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Intraventricular tumors
Amit Agarwal MD, Sangam Kanekar MD

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Semin Ultrasound CT MRI

Cite this article as: Amit Agarwal MD, Sangam Kanekar MD, Intraventricular tumors,
Semin Ultrasound CT MRI , http://dx.doi.org/10.1053/j.sult.2015.12.003

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Seminars in US, CT and MRI “Ventricles and cisterns”

Chapter 9: Intraventricular tumors

Authors:

1. Amit Agarwal MD (corresponding author)

Assistant Professor of Radiology

Penn State University
Hershey, PA 17033
7175311098
amitmamc@gmail.com

2. Sangam Kanekar MD

Associate Professor of Radiology & Neurology

Penn State University
Hershey, PA 17033
7175318051

NONE OF THE AUTHORS HAVE ANY CONFLICTS OF INTEREST OR

FUNDING SOURCE TO REPORT FOR THE PAPER

Intraventricular Tumors

Abstract

Intraventricular tumors represent a unique group of intracranial neoplasm separate from

the classic division as intra versus extraxial masses. Intraventricular tumors are unique

because of the diverse pathologic spectrum, including the entire gamut of neuroepithelial

and non-neuroepithelial tumors. Most of these tumors are clinically benign presenting

with headaches or signs and symptoms of hydrocephalus. Computed Tomography (CT)

and Magnetic Resonance Imaging (MRI) play a pivotal role in diagnosis and

neurosurgical guidance. Though, practically any intracranial tumor can have an

intraventricular location, we will be discussing the common eight tumors, which together

constitute more than 90% of intraventricular masses. Demographics, clinical and imaging

findings, are together very useful in narrowing down the differential.

Keywords: Intraventricular; Tumor; choroid plexus

Introduction

Intraventricular tumors are rare lesions that make up 0.8 to 1.6% of all intracranial

tumors, with the vast majority of them being benign. They are however more common in
1 ,2
children and comprise around 16% of childhood and adolescent intracranial tumors.

These are a histologically heterogeneous group of tumors that can be divided into

primary and secondary intraventricular tumors. ―Primary tumors‖ are neoplasms that

originate from the ependymal or subependymal lining, septum pellucidum, choroid

plexus and the supporting arachnoid tissue. This includes a wide variety of tumors unique

to the ventricles (e.g. choroid plexus papilloma) and tumors frequently seen

elsewhere(e.g. meningioma).3,4 The ventricular margins are composed of ependymal cells

with subependymal glial plate giving rise to ependymomas, subependymomas, and

subependymal giant cell astrocytomas (SEGAs). The septum pellucidum consists of two

layers of both white and gray matter, giving rise to central neurocytomas, a glial neuronal

tumor that is unique to the ventricular system. Choroid plexus is the most vascular

structure in the ventricular system and gives rise to choroid plexus papilloma and

carcinoma which are cerebrospinal fluid (CSf) secreting tumors, frequently causing

hydrocephalus. Highly vascular tumors such as meningiomas and metastases also

generally arise from the choroid plexus secondary to the inherent high vascularity of the

structure.5 ―Secondary or paraventricular tumors‖ is a term used when these neoplasms

originate from adjacent brain substance and demonstrate more than two-thirds exophytic

growth within the ventricle. 3,4

Diagnosis and Management

Clinical signs and symptoms of intraventricular tumor vary according to age and tumor

location. Majority of the clinical findings are secondary to CSF obstruction

(hydrocephalus) and subsequent increase in intracranial pressure. Infants usually present

with macrocephaly, loss of appetite and irritability. Older children and adults present with

headache and vomiting with papilledema commonly seen on examination.6 Seizures and
visual disturbances are uncommon manifestation of these tumors. Tumors of the posterior

fossa have a higher tendency to be symptomatic and cause hydrocephalus with signs of

cerebellar dysfunction including ataxia and dysmetria. Some intraventricular tumors are

asymptomatic and may be incidentally discovered on brain imaging. The best example of

this would be a subependymoma seen within the lateral ventricles on a trauma head CT.

Imaging studies are the key component in the diagnosis of intraventricular tumors.

Magnetic resonance imaging (MRI) is the preferred modality of choice for imaging

evaluation, although CT and angiogram may often be helpful in tumor characterization.

Cranial ultrasound and Doppler are useful in infants with limited role in adult population.

