Eur Radiol (2005) 15: 453–467

DOI 10.1007/s00330-004-2557-0 NEURO

Antonios Drevelegas
Extra-axial brain tumors

Received: 14 July 2004

Revised: 14 October 2004
Accepted: 15 October 2004
Published online: 31 December 2004
# Springer-Verlag 2004
A. Drevelegas
Radiology Department, Aristotele
University of Thessaloniki,
Thessaloniki, Greece
A. Drevelegas (*)
25, Nikis Street,
55236 Thessaloniki, Greece
e-mail: adrev@med.auth.gr
Tel.: +30-2310-343921
Fax: +30-2310-471056
Abstract Meningiomas, schwanno- Keywords Extra-axial . Brain
mas, metastases, maldevelopmental tumors . MRI . Meningioma .
cysts, epidermoids, dermoids and Schwannoma
bone tumors represent the vast ma-
jority of extra-axial brain tumors. The
location of extra-axial brain tumors
affects treatment planning and pre-
dicts their prognosis. Computed
tomography and particularly magnetic
resonance imaging are used for diag-
nosis and localization. In this article,
the imaging findings of the extra-axial
brain tumors are discussed.

Extra-axial tumors are the tumors of extracerebral loca-
tion. They are usually benign. The location of brain tumors
affects treatment planning and predicts their prognosis.
The multiplanar capability of MR imaging makes it the
best technique in the evaluation of extra-axial brain tumors.
Meningiomas are the most common exta-axial neoplasms
in the supratentorial compartment. Other extra-axial neo-
plasms are: schwannomas, metastatic lesions, arachnoid
cysts, epidermoids, dermoids, chordomas and eosinophilic
granulomas.
Meningiomas
Meningiomas are vascular, non-glial tumors of the central
nervous system arising from meningothelial (arachnoidal)
cells. They generally receive their blood supply from
branches of the external carotid arteries, although large
tumors will also recruit branches from the internal carotid
arteries [1, 2]. Meningiomas are the most common non-glial
primary CNS tumors and the most common extra-axial
intracranial tumors. The relative frequency of meningio-
mas regarding all intracranial tumors varies between 15%
[1, 3, 4] and 20% [1, 5, 6]. They are encountered in
middle-aged adults and are more common in women than
in men. Childhood meningiomas are uncommon and rep-
resent 1–4.2% of central nervous system tumors and 1.5–
1.8% of all intracranial meningiomas [7–11].
The presenting signs and symptoms of meningiomas,
when neurofibromatosis is excluded, are related to the tumor
location and size, they are often non-specific and vague,
primarily related to brain compression and edema from the
adjacent neoplasm [1, 12]. Signs of increased cranial pressure
(nausea, headache, vomiting) are found in 50% of the pa-
tients. Confusion, focal weakness and seizures are the most
common symptoms while paresis is the most frequently
found physical sign [1, 13, 14]. Headache has been reported
as the most common single presenting symptom, found in
36%, while normal physical examination has been reported
in 26% of patients [12].
The most common locations of meningiomas in de-
scending order of frequency are: convexity meningiomas
20–34%, parasagittal 18–22%, sphenoid and middle cra-
nial fossa 17–25%, frontobasal 10% and posterior fossa
9–15%.
454
Meningiomas are well-circumscribed globular or lobu-
lated dural-based tumors, clearly demarcated from the
brain. Histologically, meningiomas are characterized by
increased inter- and intratumoral heterogeneity. Although
by recent classifications a number of types are recognized
(and new variants are described), only a minority are found
in pure form. Meningothelial, fibrous and transitional me-
ningiomas are the most commonly found forms.
Although psammoma bodies are often found in menin-
giomas, when abundant, they characterize the tumor as
psammomatous meningioma (Fig. 1). Less commonly
found subtypes are angiomatous, microcystic [15] and
secretory meningiomas. The above-described subtypes are
grade I by WHO classification, exposing a low risk of re-
currence and aggressive growth. On the contrary, the
WHO grade II (chordoid, clear cell and atypical) menin-
giomas, and especially the WHO grade III (papillary,
rhabdoid and anaplastic,) meningiomas are more aggres-
sive with a higher risk for recurrence [16]. On non-contrast
CT, meningiomas appear as unilobular, homogeneous hy-
perdense masses in relation to brain parenchyma. After the
administration of contrast medium, they show intense and
usually homogeneous enhancement (Fig. 2). Calcification
is seen on CT in 20–27% of meningiomas [17, 18]. It is
usually microscopic or punctuated, but may be large,
conglomerate, peripheral or central (Fig. 3). Hyperostosis
of the adjacent calvarium or skull base may be seen in 18–
50%. Bone destruction is an uncommon feature found in
approximately 3% of cases (Fig. 4.)
Fig. 1 Different histological
types of meningiomas (haema-
toxylin–eosin, original magnifi-
cation ×200). a Meningothelial
meningioma, composed of nests
of cells with rounded nuclei and
indistinct cytoplasmic borders.
b Fibrous meningioma consist-
ing of parallel spindle cells and
bands of collagen. c Transitional
meningioma characterized by
the formation of whorls.
d Psammomatous meningioma
with multiple psammoma bodies
The morphologic characteristics of meningiomas on
MRI are similar to those seen on CT studies. Typically, they
are peripheral unilobular masses with broad-based dural
attachments and smooth, well-defined borders. On T1-W
images, meningiomas are usually isointense or mildly hypo-
intense to normal gray matter [19–22]. This finding con-
trasts with those from other intracranial tumors, which are
usually moderately hypointense on T1W images, due to the
increased water content of the neoplastic tissues. The rel-
atively high cellularity and low water content of most
meningiomas may account for the generally isointense
appearance on T1W images. Although the signal intensity
on T2W images varies, most tumors are reported to be
isointense to mildly hyperintense compared with gray mat-
ter. Nearly all meningiomas enhance rapidly and intensely
following contrast administration [23] (Fig. 5).
Determination of the compartment in which the lesion is
located is very important to the establishment of a correct
differential diagnosis. The extra-axial location of the me-
ningiomas is better detected on MRI than on CT.
A useful feature in confirming the extra-axial location of
the suspected meningioma is the inward bowing of the
gray-white junction of the adjacent brain parenchyma, often
called white matter buckling [24]. White matter buckling is
especially well visualized on MRI studies because of the
superior recognition of the gray and white matter of the
superficial brain on MRI examinations (Fig. 6). Other use-
ful MR characteristics, confirming the extra-axial location,
are the presence of a signal void pseudocapsule and CSF
 455

