous cell carcinoma.
• Adenoid cystic carcinoma has a high risk of local recurrence and metastasis.
Carcinoma ex pleomorphic adenoma
• Pleomorphic adenoma can undergo malignant transformation to so-called carcinoma ex
pleomorphic adenoma. The risk accumulates over many years.
• The typical patient is an elderly person with a long-standing parotid mass that is newly
associated with rapid enlargement, pain, or facial nerve palsy.
• In contrast to pleomorphic adenoma, carcinoma ex pleomorphic adenoma is hypointense on
T2-weighted images and shows low ADC values. The malignancy is infiltrative, showing ill-
defined borders and possible extension beyond the gland parenchyma.
Metastases
• Metastases to the parotid nodes (both within the gland and surrounding it) most commonly
occur from cutaneous malignancies on the lateral side of the head, usually squamous cell
carcinoma.
• On imaging, a round parotid mass larger than 6 mm, sometimes with central necrosis or ill-
defined margins, is suggestive of nodal metastasis in patients with a history of scalp or face
skin cancer or concurrent cervical nodal metastases from other primary tumors.
Lymphoma
• Salivary gland lymphomas are rare. Most are non-Hodgkin B-cell lymphomas, particularly
extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT
lymphoma).
• Sjögren syndrome is a strong risk factor, although most instances of salivary gland
lymphoma are not associated. Any new dominant parotid mass in the setting of Sjögren
syndrome should raise concern for lymphoma.
Inflammatory salivary disease

Sialadenitis and sialolithiasis
• Sialolithiasis (stones within salivary ducts or glands) is the most common cause of acute
unifocal sialadenitis, due to obstruction of the drainage and resultant gland inflammation.
• The vast majority of salivary calculi and, in turn, cases of sialadenitis, occur in the
submandibular gland and duct, due to its relatively viscous secretions and uphill drainage
course.
• Suppurative (acute bacterial) sialadenitis can occur without sialolithiasis, predominantly
involving the parotid gland in elderly patients, often in the setting of recent surgery,
intubation, dehydration, or poor oral hygiene.
• The most common causes of multifocal/bilateral sialadenitis in children are juvenile
recurrent parotitis (chronic parotitis) and mumps viral parotitis.
Iodine-related sialadenopathy
• Radioiodine sialadenitis is a common, dose-dependent side effect of iodine-131 therapy
for thyroid cancer. Patients have transient salivary gland swelling and pain with decreased
salivary flow.
• Iodide sialadenitis, also known as iodide mumps, is a rare, idiosyncratic, non-allergic
adverse reaction to iodinated contrast media administration. Patients have self-limited
painless salivary gland swelling minutes to days after contrast-enhanced CT or angiography.
HIV-related benign lymphoepithelial lesions
HIV lymphoepithelial lesions:

Axial contrast-enhanced CT
through the parotid glands
shows numerous peripherally
enhancing cystic lesions
bilaterally (arrows).
Case courtesy Mary Beth
Cunnane, MD, Massachusetts
Eye and Ear Infirmary.

• HIV infection is frequently associated with benign lymphoepithelial lesions, which are mixed
solid and cystic masses representing reactive lymphoid infiltration that causes proliferation
of ductal epithelium with cystic change.
• Benign lymphoepithelial lesions almost always involve the parotid gland. They are
the most common parotid lesions in patients with HIV infection. Concurrent cervical
lymphadenopathy is an additional clue on imaging for HIV infection.
Sarcoidosis
• Sarcoidosis occasionally involves the parotid glands with granulomatous inflammation,
typically presenting as bilateral painless gland swelling.
• Heerfordt syndrome, or uveoparotid fever, is the rare but pathognomonic presentation of
sarcoidosis as bilateral uveitis, parotitis, and facial nerve palsy.
• The panda sign of sarcoidosis is the finding on the obsolete gallium-67 scan of radiotracer
uptake in bilateral lacrimal and parotid glands, superimposed on physiologic nasopharyngeal
uptake.
Sjögren syndrome
Sjögren syndrome: Coronal post-contrast T1-weighted (left image) and axial T2-weighted MRI with fat
suppression shows numerous small, T2 hyperintense lesions in the left parotid (arrows), which demonstrate
minimal peripheral enhancement.
• Sjögren syndrome is an autoimmune disorder affecting the salivary and lacrimal glands.
• The typical patient is a middle-aged female. The disorder can be either primary or secondary
to another autoimmune disorder (most commonly rheumatoid arthritis or systemic lupus
erythematosus).
• MRI shows a salt-and-pepper or honeycomb appearance of bilateral parotid glands: multiple
areas of high signal intensity mixed with discrete areas of low signal intensity on both T1-
and T2-weighted images, which represent a combination of benign lymphoepithelial lesions
(also known as lymphoepithelial sialadenitis) with fibrosis, punctate calcifications, and fatty
infiltration.
IgG4-related disease
• IgG4-related disease is a multisystem fibroinflammatory disorder, which can involve the
submandibular and, less often, parotid glands.
• Mikulicz syndrome refers to diffuse IgG4-related chronic sclerosing sialadenitis and
dacryoadenitis.
• Küttner tumor is a term for focal IgG4-related chronic sclerosing sialadenitis involving the
submandibular gland.

Miscellaneous salivary lesions
First branchial cleft cyst (BCC)
Axial T2-weighted (left image) and T1 post-contrast MRI shows a left infra-auricular cystic lesion (arrows) along
the superficial margin of the left parotid gland, thought to represent a first brachial cleft cyst.
• Branchial apparatus (pouch or cleft) remnants include cysts, as well as sinuses and fistulas.
• Branchial cleft cysts are most common and usually appear as a simple cyst. However,
superinfection or hemorrhage can cause internal debris or wall thickening.
• First branchial cleft cysts are located between the external auditory canal and the
submandibular region, most frequently within the parotid gland.
Sialocele
Axial contrast-enhanced CT shows an

ovoid fluid-density lesion (arrow) in the
left sublingual space, adjacent to the
sublingual gland, thought to represent
a sialocele.
• Sialoceles are focal pseudocysts of saliva due to gland/duct disruption, such as due to
postobstructive rupture, trauma, or surgery.
• Sialoceles are most commonly related to the parotid gland.
Sialadenosis
• Sialadenosis refers to chronic diffuse enlargement of the major salivary glands (typically the
parotid) due to acinar hypertrophy.
• The major risk factors are nutritional and hormonal disturbances, such as diabetes mellitus,
alcohol use disorder, and eating disorders.

Central skull base and sella
Overview and anatomy of the sellar and parasellar regions
Sellar and parasellar region
• The sella turcica is a saddle-shaped depression of the sphenoid bone, which creates the
space for the pituitary gland.
• The anterior wall of the pituitary fossa is the tuberculum sellae. The posterior wall is the
dorsum sellae. The roof is the diaphragma sellae, a dural reflection.
• The parasellar region includes the cavernous sinuses, suprasellar cistern, and hypothalamus.
Pituitary gland
• The pituitary is composed of an anterior and a posterior lobe.
• The anterior pituitary (adenohypophysis) produces and secretes the following hormones:
growth hormone (GH), prolactin, follicle-stimulating hormone (FSH), luteinizing hormone
(LH), adrenocorticotrophic hormone (ACTH), and thyroid-stimulating hormone (TSH). The
anterior pituitary gland is formed from Rathke pouch, which is a superior invagination of
primitive oral ectoderm.
Rathke pouch normally involutes. Sometimes, a cleft can be left behind, which may give rise to
craniopharyngioma or Rathke cleft cyst.
• The posterior pituitary (neurohypophysis) and infundibulum (pituitary stalk) are the
projection from the hypothalamus that transports and secretes antidiuretic hormone (ADH),
vasopressin) and oxytocin. The posterior pituitary gland is formed from neuroectoderm.
The normal posterior pituitary is hyperintense on T1-weighted MRI due to stored ADH and is called the
posterior pituitary bright spot, best seen on sagittal images. Loss of the posterior pituitary bright spot has
been associated with central diabetes insipidus but also occurs in some normal patients.
The posterior pituitary normally descends from the diencephalon. Sometimes, the downward extension is
halted, resulting in an ectopic posterior pituitary, usually at the median eminence (inferior aspect of the
hypothalamus).
The combination of ectopic posterior pituitary with an absent or hypoplastic infundibulum and anterior
pituitary is known as pituitary stalk interruption (transection) syndrome.
Normal posterior pituitary bright spot (arrow) Sagittal T1-weighted MRI shows absence of the normal
on sagittal T1-weighted MRI. posterior pituitary bright spot and an intrinsically T1
hyperintense nodule within the infundibulum (arrow),
likely an ectopic posterior pituitary.
• The pituitary gland enhances on dynamic contrast-enhanced MRI in accordance with
its blood supply: first the infundibulum and posterior pituitary, followed by the anterior
pituitary, which is supplied by the hypophyseal portal system. The entire gland enhances
homogeneously between 30–60 seconds and then washes out.

Cavernous sinus
optic nerve optic chiasm
supraclinoid
carotid
cavernous CN III oculomotor nerve
superior orbital fissure

carotid pituitary all extraocular muscles except SO & LR
gland CN IV trochlear nerve
superior oblique (SO)
exit
CN VI abducens nerve
cavernous lateral rectus (LR)
sinus CN V1 ophthalmic division
sensory forehead region
sphenoid
sinus CN V2 maxillary division
sensory cheek region
exits foramen rotundum
nasopharynx
CN VI and sympathetic fibers around the carotid artery are located within the center of the cavernous sinus, while
the other cranial nerves travel within the cavernous sinus wall.
The mandibular nerve (V3) is the only segment of the trigeminal nerve that does not traverse the cavernous sinus.
It exits inferiorly from Meckel’s cave through foramen ovale.
The abducens nerve (VI) enters the petrous portion of the temporal bone through Dorello’s canal and is the only
nerve that travels in the medial venous sinusoids.
The maxillary nerve (V2) is the only nerve of the cavernous sinus that does not exit the superior orbital fissure.
Instead, it exits foramen rotundum.
• The cavernous sinuses are paired dural venous sinuses of the middle cranial fossae on either
side of the sella turcica, connected by the variable intercavernous sinuses.
• The cavernous sinus drains the (superior and inferior) ophthalmic veins and sphenoparietal
sinus.
The cavernous sinus is the most frequently involved dural sinus with infection and thrombosis (septic
thrombophlebitis). Infection may spread from the central face (“danger zone”), paranasal sinuses, teeth,
or orbits (discussed previously in the orbital infection section).
• The cavernous sinus drains via the superior and inferior petrosal sinuses to the sigmoid sinus
and jugular bulb, respectively. There are also connections to the pterygoid venous plexus
and basilar (clival) plexus.
Inferior petrosal sinus sampling (via the internal jugular vein) is performed to demonstrate pituitary ACTH
hypersecretion in cases of suspected Cushing disease.
• The internal carotid artery traverses the cavernous sinus. Rupture results in a direct
caroticocavernous fistula (discussed previously in the ocular trauma section).
• The cavernous sinus contains cranial nerves III, IV, VI, V1, and V2, and sympathetic fibers. CN
VI and sympathetics around the carotid artery are located within the center of the sinus,
while the other cranial nerves course between two dural layers within the lateral wall.
• The lateral wall of the cavernous sinus is normally concave or straight. Outward bulging
suggests involvement with a lesion, whether neoplastic, vascular, or inflammatory.
• Cavernous sinus syndrome consists of clinical signs and symptoms attributable to cavernous
sinus pathology, particularly neurologic deficits (ophthalmoplegia, facial sensory loss, Horner
syndrome) and orbital/ocular congestion (chemosis, proptosis). Pain/headache may be
present, especially in inflammatory disorders such as Tolosa-Hunt syndrome.

Suprasellar cistern
• The suprasellar cistern is the pentagonal basal cistern located above the sella, under the
hypothalamus, between the unci of the temporal lobes, and anterior to the interpeduncular
cistern.
Supratentorial mass effect with uncal herniation effaces the suprasellar cistern from the side(s).
Spontaneous intracranial hypotension reduces the height of the suprasellar cistern.
• Multiple important neurovascular structures traverse the suprasellar cistern: Optic nerves
and chiasm, infundibulum, and circle of Willis.
Intrasellar lesions
Pituitary adenoma
Microadenoma: Coronal T2-weighted (left image) and sagittal T1 post-contrast MRI (right image) shows a
subcentimeter T2 hyperintense, hypoenhancing lesion in the central pituitary gland (arrows).
• Adenomas are by far the most common intrinsic pituitary mass but can have suprasellar
extension when large.
• Adenomas are classified by size as microadenomas (<10 mm) or macroadenomas (≥10 mm).
They are also classified by hormonal production, with the most common being lactotroph
and nonfunctioning adenomas.
• Patients present with symptoms of endocrine dysfunction (hypogonadism, acromegaly,
Cushing disease, or hyperthyroidism) or, in the case of macroadenomas, mass effect (visual
field deficits due to optic pathway compression, headache).
Rarely, patients present with pituitary apoplexy, a clinical syndrome of severe headache, visual
impairment, and hypopituitarism caused by sudden hemorrhage into the pituitary. The typical cause is
pituitary adenoma.
Sheehan syndrome refers to pituitary apoplexy in postpartum women associated with hypopituitarism.
In the acute phase, imaging shows an enlarged pituitary gland possibly with high intrinsic T1 signal due to
hemorrhage. Over time, the pituitary atrophies, leaving a partially empty sella.
• Most cases are sporadic but syndromic causes include multiple endocrine neoplasia type 1
(MEN1).
• Microadenomas usually appear on MRI as foci of subtle signal abnormality within the gland
on conventional sequences, but contrast-enhanced sequences improve sensitivity. Most
microadenomas show delayed enhancement relative to the normal pituitary, which appears
hypoenhancing based on the timing of most post-contrast protocols. Dynamic imaging with
early and delayed phases is needed to detect a small subset of microadenomas.
Pituitary adenoma (continued)
• As adenomas are typically slow-growing, macroadenomas enlarge and remodel the sella.
• Pituitary macroadenomas can invade the cavernous sinus and encase the internal carotid
artery. High risk of invasion is predicted on preoperative coronal MR images when the tumor
extends laterally beyond the tangent line connecting the lateral walls of the supraclinoid and
cavernous internal carotid artery segments. Complete encasement of the internal carotid
artery certainly indicates cavernous sinus invasion but this sign occurs late.
• As adenomas are typically soft, the diaphragma sellae can indent macroadenomas that
extend into the suprasellar cistern, creating the snowman sign (also known as a figure-of-8,
dumbbell, hourglass, or bottleneck configuration). They tend not to narrow the internal
carotid artery (whereas meningiomas or metastases can narrow the carotid).
• Macroadenomas can be heterogeneous due to cystic change, necrosis, or hemorrhage.
Hemorrhagic pituitary adenoma is the most common sellar region lesion with intrinsic T1
hyperintensity, especially with a fluid level.
Macroadenoma: FLAIR (left image) and post-contrast sagittal T1-weighted MRI shows complete replacement of
the pituitary gland by an enhancing mass (yellow arrows). The optic chiasm is displaced superiorly (red arrow).
Pituitary hyperplasia
• The normal pituitary varies widely in size depending on age, sex, and hormonal status.
• Physiologic pituitary hyperplasia commonly occurs in periods of hormonal activity like
adolescence, pregnancy, and perimenopause.
• Pathological pituitary hyperplasia is usually related to end-organ insufficiency, especially
primary hypothyroidism.
• On imaging, pituitary hyperplasia appears as a homogeneously enlarged gland with a convex
superior margin.
Hypophysitis
• Hypophysitis refers to inflammatory infiltration of the pituitary gland and sometimes also
infundibulum. It is classified by histology, with lymphocytic being most common, followed by
granulomatous and plasmacytic.
• Lymphocytic hypophysitis usually occurs in women, typically in the peripartum period. It is
also a side effect of checkpoint inhibitor immunotherapy (e.g., ipilimumab and nivolumab).
• Granulomatous hypophysitis can be idiopathic or secondary to systemic disorders such as
sarcoidosis or granulomatosis with polyangiitis (Wegener’s).
• Plasmacytic hypophysitis is a rare IgG4-related disease.
• MRI shows diffuse enlargement of the pituitary gland, and often the infundibulum, with
homogeneous enhancement.