Besides conventional MR imaging, newer sequences like susceptibility-weighted imaging

(SWI) and advanced techniques including perfusion imaging and Proton (H1)

spectroscopy are increasingly being utilized for tumor characterization. This is especially

important if the mass is benign and conservative follow-up could be the optimal

treatment. 7

A systemic approach taking into consideration patient age, location of tumor and imaging

findings can substantially narrow down the differential, and in many cases suggest a

single most probably diagnosis. Patient‘s age and location are the two key concepts for

the imaging diagnosis of intraventricular tumors.8 Tumors such as Central neurocytoma

(CN) and SEGAs are predominantly located in the anterior portion of the lateral

ventricles whereas epedymomas and subependymomas are more common in the fourth

ventricle. Vascular lesions such as meningiomas and metastasis tend to occur within the
atria of the lateral ventricles as the choroid plexus is most prominent in this region.

Epedymomas and choroid plexus tumors are usually seen in the pediatric age group,
9
whereas meningiomas and CN are usually seen in middle-aged adults (30-40 years).

The demographic and major imaging features of the common intraventricular tumors are

highlighted in the Table-1. Microsurgical resection is the gold standard of intraventricular

tumor resection. Neuroendoscopic surgery has however become the first-line modality

for obtaining tumor samples from most intraventricular tumors along with simultaneous

treatment of hydrocephalus, thereby avoiding aggressive conventional surgery in few

cases. Endoscopy may also be used for complete excision of intraventricular tumors in
10
selected cases.

Neoplasm of the choroid plexus

Choroid plexus tumors (Papilloma and Carcinomas)

Choroid plexus tumors constitute about 0.5 % of adult brain tumors and 1-2% of pediatric

brain tumors, with majority (80%) being diagnosed as choroid plexus papilloma (CPP) as

compared to carcinomas (20%). The frequency of these tumors is much higher in the

infant age group, ranging from 15-20% of intracranial tumors in the first year of life.

Most common locations are the atria of lateral ventricle (50%) and the fourth ventricle
11,12
(40%). These tumors are divided on histology as typical CPP (WHO Grade I) ,

atypical CPP (WHO Grade II) and CPC (Grade III). Choroid plexus carcinomas (CPC)

are found exclusively in children. All these tumors are associated with Aicardi and Li-

Fraumeni syndromes.13 These tumors are derived from the neuroepithelial cells of the
choroid plexus and present as well-circumscribed lobulated cauliflower like masses. On

histology, CPPs resemble normal choroid tissue with fronds of fibrovascular connective

tissue, no atypical cells or significant mitotic activity. On the contrary, CPCs show classic

malignant findings of nuclear pleomorphism, high mitotic activity and invasion into the

adjacent brain parenchyma. On gross examination, hemorrhage and necrosis are

hallmarks of CPC. There is marked overproduction of CSF by all these tumors resulting

in hydrocephalus and signs of increased intracranial pressure. In a small minority of

cases, the hydrocephalus is secondary to mechanical obstruction or blockage of arachnoid

villi due to associated hemorrhage. All these changes are more prominent in CPC as

compared to CPP. 14

Neuroimaging findings are characteristic of choroid plexus tumors. These are iso to

hyperdense on CT with ―frond-like‖ appearance and calcification in around 24 % of

cases. On MR images, CPP appear as isointense to hypointense intraventricular masses

on T1-weighted sequences with variable signal intensity masses on T2-images. They are

very well-circumscribed and tend to engulf the normal choroid plexus (Fig.1).

Hydrocephalus is present in almost all the cases and is more prominent in fourth

ventricular lesions. Given the very high vascularity, these tumors tend to enhance avidly

and may show prominent intralesional flow voids on MR, with enlarged choroidal

arteries in many cases. Parenchymal invasion may be seen in CPC, however is rare with

CPP (Fig.2). Similarly, although CSF seeding can be seen with either CPP or CPC, it is

much more common with the later. Despite these differences, imaging cannot confidently
differentiate between CPP and CPC, and therefore imaging of the entire neuroaxis is

recommended in all these tumors. MR spectroscopy (MRS) has shown elevated

5, 15
myoinositol in cases of CPP and elevated choline peak in CPC (Fig. 2d). All these

tumors show markedly elevated cerebral blood flow on dynamic perfusion imaging.

