Imaging findings of intraventricular and ependymal lesions

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Journal of Neuroradiology (2013) xxx, xxx—xxx

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REVIEW

Imaging findings of intraventricular and ependymal lesions L. Vandesteen a, A. Drier a,∗, D. Galanaud a, F. Clarenc ¸on a, D. Leclercq a, C. Karachi b, D. Dormont a a

Department of Neuroradiology, Pitié-Salpêtrière Hospital, AP—HP, 47-83, boulevard de l’Hôpital, 75013 Paris, France b Department of Neurosurgery, Pitié-Salpêtrière Hospital, AP—HP, 47-83, boulevard de l’Hôpital, 75013 Paris, France

KEYWORDS Intraventricular; Ependyma; Disease; Diagnosis; MRI

Summary Intraventricular and ependymal lesions comprise a wide spectrum of tumoral, cystic, vascular, infectious and inflammatory disorders. With respect to tumoral and cystic diseases, the location, age and CT and MRI patterns are the main factors for diagnosis. The MRI findings of infectious diseases are supported by the clinical history, immune status and laboratory findings. Intracranial associated lesions may be very helpful for the diagnosis of Sturge-Weber, subependymal giant cell astrocytoma and systemic diseases, such as sarcoidosis and histiocytosis. Intraventricular vascular lesions are rare but present typical features on neuroimaging. The aim of this review is to provide a detailed description of these disorders with an emphasis on the key imaging findings and to generate a narrow differential diagnosis. We present a diagnostic approach based on the solid or cystic aspect of the intraventricular focal mass, its origin from the ventricular wall or choroid plexus and its location within the ventricular system. We also propose a differential diagnosis for ependymal dissemination: the ependymal enhancement may be due to ventriculitis from adjacent parenchymal lesions, the ependymal spread of tumors or infectious or inflammatory/systemic diseases. © 2013 Published by Elsevier Masson SAS.

Abbreviations Cho CMV

Chocholine Cytomegalovirus

∗ Corresponding author. Tel.: +33 1 42 16 55 22; fax: +33 1 42 16 35 98. E-mail address: [email protected] (A. Drier).

CNS Cr CSF CT DSC MRI MRS NAA PCNSL PNET

Central nervous system Creatine Cerebral spinal fluid Computed tomography Dynamic susceptibility contrast Magnetic resonance imaging Magnetic resonance spectroscopy N-acetyl-l-aspartate Primary central nervous system lymphoma Primitive neuroectodermal tumor

0150-9861/$ – see front matter © 2013 Published by Elsevier Masson SAS. http://dx.doi.org/10.1016/j.neurad.2013.06.004

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rCBV RGNT SFT SEGA TB VZV WHO WI

Relative cerebral blood volume Rosette-forming Gioneural Tumor Solitary fibrous tumors Subependymal giant cell astrocytoma Tuberculosis Varicella zoster virus World Health Organization Weighted-imaging

Introduction The ventricles and the ependyma may be involved in a wide spectrum of CNS disorders, either congenital or acquired, as the primary organ or as an extension of the disease. The

Figure 1

Figure 2

ventricular system may be affected by tumoral, infectious, systemic or vascular lesions. Radiologists may recognize some disease entities with typical imaging findings. The clinical presentation is most often nonspecific, with the notable exception of sudden positional headache and sudden death in colloid cysts [1,2]. Although MRI is the modality of choice for evaluation, CT, CSF analyses or biopsy with histologic examination may be necessary for a correct diagnosis. Surgical resection is usually the treatment of choice for tumoral lesions. The aim of this pictorial review is to discuss the imaging features of each intraventricular lesion and to present a diagnostic approach based on the solid or cystic aspects of the intraventricular focal mass, its origin from the ventricular wall or choroid plexus (Fig. 1) and its location within

Diagnostic approach of intraventricular focal masses: solid versus cystic lesion.

Diagnostic approach-based on the intraventricular topography and the most common lesions.

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Imaging findings of intraventricular and ependymal lesions

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Causes of ependymal enhancement.

the ventricular system (Fig. 2). We also discuss different causes of ependymal dissemination: tumor, infections and inflammatory/systemic diseases (Fig. 3).