Rathke cleft cyst
Rathke’s cleft cyst: Axial FLAIR (left image) and coronal post-contrast T1-weighted MRI shows a FLAIR
hyperintense, T1 hypointense parasellar mass (yellow arrows). The mass demonstrates faint peripheral rim
enhancement. The pituitary is displaced to the right and the optic chiasm is displaced superiorly (red arrow).
• Rathke cleft cyst is a remnant of the embryologic Rathke pouch lined with simple columnar
or cuboidal epithelium. They are typically intrasellar with or without suprasellar extension.
• Rathke cleft cysts are typically seen in middle-aged adults, twice as commonly in females.
• Rathke cleft cyst is reportedly very common in autopsy studies (up to 22% incidence), but
clinically is usually asymptomatic or discovered incidentally.
• On imaging, Rathke cleft cyst is a nonenhancing cyst without calcification. An enhancing rim
may be seen related to the pituitary tissue wrapped around the cyst (claw sign). A small,
nonenhancing intracystic nodule, likely a clump of mucin, is pathognomonic.
• The MR signal characteristics depend on the protein content of the cyst fluid. The intra-
cystic fluid may be isointense to CSF if low protein and hyperintense on T1-weighted images
if high protein. High protein content may cause incomplete nulling of the intracystic fluid on
FLAIR.
Empty sella
• The (partially) empty sella is mostly filled with CSF and possibly slightly enlarged, due to
herniation of the subarachnoid space (sometimes known as intrasellar arachnoidocele). The
small pituitary gland is flattened against the floor of the sella.
• The infundibulum sign, in which the pituitary stalk traverses this space, distinguishes empty
sella from true cystic intrasellar lesions.
• Primary empty sella can be a normal variant, especially in older patients, related to
insufficiency of the diaphragma sellae, or be caused by intracranial hypertension.
• Empty sella is one of a constellation of findings in idiopathic intracranial hypertension
(pseudotumor cerebri), which is a syndrome attributed to elevated CSF pressure in the
absence of intracranial mass or hydrocephalus.
Patients with idiopathic intracranial hypertension, who are typically female and obese, present with
headache, transient visual obscurations, and/or pulsatile tinnitus.
The main imaging findings are empty sella, papilledema/posterior scleral flattening, optic nerve sheath
dilation, bilateral transverse sinus stenosis, cerebellar tonsillar ectopia, and meningoceles of Meckel's cave
or petrous apex.
• Secondary empty sella is related to prior pituitary disease. Gland shrinkage may reflect
sequela of treated pituitary tumors, pituitary apoplexy, Sheehan syndrome, or trauma.
Suprasellar / parasellar mass
Overview
• The differential diagnosis for a parasellar/suprasellar lesion is broad, but the imaging
findings together with the patient's age and clinical presentation can usually narrow the
differential diagnosis to a few entities.
• The MOuSTACHE mnemonic may be helpful to remember the spectrum of parasellar/
suprasellar lesions, albeit not in order of prevalence:
Meningioma/Metastasis.
Optic pathway glioma.
Sellar lesion with suprasellar/parasellar extension (e.g., macroadenoma).
Teratoma and other germ cell tumors (e.g., germinoma).
Aneurysm.
Craniopharyngioma.
Hypothalamic glioma or hamartoma.
Epidermoid/dermoid cyst.
• In adults, the most common suprasellar neoplasm is pituitary macroadenoma that has
extended superiorly. The second most common suprasellar neoplasm and most common
parasellar/cavernous sinus neoplasm is meningioma. The most common nonneoplastic
parasellar mass is an arterial aneurysm.
• In children, the most common suprasellar neoplasms are craniopharyngioma, followed by
gliomas of the optic pathway or hypothalamus. A distinct subset of pediatric suprasellar
neoplasms are those arising from the infundibulum, of which the most common are germ
cell tumors and Langerhans cell histiocytosis.
Meningioma
• Meningiomas can arise anywhere along the skull base meninges, including the planum
sphenoidale, anterior clinoid processes, tuberculum sellae, diaphragma sellae, dorsum
sellae, and cavernous sinus wall.
• As with meningiomas elsewhere, these tumors show uniform, intense contrast
enhancement often with a dural tail. Meningiomas may cause adjacent hyperostosis due to
vasoactive factors.
• An important imaging finding of a parasellar meningioma is possible encasement and
narrowing of the cavernous or supraclinoid internal carotid artery.
Aneurysm
• The suprasellar/parasellar region is the most common site of giant intracranial aneurysms.
These typically arise from the supraclinoid or cavernous internal carotid artery.
• Aneurysms are an important entity to consider in the differential diagnosis of suprasellar/
parasellar tumors to avoid a catastrophic biopsy.
• Pulsation artifact or a flow void may be present on conventional MRI sequences. CTA or
MRA would be diagnostic.
Metastases
• Malignancies rarely metastasize to the pituitary gland and stalk.
• Breast cancer is the most common primary tumor to metastasize to the suprasellar/
parasellar region. Other tumors include lung cancer, lymphoma, and prostate cancer.

Craniopharyngioma
Craniopharyngioma: Noncontrast CT (left image) shows a hypoattenuating suprasellar mass (arrows)

containing coarse calcifications. The suprasellar cistern is effaced. FLAIR MRI (middle image) shows an
isointense, primarily solid suprasellar mass. Post-contrast T1-weighted (right image) MRI shows avid
heterogeneous enhancement. There is a small cystic focus anteriorly (red arrow).
• Craniopharyngiomas are benign (WHO grade I) neoplasms arising from Rathke pouch
remnants that produce keratin.
• Most craniopharyngiomas are suprasellar, although they may extend into or rarely arise
within the sella.
• Craniopharyngioma occurs in a bimodal age distribution but more commonly occurs in
children.
• In children, most craniopharyngiomas are the adamantinomatous subtype, which are
complex cystic, lobulated masses with calcifications (similar to enamel). The cyst fluid is
typically proteinaceous (described as machine oil or motor oil), which has a hyperintense
appearance on T1-weighted images.
• In adults, the papillary subtype is more common, which typically appears as a predominantly
solid, enhancing, spherical, non-calcified mass.
Germ cell tumors
• Intracranial germ cell tumors arise in the midline, with the majority in the pineal region and
next most commonly in the suprasellar region.
• The majority of intracranial germ cell tumors are germinomas. Nongerminomatous germ cell
tumors include teratoma, embryonal carcinoma, endodermal sinus tumor, choriocarcinoma,
and mixed tumors.
• The incidence peaks during adolescence.
• Imaging shows a homogeneous, intensely enhancing midline mass. The mass is hypointense
on T2-weighted images and dark on ADC map due to hypercellularity.

Glioma
Optic pathway glioma: Sagittal T1- (left image) and post-contrast axial T1-weighted MRI shows a suprasellar
mass that is slightly hypointense relative to gray matter (yellow arrows), with diffuse enlargement of the
adjacent optic chiasm (red arrow). The mass demonstrates avid heterogeneous enhancement.
• Optic pathway gliomas, as previously discussed in the orbital section, can arise anywhere
along the optic nerves, optic chiasm, and optic tracts. Hypothalamic gliomas are often
considered together with this group due to difficulty distinguishing the site of origin in the
suprasellar region.
• These tumors are isointense on T1-weighted images, hyperintense on T2-weighted images,
and usually enhance.
Langerhans cell histiocytosis (LCH)
• Langerhans cell histiocytosis is a multisystem, infiltrative neoplasm of children.
• The most common endocrine abnormality in LCH is diabetes insipidus, due to involvement
of the pituitary or its stalk.
• Infundibular thickening and enhancement is the most common central nervous system
imaging manifestation of LCH.
Epidermoid and dermoid cysts
• Epidermoid and dermoid cysts are benign congenital ectodermal inclusion cysts.
• While dermoid and epidermoid cysts most commonly occur in the posterior cranial fossa,
the most common supratentorial site is the suprasellar cistern.
• As described earlier in the chapter, epidermoid cysts follow CSF signal on T1- and T2-
weighted images, but are hyperintense on FLAIR and show restricted diffusion.
• Dermoid cysts may contain intracystic fat, which can cause chemical meningitis or
ventriculitis upon rupture.

Hypothalamic hamartoma
Hypothalamic hamartoma: Sagittal T1-weighted (left image) and axial FLAIR MRI shows a T1 isointense, FLAIR
hyperintense suprasellar mass (yellow arrows) projecting inferiorly from the hypothalamus. The optic chiasm
(red arrow) is normal, as is the anterior pituitary (blue arrow) and posterior pituitary bright spot (green arrow).
• Hypothalamic (tuber cinereum) hamartoma represents gray matter heterotopia arising
between the pituitary stalk and the mammillary bodies.
• Hypothalamic hamartoma is the most common mass causing central precocious puberty in
children. These masses are also associated with gelastic seizures (laughing spells).
• Hypothalamic hamartoma characteristically appears as a sessile or pedunculated mass at
the floor of the third ventricle that does not enhance and is isointense to gray matter.

Differential diagnosis of a suprasellar mass is highly dependent on age
Suprasellar mass in a child
Calcified, enhancing, complex cystic mass?

Distinct from the pituitary?
Craniopharyngioma
T2 hyperintense, enhancing mass?

Secondary signs of neurofibromatosis 1?
Optic pathway glioma
Avidly enhancing midline mass? (germinoma)

Contains fat? (dermoid – much less common)
Germ cell tumor
Nonenhancing, gray-matter isointense mass?
Gelastic seizures?
Precocious puberty?
Hypothalamic hamartoma
Enhancing, enlarged pituitary stalk?

Diabetes insipidus? Langerhans cell
histiocytosis hypophysitis
Suprasellar mass in an adult
Pituitary mass extending superiorly?

Expansion of the sella?
Pituitary macroadenoma extension
Intense enhancement with a normal sella?
Enhancing dural tail?
Adjacent hyperostosis?
Narrows adjacent vasculature?
Meningioma
Calcified, enhancing, complex cystic mass?

Distinct from the pituitary?
Craniopharyngioma
Nonenhancing cystic mass without calcification?

Rathke’s cleft cyst
Enhancement equal to blood pool?

Calcified rim (if thrombosed)?
Aneurysm
Enhancing, enlarged pituitary stalk?

Diabetes insipidus? Lymphocytic or granulomatous
hypophysitis
Lymphocytic hypophysitis if peripartum;
granulomatous hypophysitis otherwise.
Metastasis, lymphoma

Clivus
Anatomy and anatomic variants
• The clivus is the sloping midline aspect of the central skull base formed by the sphenoid
body and basiocciput.
• These bones join at the spheno-occipital synchondrosis, which fuses during adolescence.
• A normal variant canal located superiorly, in the midline sphenoid body, is the persistent
hypophyseal canal (if <1.5 mm) or craniopharyngeal canal (if >1.5 mm), which connects the
nasopharynx and sella.
• Two notochord-derived clival variants located inferiorly are the canalis basilaris medianus
(a long channel in the midline basiocciput) and the fossa navicularis magna (a notch in the
anterior surface of the basiocciput).
• The clivus transitions during normal aging from hematopoietic marrow with low signal on
T1-weighted MRI to fatty marrow with high T1 signal. Low T1 marrow signal in an older adult
is abnormal, which may be due to a neoplasm or diffuse systemic process.
Ecchordosis physaliphora
Ecchordosis physaliphora: Axial T2-weighted MRI (left image) and sagittal FIESTA (right image) shows a T2
hyperintense lesion (arrows) centered within the central clivus which extends intradurally into the prepontine
cistern. There is no significant enhancement (not shown).
• Ecchordosis physaliphora is a benign, ectopic notochordal remnant that projects from the
dorsum of the clivus into the posterior cranial fossa.
• On imaging, ecchordosis physaliphora appears as a small T2 hyperintense retroclival lesion,
without contrast enhancement and often with a stalk and/or small bony defect in the
adjacent clivus. Stability over time supports the diagnosis as opposed to chordoma.
Benign notochordal cell tumor
• Intraosseous benign notochordal cell tumor is a notochord-derived neoplasm that, unlike
chordoma, is limited to the bone, associated with mild osteosclerosis rather than bone
destruction, and shows minimal to no contrast enhancement.
• They are usually asymptomatic. Long-term stability supports the radiologic diagnosis.

Chordoma/Chondrosarcoma
Clival chordoma:
Sagittal T1-weighted MRI (top left image) shows
replacement of the normal clival marrow by an
isointense mass (arrows).
Sagittal post-contrast T1-weighted MRI (top right
image) shows heterogeneous enhancement of the
mass (arrows).
Axial T2-weighted MRI (bottom left image) shows
a microlobulated, hyperintense clival mass with
extension into the left petrous apex and opacification
of the left middle ear and mastoid air cells.
• Chordoma is a notochord-derived malignancy in adults that most commonly arises in the

sacrum, followed by the clivus, and less commonly the vertebral column. Chordoma is the
most common primary neoplasm of the clivus.
• Chordomas show high signal on T2-weighted MRI and usually do not calcify. Key imaging
features that distinguish chordoma from benign notochordal tumors are bony destruction,
extraosseous extension, and contrast enhancement. Posterior tumor projection often
indents the pons, creating the thumb sign on sagittal images.
• Chondrosarcoma is a cartilage-derived malignancy in adults that, within the skull base, most
commonly arises at the petroclival synchondrosis (petro-occipital fissure).
• Chondrosarcomas show high signal on T2-weighted MRI and markedly elevated ADC values
(higher than those of chordoma). CT can demonstrate the rings and arcs calcifications
characteristic of chondroid lesions.
• Because chordomas and chondrosarcomas frequently have overlapping imaging features,
location is key in diagnosis. Chordomas tend to be midline, while chondrosarcomas are
mostly centered off-midline.
Secondary malignancies
• As with other bones, the clivus can be a site of metastatic disease (e.g., breast cancer),
local extension of soft tissue tumors (e.g., nasopharyngeal carcinoma), or involvement with
hematopoietic malignancies (e.g., myeloma/plasmacytoma or lymphoma).

Pterygopalatine fossa
Anatomy of the pterygopalatine fossa
axial
pterygopalatine fossa
vidian canal pterygomaxillary fissure

vidian artery and nerve leads to masticator space
foramen ovale sphenopalatine foramen

CN V3 leads to nasal cavity via the
superior meatus
foramen spinosum
middle meningeal artery
carotid canal
axial (higher level)
inferior orbital fissure

infraorbital nerve foramen rotundum
CN V2
coronal
anterior clinoid process optic canal
superior orbital fissure foramen rotundum
vidian canal
coronal (anterior)
inferior orbital fissure

Anatomy of the pterygopalatine fossa (continued)
• The pterygopalatine fossae are inverted pyramid-shaped spaces in the deep face that are
important central stations for the spread of disease between the facial skull and middle
cranial fossa.
• The pterygopalatine fossa contains fat and neurovascular structures including the
pterygopalatine ganglion, maxillary nerve (cranial nerve V2) branches, and distal maxillary
artery branches.
• Anteriorly, the pterygopalatine fossa is bordered by the maxillary sinus.
• Posteriorly, the pterygopalatine fossa is bordered by the base of the pterygoid plates of the
sphenoid bone, through which the foramen rotundum and Vidian canal are routes to the
middle cranial fossa. The former carries the maxillary branch of the trigeminal nerve (V2),
while the latter carries the Vidian nerve (nerve of the pterygoid canal).
• Superiorly, the inferior orbital fissure is the base of the pyramid that opens anteriorly into
the orbit. It transmits the infraorbital nerve, among other structures.
• Laterally, the pterygomaxillary fissure is the exit to the masticator space or infratemporal
fossa.
• Medially, the sphenopalatine foramen is the exit to the superior meatus of the nasal cavity.
It transmits the sphenopalatine artery, among other structures.
• Inferiorly, the pterygopalatine canal is the apex of the pyramid that leads to the oral cavity
via the greater and lesser palatine foramina. They transmit the greater and lesser palatine
nerves and vessels.
Pterygopalatine fossa pathology
• The pterygopalatine fossa can be involved with neoplastic or inflammatory entities by direct
invasion or perineural spread.
Primary sites include the cheek (e.g., squamous cell carcinoma), maxillary sinus (e.g., invasive fungal
sinusitis), nasal cavity and nasopharynx (e.g., juvenile nasopharyngeal angiofibroma, nasopharyngeal
carcinoma), palate (e.g., adenoid cystic carcinoma), masticator space (e.g., rhabdomyosarcoma), or orbit
(e.g., idiopathic orbital inflammation).
• Obliteration/infiltration of the fat of the pterygopalatine fossa with soft tissue is the earliest
imaging sign of its pathological involvement. Later signs are widening or erosion of the bony
walls.
• Contrast enhancement and enlargement of the neural foramina/canals leading to the
pterygopalatine fossa indicate perineural tumor spread.