Gross total surgical resection is the treatment of choice in all the choroid plexus tumors

with excellent outcomes in CPP. 16

Meningioma

Meningiomas arise from the arachnoid cap cells within the choroid plexus and are usually

seen within the atria of the lateral ventricles. They constitute 0.5- 3.7 % of all intracranial

meningiomas.17 These tumors are usually seen in the age group pf 30-60 years with a

higher female predilection, similar to meningiomas in extra-ventricular location. Pediatric

18
meningiomas and meningiomas in the third and fourth ventricles are rare. These are

generally benign WHO Grade I tumors, very similar to convexity meningiomas, and most

commonly of the meningoepithelial type. Pediatric meningiomas have shown higher

tendency for sarcomatous transformation, especially if associated with syndromes like

Neurofibramatosis-2 (NF –II) or radiation.19 Intraventricular meningiomas (IVM)

typically present with headaches or signs and symptoms of intracranial hypertension. The

ventricular trigone is in close proximity to the hippocampus and visual pathway, and

hence seizures and visual changes have been reported with trigonal meningiomas.20
Imaging findings closely resemble dural meningiomas. They are hyperdense on CT with

calcification seen in around 50% of cases. They are iso to hypointense on T1W images

and hyperintense on T2 with avid post contrast enhancement (Fig. 3). Cystic changes are

often seen in pediatric meningiomas. Elevated alanine to creatine ratio on MRS has high
5,21
specificity for meningiomas. Dynamic perfusion images shows persistent elevated

blood volumes secondary to high vascularity and disruption of blood-brain barrier.

Microsurgical gross total resection is the treatment of choice. Catheter angiography is

used for preoperative feeding vessel embolism in few select cases.16,20

Metastases

Leptomeningeal tumor spread (carcinomatosis) along the ventricular margins is common

with primary malignancies of breast and lung. However, intraventricular metastases

5
(hematogenous) are rare accounting for 0.9 to 4.6% of all cerebral metastases. Most

common primaries in adult include lung, breast, renal and colon carcinomas. Renal

metastases are unique in the fact that they can seed the choroid plexus decades after the

primary diagnosis. In the pediatric age group, Wilms tumor, neuroblastoma and

retinoblastomas are the most common primaries. The vast majority of these lesions are

seen in the lateral ventricle. The diagnosis is straightforward when associated with

multiple parenchymal lesions and leptomeningeal disease. Differentiating solitary

ventricular metastases from other benign tumors, like meningioma, can however be

challenging. Lumbar puncture with CSf analysis can usually provide answers in such

equivocal cases. 22
Neoplasm of the ventricular wall and septum pellucidum

Ependymoma

Ependymomas are common slow-growing tumor arising from the differentiated

ependymal cells lining the ventricle and central canal. They are seen in both adults and

children with no gender preference. They constitute around 2-9% of pediatric brain

tumors and almost one-third of all brain tumors in children younger than 3 years. 23 They

are the third most common pediatric brain tumors, after astrocytoma and

medulloblastoma. Fourth ventricle is the most common location accounting for more than

60% cases and is the typical site in children. Most supratentorial ependymomas are extra-

ventricular, arising from the embryonic rest of ependymal tissue. Supratentorial location

is more common in older children and adults with almost half of these being extra-

ventricular. Classic ependymomas are benign low-grade lesions (WHO-II) lesions usually

presenting with cerebellar symptoms along with signs of raised intracranial pressure. The

more aggressive tumor type namely anaplastic ependymomas are WHO grade III lesions

with malignant features and poor prognosis. 8,9,23

On CT imaging, ependymomas are usually heterogeneously isodense lesions with

calcification seen in 50% of cases and hemorrhage seen in 10%. Tumor heterogeneity,

hemorrhage, necrosis, cystic changes and calcification are important clues in diagnosis.

On MRI, ependymomas show low T1 signal and appear heterogeneously bright on T2WI

with inhomogeneous contrast enhancement. Most of these tumors show gradient signal

drop-out secondary to calcification or hemorrhage. One of the unique imaging findings of

these tumors is the propensity to extend along the foramen of Luschka and Magendie