Intraventricular focal lesions Solid lesions arising from the ventricular wall or septum pellucidum Central neurocytoma The typical topography of a central neurocytoma is the anterior part of the lateral ventricles with a characteristic attachment to the septum pellucidum (Fig. 4). Neurocytomas can also arise from the ventricular wall [3]. Other locations are very rare. Approximately 13% are bilateral. The mean age of presentation is 29 years [4]. They are considered WHO grade II tumors [5]. In anatomopathologic studies, the lesion may be mistaken for an oligodendroglioma if the appropriate staining or immunohistochemical examination is not performed [4,6]. The typical imaging finding is a well-circumscribed intraventricular lobulated mass attached to the septum pellucidum or the ventricular wall with intratumoral cyst-like areas (two third of cases) [7]. Neurocytomas are most commonly located near the foramen of Monro, and the majority of cases are associated with hydrocephalus or monoventricular dilatation. On CT, they are normally hyperdense compared with the brain parenchyma. Calcifications may be noted in half of cases, usually punctate in character [4]. On MRI, the lesion is usually heterogeneous, mostly isointense compared with the gray matter in T1WI and hyperintense on T2WI, with a typical ‘‘bubbly’’ appearance of the cystic areas. Prominent flow voids may be observed. The solid portions present moderate enhancement after intravenous contrast administration [4,8,9]. The vascular appearance of neurocytomas on DSC perfusion study is highly variable with a rCBV ranging from 1.5 to 5.1 and a mean rCBV greater than 2 but less than 3 [10]. On MRS, the Cho/Cr and Cho/NAA

ratios are elevated, and there is a peak at 3.55 ppm that likely corresponds to inositol or glycine [11].

Ependymoma Ependymomas are common neoplasms developed from differentiated ependymal cells that line the cerebral ventricles [12] (Fig. 5). The main location is the fourth ventricle, accounting for more than 50% of reported cases. The remaining cases (of intraventricular ependymomas) occur in the third and lateral ventricles. Most of the ependymomas of the posterior fossa arise in children, with a mean age of 6 years, whereas the majority of supratentorial ependymomas occur in young adults (18—24 years) [4,13]. They are considered WHO grade II (low grade, well differenciated) or grade III (anaplastic) neoplasms, and are associated with a high rate of recurrence post-surgery and CSF dissemination ranging from 12 to 24% of cases [14,15]. Therefore, imaging of the entire neuroaxis should be performed to asses for CSF dissemination. On non-enhanced CT images, intraventricular ependymomas are usually isoattenuated, partially calcified masses. The enhancement is heterogeneous after the administration of contrast material. Calcifications are common (40—80% of cases), ranging from small punctate foci to large masses [4]. Occasionally, intratumoral hemorrhage may produce a blood-fluid level. In contrast to most posterior fossa ependymomas, supratentorial ependymomas are usually located in the cerebral parenchyma and frequently have a cystic appearance on cross-sectional images [4]. On MRI, ependymomas are typically isointense compared with the gray matter in T1WI and hyperintense in T2WI. A heterogeneous appearance is typical, reflecting the calcification, hemorrhagic, and cystic changes that are often present. After intravenous contrast administration, they present a variable enhancement but are usually intense in the soft-tissue portions [4]. WHO grade II tumors are poorly vascularized with a mean rCBV values less than 2 [10]. They usually have a suggestive profile on MRS, with high levels of myoinositol

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Figure 4 Central neurocytoma. Axial T1WI (A), axial T1WI gadolinium (B), ADC map (C), MRS TE 135 ms (D) and perfusion curve (E). ‘‘Bubbly’’ appearance of the intraventricular mass attached to the septum pellucidum (white arrow) with little to moderate enhancement after contrast administration. Restricted diffusion is noted in the ADC map related to tumor hypercellularity. The MRS shows a marked choline peak and higher Cho/Cr and Cho/NAA ratios. The perfusion curve demonstrates a non-elevated rCBV. Monoventricular dilatation is noted.