Temporal bone/lateral skull base � posterior skull base
Overview of the temporal bone
tympanic scala
cochlea
membrane oval vestibuli
via stapes
window
incoming sound wave
ossicles
amplify sound
round
scala
window tectorial membrane tympani
external ear middle ear inner ear

contents: contents: contents:
tympanic membrane cochlea
ossicles: semicircular canals
external auditory canal malleus vestibule
(EAC) incus utricle
stapes saccule
stapedius muscle vestibular aqueduct
facial nerve cochlear aqueduct
pathology: pathology: pathology:

EAC atresia hypoplasia of ossicles cochlear dysplasia
squamous cell carcinoma oval window atresia superior semicircular canal
surfer’s ear (EAC exostosis) cholesteatoma dehiscence
swimmer’s ear (acute external otitis) otitis media semicircular canal hypoplasia
malignant otitis externa mastoiditis lateral most commonly affected
first branchial cleft cyst glomus tympanicum enlarged vestibular aqueduct
keratosis obturans aberrant internal carotid artery otospongiosis/otosclerosis
dehiscent jugular bulb labyrinthitis
facial nerve schwannoma Paget disease
fibrous dysplasia
petrous apicitis
cholesterol cyst
• The temporal bone can be anatomically and functionally divided into the external (outer),
middle, and inner ear. Although some pathologies can overlap, each division tends to be
susceptible to unique pathologies.
• This anatomic and functional division parallels the pathway of sound waves into the brain.
Sound enters the external ear, is amplified by the ossicles in the middle ear, and is finally
converted into electrical impulses in the inner ear.
• An additional function of the inner ear (not drawn above) is the balance and position sense
provided by the vestibule and the semicircular canals.
• Together, the cochlea, vestibule, and semicircular canals make up the labyrinth. The osseous
wall is known as the bony labyrinth or otic capsule, while the internal structures are known
as the membranous labyrinth.

External ear
Anatomy of the external ear
• The external (outer) ear is composed of the auricle (pinna), external auditory canal (EAC),
and tympanic membrane.
• The EAC is a tube surrounded by fibrocartilage (laterally) and bone (medially) that sound
passes through before reaching the tympanic membrane.
• The bony part of the EAC is bordered posteriorly and superiorly by mastoid air cells, while
the rest is formed by the tympanic part of the temporal bone.
Mastoidectomy procedures are distinguished by whether the posterosuperior walls of the EAC are
preserved (canal wall up mastoidectomy) or removed (canal wall down mastoidectomy).
The tympanic part of the temporal bone develops in parts that normally fuse at the anteroinferior
aspect in early childhood. Occasionally, incomplete fusion leaves a patent foramen of Huschke (foramen
tympanicum), a dehiscence connecting the EAC and temporomandibular joint.
• Sound waves vibrate the tympanic membrane, which transmits mechanical energy to the
middle ear ossicles.
• The tympanic membrane is divided into two sections: the pars tensa (larger, more inferior)
and the pars flaccida (smaller, more superior).
Congenital aural atresia/stenosis
• Congenital aural atresia/stenosis is characterized by developmental narrowing or occlusion
of the EAC, often associated with malformation of the auricle (microtia), ossicles (especially
malleus and incus), and/or middle ear cavity.
• The external and middle ear malformations are related by their development from the
first branchial cleft, first and second branchial arches, and first branchial pouch. Associated
anomalies of the inner ear are uncommon due to its separate origin from neuroectoderm.
• Most cases are isolated, but aural atresia can be a part of several syndromes involving the
first and second branchial arches, especially Treacher-Collins syndrome and craniofacial
microsomia (inclusive of the prior terms hemifacial microsomia, Goldenhar syndrome, and
oculo-auriculo-vertebral spectrum).
Benign bony external auditory canal lesions
Exostosis: Axial noncontrast CT through the right and left temporal bones shows broad-based bony exostosis in
bilateral external auditory canals narrowing the canal lumen.
• EAC exostosis, also known as surfer’s ear, is a non-neoplastic, reactive bony outgrowth
projecting into the EAC seen in those who swim/surf in cold waters. It is more often sessile
and multiple.
• EAC osteoma is the most common osseous neoplasm of the temporal bone. It is more often
solitary and pedunculated.
Otitis externa (external otitis)
• Otitis externa, also known as swimmer’s ear, refers to inflammation of the EAC. The most
common cause is acute bacterial infection, most commonly with Pseudomonas aeruginosa.
• Necrotizing otitis externa, previously known as malignant otitis externa, refers to otitis
externa complicated by temporal bone osteomyelitis. The most common risk factor is
diabetes mellitus.
• Imaging of otitis externa shows EAC soft tissue thickening, enhancement, and stranding.
Specific findings of necrotizing otitis externa, as with osteomyelitis elsewhere, are cortical
bone erosion on CT and marrow replacement on MRI.
• Chronic otitis externa can result in medial canal fibrosis, which appears as crescentic soft
tissue thickening over the outer surface of the tympanic membrane.
Benign keratinous external auditory canal lesions
• Keratosis obturans is an accumulation of keratin plugs that occludes and expands the EAC
without bone involvement. The condition is more often seen in young adults and children,
sometimes associated with sinusitis and bronchiectasis.
• On imaging, keratosis obturans appears as EAC soft tissue opacification with smooth,
expansile remodeling of the bony canal. Involvement is often bilateral.
• Cholesteatoma is a collection of keratin lined by squamous epithelium, which rarely occurs
in the EAC. EAC cholesteatoma more often occurs in middle-aged to older adults.
• On imaging, EAC cholesteatoma appears as a soft tissue mass with focal bone erosion or
sequestered bone fragments. Involvement is unilateral.
External ear malignancies
• The most common external ear malignancies are skin cancers: basal cell carcinoma,
squamous cell carcinoma, and melanoma.
• Within the external auditory canal, the most common malignancy is squamous cell
carcinoma. Imaging shows an enhancing soft tissue mass with osseous erosion.

Middle ear and mastoid
Anatomy of the middle ear and mastoid
malleus incus stapes semicircular canals
facial nerve
vestibule
oval window
external
auditory
round window
canal
tympanic cochlea
membrane
Eustachian tube
chorda tympani stapedius tensor tympani

muscle muscle
• The middle ear (tympanic) cavity or cleft can be conceived of as a 6-sided box, further
divided into compartments demarcated by the upper and lower borders of the
tympanic membrane: epitympanum (attic or epitympanic recess), mesotympanum, and
hypotympanum.
• The contents include the ossicles (malleus, incus, and stapes), the tensor tympani and
stapedius muscles, and part of the facial nerve.
• The lateral wall of the middle ear cavity is the tympanic membrane, which is attached to
the manubrium (handle) of the malleus. Sound reaching the tympanic membrane conducts
through the ossicular chain and its articulations with each other (incudomallear and
incudostapedial joints). At the end, the footplate of the stapes acts as a piston on the oval
window.
• The medial wall has the cochlear promontory and two membranous interfaces with the
inner ear: the oval window, where sound energy enters, and the round window, which
decompresses that energy after it travels through the cochlea.
• The roof of the epitympanum is the tegmen tympani, which is part of the floor of the
middle cranial fossa.
• The posterior wall of the epitympanum contains the aditus (opening) to the mastoid
antrum, which leads to the mastoid air cells.
• The anterior wall of the hypotympanum contains the opening for the Eustachian tube, which
leads to the nasopharynx.
• The floor of the hypotympanum contains the jugular plate, which covers the jugular bulb.

Anatomy of the middle ear and mastoid (continued)
cochlea
apical and middle turn
basal turn
tympanic membrane
modiolus
external
auditory canal (EAC) internal
auditory canal (IAC)
round window
incudomalleolar joint
head of malleus cochlea

basal turn
IAC
body of incus
vestibule
facial nerve
tympanic segment
malleus
tegmen tympani
superior semicircular canal
Prussak’s space
lateral semicircular canal
scutum
EAC
oval window
cochlear promontory
stapes
incudostapedial joint

Arterial variants
• Arterial anatomic variants are among the causes of a red retrotympanic mass and of
pulsatile tinnitus.
• The most common of these is the aberrant internal carotid artery, which is an enlarged
collateral pathway between the internal and external carotid artery trees involving the
caroticotympanic artery and the inferior tympanic artery. CT shows a dehiscent carotid
plate, soft tissue protruding into the anterior mesotympanum and coursing down over the
cochlear promontory to the posterior mesotympanum, and an enlarged inferior tympanic
canaliculus.
Axial (left image) and coronal noncontrast CT through the left temporal bone demonstrates an aberrant
carotid artery which extends laterally into the middle ear cavity with dehiscent bony covering, and
coursing around the cochlear promontory (arrows). The ipsilateral foramen spinosum is not visualized (not
shown), suggesting the presence of a persistent stapedial artery.
• In a lateralized internal carotid artery, the petrous segment of the internal carotid
artery protrudes laterally, with a thinned or dehiscent carotid plate, into the anterior
mesotympanum. The inferior tympanic canaliculus is not involved.
• A persistent stapedial artery is a branch of the hyoid artery connecting the external and
internal carotid arteries, which normally regresses. CT shows soft tissue coursing from the
petrous segment of the internal carotid artery, up over the cochlear promontory, and along
the proximal tympanic segment of the facial nerve. The foramen spinosum is absent.
Venous variants
• Venous variants of the sigmoid sinus and jugular bulb are among the causes of pulsatile
tinnitus and, in the case of dehiscent jugular bulb, of a blue retrotympanic mass.
• Sigmoid sinus or jugular bulb dehiscence refers to a gap in the bony plates that separates
the venous structure from the mastoid air cells or middle ear, respectively.
• Sigmoid sinus or jugular bulb diverticulum refers to a focal outpouching of the vessel that
protrudes into the temporal bone, with or without bony dehiscence.
• High-riding jugular bulb describes when the dome of the jugular bulb rises to a higher than
normal position (which is inconsistently defined), with or without bony dehiscence. Hearing
or balance issues may result from encroachment on middle and inner ear structures.

Paragangliomas
• Paragangliomas are the most common primary middle ear tumors. Clinically, they typically
present with pulsatile tinnitus or conductive hearing loss and appear on otoscopic
evaluation as a red retrotympanic mass.
• Paragangliomas are extra-adrenal neoplasms of sympathetic or parasympathetic
paraganglionic tissue. In the head and neck, most arise from the parasympathetic,
noncatecholaminergic glomus cells and therefore are called glomus tumors. Most are
benign, but they can be locally aggressive. Less than 5% undergo malignant degeneration.
• Most head and neck paragangliomas are sporadic but a significant minority are associated
with a hereditary disorder: familial paraganglioma due to succinate dehydrogenase (SDH)
subunit gene mutations, multiple endocrine neoplasia type 2 (MEN2), neurofibromatosis
type 1 (NF1), or von Hippel Lindau disease (VHL).
• Paragangliomas tend to occur in a few locations in the head and neck: at the carotid
bifurcation, in the suprahyoid neck along the course of the vagus nerve, at the jugular
foramen, and in the middle ear.
Glomus tympanicum tumor is a paraganglioma isolated to the middle ear, typically centered at the
cochlear promontory along the Jacobson nerve (branch of CN IX). The jugular plate is preserved.
Glomus jugulotympanicum tumor describes a paraganglioma that involves both the middle ear cavity
and jugular foramen, eroding through the jugular plate.
• Paragangliomas are highly vascular, avidly enhancing soft tissue masses. In larger tumors,
the classic MRI pattern is the salt and pepper appearance due to intratumoral flow voids.
Preoperative angiography with tumor embolization can reduce surgical blood loss.
Glomus tympanicum: Coronal (left image) and axial post-contrast T1-weighted MRI demonstrates a
heterogeneously enhancing lesion (yellow arrows) with apparent flow voids (red arrows) within the left
middle ear.
• As paragangliomas are neuroendocrine tumors that express somatostatin receptor 2
(SSTR2), the most sensitive modality for their detection is Ga-68 DOTATATE PET-CT.

Cholesteatoma
Middle ear cholesteatoma: Coronal (left image) and axial noncontrast CT through the right temporal bone
demonstrates a soft tissue mass (yellow arrows) in the middle ear with near-complete erosion of the scutum
(red arrow) and the ossicles, consistent with a cholesteatoma. There is opacification of the mastoid air cells.
• Cholesteatoma is a mass of exfoliated keratin lined by squamous epithelium in the temporal

bone, which has been described as “skin in the wrong place.” The name cholesteatoma is
deceptive since the lesion does not contain cholesterol crystals or fat and is not neoplastic.
The histologically identical intracranial counterpart is the epidermoid cyst.
• Cholesteatomas are among the causes of conductive hearing loss and of a white mass in the
middle ear.
• Cholesteatomas are classified by etiology into acquired and congenital forms but they are
histologically identical.
Acquired cholesteatoma represents the vast majority of cholesteatomas and can occur in both children
and adults. Primary acquired cholesteatoma occurs in the setting of a tympanic membrane retraction
pocket, which may be due to Eustachian tube dysfunction. Secondary acquired cholesteatoma occurs
in the setting of tympanic membrane perforation, which may be due to chronic otitis media, trauma, or
surgery.
Congenital cholesteatoma is uncommon and likely represents persistent fetal epithelial rests. They
typically present in children without a history of tympanic membrane perforation, retraction, or surgery.
• The vast majority of cholesteatomas occur in the middle ear, although congenital
cholesteatomas may also occur elsewhere in the temporal bone (e.g., EAC, mastoid, petrous
apex).
Acquired cholesteatomas most commonly arise in the Prussak space, a part of the epitympanum lateral
to the neck of the malleus; these are known as pars flaccida cholesteatomas.
In contrast, acquired pars tensa cholesteatomas and congenital middle ear cholesteatomas are typically
medial to the ossicles.
• CT is sensitive for the detection of even a small cholesteatoma, which appears as a
well-circumscribed soft tissue mass opacifying part of the middle ear cavity. However,
opacification is nonspecific and may reflect effusion, granulation tissue, or fibrosis. Adjacent
bony erosion, such as the wall of the middle ear cavity (earliest involving the scutum in pars
flaccida cholesteatomas) or ossicles (most commonly the long process of the incus), favors
cholesteatoma.
Erosions of bone covering specific structures outside the middle ear cavity are important to identify so
that they may be protected during cholesteatoma surgery: Lateral semicircular canal, facial nerve, and
intracranial compartment (e.g., tegmen tympani, sigmoid plate).

Cholesteatoma (continued)
• MRI is more specific for evaluating cholesteatoma, particularly in the postoperative
surveillance setting, using DWI or post-contrast imaging. Similar to intracranial epidermoid
cysts, cholesteatomas are hyperintense on DWI and do not enhance. Echo planar imaging
(EPI) DWI techniques routinely used for the brain are prone to artifacts in the temporal
bone, so non-EPI DWI is preferred for evaluation for cholesteatoma.
Middle ear cholesteatoma: T1-weighted axial MRI T2-weighted axial MRI with fat suppression shows
demonstrates iso- to slightly hyperintense (compared that the lesion is slightly hyperintense (arrow).
to gray matter) signal in the left middle ear (arrow).
Post-contrast T1-weighted MRI shows no enhancement Coronal diffusion weighted image shows a focus
of the lesion (arrow). of DWI hyperintensity in the left middle ear.
Diffusion was restricted when correlated with the
ADC map (not shown).

