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23
CHAPTER
Anterior Skull Base Lesions: Imaging
Ajay Garg, Anuj Prabhakar
• Introduction
• Congenital Anterior Skull Base
Lesions
– Nasal Dermal Sinus, Dermoid
Cyst, and Epidermoid Cyst
– Nasal Glioma
– Anterior Cephalocele
– Kallmann Syndrome
• Trauma
– ClassicationofFrontobasal
Fractures
– Complications
• NontraumaticCerebrospinalFluid
Rhinorrhea
– SpontaneousCerebrospinal
FluidRhinorrhea
• Tumors
– Meningioma
– Hemangiopericytoma/Solitary
FibrousTumorsoftheDura
– Pituitary Macroadenoma
– SubfrontalSchwannomas
– Metastasis
INTRODUCTION
Anterior skull base lesions can be classied based on etiology (Table 23.1).
CONGENITAL ANTERIOR SKULL
BASE LESIONS ALSO SEE CHAPTER 20
■ Nasal dermal sinus
■ Anterior cephalocele
■ Nasal glioma
■ Kallmann syndrome.
Nasal Dermal Sinus, Dermoid Cyst, and Epidermoid Cyst
■ ese are congenital inclusion cysts.
■ Incomplete dural separation from the skin and subcutaneous tissue
during regression pulls dermal elements into the dural tract.
■ Occur along the course of the dural tract.
■ Seen in subcutaneous region of the nasal bridge from the glabella to tip
of the nose, the nasal septum, prenasal space and at level of foramen
cecum, adjacent to the crista galli, or anterior third ventricle margin.
Table 23.1: Classication of anterior skull base lesions based on etiology.
Congenital
Trauma(anteriorskullbase
fractures)
Nontraumaticcerebrospinal
uid(CSF)rhinorrhea
Infection/inammatory
Tumors
• Nasal dermal sinus, epidermoid, and dermoid cyst
• Nasal glioma
• Anterior encephalocele
• Kallmann syndrome
• Extensionofsinonasalinfection(osteomyelitis)
• Pseudotumor
• Tumorsarisingfromabove:
– Meningioma
– Pituitary adenoma
– Hemangiopericytoma
– Anteriorskullbaseschwannoma
• Tumorsfrombelow:
– Metastases
– Paget’s disease
■ Rarely sinus tract may extend up to philtrum.
■ Intracranial extension may be seen in 20%; while 80% are extracranial.
■ ese are associated with third ventricle colloid cysts, craniofacial
anomalies in 15%.
■ Present as broadened nasal root, nasoglabellar mass with pit on nasal
bridge with/without hair, and sebaceous discharge. Recurrent meningitis
may be seen, if tract is patent throughout.
■ Computed tomography:
• Large foramen cecum, bid crista galli, and deformity of cribriform
plate on bone window.
• Focal mass along nasal bridge or in the sinus tract.
■ Magnetic resonance imaging (Figs. 23.1A to F):
• Dermal sinus tract: Appears as a midline, subcutaneous, linear
T1 hypointensity within the nasal bridge and coursing toward the
prenasal space.
• Epidermoid cyst: Low signal on T1, bright signal on T2 with diusion
restriction.
• Dermoid cysts: Fat containing lesion showing T1 and T2 hyperintensity
and variable diusion-weighted imaging (DWI) signal.
Nasal Glioma
■ Synonyms: Benign congenital nasal neuroectodermal tumor/nasal
cerebral heterotopia/glial heterotopia.
■ Fibrous stalk representing the rudimentary intracranial connection can
be found in 15%.
317Chapter 23 Anterior Skull Base Lesions: Imaging
Section 6 Systemic Disorders/Surrounding Structures Involving PNS318
A
D
Figs. 23.1A to F: Nasal sinus with dermoid. T1,T2hyperintenselesion(arrowsinA,B,D,
andE)extendingfromthesubcutaneous planesinthebridgeofthenose uptotheintracranial
compartmentacross the foramencecum(arrowinE). Partial fat suppression(arrowinC).