Figure 5 Ependymoma. Sagittal T2WI (A), sagittal T1WI gadolinium (B) and axial T1WI gadolinium (C). Heterogeneous fourth ventricle mass insinuated in the right Luschka (white arrow) and in the Magendie (yellow arrow) foramens with intralesional cysts (blue arrow). After the administration of gadolinium, discrete to moderate heterogeneous enhancement is observed.

and glycine at 3.55 ppm, which are associated with elevated choline and reduced NAA peaks [16,17]. Subependymomas The majority of these benign (WHO grade I) tumors occur within the fourth (60%) and lateral ventricles in middle-aged or elderly patients. Subependymomas are typically smaller than 2 cm and asymptomatic [18]. Recurrence after surgical resection is rare [4]. The typical lesion is well-circumscribed

and appears as a solid lobular mass. On CT, they are isoattenuated to slightly hypoattenuated compared with the brain parenchyma, with or without a mild enhancement. Internal cystic areas are frequent [19], but calcifications and hemorrhage are not common, except in large lesions [18]. On MRI, they are typically homogeneous solid masses, hypointense on T1WI and hyperintense on T2WI. There is no edema observed in the adjacent brain parenchyma. Typically, they do not enhance or are minimally enhanced after intravenous

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Figure 6 Subependymal giant cell astrocytoma. Axial T1WI gadolinium (A), axial FLAIR (B) and CT scan (C). Tuberous sclerosis complex with nodular lesions situated in the foramen of Monro bilaterally with intense enhancement after contrast administration (white arrows) and associated cortical tubers (yellow arrows), subependymal calcified nodules (red arrows) and calcified cortical tubers (blue arrows).

contrast administration [19]. These tumors are poorly vascularized on DSC perfusion with a mean rCBV less than 2 [10]. Subependymal giant cell astrocytoma SEGAs are observed in 6—18% of cases of tuberous sclerosis complex [20] (Fig. 6). The presence of associated lesions, such as cortical/subcortical tubers, subependymal glial nodules and white-matter lesions, along the lines of neuronal migration may help evoke the diagnosis. SEGA is often diagnosed in the first and second decades of life. SEGAs are considered WHO grade I tumors [20]. After surgical resection, recurrence is rare [21]. This lesion is well marginated and arises from the ventricular wall near the foramen of Monro, which can be enlarged by this mass. On CT, SEGA is usually iso- or slightly hypodense compared with the normal white-matter, with frequent calcifications and strong enhancement after intravenous contrast administration. On MRI, the lesion is heterogeneous on T1WI and T2WI, with frequent hypointense foci on T2WI due to calcifications. The lesions strongly enhance after intravenous contrast administration. This strong enhancement and growth over time distinguish SEGAs from subependymal nodules, which are typically stable and do not enhance [4,22]. These tumors are poorly vascularized with a mean rCBV values less than 2 [10]. Metastasis The most frequent related primary tumors are renal cell carcinoma and lung carcinoma in adults and neuroblastoma, Wilms tumor and retinoblastoma in children [23] (Fig. 7). These lesions may reach the ventricular system by two pathways (hematogeneously and by the CSF), and the lateral ventricle is the most common site for metastatic spread [4,24]. These tumors can mimic meningiomas in imaging studies. On CT, they are isodense or hypodense compared with the brain parenchyma. On MRI, they are usually hypointense on

T1WI and hyperintense on T2WI. They strongly enhance after intravenous contrast administration [4]. DSC perfusion study, the rCBV values depend on the primary tumor. Renal and thyroid carcinomas, and melanoma metastases are all highly vascularized (mean rCBV > 3) compared with other metastases, which are intermediately vascularized (mean rCBV > 2 but < 3) [10]. PNET Primitive neuroectodermal tumors, which are embryonal tumors with high cellularity, are composed of greater than 90% undifferentiated cells [25] (Fig. 8). PNETs are most frequently intraparenchymal lesions, and an intraventricular location is less frequent, with possible CSF dissemination. They are commonly observed in children under the age of 5 years [25,26]. The tumor is usually sharply marginated and heterogeneous with different degrees of hemorrhage and necrosis. There is usually minimal peritumoral edema. On CT scans, the tumor tends to be hyperdense, and calcifications are present in approximately 50—70% of cases [26]. On MRI,

Figure 7 Metastasis. Axial T1WI (A) and axial T1WI gadolinium (B). Renal cancer metastasis: round heterogeneous lesion in the foramen of Monro with intralesional hemorrhage (hyperintensity on T1- white arrow) and heterogeneous contrast enhancement. Monoventricular dilatation secondary to trapped CSF is noted.