(Fig. 4). The entire neuroaxis should be evaluated to rule out CSf spread, which though
23, 24
less common than medulloblastoma, can be seen in around 5% of cases. Perfusion

images demonstrate markedly elevated cerebral blood volumes with poor return to

baseline. Elevated choline (Cho), lactate, glycine and myoinositol (mI) can be seen with

ependymomas, with reduced N-acetyl aspartate (NAA). Spectroscopy finding are

however not helpful in differentiating this from other posterior fossa tumors. Gross total

resection is the treatment of choice for ependymomas. 24

Subependymoma

Subependymomas are rare benign WHO grade I tumors arising from the ependymal-glial

precursor cells. These are highly differentiated tumors accounting for 0.2-0.7% of all

intraventricular tumors. These tumors usually present between the fourth and sixth

decades, though few pediatric case have been reported in literature. Majority of these

tumors are located in the fourth ventricle (50-60%) followed by the ventricular margins

or septum pellucidum of the lateral ventricle (30-40%). Differentiation from central

neurocytomas can be challenging when these lesions are small and arise from the septum

pellucidum. Imaging findings are non-specific with well circumscribed lobulated

appearance on both CT and MRI. There is associated hydrocephalus in around 80% of

cases and calcification is seen in around 30% of lesions. They are isointense on T1WI

with bright signal on T2. There is no parenchymal invasion and poor contrast
enhancement (Fig.5a-c). The latter feature can be helpful in demarcating

subependymomas from CN and SEGAs. Unlike ependymomas, these tumors are almost

always confined to the ventricles. Subependymomas have excellent prognosis after

complete resection.

Subependymal Giant Cell Astrocytoma (SEGAs)

Subependymal Giant Cell Astrocytomas (SEGAs) are slow growing WHO grade I glial-

neuronal neoplasm, occurring exclusively in patient with Tuberous Sclerosis (TS). They

are seen in 15% of patients with TS and are the most common CNS neoplasms in this

neurocutaneous syndrome.1,5 There is a wide age distribution, however SEGAs usually

present within the first two decades of life and virtually always at the foramen of Monroe.

These lesions probably arise from the subependymal nodules seen in the ventricular wall

in patients with TS. They are usually diagnosed on the basis of growth on sequential

MRIs in patient with TS or secondary to obstructive hydrocephalus. Despite the tendency

to grow in size, these are completely benign lesions with no malignant potential.6,8

On CT imaging, SEGAs are seen as isodense intraventricular mass along the foramen of

Monroe .Calcification is variable and hemorrhage is seen in few cases. Lesion is

isointense on T1WI and heterogeneously bright on T2. The calcific component may be

hypo or hyperintense on T1WI. Although SEGAs show robust enhancement, this feature

alone cannot differentiate SEGAs from benign hamartamous nodules in patients with TS.

In general, a size of > 1.3 cm and interval growth on sequential scans favors the diagnosis

of SEGAs (Fig. 6). Surgical resection is usually performed for symptomatic lesions or
lesions with documented growth on serial scans. Annual follow-up MRI should be

performed post resection. 8,11,25

Central Neurocytoma (CN)

Central Neurocytomas (CN) are low grade (WHO-II) lesions arising from progenitor

bipotential cells with capability of differentiating along the glial or neuronal line. They

arise from the subependymal plate along the septum pellucidum or the ventricular

margins. They are seen predominantly in the age group of 20-40 years and constitute

around 0.25-0.5 % of intracranial tumors. Inferior septum pellucidum and the anterior

lateral ventricle are the most common location. Neurocytomas can be extraventricular;

however the term CN is reserved exclusively for intraventricular lesions.1,5, 6

Central neurocytomas are well-circumscribed lobulated masses with intratumoral cysts

giving the characteristic ―bubbly‖ appearance. On CT, these tumors are hyperdense with

calcification seen in around 50% of cases and hemorrhage seen in few cases. On MR, the

solid components of the tumors are hyperintense on T1 and T2 weighed images. Long TR

sequences show cystic changes in two-thirds of the cases and broad attachment to the

ventricular wall or septum is almost always seen. Moderate enhancement is seen after

contrast administration (Fig. 5d-f). Presence of glycine peak (3.5ppm) has recently been

reported with these tumors, and may be helpful in differentiating it from other

intraventricular neoplasms.6, 26
Secondary Intraventricular tumors

Secondary intraventricular or paraventricular tumors are terms used for tumors arising

from the brain parenchyma with more than two-third growth within the ventricular

lumen. Theoretically, any parenchymal tumor can grow exophytically into the ventricular

lumen; however, this is more common with high grade neoplasm such as Glioblastoma

multiforme (GBM) (Fig. 7). The use of the term secondary intraventricular is becoming

obsolete and though there are case reports of intraventricular GBM in literature, these are

likely exophytically growing parenchymal tumors rather than primary intraventricular

