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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4504_Библиотеки_им_академика_М_И_Перельмана
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8.8 Primary Neoplasms
8.8.1 Extra-axial Neoplasms
Extra-axial neoplasms arise from the supporting tissues of
the meninges (meningioma) and the nerves passing from
central to peripheral (schwannoma). These are the two most
common extra-axial and most common non-glial tumors.
They occur anywhere around the cerebral convexities, along
the falx and tentorium, and on the skull base. Meningiomas
arise from the arachnoid and usually have a broad base of
attachment to the adjacent dura—giving them a hemispheric
or “globose” shape (Fig.8.7). A second morphology is the
“en plaque” meningioma—a thickening growing along the
inner table of the skull like a at bread (pita bread).
Meningiomas usually maintain a homogenous CT high
attenuation, and MR gray-matter-like signal intensity, and
enhancement as they grow larger. They are commonly associated with adjacent hyperostosis and an enhancing “dural
tail” [7]. Intra-axial vasogenic edema occurs in about 50% of
meningiomas and is only loosely correlated with histology
[8]. It is more often seen when the tumor does not have a
clear visible CSF-cleft, has high signal intensity on T2 and a
pial blood supply (rather than dural-only) (Fig.8.8) [9]. On
perfusion imaging, they usually have increased rCBV and
rCBF—while showing prolonged MTT.
Schwannomas arise from the peripheral portions of the
cranial nerves [3–12]—so they are ventral to the brainstem,
F. Bonneville et al.
Fig. 8.8 Meningioma. Axial T2-weighted MR shows a bi-frontal softtissue mass centered on the falx, with non-specic gray-matter signal
intensity. There is bi-frontal intra-axial vasogenic edema that skirts the
gray matter of the lenticular nuclei. Meningiomas easily inltrate
through the dura (not a sign of malignancy)—while other lesions
(metastasis) usually do not
most commonly in the posterior fossa. The most common
site of origin is the inferior division of the vestibular nerve,
at the apex of the internal auditory canal (IAC)—VS (vestibular Schwannoma). The tumors will compress the adjacent cochlear nerve—causing high-frequency hearing loss;
but, vestibular dysfunction may be retained. They grow out
of the IAC into the cerebellopontine angle (CPA) cistern—
where they present the bulk of the mass (Fig.8.9). Like
meningiomas VS will show avid enhancement. However,
unlike meningioma, large schwannomas become
heterogenous from benign cystic/necrotic degeneration.
There are no imaging signs that reliably predict tumor
growth, but larger tumors at presentation tend to grow
faster [11].
Fig. 8.7 Meningioma. Coronal T1-weighted MR after gadolinium.
This globose meningioma shows a sharply-demarcated, hemispheric,
extra-axial lesion with overlying calvarial thickening (hyperostosis).
The nearby adjacent dura is slightly thickened with avid enhancement—the “dural tail.” This represents a reactive process, not neoplastic inltration
Key Point
Meningiomas usually remain homogeneous, even
when large. Vestibular schwannomas are distinguished
by location at a nerve (e.g., arising within the internal
auditory canal); and, they often become heterogeneous
as they grow and enlarge. Almost all extra-axial and
non-glial neoplasms show contrast enhancement.
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Fig. 8.9 Vestibular schwannoma. Axial T1-weighted MR after gadolinium shows a heterogeneously enhancing left-sided mass in the cerebellopontine angle cistern with a component inside an enlarged internal
auditory canal
8.8.2 Intra-axial Neoplasms
The overwhelming majority of primary intra-axial neoplasms arise from the glia—or glial cell precursors, and the
2021 WHO classication of brain tumors is heavily based on
molecular features, in particular the presence of IDH and
1p/19q mutations [13]. Glial CNS neoplasms are discussed
elsewhere in details in the course.
Here, we would merely like to highlight a few imaging
features that are important for the differential diagnosis: A
T2/FLAIR mismatch is a sensitive sign for an IDH mutant
astrocytoma (but it is present only in about 50% of these
tumors, so that absence of this sign does not exclude an
astrocytoma) [14] (Fig. 8.10). Oligodendrogliomas (IDH
mutant 1p19q deleted) show frequently intratumoral calcication and are commonly located in the frontal lobes with
involvement of the cortex and subcortical white matter
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(Fig. 8.11). The classical picture of GBMs is that of an
irregularly enhancing tumor often with a necrotic center, surrounding white matter inltration/edema. However, with the
increased molecular diagnosis of GBMs (IDH wild-type), it
has become apparent that GBMs can also present as nonenhancing inltrative tumors. A further entity of note are
gliomas with H3 K27 mutations, which involve usually midline structures [15] (Fig.8.12).
Lymphoma is another common CNS neoplasm, which is
important to distinguish from glial neoplasm. The majority
(80–85%) of primary CNS lymphomas are diffuse large
B-cell Lymphomas, Epstein–Barr virus negative (EBV-).