Subtleenhancementalongtheintracranialmargin(arrowinF).
B
E
C
F
■ Detected at birth or in infancy and grow with the child.
■ Composed of dysplastic, neuroglial tissue, and brovascular tissue.
■ e mass may be seen along the nasal dorsum in the region of glabella
(most common) or slightly o midline as a medial canthal lesion.
■ e tumor might also be intranasal (30%), arising from the lateral nasal
wall, middle turbinate, or nasal septum or mixed intra and extranasal
masses (10%).
■ Often misdiagnosed initially as capillary hemangiomas.
■ Present with nasal airway obstruction.
■ Appears as a solid soft tissue mass in the nasal dorsum or cavity without
intracranial extension.
■ Computed tomography:
• inning of nasal bones
• Midline brous pedicle showing an intracranial connection
• Defect in cribriform plate
• Nonenhancing heterogeneous soft tissue density mass
• Cisternography does not reveal any communication between the
lesion and the brain.
■ Magnetic resonance imaging:
• Well-circumscribed, rounded, or polypoid in shape that is iso to
hypointense on T1W and hyperintense on T2W
• Areas of cysts and myxoid degeneration
• Peripheral enhancement of the surrounding nasal mucosa is seen
• e mass itself does not enhance.
Fig. 23.2: Nasofrontal encephalocele.Herniationofthebrainparenchymawithmeninges
(small arrow) through a midline defect between the frontal and nasal bones (large white
arrow).
■ Can be dierentiated from hemangioma using magnetic resonance
imaging (MRI) or Doppler, which shows low diastolic ow in nasal
gliomas.
Anterior Cephalocele
■ Due to incomplete separation of neural and surface ectoderm at the site
of closure of the rostral neuropore in the 4th week of gestation resulting
in a midline mesodermal defect.
■ Classication based on location:
• Nasofrontal cephalocele: It projects out via fonticulus frontalis. Present
as glabellar mass (Fig. 23.2).
• Nasoethmoidal cephalocele: It projects via foramen cecum into the
prenasal space. Present with lesion at the nasal root/intranasally (Figs.
23.3A and B).
• Naso-orbital encephalocele: It projects via foramen cecum, behind
the frontal processes of the maxillary bones into both orbits, and
displacing globes laterally. Present with a medial canthal region mass.
• Basal encephaloceles including spheno-orbital, transethmoidal,
sphenoethmoidal, sphenomaxillary, and transsphenoidal encephaloceles (Fig. 23.4).
■ Classication based on content:
• Meninges only (meningocele)
• Cerebrospinal uid (CSF), meninges, and brain (meningo-
encephalocele)
• Dura, dysplastic neural tissue, and brous tissue (atretic cephalocele)
• Glial-lined cysts containing CSF (glioceles).
■ ese are not linked to neural tube defects.
319Chapter 23 Anterior Skull Base Lesions: Imaging
Section 6 Systemic Disorders/Surrounding Structures Involving PNS320
A B
Figs. 23.3A and B: Nasoethmoidal encephalocele. Hypodense lesion (large arrows) extending
acrossadefectintherightcribriformplate(smallarrows)belowthenasalbone.
Fig. 23.4: Transsphenoidal encephalocele. Well-dened T2 hyperintense lesion with
central hypointensity, in the nasal cavity. Extension across the sphenoid bone (arrows)
anterior to the dorsum sellae. Herniating gliotic brain parenchyma is seen at the site of
intracranialcommunicationandwithinthelesion.
■ Broadening of the nasal bridge, hypertelorism, and enlargement with
crying/jugular compression (positive Furstenberg sign) are seen.
■ Associated anomalies include: Anophthalmia, arrhinencephaly, microphthalmos, corpus callosum anomalies, interhemispheric lipomas, arachnoid cysts, colloid cyst, cerebral cortical malformations, and hydrocephalus.
■ Mass with intracranial extension across a bony defect is seen on imaging.
■ Computed tomography:
• Widening of the foramen cecum
• Deformity or absence of the normal crista galli and cribriform plate.