neoplasm. It is important to demarcate an intraventricular tumor from a parenchymal

tumor with exophytic growth due to the completely different set of tumor pathology at

these locations. Although this can be challenging at times, a confident diagnosis can

usually be made for most cases, after utilizing the three planes on MRI.27, 28

Non-neoplastic lesions

Besides neoplastic lesions, a number of non-neoplastic ―masses‖ can be seen within the

ventricular system. They can be cystic lesions such as colloid cyst, simple intraventricular

cysts (including arachnoid cysts, ependymal cysts and large choroid plexus cysts) and
29
xanthogranulomas of the choroid (Fig. 8). Congenital lesions like cavum septum

pellucidum and cavum velum interpositum can be incidentally discovered on head

imaging. Infective lesions like neurocysticercosis and tuberculomas can present as

intraventricular cyst, more commonly seen in the developing countries. Apart from

colloid cyst and infective lesions, these lesions are almost always asymptomatic with no

definite indication for treatment or imaging follow-up. 29,30

Summary

Intraventricular tumors represent a histologically wide group of neoplasm with

overlapping clinical and imaging findings. However, using a combination of patient

demographics, tumor location and imaging features, we can substantially narrow down

the list of differentials. Though rare in adults, these tumors are common in the pediatric

age group, especially in infants. Microsurgical resection is the gold standard for treatment

and MRI is the imaging modality of choice for this group of tumors.

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tumors. Eur J Radiol. 2012;81:e688-96.

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OD, Cavenee WK, editors. WHO Classification of Tumours of the Central Nervous
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occurring before 1 year of age: a retrospective reviews of 22 cases in an 11-year period
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(CHLA) experience, 1991-2010. Pediatr Blood Cancer 2012; 58(6):905–909
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ventricle, in Vinken PJ, Bruyn GW (eds): Handbook of clinical neurology. New York,
Elsevier, 1974, pp 555-595.

15. Krieger MD, Panigrahy A, McComb JG, Nelson MD, Liu X, Gonzalez-Gomez I,
Gilles F, Bluml S: Differentiation of choroid plexus tumors by advanced magnetic
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& Williams, 2005; 603–610.

17. Liu M, Wei Y, Liu Y, Zhu S, Li X. Intraventricular meninigiomas: a report of 25

cases. Neurosurg Rev 2006;29(1):36–40

18. Baumgartner JE, Sorenson JM: Meningioma in the pediatric population. J Neurooncol
29:223-228, 1996.

19. Greene S, Nair N, Ojemann JG, et al. Meningiomas in children. Pediatric

neurosurgery. 2008;44:9–13.

20. McDermott MW: Intraventricular meningiomas. Neurosurg Clin N Am. 2003;14:559-

569.

21. Reddy DR, Kolluri VRS, Rao KS, et al. Cystic meningiomas in children. Childs Nerv
Syst 1986;2(6):317–319.

22. Della Puppa A, Dal Pos S, Zovato S, et al. Solitary intra-ventricular brain metastasis
from a breast carcinoma. J Neurooncol. 2010 Mar;97(1):123-6.

23. Yuh EL, Barkovich AJ, Gupta N. Imaging of ependymomas: MRI and CT. Childs
Nerv Syst 2009;25:1203–13.

24. Merchant TE, Fouladi M: Ependymoma: new therapeutic approaches including

radiation and chemotherapy. J Neurooncol. 2005;75:287-299.
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concepts, management, and future directions. Childs Nerv Syst. 2014 Apr;30(4):561-70.

26.Shah T, Jayasundar R, Singh VP, Sarkar C. In vivo MRS study of intraventricular

tumors. J Mag Res-on Imaging 2011;34(5):1053–1059.

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Table-1

Tumor Patient age Location Imaging hallmark

Choroid plexus CPP are more common in 50% lateral Hyperdense on CT,
tumors (CPP and children, usually <10 ventricles, 40 % in avidly enhancing,
CPC) years. Carcinomas occur fourth ventricle lobulated, frond like
exclusively in children appearance
and infants
Meningioma 40-60 years, with female Atria of lateral Hyperdense on CT with
predilection(similar to ventricle in calcification in 50% and
dural meningiomas) avid enhancement