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Figure 8 PNET. Axial DWI (A), axial T1WI gadolinium (B), MRS (TE 135 ms) (C) and perfusion curve (D). Heterogeneous mass in the trigone of the lateral ventricle with restricted diffusion and heterogeneous intense contrast enhancement. On the perfusion curve, the lesion is hyperperfused with an augmented rCBV (5 ×). On MRS, the Cho/Cr and Cho/NAA ratios are elevated.

areas of restricted diffusion in the solid portions of the tumor are present and may be suggestive of the diagnosis [27]. Perfusion imaging shows increased rCBV [28]. After the administration of contrast media, enhancement is heterogeneous [25,26]. On MRS, high levels of choline, lipids and myo-inositol are observed [17]. A significant elevation of Tau at 3.3 ppm is also usual [29]. Gliomas Intraventricular gliomas are rare, accounting for 1% or less of all intracranial neoplasms [30]. They arise from the ventricular wall or septum pellucidum. They occur mainly in the lateral ventricles, with the exception of the chordoid glioma that has a predilection for the third ventricle. Astrocytomas present the same imaging findings as their intra-axial counterparts, and they may invade and infiltrate the adjacent parenchyma. The chordoid glioma is a new clinicopathologic entity, considered to be a low-grade glioma that occurs in the region of the hypothalamus and anterior third ventricle and that has recently been added to the WHO classification [31,32]. In the study of Brat et al., the mean age of diagnosis was

46 ± 13 years [32]. Imaging findings suggestive of this lesion include an ovoid shape with regular non-infiltrative contours that is hyperdense on CT, isointense on T1WI, and relatively hypointense on T2WI and has intense homogeneous enhancement. A case report of a chordoid glioma reported a rCBVmax at 1, significantly lower than in meningiomas or malignant gliomas, with a breakdown of the blood-brain barrier [33]. When there is associated edema, it usually extends into the optic tracts and helps differentiate this lesion from the most frequent optic/hypothalamic glioma that tends to infiltrate the optic tracts. Another difference is that the latter occurs in younger patients.

Solitary fibrous tumor SFTs are infrequent benign neoplasms of mesenchymal origin, initially described in the visceral pleura. Intracranial SFTs are rare lesions and usually develop from the meninges. Intraventricular and parenchymal SFTs are rare. Pathological and immunohistochemical descriptions of these tumors are now well-established and usually allow the differentiation among SFTs, meningiomas, hemangiopericytomas and other extra-axial lesions.

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Figure 9 Choroid plexus papilloma. Coronal T2WI (A), sagittal T1WI (B) and sagittal T1 gadolinium (C). Discrete lobulated mass centered in the fourth ventricle with an intermediate signal on T2WI and presenting an intense enhancement after the administration of gadolinium. The cystic formation in the posterior aspect of this mass is most likely related to trapped CSF.

On CT, SFTs are usually isodense with intense enhancement after contrast injection. Intratumoral calcifications may exist but are rare [34]. On MRI, SFTs are heterogeneous, presenting areas with low signal on T2WI with intense homogenous enhancement after intravenous contrast administration that corresponds to fibrosis with abundant collagen [34—36]. The other components of the lesion are hypercellular on histology and correlated with a heterogeneous T2 hypersignal and heterogeneous enhancement after contrast administration. These different components and signals give the lesion a ‘‘Yin-Yang’’ pattern as previously described [37]. Rosette-forming gioneural tumor RGNT is considered WHO grade I and it was included as a distinct glioneural neoplasm in 2007 WHO classification of tumors of the central nervous system [15,38,39]. At histologic examination, the tumor presents a lowgrade glial component that resembles pilocytic astrocytoma and a neurocytic component. Mitotic activity and necrosis are absent. These tumors probably arise from progenitor pluripotential cells of the subependymal plate [15]. RGNT predominantly occurs in young adults and the typical location is within the fourth ventricle [15,39]. The lesion is well-circumscribed, with solid and cystic components centered in the fourth ventricle. Heterogeneous enhancement is usually seen on contrast-enhanced studies. Hemorrhage and calcification may be present [15,39].

Solid lesions arising from choroid plexus Choroid plexus papilloma and carcinoma Choroid plexus papilloma and carcinoma are both papillary neoplasms derived from the choroid plexus epithelium [40] (Fig. 9). Choroid plexus papillomas are benign, slowgrowing lesions with a good prognosis. They are considered WHO grade I lesions. In contrast, choroid plexus carcinomas are malignant tumors classified as WHO grade III, and occur quasi exclusively in very young children (< 5 years). They grow rapidly, and the outcome is poor, especially when brain invasion is present. CSF dissemination occurs in both choroid plexus papillomas and carcinomas but is much more common in patients with carcinoma [41,42].