■ Magnetic resonance imaging:
• T1: Variable hypointense CSF with isointense tissue
• T2: Bright CSF signal and gliosis within the herniated tissue
• Meningeal enhancement may be seen in case of inammation/
infection. No enhancement within the herniated tissue.
Table 23.2: Dierences between dermoid cyst and encephalocele.
Dermoid cyst Encephalocele
Thisisacongenitalinclusioncystformed
duetoincompleteseparationofthedural
and dermal elements
Noenlargementwithcrying/jugular
compression
Hairandsebaceousdischargewithsinus
openingareseenonthesurface
Intracranialextensionmayormaynotbe
seen
FatcontaininglesionshowingT1andT2
hyperintensity on imaging
(CSF:Cerebrospinaluid;MRI:Magneticresonanceimaging).
Thisisanextracranialherniationof
meningeswith/withoutbrainacrossabony
defect
Enlargementwithcrying/jugular
compression is seen
Nohair/sebaceousdischarge/sinus
opening seen
Masswithintracranialextensionacrossa
bonydefect
BrightCSFsignalwithgliotictissueseen
withinthelesiononMRI
Table 23.2 describes the dierences between dermoid cyst and
encephalocele.
Kallmann Syndrome
■ Hypogonadotropic hypogonadism and anosmia/hyposmia.
■ Due to abnormal development of olfactory axon ending and gonadotropin-releasing hormone (GnRH) neuron migration.
■ All modes of inheritance have been described. X-linked is the most
common.
■ Associated anomalies include: Cardiovascular abnormalities, renal
agenesis, cryptorchidism, midline defects, sensorineural deafness, small
anterior lobe of the pituitary gland, short fourth metacarpal and facial
anomalies, and septo-optic dysplasia.
■ Low levels of the gonadotropin hormones are seen.
■ Computed tomography:
• Ethmoid bone abnormalities in the form of reduction in the height,
width, and surface area of olfactory fossa.
• Flattening of the ethmoid oor with loss of normal gull wing
appearance of the ethmoid.
■ Magnetic resonance imaging of the olfactory region:
• Unilateral or bilateral hypoplasia or aplasia of the olfactory bulbs
• Hypoplastic olfactory sulci
• Hypoplastic anterior pituitary
• Abnormalities of the olfactory tracts.
321Chapter 23 Anterior Skull Base Lesions: Imaging
TRAUMA ALSO REFER TO CHAPTER 17
■ Direct frontal trauma results in frontobasal injuries, involving the upper
facial third (frontal bone/sinus and superior orbital rim), and anterior
skull base (cribriform plate, ethmoid roofs, and planum sphenoidale).
Section 6 Systemic Disorders/Surrounding Structures Involving PNS322
A B
Figs. 23.5A and B: Frontobasal fracture type 1.Pictorialrepresentations(A)and(B)show
a longitudinal fracture (red line) of the cranial base that is parallel to the cribriform plate.
Fracturelinesubsequentlyextendsposteriorlytoseparatetheanteriorandmiddlefossafrom
theposteriorfossa.
Classication of Frontobasal Fractures
8
■ Type I frontobasal fractures (Figs. 23.5A and B):
• Generally associated with a relatively lower impact frontal injury
• Linear fractures that initially parallel the cribriform plate
• May extend posteriorly along the sella and petrous ridge to separate
the anterior and middle cranial fossa from the posterior cranial fossa
• Medially located, involving the medial third of the supraorbital rim
• Less frequently associated with complications.
■ Type II fractures (Figs. 23.6A and B):
• Lateral vertical linear fractures of the frontal calvarium and anterior
skull base
• Involve the lateral two-thirds of the supraorbital rim, squamous
portion of the temporal bone, orbital roof, lateral orbital wall, or
orbital apex
• Occur due to higher velocity impact
• Frequently associated with CSF leak and intracranial injury
• Associated with midface injuries.
■ Type III fractures (Fig. 23.7):
• Combined central and lateral frontobasilar fractures
• Comminution of the entire frontal bone, orbital roof, and lateral
cranial vault may be seen
A B
Figs. 23.6A and B: Frontobasal fracture type 2.Pictorialrepresentations(A)and(B)show
alinearfracture(redline)involvingthefrontalboneinadditiontoextensionintotheskullbase.