Cholesterol granuloma
Petrous apex cholesterol granuloma: Axial T1-weighted (left image) and T2-weighted (right image) shows
a lobulated T1 hyperintense, heterogeneously T2 hyperintense, expansile lesion in the left petrous apex
(arrows). There is no associated restricted diffusion (not shown).
• Cholesterol granuloma is a unique type of granulation tissue associated with friable blood
vessels. Histologically, it represents a giant cell reaction to cholesterol crystals.
• Cholesterol granulomas are most commonly located in a pneumatized petrous apex but can
occur in any obstructed air space such as the mastoid and middle ear cavities.
• Cholesterol granulomas in the middle ear may present on otoscopy as a blue retrotympanic
mass or as hemotympanum.
• Cholesterol granuloma can expand and thin the surrounding bone. On MRI, the lesions
are typically hyperintense on T1-weighted images due to blood products and do not show
restricted diffusion, unlike cholesteatoma.
Otomastoiditis
• Otomastoiditis refers to infection or inflammation in the middle ear and mastoid cavities.
Various terms are used clinically to classify this spectrum based on duration (acute or
chronic), presence and type of fluid (suppuration or serous effusion), and presence of
tympanic membrane perforation and/or cholesteatoma.
• An imaging finding of fluid in the middle ear and mastoid is common and not specific for
clinically significant inflammation or infection. Otomastoiditis remains a clinical diagnosis,
while imaging is reserved to detect complications such as those below.
• Coalescent mastoiditis is the advanced stage of acute mastoiditis in which osteitis is
present, defined on CT by resorption of the bony septae and thus merging of adjacent
opacified mastoid air cells.
Subperiosteal abscess results from coalescent mastoiditis that has eroded through the external mastoid
cortex but remains contained by periosteum, usually in the postauricular region. Further progression
through the periosteum is called a subcutaneous abscess.
Erosion through the mastoid tip can result in abscess tracking either along the sternocleidomastoid
muscle, called Bezold abscess, or along the posterior belly of the digastric muscle, called Citelli abscess.
• Intracranial complications are the main cause of mortality in acute and chronic
otomastoiditis, including meningitis, epidural abscess, subdural empyema, cerebritis, brain
abscess, and dural venous sinus thrombosis.
• Involvement of the inner ear (labyrinthitis) and petrous apex (petrous apicitis) are discussed
later in this temporal bone section.
• Intratympanic sequelae of chronic otitis media that can contribute to hearing loss
include middle ear effusion, granulation tissue, cholesteatoma, cholesterol granuloma,
post-inflammatory ossicular fixation (including tympanosclerosis), and ossicular erosion
(especially at the long process of the incus).
Intratemporal facial nerve
Anatomy of the intratemporal facial nerve
• The portion of the facial nerve within the temporal bone is divided into three segments:
Labyrinthine segment: courses from the internal auditory canal to the geniculate ganglion (anterior
genu), which is located superior to the cochlea.
g Greater superficial petrosal nerve innervates salivation.
Tympanic (horizontal) segment: courses posteriorly under the lateral semicircular canal to the posterior
genu.
Mastoid (descending) segment: courses inferiorly to the stylomastoid foramen.
g Nerve to stapedius.
g Chorda tympani (taste to anterior 2/3 of tongue).
• The portions of facial nerve that may normally enhance (related to its peri/epineural
vascular plexus) on MRI are the geniculate ganglion, tympanic segment, and mastoid
segment.
• Enhancement proximal to the geniculate ganglion, such as in the labyrinthine segment, or
extracranial portion is abnormal.
Facial nerve schwannoma
cochlea
vestibule
Facial nerve schwannoma: Axial CT through the temporal bone in a child shows subtle enlargement of the
tympanic segment of the left facial nerve canal (arrows).
• Within the temporal bone, schwannomas of the facial nerve (CN VII) tend to be slow
growing and most commonly involve the geniculate ganglion, followed by the labyrinthine
and tympanic segments.
• The majority of patients with facial nerve schwannoma present with facial nerve
palsy; however, up to 30% present without facial nerve symptoms. Larger facial nerve
schwannomas can interfere with ossicular function, causing conductive hearing loss.
• On CT, the typical finding of a facial nerve schwannoma is enlargement of the bony
canal through which the involved portion of the facial nerve passes. There is typically no
calcification. The tumor usually demonstrates brisk contrast enhancement on MRI.
Facial nerve venous malformation
• Facial nerve venous malformations, previously described as hemangiomas, are perineural
vascular lesions involving the petrous temporal bone.
• Facial nerve venous malformation is most commonly seen in the region of the geniculate
ganglion, followed by the IAC, and least commonly at the posterior genu.
• This lesion characteristically has an expansile honeycomb appearance with intralesional
bone spicules on CT, a pattern previously termed ossifying hemangioma. On MR, the
lesion is characterized by heterogeneous signal intensity on T2-weighted imaging and avid
enhancement.
Idiopathic and infectious causes of facial nerve enhancement
Axial post-contrast T1-weighted MRI demonstrates right facial nerve enhancement in the IAC (yellow arrow)
and faint cochlea enhancement (red arrow), consistent with Ramsey Hunt syndrome in this patient with right
facial weakness, sensorineural hearing loss, and a rash in the EAC.
• In addition to schwannoma and venous malformations, the differential diagnosis for
abnormal facial nerve enhancement includes infectious etiologies such as Lyme disease and
herpes zoster oticus (Ramsay Hunt syndrome) and idiopathic facial neuropathy.
• Idiopathic facial neuropathy, eponymously named Bell’s palsy, is the most common
syndrome of acute-onset, unilateral facial weakness.
Herpes simplex virus type-1 reactivation within the geniculate ganglion has been proposed as an etiology,
resulting in demyelination and inflammation of the facial nerve. Facial paralysis is usually preceded by a
viral prodrome.
History and physical examination is generally sufficient for diagnosis. Imaging is generally performed to
rule out other etiologies in patients presenting with atypical symptoms, recurrent symptoms, or slow
recovery. The majority of patients have a complete recovery within 6 months.
MRI demonstrates a uniformly enhancing, normal sized or mildly thickened facial nerve commonly
extending from the intracanalicular segment to the tympanic segment. Enhancement may persist
following clinical improvement.
• Enhancement of the facial nerve accompanied by enhancement in the internal auditory
canal and labyrinth, and vesicles within the EAC are suggestive of Ramsay Hunt syndrome.
• Lyme disease is caused by Borrelia burgdorferi. Clinically, these patients present with a rash
and can have arthritis and myocarditis.
Perineural tumor spread along the facial nerve
• Parotid malignancies such as lymphoma and adenoid cystic carcinoma and adjacent skin
malignancies that secondarily invade the parotid gland have a propensity for perineural
spread along the facial nerve.
• Facial nerve involvement occurs more frequently and in earlier stages in the extratemporal
portion of the facial nerve. Proximally, the stylomastoid foramen segment and the
descending segments can be involved.
• MRI demonstrates enlargement of the facial nerve with patchy enhancement, enlargement
of the stylomastoid foramen, or loss of the normal fat signal surrounding the nerve within
the foramen.

Inner ear
Anatomy of the inner ear
• The inner ear is situated within the petrous portion of the temporal bone and comprises
the otic capsule (also known as the bony labyrinth). The otic capsule is the osseous
superstructure containing the fluid-filled spaces of the cochlea, vestibule, and semicircular
canals. The otic capsule is the densest bone in the body.
• The cochlea is a conical structure consisting of a bony two-and-a-half turn spiral canal,
including the basal, middle and apical turns, around a central core called the modiolus. The
modiolus contains the cells of the spiral ganglion and corresponds to the exit of the cochlear
nerve towards the internal auditory canal.
• The spiral of the cochlea is separated by osseous spiral lamina and consists of the scala
tympani, scala media, and scala vestibuli.
• The scala media, also known as the cochlear duct, separates the scala vestibuli and the
scala tympani, contains endolymph and the organ of Corti, the receptor organ for hearing
comprised of sensory epithelium containing numerous neuroepithelial hair cells, which send
electrical impulses to the spiral ganglia of the cochlea.
• The scala tympani and scala vestibuli contain perilymph. They communicate at the apex of
the modiolus by a small opening, the helicotrema.
Hydraulic pressure created in the perilymph by the vibrations of the stapes against the oval window
ascends to the apex of the cochlea by the scala vestibuli. Pressure waves descend back to the basal turn
through the scala tympani. The vibrations from the scala tympani are transmitted through the round
window, where the energy is dissipated.
• The cochlear aqueduct, also known as the cochlear canaliculus, extends from the scala
tympani to the subarachnoid space, opening on the inferior surface of the petrous portion
of the temporal bone. This theoretically allows for equilibration between the perilymphatic
space and the subarachnoid space.
• The vestibule is an ovoid perilymphatic space which is continuous with the cochlea
anteriorly and the semicircular canals posteriorly, and contains the utricle and saccule, the
sense organs involved in balance. The semicircular canals are oriented orthogonal to one
another.
• The vestibular aqueduct connects the crus commune (the common channel of the
superior and posterior semicircular canals) to the posterior cranial fossa and contains the
endolymphatic duct and sac.
• The endolymphatic duct arises from the utricle and saccule and ends in a blind pouch, the
endolymphatic sac, at the posterior margin of the petrous ridge. The endolymphatic sac
acts as a reservoir for endolymph and the site for reabsorption into the epidural space.
Congenital anomalies
• Congenital anomalies of the inner ear are divided into two broad categories: malformations
that involve only the membranous labyrinth and malformations that involve both the
osseous and membranous labyrinth (e.g., malformed otic capsules).
• Several types of membranous labyrinth malformation have been described, the classification
of which is not useful radiologically as differentiation is made on histopathologic
examination.
• Conversely, radiologic identification and characterization of malformations of both the
osseous and membranous labyrinth significantly impacts management strategy and
prognosis and will be discussed in more detail.

Type II incomplete partition (Mondini deformity)
Axial noncontrast CT through the left temporal

bone shows cochlear hypoplasia with 1.5 turns
and a cystic apex representing fusion of the
middle and apical turns (yellow arrow). The
modiolus is deficient and the lateral interscalar
septum is absent. An ipsilaterally enlarged
vestibular aqueduct is also present (red arrow).
• The most common form of congenital cochlear dysplasia, accounting for more than 50% of
all cochlear deformities. It consists of a cochlea with 1.5 turns and absence of the interscalar
septum and osseous spiral lamina. The basal turn appears normal and the middle and apical
turns coalesce to form a cystic apex.
• Although the correct nomenclature for this anomaly is incomplete partition type II, it is
commonly and historically referred to as the Mondini deformity. The use of the eponym
Mondini to describe cochlear dysplasia is controversial and probably best avoided, as there
is confusion amongst radiologists regarding the exact malformation originally described.
• There is strong association with an enlarged vestibule and enlarged vestibular aqueduct and
normal semicircular canals.
Type I incomplete partition (cystic cochleovestibular malformation)
• Type I incomplete partition accounts for about 6% of all cochlear malformations. It is
characterized by a complete absence of the modiolus, a cystic appearance of the cochlea,
and a dilated appearance of the vestibule, forming a figure 8. The cochlea and vestibule are
distinct, distinguishing from a common cavity.
Common cavity
• A common cavity accounts for about 25% of all cochlear malformations. It is defined by the
absence of the normal differentiation between the cochlea and vestibule.
Cochlear hypoplasia
• Cochlear hypoplasia accounts for about 15% of all cochlear malformations. This results in
aberration in the development of the cochlear duct during the sixth week of gestation. It
is defined by the presence of a small cochlear bud arising from an abnormally small and
deformed vestibule, usually with only one or a partial turn. Frequently it is accompanied by
an abnormally small IAC.
Cochlear aplasia
• Cochlear aplasia is rare and accounts for about 3% of all cochlear malformations. It is
characterized by an absent cochlea with a normal or deformed vestibule and semicircular
canals.

Complete labyrinthine aplasia (Michel aplasia)
Axial noncontrast CT through the right temporal

bone demonstrates absence of the cochlea,
a dysplastic vestibule (yellow arrow), and
hypoplastic semicircular canals (not shown).
The IAC is small and stenotic (red arrow).
• Michel aplasia is the most severe form of inner ear deformity and is defined by complete
absence of the inner ear structures. On CT, an atretic IAC is seen without visualization of CN
VIII. It is extremely rare, and accounts for only 1% of all inner ear malformations.
• This can be unilateral or bilateral; however, when unilateral, the contralateral side is
frequently also dysplastic.
• This is frequently associated with abnormalities in structures arising from the otic capsule,
including hypoplasia of the petrous bone, absence of the round and oval windows, flattening
of the medial wall of the inner ear cavity.
Enlarged vestibular aqueduct syndrome
Axial noncontrast CT through the left temporal

bone demonstrates an enlarged vestibular
aqueduct (yellow arrow). Note size comparison
to the adjacent semicircular canal (red arrow)
• When CT imaging is positive for workup of unexplained sensorineural hearing loss, the
most common finding is an enlarged vestibular aqueduct. The pathophysiology behind
the association with an enlarged vestibular aqueduct and sensorineural hearing loss is
not known. Multiple studies have shown that the probability of progressive hearing loss
increases linearly with increasing width.
• There is an association with other inner ear anomalies, such as modiolar deficiency and
incomplete partition type II.
• The measurement criteria are referred to as the Cincinnati criteria, which defines
enlargement as >1.9 mm at the operculum and/or >0.9 mm at the midpoint in a child.
• As an internal reference, the vestibular aqueduct should not be larger than the posterior
semicircular canal, which is often seen at the same level in the axial plane.

Causes of conductive hearing loss
Otospongiosis (otosclerosis)
Fenestral otospongiosis: Axial noncontrast CT Retrofenestral otospongiosis: Axial noncontrast

through the right temporal bone demonstrates focal CT through the left temporal bone shows focal
demineralization in the bone anterior to the oval demineralization of the cochlear capsule (yellow
window (yellow arrow) at the fissula ante fenestram arrow). There is also demineralization of the fissula
(red arrow). ante fenestram (fenestral otospongiosis, red arrow).
• Otospongiosis, otherwise known as otosclerosis, is a primary bone dysplasia of the otic
capsule characterized by replacement of normal endochondral bone by irregular spongy
bone. Otospongiosis occurs most commonly in young and middle-aged women and is
bilateral 85% of the time.
• Patients present with predominantly conductive hearing loss earlier on, and a mixed
conductive and sensorineural hearing loss later in the disease process.
• The two main types of otospongiosis are fenestral and retrofenestral types.
The fenestral type of otospongiosis is more common, occurs at the fissula ante fenestram (located
directly anterior to the oval window), and usually affects the oval window.
The retrofenestral (cochlear) type is thought to represent a more severe form with involvement of the
otic capsule separable from the oval window, typically involving the cochlear capsule, with possible
extension to the vestibule, semicircular canals, and IAC. Involvement of the cochlear promontory can
result in a red-tinged appearance on otologic examination, termed the Schwartze sign.
• CT is the best imaging modality for evaluation of otospongiosis. In the earlier, vascular
phase, there is replacement of dense bone with demineralized bone, resulting in a less
dense appearance. In a later, less active phase, the bone becomes more dense and sclerotic.
• The differential diagnosis of cochlear demineralization includes retrofenestral otospongiosis,
osteogenesis imperfecta in a child, fibrous dysplasia in a young adult, and Paget disease in
an older adult.
Round window occlusion
• Round window occlusion can occur with inflammatory tissue, bone lesions, high-riding
jugular bulb, or congenital absence.
• These abnormalities can result in conductive hearing loss by adding resistance to acoustic
energy entering the cochlea and requiring more energy to displace the basilar membrane.
Superior semicircular canal dehiscence
• A bony defect in the superior semicircular canal results in dispersion of sound energy along
the canal, creating a “third window” with less energy available to the cochlea. The resultant
drop in sound wave amplitude leads to conductive hearing loss. The abnormal movement of
the endolymph can lead to a variety of vestibular and cochlear symptoms referred to as the
“third window phenomenon.”

Infectious and inflammatory conditions of the inner ear
Labyrinthitis
Acute labyrinthitis: Axial post-contrast T1-weighted MRI demonstrates increased enhancement within the
inner ear (arrow).
• Labyrinthitis is inflammation of the inner ear, which may be infectious or autoimmune.
• Labyrinthitis has been divided into three stages of chronicity based on the imaging (primarily
MR) characteristics.
• Acute labyrinthitis is the earliest stage, presenting as pus in the inner ear. The only MRI
signal abnormality of acute labyrinthitis is enhancement of the affected inner ear structures.
The main differential consideration is a cochlear or intra-labyrinthine schwannoma. A schwannoma tends
to be focal and discrete, while labyrinthitis may produce more diffuse enhancement.
• Fibrous labyrinthitis represents the replacement of endolymph and perilymph with fibrous
strands that cause decreased signal intensity on T2-weighted images. There may be mild
(but decreased) residual post-contrast enhancement of the affected structures.
• Labyrinthitis ossificans is the final stage of the disease. Calcified debris replaces the
normal endolymph and perilymph. CT is the best way to image labyrinthitis ossificans,
as the calcification causes decreased signal intensity on T2-weighted MRI and lack of
enhancement.
Labyrinthitis ossificans: Coronal noncontrast CT

through the right temporal bone demonstrates
partial mineralization of the anterior limb of the
superior semicircular canal (arrow).