These can be solitary or multiple (30–50%) and are usually
hypointense to gray matter on T2W imaging, have a low
ADC, and enhance homogeneously [16] (Fig.8.13). On MR
perfusion imaging, lymphomas show typically a mildly elevated rCBV (much less than, e.g., GBMs) and a marked T1
leakage effect. EVB + B-cell lymphomas account for
approximately 10% of lymphomas and are associated with
immune deciency (e.g., post-transplant, autoimmune conditions, HIV), show irregular ring enhancement, have variable ADC values, and may contain hemorrhagic components.
Other forms of lymphoma include secondary CNS lymphoma (usually with ependymal and meningeal involvement), intravascular B-cell lymphoma, dural lymphoma, and
lymphomatosis cerebri.
Intraventricular neoplasms include colloid cysts (at the
foramen of Monro/third ventricle), meningiomas (typically
in the trigone of the third ventricle), choroid tumors and
ependymomas (lateral ventricle in children, fourth ventricle
in adults), central neurocytoma (lateral ventricle, involvement of the septum pellucidum), and metastases (choroidal/
ependymal). Neurocytomas that occur in younger adults
show frequently restricted diffusion and contain calcications (Fig.8.14).
Tumor mimics are important in the differential diagnosis
and we include here a pictorial panel with detailed descriptions of such lesions of vascular origin (Figs.8.15, 8.16, and
8.17), inammatory origin (Figs. 8.18 and 8.19), or infec-
tious origin (Figs.8.20 and 8.21).
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Fig. 8.10 Low-grade
astrocytoma (grade 2) in a
47-year-old male patient
present new onset epilepsy.
(a) Axial T2W, (b) FLAIR,
(c) T1 post-contrast, and (d)
rCBV map of DSC perfusion
imaging. A left temporal and
insular mass lesions appear
homogeneously hyperintense
on T2 w images. The FLAIR
image shows a hyperintense
rim with a hypointense center
(T2/FLAIR mismatch), which
is typical for an IDH mutant
astrocytoma. Post-contrast
T1W image shows no
enhancement, and the rCBV
does not contain any areas of
increased rCBV
F. Bonneville et al.
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Fig. 8.11 Oligodendroglioma in a 57-year-old male patient presenting
with epilepsy. (a) Axial CT, (b) axial T2-weighted image, (c) FLAIR,
(d) post-contrast T1-weighted, (e) SWI image, and (f) rCBV map of
DSC perfusion. A heterogenous T2/FLAIR hyperintense left frontal
mass involving cortex and subcortical white matter contains punctate
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Fig. 8.12 Biopsy-proven lymphoma in a 64-year-old female patient
with progressive cognitive decline and headaches. (a) Axial
T2-weighted, (b) FLAIR, (c) T1 post-contrast, and (d) ADC map demonstrate a mass lesion in the splenium with surrounding oedema. The
calcication (a) which causes signal drop out on the SWI sequence (e).
There is faint enhancement (d) and mildly raised rCBV (f). This is an
oligodendroglioma. Mild enhancement and mildly elevated rCBV values can also be seen in low-grade (WHO grade 2) oligodendrogliomas
due to the typical intratumoral “chicken wire” vessels
mass is of intermediate intensity on T2W and FLAIR images (a and b),
enhances homogenously (c), and has a relatively low ADC.These features in this location suggest a primary CNS lymphoma
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F. Bonneville et al.
Fig. 8.13 Glioblastoma in a 59year-old male patient with cognitive
decline. (a) Axial T2-weighted, (b) FLAIR, (c) T1 post-contrast, and
(d) ADC map. There is a mass lesion in the splenium which is predominantly hyperintense on T2 and FLAIR images (a and b). These images
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Fig. 8.14 Central neurocytoma in a 42-year-old man with intracranial
hypertension, headaches, and blurry vision. (a) Axial T2-weighted
image, (b) axial T1 pre-contrast, (c) ADC map, and (d) SWI image
demonstrate an intraventricular heterogeneous mass lesion, involving
also contain some vascular ow voids. Following IV gadolinium, the
mass enhances heterogeneously with a characteristic necrotic center
(c). The ADC map is heterogeneous but contains predominantly areas
of increased ADC values. Biopsy conrmed a glioblastoma
the septum pellucidum and extending in the right ventricle.