323Chapter 23 Anterior Skull Base Lesions: Imaging
MISSING
Fig. 23.7: Frontobasal fracture type 3. Pictorial representation shows a comminuted
fracture(blacklines)ofthefrontalboneinvolvingalateralandacentralarea,associatedwith
comminutedfractureoftheorbitalroofalso.Alinearfracture(redline)extendsintothemiddle
andposteriorcranialfossa.
• Associated with midface injuries
• Related to a higher velocity impact from lateral/inferior frontal/
supraorbital direction
• Most often associated with complications such as intracranial injury
and CSF leak (25% of cases).
Section 6 Systemic Disorders/Surrounding Structures Involving PNS324
Complications
■ Skull base fractures often require repair only if there is associated
intracranial injury requiring decompression, persistent CSF leak or
signicant cranial nerve, vascular injury, or to prevent mucocele
formation.
■ Associated complications are:
• Cerebrospinal uid leak
• Olfactory nerve injury
• Frontal lobe contusion
• Intraorbital injuries.
■ Post-traumatic CSF leak is a complication of anterior skull base fracture.
It has been described in detail in Chapter 18.
■ Olfactory nerve injury:
• Anosmia occurs
• Incidence is 7%
• Increased risk in medial fractures along the cribriform plates
• Associated with traumatic CSF leak
• Only 10% of all patients with traumatic anosmia are estimated to
recover sense of smell, months to years after the injury.
NONTRAUMATIC CEREBROSPINAL FLUID RHINORRHEA
■ May be spontaneous or secondary leaks.
Spontaneous Cerebrospinal Fluid Rhinorrhea
(also See Chapter 18)
■ Occur in the absence of congenital abnormality, underlying lesion,
previous trauma, or surgery.
■ Spontaneous leaks may be more common than was previously
considered, ranging from 20.8% to 40% of CSF leaks.
■ Clinically leak should be conrmed with beta-2 transferrin testing.
■ Mostly caused by underlying idiopathic intracranial hypertension (IIH)
(discussed in Chapter 18).
TUMORS
Meningioma
■ It is the most common intracranial lesion aecting the anterior skull base.
■ Are more common in females.
■ Classied into olfactory groove meningioma, planum sphenoidale
meningioma, or tuberculum sellae meningioma based on the site of the
dural attachment.
■ Olfactory groove meningiomas may extend through the cribriform plate
into the ethmoid sinuses and nasal cavity.
■ Symptoms may occur late in the course of the disease as the frontal lobes
are able to tolerate more compression.
■ Behavioral changes, personality changes, headache, and anosmia may
be seen.
■ Visual symptoms and seizures may also occur.
■ Planum sphenoidale and tuberculum sellae meningiomas may present
with headache, visual eld defects, and endocrinopathies secondary to
pituitary stalk compression.
Imaging
■ Appear as well circumscribed, smooth, or lobulated lesions with variable
amount of perilesional edema.
■ Computed tomography:
• Isoattenuating to hyperattenuating mass
• Intratumoral calcications may be present
• Hyperostosis may be seen in the adjacent bone.
■ Magnetic resonance imaging (Figs. 23.8A to C):
• Well-circumscribed lesions that are isointense to brain on both T1W
and T2W images.
• Show intense and homogeneous gadolinium enhancement with an
adjacent linear dural tail in 58–72% of cases.
325Chapter 23 Anterior Skull Base Lesions: Imaging
A
C
B
Figs. 23.8A to C: Planum sphenoidale
meningioma.Well-denedextra-axial
T1 isointense to mildly hyperintense
lesion in the midline (arrow). The
lesion is isointense to gray matter on
T2withareasofcentralhyperintensity.
Cerebrospinal uid (CSF) cleft is
seen along the margin of the lesion
(small arrow). Intense enhancement
with few nonenhancing areas within.
Attachment to the planum sphenoidale
(arrowheads).
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