Fig. 2 Typical meningioma.

NCCT shows a well-marginated,
high density mass with punctu-
ate calcifications (a), which en-
hances homogeneously after the
administration of contrast mate-
rial (b)

Fig. 3 Calcification patterns of

meningiomas in NCCT. a Ring-
like peripheral calcification.
b Dense confluent calcifica-
tions. c Multiple psammomatous
calcifications (arrowheads) with
partial rim-like calcification
(arrow). d Almost completely
calcified meningioma
456

Fig. 4 Axial post-contrast

(a) and coronal (b) CT images
show lobulated bilaretaral fal-
cine mass with intense homo-
geneous enhancement. Note the
destruction of the calvarium and
the extracranial extension of the
mass

cleft. The pseudocapsule consists of linear signal void rep-
resenting the dura itself, interposed between the tumor and
the brain parenchyma, as well as of punctuate foci of signal
void owing to the displaced vessels (Fig. 7) [20, 21].
The CSF cleft trapped between the cortex and the
meningioma demonstrates low-signal intensity on T1W
images and high-signal intensity on T2W images (Fig. 8).
About 60% of meningiomas show a linear enhancement
along the dura matter on either side of the tumor called the
“dural-tail sign” (Fig. 9).
This sign is not specific to meningioma, and is also
observed in several conditions including glioma, [25, 26]
brain metastasis [27], acoustic neuroma [28, 29], lympho-
ma [30, 31], adenoid cystic carcinoma [32], sarcoidosis
[30] and aneurysm [33]. The precise pathologic explana-
tion for the “dural tail” sign is questionable as to whether
there is correlation with dural invasion of intracranial me-
ningiomas or only reactive thickening of the dura mater.
Some reports have found reactive vascular changes [34,
35], whereas other describe neoplastic invasion into the
subarachnoid or subdural space [36, 37].
En plaque meningiomas are a variant of primary neur-
axial meningiomas, which may infiltrate both the dura and
the bone cloaking the inner table of the skull. Other im-
aging features of meningiomas include peritumoral edema,
cystic changes, lipomatous transformation and intracranial
hemorrhage [38].