Ependymoma Both adults and children , Fourth ventricle in > Tumor heterogeneity,
one-third of all brain 60% cases hemorrhage, necrosis,
tumors in children < 3yrs cyst and calcification
Subependymoma 40-60 years. Fourth ventricle (50- Poorly enhancing,
60%) and lateral calcification in 30%
ventricular margins
or septum (30-40%)
SEGA First two decades of life Virtually always at Robust enhancing lesion
the foramen of seen exclusively in
Monroe patients with Tuberous
sclerosis
Central Predominantly in the age Inferior septum Lobulated enhancing
neurocytoma group of 20-40 years. pellucidum and the mass with ‗bubbly‖
anterior lateral appearance due to
ventricle are the most intratumoral cyst.
common location Glycine peak (3.5 ppm)
Legends

Figure 1: Choroid plexus papilloma. (a) Axial noncontrast CT image shows a

circumscribed lobulated hyperdense mass with calcific foci in the atrium of the right

lateral ventricle. (b) Axial T2WI and contrast-enhanced T1WI (c) shows ―frond like‖

appearance and avid enhancing mass with ventricular dilatation.

Figure 2: Choroid plexus carcinoma. Two axial FLAIR images (A,B) show a large

infiltrative mass with prominent feeding arteries (seen as prominent flow voids) and

extensive parenchymal edema. Extent of parenchymal edema can be compared with the

prior case of CPP. (C) Post-contrast T1WI image shows avid enhancement of the mass

and areas of parenchymal invasion. (D) MR spectroscopy reveal elevated choline peak,

prominent myoinositol peak and reduced NAA levels.

Figure 3: Intraventricular meningioma. (A) Homogenous round T2 bright lesion is noted

in the trigone of left lateral ventricle with restricted diffusion (B) and homogenous

contrast enhancement.

Figure 4: Classic imaging findings of ependymoma in a child. (A) Complex solid-cystic

mass within the fourth ventricle is seen on the T1 sagittal image with obstructive

hydrocephalus. (B) T2W image shows the complex cystic nature of the mass with

heterogeneous enhancement after gadolinium administration (C). Extension of the mass

along the foramen of Luschka is one of the classic imaging findings in ependymomas,

seen in this patient on both, T2 and post-contrast images.

Figure 5: Subependymoma and central neurocytomas in two different patients. (A,B,C)

Complex cystic mass noted within the right anterior lateral ventricle attached to the

septum pellucidum. Lesion is barely perceptible on the T2WI (B) with no contrast

enhancement (C) and proved to be subependymoma on pathology. Axial CT (D), axial

T2WI (E) and post contrast (F) images in the second patient with pathologically proven

neurocytomas shows a partially calcific mass attached the septum. However, in contrast

to subependymoma, intense enhancement is seen in this within this lesion.

Figure 6: Subependymal Giant Cell Astrocytoma (SEGAs). (A) Axial FLAIR image

shows multiple subcortical and subependymal tubers in this patient with Tuberous

sclerosis complex. (B) Axial post-contrast image (2010) show enhancement of multiple

subependymal tubers. (C)Follow up MRI after 3 years (2013) shows significant interval

growth of the lesion along the foramen Monroe suggesting the diagnosis of SEGA.

Enhancement alone cannot differentiate SEGA from tubers and size >1.3 cm along with

growth on sequential scans are considered important diagnostic clues.

Figure7: Secondary intraventricular tumor (Glioblastoma Multiforme). (A, B)

Heterogeneous T2/FLAIR hyperintense mass noted in the right lateral ventricle with

extensive adjacent parenchymal signal changes. Lesion shows peripheral enhancement

with central necrosis (C, D) and was seen arising from the right thalamus on surgery,

with exophytic growth into the ventricle. Histopathology showed GBM.

Figure 8: Non-neoplastic cyst (Xanthogranulomas, ependymal cyst, colloid cyst). (A)

Incidental bilateral xanthogranulomas within the trigone of the lateral ventricle with

restricted diffusion. (B) Smooth walled cystic lesion along the margins of the right lateral

ventricle representing a benign ependymal cyst. (C) Classic location of a colloid cyst

along the foramen of Monroe with intrinsic T1 hyperintensity .

Fig. 1a
Fig.1b
Fig. 1c
Fig. 2a
Fig. 2b
Fig. 2c
Fig. 2d
Fig. 3a
Fig. 3b
Fig. 3c
Fig. 4a
Fig. 4b
Fig. 4c
Fig. 5a
Fig. 5b
Fig. 5c
Fig. 5d
Fig. 5e
Fig. 5f
Fig. 6a
Fig. 6b