Heterogeneity with areas of spontaneous T1 hyperintensity, low ADC,
and hypointensity on SWI is suggestive of the diagnosis
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Fig. 8.15 Subacute stroke in
a 57-year-old man with
subacute vertigo and
headaches since 7days. (a)
Axial FLAIR shows abnormal
heterogeneous corticosubcortical hyperintensity in
the left cerebellar hemisphere,
better delineated on (b) axial
diffusion-weighted Image. (c)
Axial post-contrast
T1-weighted image reveals
peripheral enhancement,
erroneously suggesting a
tumor. (d) Coronal
T2-weighted image
demonstrates sharp borders of
this cortico-subcortical lesion,
not crossing the midline,
strictly limited to the PICA
territory, which is in favor of
an ischemic stroke
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Fig. 8.16 Giant thrombosed
aneurysm in a 72-year-old
woman with cognitive
impairment and headaches.
Axial T1-weighted images (a)
before and (b) after
gadolinium injection reveal a
huge non-enhancing mass
lesion in the left frontal lobe
with mass effect on the
ipsilateral ventricle and
minimal midline shift.
Spontaneous hyperintensity at
the periphery of the lesion is
suggestive of thrombus. (c)
Axial FLAIR demonstrates
heterogeneous hypointensity
of the mass lesion, which is in
favor of a thrombosed
aneurysm, as conrmed by
(d) anteroposterior view of
left internal carotid artery
digital subtracted angiogram
F. Bonneville et al.
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Fig. 8.17 Giant cavernoma in a 29-year-old man with seizures. (a)
Axial FLAIR reveals a giant right frontal heterogeneous mass lesion in
the right frontal lobe, surrounded by vasogenic edema. (b) Axial
T1-weighted image demonstrates spontaneous hyperintensity of this
multilobulated mass, formed by a cluster of multiple dilated “caverns,”
lled with blood, as conrmed by the marked hypointensity observed
on (c) axial gradient echo T2* image
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Fig. 8.18 Behcet’s disease in a 31-year-old man with right hemiparesia
and confusion. (a) Coronal FLAIR, (b) axial enhanced T1-weighted image,
(c) DWI image, and (d) ACD demonstrate a partially enhancing lesion cen-
Fig. 8.19 Sarcoidosis in a
42-year-old woman with left
hemiparesis. (a) Coronal
post-contrast T1-weighted
image reveals a dura-based
mass lesion mimicking a
meningioma. The lack of
adjacent bony reaction and of
typical dural-tail sign is
suspicious. (b) Coronal T2
demonstrates mark
hypointensity, a feature that
may suggest chronic
inammation, as observed in
systemic diseases, and in
particular in sarcoidosis
tered on the left basal ganglia extending across the midline and inferiorly
into the midbrain. There is patchy enhancement and partially restricted diffusion. This is an inammatory mass in the context of Behcet’s disease
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Fig. 8.20 Bacterial abscess in a 48-year-old woman with seizures. (a)
Axial T2-weighted image, (b) Axial post-contrast T1-weighted, (c)
DWI and (d) ADC map, (e) SWI image with minimal intensity projection, and (f) phase images of SWI sequence. There is a ring-enhancing
lesion in the left temporal lobe with surrounding oedema (a and b)
showing central restricted diffusion (c and d) and a double rim sign on
SWI images (e and f). These features a typical for a bacterial abscess
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Fig. 8.21 Toxoplasmosis abscess in a 32-year-old HIV man. (a) Axial
T2-weighted image, (b) axial contrast-enhanced T1-weighted image,
(c) DWI, and (d) ACD map. There is a ring-enhancing (b) mass in the
left superior frontal gyrus with surrounding oedema. T2W images dem-
onstrate a “target sign.” The lesion shows predominantly increased
water diffusion (c and d). This is a toxoplasmosis abscess, which shows
typically increased water diffusivity, as opposed to bacterial abscesses
that show restricted water diffusion
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8.9 Concluding Remarks
There are multiple tools for triangulating a short differential
diagnosis list; and, it is important to use “pattern analysis”
rather than simple “pattern recognition.” Key features include
lesion location, relative “volume effect”; secondary vasogenic edema; homogeneity or heterogeneity of the lesion;
and patterns of contrast enhancement (homogeneous, patchy,
closed or open ring). Multiple lesions usually represent a
systemic process: inammatory, toxic, metabolic, genetic,
or, hematogenous dissemination. Extra-axial masses are
non-glial, while intra-axial neoplasms may be metastatic
from extra-CNS sources, or primary gliomas.
Take Home Messages
• Some of the primary gliomas have distinctive features, such as a T2-FLAIR mismatch in IDH mutant
astrocytomas and calcication in
oligodendrogliomas.
• Enhancement is not a reliable indicator for tumor
grade.
• Primary CNS lymphomas have a different appearance in immunocompetent and immunocompromised patients.
• Extra axial lesions are commonly meningiomas,
schwannomas, and congenital cysts but metastases,
inammatory lesions (e.g., sarcoidosis), and
myeloma are in the differential diagnosis.
• Important non-neoplastic tumor mimics include
tumefactive MS, ADEM, abscesses, and vascular
lesions.
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