Fig. 5 Typical MR findings in a parasagittal meningioma. Axial T1WI (a) and coronal T2WI (b) show a well delineated, isointense mass on
both sequences. After administration of contrast medium (c), the mass shows intense and homogeneous enhancement

Fig. 6 Large parietal meningioma. Sagittal T1WI shows an extra-
axial isointense mass compressing the adjacent cortical convolutions
(arrows)
Diffusion-weighted MRI, perfusion MRI and proton MR
spectroscopy may be used in the diagnosis of meningio-
mas. On diffusion-weighted MR images the atypical and
malignant meningiomas tend to be markedly hyperintense
and exhibit marked decreases in the diffusion constant
(DAV) or ADC values when compared with normal brain
parenchyma, while the benign meningiomas have a var-
iable appearance on diffusion-weighted images and tend to
have higher (DAV) values compared with normal brain. On
perfusion MRI the meningiomas are hyperperfused. In MR
spectroscopy, the meningiomas are characterized by the
presence of alanine, low creatine and N-acetyl-aspartate,
high choline and glutamine and absence or low quantities
of lipids [39] (Fig. 10).
Fig. 7 Frontal meningioma.
a Axial T2WI shows a rim-like
low signal intensity (arrows)
representing the dural pseudo-
capsule. b T1WI at a lower level
shows the signal voids (arrows)
at the periphery of the mass due
to the displaced vessels
457
Schwannomas
The schwannoma is a benign tumor, composed entirely of
Schwann cells. The neurofibroma is a well-differentiated
nerve sheath tumor composed predominantly of Schwann
cells and, to a lesser extent, fibroblasts and perineural
cells. Neurofibromas of cranial nerves are extremely rare
[2, 40]. Schwannomas are the second most common extra-
axial intracranial tumors, preceded only by meningiomas.
They constitute 5–10% of all intracranial neoplasms. The
peak incidence is between the third and sixth decade.
Macroscopically, schwannomas are typically well cir-
cumscribed and more often globular than fusiform in con-
figuration. In small lesions, the parent nerve can be detected
within the tumor, but in larger tumors the relationship
between the nerve and the tumor becomes obscured. The
schwannoma is surrounded by a thick, completely collag-
enous capsule.
Microscopically, two patterns can be distinguished, ac-
cording to the morphology of the tumor cells and their
spatial arrangements: the Antoni A and B types as de-
scribed in 1920 by Antoni [6, 41]. In the Antoni A type,
tumor texture is compact and composed of interwoven
bundles of long bipolar spindle cells. The type B Antoni
architecture is often intermingled with type A, and has a
loose texture and polymorphism. Mucinous and cystic
changes occur and when confluent, large cysts develop.
Like their intraspinal counterparts, the intracranial schwan-
nomas show a predilection for the sensory nerves, and
most often involve the vestibular division of the eight
nerve. The fifth cranial nerve is the second most common
site of origin. Schwannomas of the jugular foramen usually
originate from the ninth nerve. The facial nerve schwan-
noma can be located in the internal auditory canal (IAC) or
in the facial canal.
458
Fig. 8 Parasagittal meningio-
ma. a Axial T1- and b T2-
weighted images show a CSF
cleft surrounding the tumor that
exhibits low signal on T1 and
high signal intensity on T2WI
(arrows)
The intracanalicular vestibular schwannoma is char-
acterized on MR imaging by the absence of the normal
CSF signal in the IAC, and by the distorted anatomy of the
neural bundle complex. Instead, an intracanalicular mass is
seen, not always associated with an enlargement of the
IAC, and with variable extension into the cerebellopontine
angle cistern. The tumor enhances after gadolinium. With
conventional CT these lesions cannot be reliably diag-
nosed (Fig. 11).
The intralabyrinthine vestibular or cochlear schwanno-
ma is characterized on T2-W MR images by the absence
of the normal fluid signal in the involved part of the
labyrinth. The diagnosis relies on the use of high res-
olution, ultra-thin section heavily T2-W images. These can
be obtained by using ultra-thin 3D FT FSE T2W images or
by using a 3D gradient echo sequence such as constructive
interference in steady (CISS) sequence.
Fig. 9 Post-contrast T1WI of different meningiomas. Axial (a), coronal (b), and sagittal (c) images show different types of “dural-tail”
enhancement (arrows)
Moreover, the tumor enhances after intravenous gado-
linium injection. Therefore, it is important to perform thin
section T1-W images both before and after gadolinium
injection. The T1W images without gadolinium can used
for the differential diagnosis with intralabyrinthine haem-
orrhage [42, 43] (Fig. 12).
The large vestibular schwannoma is located in the IAC
with extension the cerebellopontine angle, centered around
the IAC. The resulting appearance is that of a scoop of ice
cream on the top of an ice cream cone. The signal intensity
(SI) depends on the histological composition of the tumor.
Antoni type A lesions tend to present a homogeneous SI,
are hypointense on T2-W images and enhance homoge-
neously. Antoni type B lesions contain more extracellular
fluid and therefore present a higher SI in the T2W image;
they often contain intratumoral cysts or necrotic foci. A
nearly complete cystic schwannoma is rare [44]. Associ-
 459