Cerebellopontine angle (CPA) mass
Overview and anatomy of the CPA
clivus
porus acousticus
internal acoustic meatus basilar artery
cochlea
AICA
vestibule & cerebello-
semicircular canals pons pontine
t-bone angle cistern
facial nerve
flocculus of
vestibulocochlear nerve cerebellum
lateral recess
4th ventricle
cerebellum 4th ventricle
• The cerebellopontine angle (CPA) is a region between the pons and cerebellum and the
posterior aspect of the petrous temporal bone. Important structures of the CPA include the
fifth (trigeminal), seventh (facial), and eighth (vestibulocochlear) cranial nerves, and the
anterior inferior cerebellar artery (AICA).
• Most lesions of the CPA are extra-axial and located in the CPA cistern itself, although some
may arise in the internal auditory canal (IAC), temporal bone, or rarely intra-axially from the
pons or cerebellum. CPA masses are more common in adults.
Schwannoma
Vestibular schwannoma: Axial T2- (left image) and T1-weighted post-contrast MRI demonstrate a
heterogeneously enhancing mass in the left cerebellopontine angle with an ice cream cone appearance that
indents the cerebellar-pontine junction (yellow arrow) and protrudes into the internal acoustic meatus (red
arrow). The porus acousticus is slightly widened (blue arrows).
• Schwannoma of the vestibulocochlear nerve, also known as a vestibular schwannoma, is by
far the most common cerebellopontine angle mass, representing greater than 75% of all CPA
masses.
• Most frequently present in the fifth to seventh decades of life in sporadic cases and in the
second decade of life in the setting of neurofibromatosis type II, which is associated with
bilateral vestibular schwannomas.
• Vestibular schwannoma is isoattenuating to the cerebellum on CT, hyperintense on T2-
weighted images and avidly enhances. The characteristic ice cream cone appearance
describes the “cone” protruding through (and widening) the porus acousticus and the “ice
cream” exerting mass effect on the cerebellar-pontine junction. Schwannoma may become
cystic, especially when larger.
• Schwannomas of other cranial nerves in the CPA, including the facial or trigeminal nerves,
are less common. Trigeminal schwannoma may extend into Meckel’s cave.
Meningioma
Prepontine/left CPA meningioma: Axial T2-weighted
MRI (top left image) demonstrates a circumscribed,
hyperintense, prepontine mass (yellow arrows).
Axial pre-contrast T1 (bottom left image) and post-
contrast T1-weighted (bottom right image) MRI
shows that the mass avidly enhances and extends
from the prepontine cistern into the left CPA and left
porus acousticus (red arrow). There is also extension
into Dorello’s canal on the left (green arrow), likely
causing cranial nerve VI palsy. There is flattening of
the pons. The basilar artery is nearly 180° encased
and mildly narrowed (blue arrow).
Case courtesy Gregory Wrubel, MD, Brigham and
Women’s Hospital.
• Although meningioma is overall the most common extra-axial mass in adults, it is only the
second most common mass of the CPA, representing approximately 10–15% of all CPA
masses.
• Meningiomas often feature a short segment of dural enhancement and may induce
adjacent bony hyperostosis. Approximately 20% calcify, in contrast to schwannomas where
calcification is rare.
• In contrast to schwannoma, a CPA meningioma seldom enlarges the porus acousticus.
Arachnoid cyst
• An arachnoid cyst is a benign CSF-filled lesion that is usually congenital.
• An arachnoid cyst will follow CSF on all sequences. Unlike an epidermoid cyst, an arachnoid
cyst does not have restricted diffusion.
Aneurysm
• Vertebrobasilar aneurysm (arising from the posterior inferior cerebellar artery, anterior
inferior cerebellar artery, vertebral artery, or basilar artery) may appear as a well-defined,
avidly enhancing CPA lesion and may be initially mistaken for a schwannoma or meningioma
on contrast-enhanced CT.
• On MRI, clues to a vascular etiology include flow void and pulsation artifacts. MRA or CTA
are diagnostic.

Epidermoid cyst
Epidermoid cyst:
Axial T2-weighted MRI (top left image) shows a
lobulated mass (arrows) in the left cerebellopontine
angle. The mass is isointense to CSF.
ADC map (top right image) and DWI (left image)
show that the mass (arrows) is dark on ADC and
bright on DWI, consistent with reduced diffusivity.
Case courtesy Gregory Wrubel, MD, Brigham and
Women’s Hospital.
• An epidermoid cyst is a congenital lesion arising from ectopic ectodermal epithelial tissue.
• Epidermoid cysts progressively enlarge from desquamation of keratinized epithelium lining
the cyst. The mass characteristically insinuates in between structures, encasing cranial
nerves and vessels. Gross pathology features a characteristic “cauliflower-like” surface.
• On CT, epidermoid cyst may mimic arachnoid cyst and appear as a CSF-attenuation cystic
structure. On MRI, an epidermoid cyst has similar signal characteristics as CSF on T1- and T2-
weighted images. Unlike arachnoid cyst, an epidermoid does not usually suppress on FLAIR
sequences.
• An epidermoid cyst is hyperintense on diffusion-weighted images, believed to be a
combination of reduced diffusivity and T2 shine through, in contrast to arachnoid cysts.
Post-surgical DWI follow-up is critical to detect any residual focus, which will be DWI bright.
• Rarely, epidermoids may exhibit signal hyperintensity on unenhanced T1-weighted imaging,
also known as “white epidermoids.”
Intra-axial neoplasm
• Less frequent benign lesions that can be seen in the IAC/CPA include lipomas and dermoids.
• A posterior fossa intra-axial neoplasm, such as a hemangioblastoma or glioma, may invade
laterally into the CPA. Other malignancies such as lymphoma, melanoma, and metastases
can also be rarely seen.
• Medulloblastoma tends to occur in the midline in children, though lateral involvement of
the cerebellar hemispheres can be seen in older children or young adults.
• Ependymoma may extend into the CPA by squeezing through the lateral fourth ventricular
foramina (of Luschka).
• Tumors related to the petrous bone (e.g., chondrosarcoma or endolymphatic sac tumors)
may extend to the CPA.

Temporal bone fractures
• Temporal bone fractures have been historically described by their orientation with respect
to the long axis of the petrous pyramid–longitudinal versus transverse–which classically
leads to conductive versus sensorineural hearing loss, respectively. However, this traditional
system does not correlate with clinical outcome or potential complications.
• A newer classification system has been proposed, classifying fractures depending on
whether the otic capsule is spared or violated.
Otic capsule-sparing temporal bone fracture
Axial CT through the temporal bone

shows a nondisplaced fracture (arrow)
extending through the axis of the
petrous portion of the temporal bone.
The otic capsule is spared.
• Otic capsule-sparing temporal bone fractures are much more common than otic capsule-
violating features, accounting for 94–97% of temporal bone features.
• Otic capsule-sparing temporal bone fracture results from a temporoparietal blow and has an
increased incidence of conductive hearing loss secondary to ossicular injury.
• The most common cause of conductive hearing loss is related to hemotympanum or
tympanic membrane rupture, which should resolve within a month of injury. Persistent
conductive hearing loss should prompt evaluation for ossicular injury.
• The most frequently injured ossicle is the incus because it has the least ligamentous
support. Ossicular dislocation is more common than ossicular fracture.
Otic capsule-violating temporal bone fracture
• Otic capsule-violating temporal bone fracture is much less common. It can involve the
vestibule, semicircular canals, cochlea and/or facial nerve.
• It is often the result of an occipital blow and has a higher incidence of facial nerve paralysis,
sensorineural hearing loss, and CSF fistula.
Complications of temporal bone fracture
Facial nerve injury
• Facial nerve transection results in immediate facial paralysis.
• Delayed facial nerve injury can present secondary to contusion, edema, or hematoma.
• Severity and onset helps guide clinical management. Delayed onset incomplete facial
paralysis may be treated with steroids and observation while surgical exploration is
considered if there is concern for transection.
• Important CT findings include: Bone fragments impinging on the facial nerve, extension of
fracture to the nerve, and ossicles or hematoma impinging on the facial canal.

CSF leak
• CSF leak is a complication seen in 11–45% of temporal bone fractures and is seen 2–4 times
more frequently in otic capsule-violating temporal bone features.
• CSF leak is seen in fractures that involve the tegmen.
• Clinically, patients present with CSF otorrhea and rhinorrhea, fullness in the ear, and
conductive hearing loss.
• Most cases occur in the first week after trauma and resolve with conservative medical
management (strict bed rest).
Labyrinthitis ossificans
• Labyrinthitis ossificans occurs when fluid-filled lumen of the otic capsule following trauma is
replaced by fibrous tissue (earlier stage) or bone (later stage).
• Clinically this presents with sensorineural hearing loss and loss of vestibular function.
Vascular injury
• Arterial injury can occur in the form of dissection, pseudoaneurysm, arteriovenous fistula,
transection or occlusion.
• Presence of carotid canal fracture is highly suggestive of injury to the passing internal carotid
artery and should be evaluated with CT angiography.
• Venous injury can manifest as venous sinus thrombosis or transection. CT venogram should
be performed in cases where the fracture line traverses the venous sinuses. Complications
of venous sinus thrombosis such as venous infarcts or hematomas should also prompt
definitive evaluation.
Petrous apex
Anatomy of the petrous apex
• The petrous apex is the most medial portion of the temporal bone
• The petrous apex is a bridge between the suprahyoid neck inferiorly and the intracranial
compartment above, and is adjacent to several important structures such as Dorello's canal,
Meckel's cave, and the petrous portion of the internal carotid artery.
Cranial nerve VI passes through Dorello's canal.
Meckel's cave is the site of the trigeminal ganglion.
• Normally, the petrous apex is composed of bone marrow and dense bone. The petrous
apex is pneumatized in approximately 10% of the population, which increases the risk for
development of a cholesterol cyst or apical petrositis.
Cholesterol cyst (cholesterol granuloma)
• A cholesterol cyst is a foreign body giant cell reaction to cholesterol crystals. It is thought
to be initially instigated as a reaction to an obstructed air cell and therefore occurs more
commonly in a pneumatized petrous apex.
• A cholesterol cyst is the most common primary petrous apex lesion but may also occur in
the mastoid portion of the temporal bone or the middle ear.
• MR imaging of a cholesterol cyst shows an expansile mass with internal hemorrhage and
fluid which does not suppress on fat suppression, unlike fatty marrow.
Congenital cholesteatoma
• While acquired cholesteatomas are located within the middle ear, congenital cholesteatoma
can be located anywhere in the temporal bone, including the petrous apex.
• MR imaging will typically show restricted diffusion.

Apical petrositis (petrous apicitis)
• A relatively rare complication of infectious otomastoiditis, apical petrositis is also known as
petrous apicitis and results when infection extends medially into a pneumatized petrous
apex.
• In the early stages of apical petrositis, there is opacification of the petrous apex air cells with
progressive bony demineralization and resorption, resulting in localized osteomyelitis of the
skull base.
• The classic Gradenigo triad is not commonly seen, but is comprised of otomastoiditis, facial
pain due to trigeminal neuropathy at Meckel's cave, and lateral rectus palsy from sixth
cranial nerve palsy at Dorello's canal.
• Vascular complications of apical petrositis include internal carotid arteritis and dural venous
thrombosis.
Schwannoma
• A petrous apex schwannoma may originate from cranial nerves V, VII, or VIII. Imaging shows
a circumscribed, smoothly expansile, enhancing mass that may cause bony remodeling.
Large tumors may become cystic and contain fluid levels.
Langerhans cell histiocytosis (eosinophilic granuloma)
• Langerhans cell histiocytosis (LCH) is a neoplastic proliferation of eosinophils and Langerhans
cells. The temporal bone is the most common site of skull base involvement.
• CT shows a well-circumscribed destructive lesion, usually with nonsclerotic margins.
• MRI shows the LCH lesions as soft-tissue masses surrounded by bone marrow and soft tissue
edema. Marked enhancement is characteristic.
Chondrosarcoma
• Chondrosarcoma is a malignant neoplasm that characteristically arises in the midline from
the clivus or slightly off-midline from the petro-occipital fissure. CT often shows a tumor
with a ring-and-arc chondroid matrix, although internal matrix is not always seen. MRI
shows a lobular, cauliflower-shaped, hyperintense mass on T2-weighted images.
Chordoma
• Chordoma (subsequently discussed in the section on clival lesions) most commonly arises
from the clivus but may expand laterally to secondarily involve the petrous apex. In some
circumstances it can be difficult to distinguish between chordoma and chondrosarcoma.
Endolymphatic sac tumor
Axial noncontrast CT (left image) demonstrates a destructive mass with internal calcification (arrows) centered
at the posterior wall of the right mastoid air cells in region of the vestibular aqueduct, and involves the right
IAC, semicircular canals, and middle ear cavity. Location of the mass suggests an endolymphatic sac tumor.
Subsequent MRI shows the mass is intrinsically T1 hyperintense (axial T1-weighted image on the right),
heterogeneously T2 hyperintense, and does not enhance.

Endolymphatic sac tumor (continued)
• Endolymphatic sac tumor is a locally invasive papillary cystadenomatous tumor.
• Most cases are sporadic, but a minority of cases are associated with von Hippel-Lindau.
• Endolymphatic sac tumor most frequently involves the region of the vestibular aqueduct
in the retrolabyrinthine petrous bone. On CT, the affected bone has a moth-eaten, lytic
appearance with intratumor bone spicules. On MRI, the presence of blood products results
in intrinsic T1 hyperintensity. Enhancement is usually heterogeneous.
Differential diagnosis of a petrous apex lesion
Petrous apex lesion
mnemonic: ACGME’S MC
benign
Fluid within petrous apex?
Apical petrositis
Bony erosion?
Restricted diffusion?
Congenital cholesteatoma
No restricted diffusion?
T1 hyperintense?
Cholesterol granuloma
Dural tail?
Meningioma
Well-circumscribed lytic
lesion in a child?
Eosinophilic granuloma
Smoothly enhancing?
Adjacent bony remodeling?
Intralesional cysts?
Schwannoma
malignant
Aggressive appearing?
Metastasis/Myeloma
Aggressive appearing?
Hyperintense on T2?
Chondrosarcoma/Chordoma

Posterior skull base
Anatomy of the posterior skull base
• The posterior skull base is bounded by the posterior clivus anteriorly, the posterior aspect of
the petrous temporal bone and condylar part of the occipital bone laterally, and the mastoid
temporal bone and squamous occipital bone posteriorly.
• The foramen magnum is formed within the occipital bone and transmits the medulla
oblongata, vertebral arteries, anterior/posterior spinal arteries, and spinal accessory nerve.
• Important foramina within the posterior skull base include jugular foramen and the
hypoglossal canal, which are separated by the jugular tubercle.
• A fibrous or bony septum divides the jugular foramen into anteromedial pars nervosa and
posterolateral pars vascularis.
Pars nervosa transmits cranial nerve IX (glossopharyngeal nerve) with its tympanic branch, Jacobson
nerve, and the inferior petrosal sinus (mnemonic Nervosa Nine).
Pars vascularis is larger and transmits the internal jugular vein, posterior meningeal artery, cranial nerves
X (vagus nerve) and XI (accessory nerve), and Arnold nerve (auricular branch of CN X).
• The hypoglossal canal transmits the cranial nerve XII (hypoglossal nerve).
General approach to the posterior skull base
• A large subset of lesions within the posterior skull base are not specific to the posterior skull
base and can be seen elsewhere. These include:
Fibro-osseous lesions such as fibrous dysplasia, Paget’s disease.
Cartilage/bone tumors such as chordomas, chondrosarcomas, osteosarcomas, plasmacytomas, multiple
myeloma, LCH.
Vascular malformations.
Metastases.
• The most common lesions localized to the jugular foramen are glomus jugulare tumors,
schwannomas, and meningiomas.
Glomus jugulare tumors make up 80% of primary neoplasms arising from the jugular foramen. The typical
patient is a woman in late middle age presenting with pulsatile tinnitus and conductive hearing loss.
Imaging findings are similar to glomus tumors in other areas of the head and neck, as described previously.
Bony changes of the jugular bulb can be used to differentiate these lesions on CT. Classically, glomus
jugulare tumors cause permeative erosion, schwannomas cause smooth remodeling, meningiomas cause
hyperostosis.
Glomus jugulare tumor: Axial CT through the mastoid air cells shows permeative, moth-eaten bony
destruction centered on the right jugular foramen (arrows).
• Cerebellopontine angle tumors also localize to the posterior skull base and are discussed
earlier in the chapter.