Fig. 10 Right parietal meningioma. a Gd-enhanced image. b On marked increase in choline (cho) and a significant decrese of creatine
ADC, the tumor is partially hyperintense and the diffusion constant is (Cr) and N-acetyl-aspartate (NAA) levels. The peaks to the right of
higher than normal brain values. c Relative cerebral volume map NAA correspond to lipids, lactate and alanine
shows typical high perfusion (red color). d Spectrum demonstrates

Fig. 11 a Axial 1 mm over-

lapping sections, 3D TSE T2W.
b Coronal 1.5 mm 3D FT GE
T1W after Gd. Intracanalicular
vestibular schwannoma. Very
small nodular tumor, located
inferoposterior in the IAC,
clearly related to the inferior
vestibular part of the nerve
(arrows)
460

Table 1 Radiological differential diagnosis between schwannoma

and meningioma in the cerebellopontine angle
Schwannoma Meningioma

Intracanalicular com- Almost always Rare

ponent (95%)
Centered around the Yes No, eccentric
IAC
Calcifications No Possible
Necrotic/cystic parts Frequent Rare
Dural tail sign Possible Possible
Secondary arachnoid Possible in large No
cyst tumors
Influence on the bone Enlargement of Hyperostosis, enostosis,
the IAC invasion
Supratentorial exten- No Possible
Fig. 12 Coronal 1.5 mm overlapping sections, 3D FT GE T1W sion
after Gd. Intralabyrinthine cochlear schwannoma. Pathological en- Contact with facies Sharp angle Broad based contact
hancement of the left cochlea (arrow)
posterior

ated arachnoidal cysts or loculations are encountered
around the tumor in 5–10% of cases [44, 45]; they are
especially observed in large schwannomas (Fig. 13). Intra-
tumoral calcifications are rare and, when found, should
favor the diagnosis of meningioma. The main differential
diagnosis of acoustic schwannoma is CPA meningioma
and is described in Table 1.
The trigeminal nerve schwannoma can be located in
every segment of the nerve: the cisternal segment in the
prepontine and cerebellopontine cistern, Meckel’s cave,
cavernous sinus, the superior or inferior orbital fissure. From
Meckel’s cave extension below the skull base through oval
foramen is possible. Frequently, the tumor presents a dumb-
bell configuration, with part of the lesion located in Meckel’s
cave (supratentorial) and part of the tumor extending into
the medial cerebellopontine angle cistern (infratentorial)
(Fig. 14). The imaging characteristics are the same as for the
vestibular schwannoma, but intratumoral cysts are more fre-
quent [46].
The jugular foramen schwannomas are usually large at
presentation with an extension in the posterior cranial fossa

Fig. 14 Trigeminal nerve schwannoma. Axial SE T1W after Gd.

Fig. 13 Axial 1.5 mm overlapping sections, 3D FT GE T1W after
Gd. Large vestibular schwannoma with an intratumoral cyst and a
large secondary arachnoidal cyst (non-tumoral)
Trigeminal nerve schwannoma. The tumor has a solid, enhancing
part and a cystic part. There is a dumbbell shape with a component
in Meckel’s cave and in the medial cerebellopontine angle cistern.
Notice the cystic extension through the oval foramen, following the
maxillary division of the nerve