Mucosal spaces: oral cavity, pharynx, larynx
• The oral cavity is a space defined by the anterior 2/3 of tongue, bounded superiorly by the
palate and inferiorly by the floor of mouth.
• The pharynx is a muscular tube extending from skull base to the thoracic inlet. It is the
anatomic center of the head and neck, around which the other suprahyoid spaces wrap. It is
divided into the following distinct anatomic regions:
Nasopharynx: Top of pharynx behind the nasal cavity.
Oropharynx: From the level of the palate to the hyoid bone, behind the oral cavity. The posterior 1/3 of
tongue is part of the oropharynx.
Hypopharynx: From the hyoid bone to the esophagus, including the piriform sinuses and soft tissue
lateral to the larynx.
• Mucosal squamous cell carcinoma (SCC) arises from the squamous lining of the pharynx,
larynx, and sinonasal cavity.
• The TNM staging system is used to classify SCC. “T” refers to the primary tumor extent, “N”
to regional lymph nodes, and “M” for distant metastases. The criterion for T and N stage
is individualized to each site (nasopharynx, oropharynx, and hypopharynx) and in the case
of the larynx to each subsite (supraglottic, glottic, and subglottic). Regardless of subtype,
tumor size and lymph nodes are reported using the longest diameter, which is in contrast
with lymph node measurements in other parts of the body. An exhaustive discussion of
TNM staging is beyond the scope of this book, however some key points and differentiating
factors are discussed below.
Nasopharynx
Overview and anatomy
• The nasopharynx is located posterior to the nasal cavity and extends from the most cranial
aspect of the pharynx (at the skull base) to the level of the soft palate.
• In the midline of the nasopharynx is the nasopharyngeal tonsillar tissue, also known as the
adenoid. This is where nasopharyngeal lymphoma can arise.
Nasopharyngeal SCC
• Most nasopharyngeal carcinomas arise from the fossa of Rossenmuller, which is adjacent
to the opening of the Eustachian tube. The proximity explains why nasopharyngeal tumors
result in middle ear effusion at the time of presentation.
• Nasopharyngeal SCC frequently demonstrates minimal mucosal disease and may have
significant extra-mucosal extension, most frequently to the parapharyngeal space and then
the retropharyngeal space.
• T staging of nasopharyngeal carcinoma is primarily defined by tumor extent/ invasion, and
less on the size of the lesion as in other sites. T1 tumor is confined to the nasopharynx while
extension to the parapharyngeal spaces, infiltration into surrounding muscles, the bony skull
base, or intracranial extension results in a higher T stage. Given the importance of detection
of skull base infiltration and intracranial extension of disease, MR is the preferred staging
tool.
• Lymph node metastases are common, and most frequently initially preferentially involve the
retropharyngeal and high jugular (level II) nodes.
• Treatment is most frequently non-surgical and a combination of chemotherapy or radiation,
depending on the TNM stage.

Thornwaldt cyst
• A Thornwaldt cyst is a notochordal remnant that is usually asymptomatic, but may be a
cause of halitosis. The typical location of a Thornwaldt cyst is in the midline nasopharynx.
Axial T1-weighted (left image) and T2-weighted (right image) MRI show a well-circumscribed, T1 hyperintense
T2 hypointense lesion in the midline nasopharynx, consistent with a Thornwaldt cyst containing proteinaceous
material.
Oropharynx
• The oropharynx includes the posterior and superior pharyngeal walls from the level of
the soft palate to the hyoid bone, and includes the posterior 1/3 of the tongue (i.e., base
of tongue), the vallecula, the palatine tonsils. The tongue base is the site of the lingual
tonsillar tissue. The circumvallate papillae defines the anterior border of the oropharynx and
separates the oropharynx from the oral cavity.
• The soft palate is part of the oropharynx and the hard palate is part of the oral cavity.
Oropharyngeal SCC
• The most common locations for oropharyngeal SCC are the anterior portion of the tonsil and
the tongue base.
• In contrast to nasopharyngeal SCC, there are two TNM staging classifications for
oropharyngeal SCC, depending on the p16 or high-risk HPV status. P16+/HPV-associated
oropharyngeal SCC has a much better prognosis despite the tendency to have early nodal
metastases and the staging scheme accounts for this. Additionally, unlike nasopharyngeal
SCC, the T-staging of the oropharynx is largely based on size criteria (T1–T3).
• Evaluation of the pre-epiglottic fat space is important as involvement of this area results
in upstaging to T3. Other areas that must be specifically addressed during staging include
mandibular invasion, prevertebral muscle invasion which precludes surgical resection,
pterygopalatine fossa invasion which raises the possibility of perineural spread, bilateral
involvement of the base of tongue which has implications for surgical resection, and
lymphadenopathy.
• Treatment is dependent on the stage, with single-modality treatment with surgery or
radiation in early-stage cancers and combined treatment in higher-stage disease.

Oral cavity
submandibular sublingual gland lingual septum
gland
genioglossus
geniohyoid
mylohyoid
hyoglossus
anterior diagstric
sublingual space
submandibular space

• The oral cavity includes the lips, the anterior 2/3 of the tongue, the buccal mucosa, the
gingiva, the hard palate, the retromolar trigone, and the floor of the mouth.
• The floor of the mouth, a substitute of the oral cavity, is bound by the mylohyoid muscle
inferiorly, the tonsillar pillar posteriorly, and the mandible anteriorly, and includes the
sublingual spaces and the deep portion of the submandibular gland as described below.
• The sublingual spaces are a subsite of the floor of mouth and are bound by the intrinsic
muscles of the tongue superiorly, the mylohyoid muscle inferolaterally, the mandible
anteriorly, and the geniohyoid/genioglossus muscles medially. Important structures
that run in the sublingual space include the lingual nerve (branch of the trigeminal), the
glossopharyngeal and the hypoglossal nerve, as well as the sublingual gland and duct.
• Directly inferior to the sublingual space is the U-shaped submandibular space. The
sublingual space is separated from the submandibular space by the mylohyoid muscle
anteriorly, although the sublingual space is contiguous with the submandibular space
posteriorly.
Retromolar trigone (arrow) on axial contrast-

enhanced CT, a triangular region bounded
anteriorly by the last mandibular molar,
posteromedially by the anterior tonsillar pillar,
laterally by the buccal mucosa.

Oral cavity SCC
• SCC is the most common malignancy which occurs in the oral cavity and risk factors are
similar to SCC of other subsites, such as smoking, chewing tobacco, and HPV exposure,
although HPV exposure is much less strongly associated in comparison to oropharyngeal
SCC.
• The lip is the most common site of SCC of the oral cavity. Many of these lesions are easily
assessed through direct inspection and imaging is indicated to evaluate for osseous invasion
or lymph node metastases.
• Oral cavity SCC staging is also largely based on the size of the lesion for determination of
T1–T3 and unlike oropharyngeal SCC, there is only one staging scheme.
• Key areas to evaluate in staging of oral cavity SCC include evaluating for mandibular/
maxillary invasion and involvement of the retromolar trigone. Involvement of the
retromolar trigone cannot be determined clinically and provides access to numerous
routes of spread. Other key areas of involvement include the pterygomandibular raphe,
which provides access to the floor of the mouth and masticator space, extension to the
oropharynx, extension to the larynx.
• For primary oral tongue lesions, it is important to assess for extension across midline and
involvement of the intrinsic muscles of the tongue.
Dermoid/epidermoid
• A dermoid is a teratomatous lesion which contains at least two germ cell layers, while an
epidermoid contains only ectoderm.
• On CT, both dermoid and epidermoid will appear as a fluid-attenuation lesion, most
commonly in the midline of the floor of the mouth. A pathognomonic MRI finding of
dermoid is the sack of marbles appearance resulting from floating fat globules. In the
absence of this finding, epidermoid and dermoid can be indistinguishable in this location on
MRI.
Ranula
• A ranula is a mucous retention cyst that
arises from the sublingual gland as a sequela
of inflammation. All ranulas arise from the
sublingual gland or adjacent minor salivary
glands and hence begin in the sublingual
space.
• A plunging ranula extends from the
sublingual space into the submandibular
space by protruding posteriorly over the
free edge of the mylohyoid or by extending
directly through a defect in the mylohyoid.
Ranula: Contrast-enhanced axial CT at the level of
• A dermoid cyst may also present below the the mandible shows a cystic lesion (arrow) in the left
mandible, but is typically midline, rather than sublingual space.
the eccentric location of a plunging ranula.

Thyroglossal duct cyst (TDC)
Infected thyroglossal duct cyst: Sagittal (left image) and axial enhanced CT in an intubated 13-month-old show
a thick-walled peripherally enhancing cystic structure (arrows) in the midline, inferior to the mylohyoid.
• A thyroglossal duct cyst (TDC) represents persistence of the thyroglossal duct. The
thyroglossal duct follows the midline descent of the embryonic thyroid gland from the base
of the tongue (foramen cecum) to its normal position in the neck. Most thyroglossal duct
cysts present in childhood as an enlarging neck mass which elevates with tongue protrusion.
• The majority of TDCs (65%) are infrahyoid, the rest found at the level of the hyoid or above.
Most TDCs are midline, but they may occur slightly off midline, especially when infrahyoid.
• Thyroid carcinoma (papillary type) is a rare complication seen in 1% of TDCs.
Lingual thyroid
• Lingual thyroid is ectopic thyroid tissue that has incompletely descended during embryologic
development and remains at the floor of the mouth. Usually, the ectopic gland is the only
functioning thyroid tissue, so the neck should be evaluated to confirm lack of normal gland.
• Lingual thyroid is much more common in females.
• Lingual thyroid is susceptible to standard thyroid pathology, including thyroiditis and cancer.
Lymphatic malformations
• Lymphatic malformations are congenital abnormalities that result when the embryologic
lymphatics fail to connect to developing veins. There are three types of lymphatic
malformations, classified by the size of the intra-lesional cystic spaces.
• Cystic hygroma is the most common type of lymphatic malformation, the majority being
present at birth and associated with chromosomal anomalies including Turner and Down
syndromes. A cystic hygroma features large lymphatic spaces. The most common location is
in the posterior triangle of the neck.
• Cavernous lymphangioma has smaller lymphatic spaces than a cystic hygroma, while a
capillary lymphangioma has the smallest cystic spaces.

Odontogenic lesions
Dentigerous cyst
Sagittal (left image) and coronal (right image) contrast-enhanced CT show an unilocular lucent lesion (arrows)
at the crown of the unerupted left third mandibular molar, consistent with a dentigerous cyst.
• A dentigerous cyst is the most common type of non-inflammatory odontogenic cyst and
forms when fluid accumulates between the follicular epithelium and the crown of an
unerupted tooth.
• This manifests as a well-defined, unilocular osteolytic lesion around the crown of an
impacted tooth, most frequently around the crown of a mandibular third molar.
Radicular (periapical) cyst
• A radicular cyst is the most common odontogenic lytic lesion. It occurs in either the
mandible or the maxilla and is associated with an infected tooth.
• This can progress to bony dehiscence which results in extension of the inflammation to
neighboring tissues and can progress to a soft tissue abscess.
Ameloblastoma
Coronal (left image) and axial (right image) noncontrast CT demonstrate an expansile, mixed-density,
peripherally calcified mass in the left maxillary sinus associated with the root of an anterior left maxillary molar
(arrow). Biopsy showed ameloblastoma.
• Ameloblastomas are benign epithelial neoplasms and exhibit locally aggressive behavior.
• These most commonly (80%) occur in the ramus and posterior body of the mandible.
Ameloblastoma (continued)
• These classically and more frequently appear as multilocular lytic lesions with mixed cystic
and solid regions.
• However, 40% of the time, these can appear unilocular and are indistinguishable from
odontogenic keratocysts or dentigerous cysts. In comparison to odontogenic keratocyst, an
ameloblastoma is more likely to be predominantly cystic, while odontogenic keratocysts
have debris resulting in a more heterogeneous appearance on T2-weighted imaging on MRI
and lower mean value on ADC.
Odontogenic keratocyst
Sagittal (left image) and axial (right image) contrast-enhanced CT show an unilocular expansile lucent lesion
(arrows) in the left mandibular body abutting the root of a left mandibular molar. Pathology upon resection
showed odontogenic keratocyst.
• A keratocystic odontogenic tumor is a benign unilocular expansile lucent lesion, most
frequently seen in the body and ramus of the mandible. As described above, it is more
likely to be heterogeneous on T2 and is not associated with buccolingual expansion in the
mandible. However, when it is multilocular, it cannot be reliably distinguished from an
ameloblastoma based on imaging.

Differential diagnosis of lytic odontogenic lesions
Lytic odontogenic lesions
Unilocular, around crown of unerupted tooth,

more homogeneous on T2, associated with
more buccolingual expansion in the mandible
Dentigerous cyst
Unilocular, in posterior jaw, more

heterogeneous on T2, not associated with
buccolingual expansion in the mandible
Odontogenic kerotocyst
Multilocular, mixed cystic/solid, associated

with more buccolingual expansion in the
mandible
Ameloblastoma
Unilocular, centered around the apex of an

infected tooth
Radicular cyst
Hypopharynx
• The hypopharynx is the inferior continuation of the oropharynx. It surrounds the larynx
on three sides and extends to the level of the inferior border of the larynx, and continues
inferiorly as the cervical esophagus. The hypopharynx can be divided into three regions: the
piriform sinuses, the posterior pharyngeal wall, and the posterior cricoid region.
• The aryepiglottic folds separate the hypopharynx from the supraglottic larynx. Tumors
arising from these folds are staged as supraglottic tumors (described in the larynx section
below).
Hypopharyngeal SCC
• Most hypopharyngeal SCCs arise in the pyriform sinus. Staging of hypopharyngeal SCC is
dependent on both the lesion size and invasion of adjacent structures.
• Important imaging findings to evaluate for during staging include: Fixation of the
hemilarynx; assessment of local invasion including potential involvement of the esophageal
mucosa, thyroid/cricoid cartilage, hyoid bone, and prevertebral fascia; and vascular
involvement such as encasement of the carotid artery or mediastinal structures.

Larynx
epiglottis
aryepiglottic fold
piriform sinus
posterior to aryepiglottic folds
false vocal cords

laryngeal
vestibule paraglottic fat
supraglottic
larynx
hyoid bone
thyroid cartilage
laryngeal ventricle
glottis thyroarytenoid
and vocalis muscles
subglottic true
larynx vocal ligament
vocal cords
thyroid gland
cricoid cartilage
trachea
trachea
• The larynx connects the oropharynx airway to the tracheal airway.

• The cartilaginous components of the larynx include the epiglottis, thyroid cartilage, cricoid
cartilage, and arytenoids.
The cricoid cartilage is a complete ring which provides the foundation for the laryngeal skeleton.
• The entire larynx, including the epiglottis, aryepiglottic folds and false vocal cords, is lined
with mucosa.
The aryepiglottic folds are an extension of the mucosa covering the epiglottis and mark the entrance to
the larynx. The aryepiglottic folds connect the epiglottis anteriorly to the arytenoids posteriorly.
The false vocal folds are mucosal infoldings superior to the laryngeal ventricle. They can be identified on
cross-sectional imaging by the presence of the paraglottic fat laterally.
• The supraglottic larynx extends from the epiglottis to the ventricle. The false vocal cords,
the aryepiglottic folds, the suprahyoid epiglottis, infrahyoid epiglottis, and the arytenoid
cartilages are within the supraglottis and considered subsites for the purposes of staging SCC
as discussed below.
• The glottis includes the true vocal cords, the anterior and posterior commissures, and
extends 1 cm below the vocal cords. The thyroarytenoid muscle, vocalis muscle, and the
innermost vocal ligament form the bulk of the vocal cords.
The true vocal cords are identified in the axial plane by CT or MRI by identifying the transition of
paraglottic fat to muscle (thyroarytenoid muscle) within the wall of the larynx.
• The subglottic larynx begins 1 cm inferior to the apex of the laryngeal ventricles and extends
to the first tracheal ring. The cricoid cartilaginous ring is within the subglottic larynx.

Vocal cord paralysis
• Vocal cord paralysis is most commonly due to iatrogenic trauma from neck surgery, but
may be secondary to a mass along the course of the vagus or recurrent laryngeal nerves.
Other conditions include stroke, infection, laryngeal neoplasm, MS and neuro-degenerative
disease.
• The most common mass to cause left vocal cord paralysis is a mediastinal or thoracic mass;
however, enlargement of the left atrium or pulmonary arteries may cause cardiovocal
syndrome due to recurrent laryngeal nerve compression.
• The CT imaging of vocal cord paralysis shows a thickened, medialized aryepiglottic fold and
enlargement of the piriform sinus on the affected side.
• The left recurrent laryngeal nerve is the most commonly affected nerve. Imaging for vocal
cord paralysis should extend from the skull base to the level of the left pulmonary artery to
cover the full course of the vagus and the left recurrent laryngeal nerves.
• The recurrent laryngeal nerve innervates all laryngeal musculature except the cricothyroid
muscle, which is innervated by the superior laryngeal nerve.
Laryngocele
• A laryngocele is a dilation of the laryngeal ventricle, which may be caused by high laryngeal
pressures. Trumpet players, glassblowers, and patients with COPD have increased risk of
developing a laryngocele. A laryngocele may be filled with air or fluid.
• An important differential consideration is ventricular obstruction by neoplasm (most
commonly squamous cell carcinoma), which typically causes a fluid-filled laryngocele.
Laryngeal SCC
Supraglottic SCC: Axial noncontrast CT through the neck (left image) in a patient presenting with hoarseness
demonstrates nodular thickening of the right false cord (yellow arrow) effacing the paraglottic fat. Subsequent
F-18 FDG PET shows uptake correlating to this nodule (yellow arrow) as well as uptake in a right level III lymph
node (red arrows) concerning for metastatic involvement.
• Laryngeal SCC is the most common laryngeal malignancy.
Less common tumors of the larynx (such as lymphoma and chondrosarcoma) are submucosal and
therefore not visible on laryngoscopic exam.
• The majority of laryngeal SCC arise from the glottis.
• There are three staging schemes for laryngeal SCC, specific to the supraglottic, glottic, and
subglottic subsites.
• Staging of the supraglottic SCC is dependent on the number of subsites of the supraglottis
that are described (listed above), vocal cord mobility, and involvement of adjacent
structures.

Laryngeal SCC (continued)
Treatment of supraglottic SCC can vary from laser epiglottectomy, various types of supraglottic
laryngectomy to total laryngectomy. Involvement of several key structures guides surgical management
including the laryngeal ventricle, thyroid cartilaginous invasion, posterior cricoid, or anterior commissure
invasion, involvement of bilateral arytenoid cartilage, which are contraindications to supraglottic
laryngectomy.
Other areas which have relevance in staging include the paraglottic space, the inner cortex of the thyroid
cartilage, involvement of the prevertebral space, encasement of the carotid artery or involvement of
mediastinal structures.
Local spread to the paraglottic spread is particularly relevant in supraglottic tumors.
• Staging of glottic SCC is also dependent on vocal cord mobility, cartilaginous involvement,
and extension to relevant structures described above.
Patients with SCC of the glottis present early because of voice changes.
Key consideration for staging glottic SCC is evaluation for contralateral involvement, since this precludes
sparing of the contralateral side as well as the degree of vertical involvement.
Transglottic tumors, which cross the laryngeal ventricle to involve both the false and true vocal cords,
portend a worse prognosis.
• Subglottic SCC constitutes less than 5% of laryngeal carcinomas. These lesions can be
difficult to identify endoscopically given obscuration from apposed true cords. Staging is
similar to the supraglottic and glottic types described above. Prognosis for subglottic lesions
is poor as they present at a much more extensive stage.
Laryngeal hemangiomas
• Laryngeal hemangiomas occur most commonly in the subglottic larynx in infants. These are
frequently associated with cutaneous lesions. They frequently regress in infants, however
given risk of airway compromise can be treated with laser therapy.
• Laryngeal hemangiomas in adults are very rare, with only case reports in the literature.
These do not regress spontaneously and are surgically treated.
Laryngeal trauma
• Blunt trauma to the neck may compress
the larynx against the cervical spine,
with injury to the posterior soft tissues
due to the sandwich effect.
• Fractures of the thyroid and cricoid
cartilage may be difficult to detect
in young patients with incomplete Thyroid cartilage fracture: CT in bone windows shows a
minimally displaced fracture of the thyroid cartilage (arrow).
ossification.
Case courtesy Mary Beth Cunnane, MD, Massachusetts Eye
• Iatrogenic trauma from intubation can
and Ear Infirmary.
cause arytenoid cartilage dislocation.
Other malignant neoplasms of the mucosal spaces
Lymphoma
• Lymphoma can arise from the adenoids of the nasopharynx. Most frequently this is non-
Hodgkin’s lymphoma and affects a younger population.
Sarcomas
• Any type of sarcoma can be found in the larynx, including synovial sarcomas,
chondrosarcomas, rhabdomyosarcomas, and liposarcomas. Chondrosarcomas are generally
centered in either the cricoid or thyroid cartilage and have characteristic popcorn-like
calcifications that are best seen on CT.

Extra-mucosal neck spaces
Overview of head and neck spaces
• The complex layers of cervical fascia create several spaces in the suprahyoid neck.
Knowledge of these spaces is useful in creating differential diagnoses for neck masses, as
specific lesions tend to arise in characteristic locations.
Retropharyngeal space
pharyngobasilar fascia pharynx

retropharyngeal space
alar fascia
danger space
prevertebral fascia
prevertebral space
the prevertebral space

is the anterior component
of the perivertebral space
• The retropharyngeal space is a potential space located posterior to the pharynx, separated
from the pharynx by the pharyngobasilar fascia. The retropharyngeal space extends from
the base of the skull to the upper mediastinum. Directly lateral to the retropharyngeal space
are the carotid and parapharyngeal spaces.
• The alar fascia is directly posterior to the retropharyngeal space. The alar fascia separates
the retropharyngeal space from another potential space, the danger space, which acts as a
trapdoor for infection to travel all the way from the neck to the diaphragm.
• The prevertebral space (the anterior component of the perivertebral space in the
suprahyoid neck) is located just anterior to the vertebral body and is bounded anteriorly by
the prevertebral fascia.
• Benign and inflammatory lesions of the retropharyngeal space:
A medially deviated internal carotid artery may mimic a mass on endoscopic evaluation or may be
injured during spine surgery.
Lipomas, fibromyxomas, and venous malformations can occur in the retropharynx.
Spread of infection into the retropharynx can result in a retropharyngeal abscess, discussed later in this
chapter.
• Malignant lesions of the retropharyngeal space:
Primary malignant lesions are uncommon. The most common malignant lesion is malignant
lymphadenopathy, most frequently associated with nasopharyngeal SCC. Other primary tumors which
are associated with retropharyngeal lymphadenopathy include: Papillary thyroid carcinoma, melanoma.
Contiguous spread of primary tumors in the nasopharynx can involve the retropharyngeal space, such as
nasopharyngeal SCC and rhabdomyosarcoma.

Carotid space
Anatomy of the carotid space
carotid space
vagus nerve (X) (yellow circle)
ICA
carotid jugular
sheath vein
Other cranial nerves passing through the carotid space:

glossopharyngeal nerve (IX)
spinal accessory nerve (XI)
hypoglossal nerve (XII)
• The carotid space, or post-styloid parapharyngeal space, is an incomplete fascial ring

surrounding the carotid artery and jugular vein. The carotid space extends from the skull
base to the aortic arch.
• The contents of the carotid space include the carotid artery, carotid body, jugular vein,
and several cranial nerves. The vagus nerve (cranial nerve X) is the only cranial nerve that
remains within the carotid space the entire way into the thorax. In contrast, cranial nerves
IX, XI and XII pass transiently through the carotid space. Though there are lymph nodes
surrounding the carotid space, there are no lymph nodes contained within it.
• The pattern of displacement of vascular structures in the carotid space is the key to
generating a differential diagnosis for a carotid space mass.
Differential diagnosis of a carotid space mass
• Paraganglioma
Paragangliomas that occur in the carotid space include
paraganglioma of the carotid body and paraganglioma
of the vagal nerve. These demonstrate imaging
characteristics similar to paragangliomas elsewhere in the
head and neck, described previously.
Paraganglioma of the carotid body (carotid body tumor or
glomus caroticum tumor) splays the external and internal
carotid arteries at the carotid bifurcation.
Paraganglioma of the vagal nerve (glomus vagale tumor)
displaces the internal and external carotid arteries
anteromedially.
• Schwannoma
Similar to glomus vagale tumor, schwannoma (also most
commonly of the vagus nerve) also displaces the carotid
arteries anteromedially. Schwannoma, however, is not Carotid body tumor: Axial contrast-
nearly as vascular as paraganglioma and does not have enhanced CT shows an avidly enhancing
internal flow voids. mass (yellow arrows) surrounding and
• Neurofibroma splaying the right internal (red arrow) and
external carotid (blue arrow) arteries.
Neurofibromas are almost always associated with
neurofibromatosis type l. Neurofibroma and schwannoma Case courtesy Mary Beth Cunnane, MD,
are indistinguishable by MRI. Massachusetts Eye and Ear Infirmary.

Parapharyngeal space (PPS)
Anatomy of the parapharyngeal space
parapharyngeal
space
masticator
space
parotid
gland
carotid
space
• The prestyloid parapharyngeal space (PPS) is a triangular fat-filled space containing

lymphatics, branches of the internal maxillary artery, ascending pharyngeal artery, and the
mandibular (V3) nerve.
• The direction of displacement of the parapharyngeal space fat by a mass in an adjacent
compartment is predictable and helpful in determining from which compartment a given
mass originates.
Masticator space lesions (e.g., masticator abscess) displace the PPS posteromedially.
Parotid lesions (e.g., pleomorphic adenoma) displace the PPS anteromedially.
Carotid space lesions (e.g., paraganglioma) displace the PPS anteriorly.
• Benign and inflammatory lesions involving the prestyloid parapharyngeal space:
Parapharyngeal abscesses most frequently result from infections that arise in adjacent spaces, most
commonly from the palatine tonsil, pharynx or are odontogenic in origin.
Second branchial cleft cysts, discussed later, can present in the parapharyngeal space.
Benign tumors, most frequently pleomorphic adenoma, arising from the deep portion of the parotid
gland or salivary rests within the parapharyngeal fat can present as a mass in this space.
Rarely schwannomas, usually arising from the sympathetic plexus or the mandibular (V3) nerve, can arise
in this space.
• Malignant lesions of the prestyloid parapharyngeal space:
Malignant tumors are rare and when they occur are most frequently salivary gland in origin, such as
mucoepidermoid carcinoma, adenoid cystic carcinoma, and acinic cell carcinoma.
Secondary invasion can be seen, most commonly from the pharynx, such as SCC or minor salivary gland
carcinoma, and lymphoma, or the skull base, chordoma, chondrosarcoma, osteoma, osteochondroma,
which are discussed elsewhere.

Perivertebral space
Anatomy of the perivertebral space
perivertebral space
VA
vertebral body
spinal
canal
paraspinal
muscles
• The perivertebral space is formed by the deep layer of deep cervical fascia which wraps
entirely around the prevertebral and paraspinal muscles. The anterior perivertebral space is
synonymous with the prevertebral space. The perivertebral space is in the suprahyoid neck;
the paravertebral space is the analogous region in the thoracolumbar spine.
• The perivertebral space includes the longus colli-capitis muscle complex, the paraspinal
muscles, the vertebral bodies, the neurovascular structures within the spinal canal, including
the spinal column, exiting nerves, the vertebral arteries, as well as the brachial plexus.
• Differential diagnosis of a benign lesion in the perivertebral space:
Congenital lymphatic lesions (discussed later).
Nerve sheath tumors arising from cervical nerve roots.
Hemangiomas of the musculature.
Benign bony tumors.
• Malignant lesions in the perivertebral space:
Malignant lesions are most frequently centered on the vertebral bodies, and therefore most frequently
are metastases.
Other differential considerations include primary vertebral body malignancies, soft-tissue malignancies
arising from the perivertebral musculature such as lymphoma, rhabdomyosarcoma.

Masticator space
Anatomy of the masticator space
masticator space
m
pterygoid
as
se
plate
tte
te
r
m
ma
po
lat
ndi
er
ra
al
s li
b
pt
le
pt me er
yg
er dia o
yg l id
oi
d
• The masticator space is located directly anterior to the parotid and contains the muscles
of mastication, the mandible, and cranial nerve V3. Cranial nerve V3 (mandibular division)
exits the skull through foramen ovale and innervates the muscles of mastication. If there is a
lesion in the masticator space, it is important to assess for perineural spread along V3.
• The temporomandibular joint also falls within the masticator space.
• The majority of abnormalities that occur in the masticator space are a result of extension
from neighboring spaces, such as the oral cavity, the parotid space, or the parapharyngeal or
retropharyngeal spaces.
Infections of the masticator space
Masticator/submandibular abscess: Axial (left image) and coronal contrast-enhanced CT shows a peripherally
enhancing irregular fluid collection (arrows) abutting the angle of the right mandible, with associated stranding
of the subcutaneous fat.
• Infections of the masticator space are more common than tumors.
• Most infections are odontogenic in origin. Less commonly, extension of infection from
parotid gland sialadenitis, extension of a palatine tonsillar abscess, or extension of a severe
retropharyngeal space infection can be seen.

• A masticator space abscess appears as an irregular, thick-walled, peripherally enhancing
fluid located inferior to the mandible. Adjacent fat-stranding is usually present.
Approach to tumors and non-neoplastic masses in the masticator space
• Masses within the masticator space can be organized as masses arising from bone
(mandible), arising within the nerve (branches of the mandibular nerve) or arising within the
muscles of mastication.
• Lesions arising from the mandible:
Primary bone tumors arising from the mandible include osteoblastoma, osteosarcoma, chondrosarcoma.
Odontogenic lesions such as dentigerous cyst, keratocyst, or ameloblastoma can be seen in the mandible,
and are more completely discussed in the oral cavity section.
• Lesions arising within nerve:
Anatomically, after exiting the skull base from the foramen ovale, V3 lies along the medial margin of the
lateral pterygoid muscle.
Schwannomas of V3 can smoothly expand the foramen ovale and present as a well-defined mass in the
masticator space, with imaging characteristics similar to those of schwannomas elsewhere in the head
and neck as described previously.
• Lesions arising within muscle:
Venous malformations (previously known as hemangiomas and lymphangiomas) can be seen, usually
within the masseter muscle when present.
Malignant masses arising from muscle include rhabdomyosarcoma, lymphoma, and metastases.
Temporomandibular joint anatomy & pathology

Right TMJ, closed mouth position Right TMJ, open mouth position
Left TMJ, closed mouth position Left TMJ, open mouth position
Sagittal T2-weighted MRI of normal and abnormal temporomandibular joints:
Images of the right TMJ demonstrate normal disc position, shape, and signal on closed mouth view, and slightly
limited disc mobility on open mouth image with abnormal retrocondylar T2 hyperintense signal representing a
small joint effusion.
Images of the left TMJ show an abnormally small condyle, and an anteriorly dislocated disc which appears
thickened with intermediate T2 signal. On open mouth view, there is lack of normal mobility without change in
disc position possibly representing “stuck disc” due to adhesions.
• The temporomandibular joint (TMJ) can get dislocated and anterior meniscal dislocations
are the most common.
• Similar to other synovial joints, the TMJ can be affected by degenerative osteoarthritis and
inflammatory arthritis such as rheumatoid arthritis and juvenile idiopathic arthritis, as well
as crystalline arthropathies, which are discussed in greater detail in the “Musculoskeletal”
chapter.
• The TMJ can be affected by lesions such as pigmented villonodular synovitis, synovial
chondromatosis and chondroid masses.

Other benign lesions/masses of the masticator space
Second branchial cleft cyst
Second branchial cleft cyst: Coronal (left image) and axial contrast-enhanced CT shows a water-attenuation
cystic lesion (yellow arrows) at the angle of the left mandible with minimal peripheral wall enhancement. This
cyst is in the classic location of a second branchial cleft cyst: Posterior to the submandibular gland (red arrow),
anterior to the sternocleidomastoid muscle (blue arrow), and closely associated with the carotid sheath.
• A branchial cleft cyst is a congenital anomaly arising from the embryologic branchial
apparatus. There are 4 types of congenital branchial cleft cysts, with the second type being
the most common type.
• A second branchial cleft cyst may occur at any point along the path extending from the
palatine tonsil to the supraclavicular region, but occurs most commonly near the angle of
the mandible.
• The classic second branchial cleft cyst displaces the sternocleidomastoid muscle posteriorly,
displaces the carotid artery and internal jugular vein medially and the submandibular gland
anteriorly.
• The cyst may become superinfected, suggested by wall enhancement and adjacent
inflammatory changes within the surrounding soft tissues.
Although second branchial cleft cysts are frequently in the posterior submandibular space, an infected
second branchial cleft cyst would not typically be confused with a submandibular abscess. Submandibular
abscess is usually due to dental disease, typically located immediately inferior to the mandible.
• Branchial cleft cysts are uncommon in older adults. A cystic metastasis (e.g., from papillary
thyroid cancer or base of tongue/tonsillar SCC) should be considered instead, especially if
the cyst is irregular or has a mural nodule.
• On imaging, there is opacification of the middle ear and mastoid air cells, often with bony
erosion of the mastoid.