and below the skull base in the carotid loge (Fig. 15). The
most common clinical presentation is hearing loss or
symptoms relating to a posterior fossa mass. Glossopha-
ryngeal deficit points to a large extension below the skull
base. The tumor causes an enlargement of the jugular fo-
ramen, with rounded, sharp and sclerotic rims, without
bony invasion or osteolysis on CT. In the differential di-
agnosis, large vestibular schwannomas should be consid-
ered: they can grow into the jugular foramen, but are
associated with erosion and enlargement of the IAC.
Conversely, a jugular foramen schwannoma may have a
significant extension in the cerebellopontine angle but the
IAC remains normal. Jugular foramen schwannomas tra-
ditionally present a low SI on T1W and a high signal on
T2W images. The enhancement is strong or moderate.
Cystic components are less frequent than in the trigeminal
nerve schwannoma. In the differential diagnosis, the fol-
lowing lesions must be considered: meningioma, glomus
jugulotympanicum, metastasis, lymphoma, giant cell tumor.
The facial nerve schwannoma can arise in the IAC, at
the level of the ganglion geniculi, in the middle ear or in
the facial canal. Because the facial nerve is located in the
anterosuperior quadrant of the IAC, bony erosion in this
vicinity favours a facial rather than a vestibular schwan-
noma, as would extension of the mass in the labyrinthine
segment of the facial canal. A facial nerve schwannoma
causes enlargement of the facial canal with possible ero-
sion and extension in the middle ear as a soft tissue mass
[47] (Fig. 16).
Fig. 15 Jugular fossa schwannoma. Gd-enhanced sagittal SE T1WI.
An enhanced fusiform soft tissue mass extends from the right
cerebello-pontine angle through the pars nervosa of the jugular
foramen into the right parapharyngeal space
461
Fig. 16 Axial CT scan through the left petrous bone (1 mm slice
thickness). Facial nerve schwannoma. A soft tissue mass involves
the geniculate ganglion and the proximal tympanic segment of the
left facial nerve. The tumor causes bone erosion with scalloping and
enlargement of the geniculate fossa, and extends into the tympanic
cavity, where it abuts the auditory ossicles (arrow)
Metastases
Metastases (calvarial, dural or leptomeningeal) are the sec-
ond most common extra-axial neoplasms in the supraten-
torial compartment.
Calvarial metastases may appear in many patients with
malignant tumors. Carcinomas of the lung, breast, kidney
and prostate are the most frequent primary neoplasms.
Calvarial metastases appear on plain radiographs as os-
teolytic or osteosclerotic lesions. CT with bone window
algorithm is very sensitive in detecting calvarial metasta-
ses. Contrast-enhanced MRI is used to detect subtle intra-
diploic lesions and to determine extension of the metastatic
lesion of the calvarium into the epidural space with in-
volvement of the underlying dura or brain. These metas-
tatic lesions demonstrate prolonged T2 relaxation times
and therefore are hyperintense on T2-weighted images with
fat suppression contrasted against the normally hypoin-
tense calvarium [48].
Dural metastases may usually occur as an extension of
the tumor to the dura from the adjacent calvarial metas-
tases. Occasionally, dural metastases may occur without
associated bony involvement. The most common primary
tumors associated with dural metastases are breast, lung,
prostate, melanoma and neuroblastoma. Lymphoma and
leukemia are other common tumors. On CT, dural metas-
tases appear as isodense areas of dural thickening and
enhancement. Post-contrast T1-weighted MRI is more sen-
sitive in depicting meningeal involvement (Fig. 17). Since
the inner table of the skull is hypointense on MRI the
462

abnormally enhancing dura clearly stands out between the

CSF and the bone of the skull [49].
Leptomeningeal metastases or meningeal carcinomatosis
is usually the result of hematogenous spread from extra-
cranial malignancies. Anaplastic astrocytoma, glioblastoma
multiforme, ependymoma and medulloblastoma may also
show leptomeningeal dissemination through the CSF. Post-
contrast T1-weighted and FLAIR studies offer the best im-
aging method to demonstrate such lesions. Leptomeningeal
metastases presents with increased enhancement in the sub-
arachnoid spaces of the cortical sulci, the fissures and the
cisterns.
Nodular formations can also develop in the subarach-
noid spaces that may invaginate within the adjacent brain
parenchyma. The pattern of leptomeningeal infiltration is
identical to that described on the CT but the intensity of
enhancement and thus the sensitivity is greater in the post
contrast MR studies (Figs. 18, 19) [50–52]. A major draw
back in the diagnosis of meningeal carcinomatosis by
either CT or MRI is that the changes described above lack
specificity. Indeed, abnormal enhancement of the lepto-
meninges identical to carcinomatosis occurs in a variety of
infections including viral, bacterial or fungal diseases [53].
Inflammatory processes such as sarcoidosis or Langerhans Fig. 18 Post-contrast T1-weighted MRI scan of the brain in a
patient with metastatic breast carcinoma. There is evidence of men-
histiocytosis also present with abnormal enhancement of ingeal carcinomatosis manifested by abnormal enhancement of the
the leptomeninges. In the case of dural involvement the leptomininges over the convexity of the right cerebral hemisphere
differential diagnosis is even broader. Besides the infec-
tious or the specific inflammatory processes already dis-
cussed, the dura enhances in response to inflammatory
reaction that occurs following previous subarachnoid hem-
orrhage. Furthermore, the dura enhances in response to a