Cervical lymph nodes
structures defining the boundaries cervical lymph node levels
of cervical lymph node levels and their boundaries
submandibular posterior margin of
gland submandibular
gland
medial margin posterior margin of

anterior of ant. digastric IIB internal jugular vein
digastric IIA
IA
anterior margin of
hyoid bone
trapezius
carotid artery SCM inferior margin
of hyoid bone III posterior margin of
thyroid cartilage sternocleidomastoid
VA
cricoid cartilage trapezius
internal jugular inferior margin VB
anterior IV
vein of cricoid cartilage posterior margin of
scalene
anterior scalene
anterior margin
clavicle of carotid artery clavicle
cervical lymph node levels superimposed on boundary structures
posterior margin
of submandibular gland
mandible
medial margin
of anterior digastric IIB
IB IIA posterior margin of
IA internal jugular vein
inferior margin
of hyoid bone anterior margin of
trapezius
thyroid
cartilage III posterior margin of
sternocleidomastoid
VA
inferior margin
of cricoid cartilage
anterior margin
of carotid artery IV VB
posterior margin of
anterior scalene
clavicle

Cervical lymph node levels
Overview of cervical lymph nodes
• The cervical lymph nodes are divided into 7 levels as recommended by the American Joint
Committee on Cancer (AJCC), with consistent agreement between surgeons, oncologists,
and radiologists. The lymph node levels are not defined by fascial planes, but instead are
defined by anatomic landmarks and organized by patterns of lymphatic spread.
• In an adult, 90% of head and neck cancers are SCC: The role of the radiologist is not to
provide a differential, but to stage the disease. The degree of lymph node involvement has a
substantial prognostic value. For instance, a single metastatic lymph node decreases survival
from SCC by 50% over an equivalent period.
• Cystic lymph nodes can be seen in the setting of papillary thyroid cancer and SCC of the
head and neck.
Level I
• Level I lymph nodes include submental and submandibular nodes, which are superior to the
hyoid bone and inferior to the mandible and mylohyoid.
• IA nodes are submental, lying between the medial margins of the anterior bellies of the
digastrics. IB nodes are submandibular, lateral to the medial margin of the anterior belly of
the digastric and extending to the posterior margin of the submandibular gland.
Level II
• Level II lymph nodes are upper internal jugular nodes, extending from the skull base to the
inferior margin of the hyoid bone.
• IIA nodes are anterior to the posterior margin of the internal jugular vein (IJV). IIB nodes are
posterior to the IJV but anterior to the posterior margin of the sternocleidomastoid muscle.
Level III
• Level III lymph nodes are middle jugular nodes, extending craniocaudally from the inferior
aspect of the hyoid to the inferior aspect of the cricoid cartilage. The posterior edge of the
sternocleidomastoid is the shared posterior margin for both level III and level IIB nodes.
Level IV
• Level IV nodes are inferior jugular nodes, extending from the inferior aspect of the cricoid
cartilage to the clavicle. Superiorly, the posterior border is the posterior aspect of the
sternocleidomastoid muscle (similar to level III and IIB nodes). Inferiorly, the posterior
border is the posterior aspect of the anterior scalene muscle.
Level V
• Level V lymph nodes are posterior cervical nodes.
• VA nodes are superior, extending from the skull base to the inferior cricoid cartilage.
• VB nodes are inferior, extending from the inferior cricoid cartilage to the clavicle.
Level VI
• Level VI nodes are pretracheal nodes, which are often simply called “pretracheal”. They
are located anteromedially in the lower neck and bounded laterally by the carotid sheaths.
Level VI extends craniocaudally from the inferior aspect of the hyoid bone to the top of the
manubrium.
Level VII
• Level VII nodes are superior mediastinal nodes, which are also commonly described by
their location. They are inferior to level VI and medial to the carotid sheaths, extending
craniocaudally from the superior aspect of the manubrium to the brachiocephalic vein.

Neck infections and inflammation
Ludwig angina
• Ludwig angina is cellulitis of the floor of the mouth. It is an infection that can involve the
submental, sublingual, and submandibular spaces.
• The tongue may be posteriorly displaced, so ensuring airway patency is a clinical priority.
• On imaging, there is stranding and swelling at the floor of the mouth.
Retropharyngeal abscess
Retropharyngeal abscess:
Lateral neck radiograph (top left image) demonstrates

marked thickening of the prevertebral tissues
(arrows).
Sagittal (bottom left image) and axial contrast-

enhanced CT demonstrate a peripherally enhancing
fluid collection in the retropharyngeal space (arrows),
causing effacement of the right oropharynx.

• Retropharyngeal infection may cause airway compromise.

• In children, retropharyngeal infection is most often from spread of an upper respiratory tract
infection, such as pharyngitis, which may cause the retropharyngeal lymph nodes that drain
the pharynx to become suppurative and rupture.
• In adults, retropharyngeal infection is most often due to penetrating injury, such as fish bone
ingestion or instrumentation.
Peritonsillar abscess
• Peritonsillar abscess is a complication of peritonsillar lymph node suppuration, causing the
characteristic hot-potato voice.
Lemierre syndrome
• Lemierre syndrome is venous thrombophlebitis of the tonsillar and peritonsillar veins, often
with spread to the internal jugular vein. Immunocompetent adolescents and young adults
are typically affected.
• The most common infectious agent is the anaerobe Fusobacterium necrophorum, which is
part of the normal mouth flora.
Lemierre syndrome (continued)
• Imaging shows enlargement, thrombosis, and mural enhancement of the affected veins.
• Pulmonary septic emboli may be present.
Tuberculous adenitis (scrofula)
• Tuberculous adenitis is usually seen in patients of Asian descent who present with painless
neck masses. Imaging findings are classically bilateral necrotic lymph nodes, often in
the level V posterior triangle distribution, occasionally multiloculated with ring-like
enhancement. Sinus tracts to skin can form at the late stage. The nodes classically calcify
after treatment.
Cat scratch fever
• Cat scratch fever is an infection caused by Bartonella henselae and can present with
fever, malaise, and regional lymphadenopathy. It can be self-limited or can progress to
encephalopathy and neuropathy.
Thyroid and parathyroid

Diffuse thyroid disease
Hashimoto thyroiditis (chronic lymphocytic thyroiditis)
• Hashimoto thyroiditis is an autoimmune disease that is thought to be due to autoantibodies
to thyroglobulins. It is the most common cause of hypothyroidism.
• The diagnosis is often made serologically. Patients are often euthyroid early in disease, but
eventually become hypothyroid due to replacement of functioning thyroid parenchyma.
• Ultrasound may show either a diffusely micronodular gland or a heterogeneous coarsened
gland without a measurable nodule. The isthmus is characteristically thickened. In its end
stage, the gland becomes atrophic.
• Patients with Hashimoto thyroiditis are at increased risk of thyroid lymphoma.
Graves disease
Graves disease: Sagittal grayscale ultrasound of the thyroid (left) demonstrates a diffusely enlarged gland with
coarsened, heterogeneous echotexture. Color Doppler (right image) shows markedly increased Doppler flow
representing the thyroid inferno sign.
Case courtesy Julie Ritner, MD, Brigham and Women’s Hospital.
• Graves disease causes autoimmune activation of the TSH receptor, stimulating thyroid
hormone synthesis and secretion. Patients clinically present with thyrotoxicosis.
• Ultrasound may show diffuse enlargement of the gland, a coarsened echotexture and
hypervascularity. The borders of the gland are often lobulated.

Graves disease (continued)
• The key color Doppler finding is the thyroid inferno sign, which represents marked
hypervascularity caused by arteriovenous shunting and enlarged peripheral vessels.
• Because of significant overlap in sonographic findings with Hashimoto thyroiditis, correlation
with laboratory findings is required.
Subacute thyroiditis (de Quervain thyroiditis)
Subacute (de Quervain) thyroiditis: Sagittal grayscale thyroid ultrasound (left image) demonstrates patchy
areas of decreased echogenicity with no discrete nodule. Color Doppler (right image) does not demonstrate
increased vascularity, in contrast to Graves disease. Case courtesy Julie Ritner, MD.
• Subacute (de Quervain) thyroiditis is granulomatous inflammation of the thyroid, thought to

be viral in origin. It is the most common cause of a painful thyroid mass. The gland is usually
tender and adjacent cervical adenopathy is common.
• Patients may present with transient hyperthyroidism due to follicular rupture and release
of thyroid hormones, followed by hypothyroidism after depletion of hormone stores. It is
usually diagnosed clinically.
• Ultrasound findings include ill-defined, patchy areas of decreased echogenicity in the
involved regions. Vascularity is normal or decreased.
• Subacute thyroiditis is treated with steroids. Follow-up ultrasound appearance can show a
dramatic response to treatment.
Multinodular gland
• The term multinodular gland is preferred over multinodular goiter because goiter is a
generic term for an enlarged gland, which can have numerous causes.
• On imaging, a multinodular gland will appear enlarged with innumerable mixed cystic and
solid nodules.
Thyroid nodule and thyroid cancer

Approach to a thyroid nodule
• There are no definitive ultrasound features that distinguish benign from malignant nodules.
• The American Thyroid Association (ATA) has developed guidelines for assessment of thyroid
nodules on ultrasound. These guidelines stress use of the sonographic pattern and size for
risk stratification and subsequent decision-making regarding FNA.
• High-suspicion sonographic features include: microcalcifications, hypoechogenicity with
irregular margins, taller-than-wide shape.
• Intermediate suspicion sonographic features include hypoechogenicity with regular margins.
• Low and very-low suspicion sonographic features include hyperechoic or isoechoic solid
nodules with regular margins, spongiform echotexture, partially cystic nodules with
eccentric solid mass.

Approach to a thyroid nodule (continued)
• The American College of Radiology white papers have published guidelines on management
of incidental thyroid nodules detected on CT or MRI. In the absence of suspicious features
on CT or MRI, a thyroid ultrasound is recommended when nodules ≥1 cm in patients <35
years old, and when nodules >1.5 cm in patients >35 years old. Nodules that do not meet
size criteria do not require further evaluation.
Thyroid cancer
Thyroid carcinoma: Sagittal (left image) and transverse grayscale images through the left lobe of the thyroid
demonstrate a solid nodule (calipers) with irregular borders containing punctate calcifications (arrows).
Case courtesy Julie Ritner, MD, Brigham and Women’s Hospital.
• Papillary cancer is by far the most common histologic subtype of thyroid cancer, and confers
the best prognosis. Lymphangitic spread is common, and therefore cervical, sometimes
cystic, lymphadenopathy is common. Lymph nodes may also be calcified, colloid-containing,
or vascular.
• Follicular carcinomas tend to spread hematogenously and have the next best prognosis.
• Medullary subtypes are less common and more aggressive and are associated with MEN II
syndrome. The anaplastic subtype is very rare and has the worst prognosis.
• Non-Hodgkin lymphoma can also occur in the thyroid and usually presents as a solid nodule.
Parathyroid
Anatomy
• Parathyroid glands are usually found adjacent to the thyroid gland. Most patients have four
glands, but there may be between two and six.
• Ectopic locations of the parathyroid glands include the upper mediastinum, in the
tracheoesophageal groove, or at the thoracic inlet.
Indications for imaging
• The most frequent indication for parathyroid imaging is workup of hypercalcemia for
identification of a parathyroid adenoma and/or hyperplasia.
• Patients frequently go straight to curative surgical exploration. In this population, up to
10% of patients develop persistent or recurrent disease after initial surgery. Therefore,
parathyroid localization is more frequently indicated in the re-operative setting.
• MEN I is associated with parathyroid adenomas or hyperplasia.
• Malignant neoplasms of the parathyroid (parathyroid carcinoma) are rare and distinction
can be made with benign adenomas based on rapid growth, local aggressive behavior, and
presence of lymph node metastases.

Imaging modalities
• Imaging options include ultrasound, four-dimensional (4D) CT, or PET.
• Ultrasound is usually the first-line modality. Parathyroid adenomas appear round, well-
circumscribed, homogeneous, and hypoechoic relative to thyroid tissue. Pros of using
ultrasound are the low-cost and lack of radiation. Limitations include operator dependence,
insensitivity for detection of multigland parathyroid disease, and the inability to localize
parathyroid tissue in sonographically inaccessible locations, such as the mediastinum,
tracheoesophageal groove, retroesophageal or retroclavicular locations.
• 4DCT consists of performing noncontrast, arterial, and delayed phases to capitalize on the
perfusion kinetics of adenomas.
Parathyroid adenomas classically are hypodense in comparison to normal thyroid tissue on noncontrast,
demonstrate enhancement greater than thyroid on early (35 sec) arterial phase, and washout more than
thyroid in the delayed phase. However, less than half of parathyroid adenomas follow this pattern.
Large adenomas may show heterogeneous enhancement and atypical enhancement patterns.
Classic parathyroid adenoma:

Axial 4DCT shows a mass (arrows)
posterior to the left thyroid lobe
in the left paraesophageal region
which is hypodense to thyroid
on noncontrast phase, hyper-
enhancing compared to thyroid on
arterial phase.
Noncontrast CT Arterial phase CT
Noncontrast CT Arterial phase CT Delayed phase CT

Atypical parathyroid adenoma: Axial 4DCT shows an oval nodule (arrows) posterior to the right thyroid lobe
which is hypodense to thyroid on noncontrast phase as well as arterial phase, and isodense to thyroid on delay
phase. This biopsy-proven parathyroid adenoma does not follow the classical enhancement pattern but is
otherwise typical in appearance with regards to morphology and location.
• Greatest advantage of 4DCT is for localization of small, multinodular, and/or ectopic

adenomas including those located far-posterior to thyroid (paraesophageal). However, the
greatest limitation is the high radiation exposure.
• Tc-99m sestamibi is the PET tracer that is taken up by parathyroids, and is discussed in
greater detail within the “Nuclear Imaging” chapter.
• MRI is occasionally used as second-line modality to identify lesions that have been
otherwise poorly localized by prior studies.

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Paranasal sinuses, nasal cavity, � anterior skull base

Overview of the sinonasal tract and anterior skull base

Neuro Head & Neck: 754

A right-side Haller cell on axial and coronal CT (arrows).

Neuro Head & Neck: 755

Onodi cell on sagittal and coronal CT (arrows).

Neuro Head & Neck: 756

Coronal CT shows opacification

Neuro Head & Neck: 757

Neuro Head & Neck: 758

Neuro Head & Neck: 759

Mucocele of the frontal sinus:

Neuro Head & Neck: 760

Neuro Head & Neck: 761

Neuro Head & Neck: 762

Encephalocele: Axial T2-weighted MRI shows focal

Neuro Head & Neck: 763

Neuro Head & Neck: 764

Neuro Head & Neck: 765

Neuro Head & Neck: 766

sphenoid greater wing lacrimal bone

zygomatic bone nasal bone

superior orbital fissure nasal septum

inferior orbital fissure palatine bone

infraorbital foramen maxilla

Neuro Head & Neck: 767

Axial T2 anterior segment

*optic nerve/sheath complex

lateral rectus muscle

medial rectus muscle

Coronal T1 superior oblique muscle

levator palpebrae superioris +

superior ophthalmic vein

medial rectus muscle

Neuro Head & Neck: 769

Neuro Head & Neck: 771

Neuro Head & Neck: 772

Thyroid orbitopathy, fatty type: Coronal (left image)

Neuro Head & Neck: 773

Neuro Head & Neck: 774

Neuro Head & Neck: 776

Neuro Head & Neck: 777

Low-grade optic nerve glioma in a young adult:

Neuro Head & Neck: 778

Optic nerve-sheath meningioma: Axial

Neuro Head & Neck: 780

Retinopathy of prematurity: Noncontrast

• Retinopathy of prematurity (ROP) is a disorder of retinal neovascularity in preterm infants,

Neuro Head & Neck: 781

Axial contrast-enhanced CT shows a

Neuro Head & Neck: 782

Retinal detachment: Axial noncontrast

• Choroidal detachment takes an hourglass configuration that diverges as it approaches the

Choroidal detachment in two different patients:

Neuro Head & Neck: 783

Neuro Head & Neck: 784

frontal sinus fractures

Frontal sinus fractures

Core Radiology - Head & Neck Imaging

Core Radiology - Head & Neck Imaging

Core Radiology - Head & Neck Imaging