Fig. 17 Coronal post contrast T1-weighted MRI scan of the brain in

a patient with metastatic prostate carcinoma to the skull. Three
destructive metastatic lesions are seen in the skull. Associated soft
tissue tumors are also present extending into the epidural space and
compressing the brain parenchyma. The abnormal enhancement of
the dura (arrows) represents tumor invasion
Fig. 19 Post-contrast T1-weighted MRI scans of the brain in a
patient with melanoma. Enhancing masses are noted in both
cerebello-pontine angles mimicking acoustic schwannomas (ar-
rows). This abnormality represents part of the spectrum of meningeal
carcinomatosis

variety of neoplastic or non-neoplastic diseases that in-
volve the calvarium. In the case of metastatic or primary
tumors of the calvarium inflammatory reaction often de-
velops in the dura even in the absence of dural involve-
ment by the neoplasm.
Previous published reports suggest that the sensitivity of
contrast enhanced MRI is rather poor, since positive re-
sults consistent with meningeal carcinomatosis are elicited
in only 36–66% of patients with positive CSF cytology.
These findings are hardly surprising, considering the fact
that only a few malignant cells in the CSF are sufficient for
establishing this diagnosis by cytology. On the other hand,
the superior sensitivity of CSF cytology is secured only if
multiple spinal taps are performed [48].
Arachnoid cysts
These non-neoplastic cysts are loculated collections of CSF
within a reduplication of arachnoidal membrane. They are
thought to be part of a continuum of epithelial cysts at the
more benign end of the spectrum behaviorly. They tend to
present at an older age, usually the 5th decade, with head-
aches, visual field defects and impotence [54]. They are
most frequently located in the middle cranial fossa. Other
sites include the suprasellar area, the frontal convexity, the
quadrigerminal cistern and the foramen magnum. Arach-
noid cysts show on CT density similar to that of CSF.
Erosion of the adjacent calvarium is often present. They are
well defined, with no calcification and no enhancement
[54, 55]. On MRI arachnoid cysts show CSF signal inten-
sity on all pulse sequences.
Epidermoids and dermoids
Epidermoids and dermoids are uncommon, slow growing
masses that account of 1% of all intracranial neoplasms
Fig. 20 Epidermoid cyst. a Post-contrast CT shows a hypodense
lesion compressing the right cerebellar hemisphere. On NCT1WI
(b) and T2WI (c), the same lesion shows signal intensity similar to
463
[56]. These lesions are similar in their development, his-
tology, behavior and imaging and for this reason are dis-
cussed together. As previously discussed, epidermoids and
dermoids along with Rathke cleft cysts, arachnoid cysts
and craniopharyngiomas are considered by some to rep-
resent a continuum of ectodermally derived cystic epithe-
lial lesions [57]. Both lesions are generally considered
developmental/congenital masses rather than neoplastic,
arising from ectodermal heterotopia. Both cysts are lined
with stratified squamous epithelium, with dermoids adding
mesodermal elements such as hair, sebaceous and sweat
glands.
Epidermoids are slightly more common than dermoids
intracranially. They typically spread along the basal sur-
faces, with the cerebellopontine angles being the most
common location, followed by the parasellar [58–60].
They are extra-axial lesions with only 1.5% being intra-
cerebral [61]. They are overwhelmingly benign, although
they rarely can be malignant. Average age of presentation is
37.3, with a male to female ratio of 3:2 [56]. The symp-
tomatic onset is generally slow, lasting 2 years or more,
although for suprasellar lesions it is much shorter [61].
Presenting symptoms may include headaches, visual prob-
lems, cranial nerve symptoms and seizures, which typically
indicate rupture. Rupture can produce aseptic meningitis,
which can be lethal although not necessarily so. Epider-
moids on CT appear as hypodense masses, with irregular
boarders and rare contrast enhancement (Fig. 20a). Dense
lesions have been reported [62] and calcification is oc-
casionally seen [60]. On MR, they typically are of low
signal on T1- and of increased signal on T2-weighted im-
ages, following that of CSF on all pulsing sequences [56]
(Fig. 20b, c). They can demonstrate increased signal on
T1-weighted images, which is due to a high lipid content
[60]. Epidermoid and arachnoid cysts can also be dis-
criminated on the basis of diffusion-weighted images. On
conventional spin echo images both show long T1 and T2
images. On diffusion-weighted images, epidermoid cysts
that of CSF. d DWI shows an inhomogenous high signal intensity
indicative of restricted diffusion
464

Fig. 21 Dermoid cyst. a Sagit-

tal T1- and b axial T2-weighted
images show a suprasellar het-
erogeneous mass. The high sig-
nal areas on T1WI are due to the
presence of fatty material

show high signal intensity due to restricted motion of pro-
tons by the presence of membranes of densely layered
epithelium, while arachnoid cysts are hypointense due to
their free water motion [63, 64] (Fig. 20d).
Dermoids are midline lesions, occurring in the parasel-
lar, frontobasal region or posterior fossa [62]. Average age
of presentation is 36.2, with a male to female ratio of 3:1
[56]. The complications of dermoids are similar to epider-
moids. They can present with headaches, seizures, men-
ingeal signs and TIAs [65, 66]. Most of these symptoms
are indicative of rupture, which produces a chemical or
aseptic meningitis and which can be lethal [65, 67].
The CT appearance of dermoids is similar to epider-
moids. Their MR appearance depends on the amount of fat
present, although generally they are of increased signal on
both T1- and T2-weighted images [56] (Fig. 21). CT or
MR can both make the diagnosis of rupture although MR
is the preferred preoperative study [66].
Treatment is surgery, with 86% being in good or
excellent condition post-operatively. The 20-year survival
of epidermoids is 92.8%, with good survival even with
recurrence [56]. Epidermoids have a classic mother-of-
pearl appearance at surgery.
structures. On T1-weighted images chordoma is iso- or
hypointense and replaces the hyperintense clival fatty
marrow. On T2-weighted images it is inhomogeneous and
hyperintense. After the administration of contrast medium,
chordoma shows heterogeneous enhancement (Fig. 22).
The differential diagnosis include metastasis, craniopha-
ryngioma, chondrosarcoma, pituitary tumors and nasopha-
ryngeal carcinoma.
Eosinophilic granuloma belongs to the group of dis-
orders called histiocytosis X. They are characterized by
histiocytic proliferation. The other two conditions are
Hand–Schuller–Christian and Letterer–Siwe disease. Eo-
sinophilic granuloma represents approximately 70% of the
total number of histiocytosis X. Although it can affect any
skeletal site, the most common locations are skull, man-

Bone tumors

Chordoma is locally aggressive but slow-growing tumor

and is thought to derives from notochordal remnants. It
invades adjacent soft tissue structures and metastasize in-
frequently. Chordoma occurs in the late middle age and
most commonly arises in the sacrococcygeal (50–60%) or
sphenooccipital regions (25–40%) [68–70]. The latter usu-
ally causes destruction of the clivus and spreads into the
middle or posterior cranial fossa compressing the brain-
stem or the nasopharynx. CT demonstrates clearly the mass Fig. 22 Chordoma. Sagittal post-contrast T1-weighted image shows
and the bony component of the tumor. MRI depicts better a heterogeneously enhanced lesion which causes destruction of the of
the extent of the lesion and its relation to the adjacent the clivus
 465

Fig. 23 Eosinophilic granuloma of the skull. Axial T1-weighted image (b). On post-contrast T1-weighted image (c) the lesion shows
image (a) shows an isointense destructive lesion of the left temporal a heterogeneous enhancement. Note also the epidural extension of
bone extending into the orbit, which is hyperintense on T2-weighted the tumor

dible, spine, ribs and long bones. In the skull, the tumor weighted images. After the administration of contrast me-
appears as a lytic lesion with epidural extension. The dium, intense enhancement is seen (Fig. 23) [70].
tumor appears hypointense on T1 and hyperintense on T2-

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