Both neoplasms present similar characteristics on CT and MR imaging and may be indistinguishable. They most commonly occur in the atrium of the lateral ventricle in children and in the fourth ventricle in adults and present as a large lobulated mass with a ‘‘cauliflower’’ appearance [40]. Calcifications are present in approximately 24% of cases with variable degrees, ranging from scattered punctate foci to calcifications involving the entire mass [4,43]. On MRI, they present variable intensity on T1WI and T2WI. Flow voids are common [4], and intense enhancement after contrast media administration is the rule. A heterogeneous lesion with necrosis, parenchymal invasion and edema is more suggestive of choroid plexus carcinoma than of choroid plexus papilloma. On DSC perfusion, these tumors are hyperperfused with a rCBV greater than 3 because they are originated from a highly vascular structure as the choroid plexus [10]. Meningioma Intraventricular meningiomas are considered in some reports as the most common atrial mass in the adult population, but they are rare and represent only 0.7% of all meningiomas (Fig. 10). They are benign tumors, classified as WHO grade I. They typically occur in the adult population older than 30 years. They are believed to arise from arachnoid cap cells trapped within the choroid plexus, tela choroidea or velum interpositum. They are usually seen as a well-defined, circumscribed mass situated in the atrium of the lateral ventricles, less frequently within third ventricle and very rarely in the fourth ventricle [4]. The imaging findings are similar to those of other intracranial meningiomas. On CT scans, meningiomas are hyperdense compared with the cerebral parenchyma and are partially calcified in 50% of cases. On MRI, they are isointense to hypointense compared with the gray matter on T1WI and iso-, hypo- or hyperintense on T2WI, although a low signal has been described as a key feature of this lesion [4,44]. Cyst-like areas may be noted. After intravenous contrast agent administration, intense homogeneous or heterogeneous enhancement is observed [45]. These lesions are highly vascularized with mean rCBV values greater than 3 [10]. Typical MRS demonstrates a high choline peak, undetectable NAA and creatine peaks as well as the occasional

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Figure 10 Meningioma. Axial T1 gadolinium (A), coronal T2 (B) and MRS (TE 35 ms) (C). Round, well-defined lesion with homogeneous enhancement after contrast administration in the trigone of the lateral ventricle. Perilesional edema is noted in the adjacent white-matter. MRS demonstrates elevated peaks of choline, glutamate (Glx—2.35 ppm) and Alanine (Ala—1.46 ppm), without a significant lipid peak.

presence of alanine [46,47]. High levels of glutamate are also considered a typical aspect [17]. Infectious diseases The infection of the choroid plexus is usually associated with encephalitis, meningitis or ependymitis. A definitive diagnosis is made by CSF analysis. Cryptococcus, tuberculosis and choroid plexitis secondary to pyogenic abscess ruptured in the ventricular system are the most common agents involved in choroid plexitis (Fig. 11) [48—50]. Cryptococcus neoformans is the most common CNS fungal infection in patients with AIDS. Granuloma formation, known as cryptococcoma, in the choroid plexus is rare and is relatively specific for CNS cryptococcosis [48]. Choroid plexus cryptococcoma presents as an enlarged choroid plexus with intense enhancement (Fig. 12). ‘‘Gelatinous pseudocysts’’ in the basal ganglia corresponding to dilatation of the perivascular spaces with a signal intensity similar to that of the CSF; meningeal, perivascular and ependymal

Figure 11 Pyogenic abscess and choroid plexitis. Axial DWI (A) and T1WI gadolinium (B). Typical abscess in the left occipital lobe with ring enhancement and restricted diffusion. Fistulization of the abscess in the ventricular system with ventriculitis (ventricular wall enhancement — white arrow) and choroid plexitis (abnormal engorged choroid plexus with intense enhancement — yellow arrow).

enhancement; and intraparenchymal cyptococcomas may be associated. Choroid plexitis is a rare feature of tuberculosis and is usually associated with the other classical imaging findings, such as basal leptomeningitis, basal ganglia infarction and parenchymal tuberculomas [50]. The mechanism of choroid plexitis is the same as the mechanism of ventriculitis, which is discussed later in this article. Sturge-Weber syndrome Sturge-Weber syndrome, also known as encephalotrigeminal angiomatosis, is characterized by a nevus flammeus ‘‘portwine stain’’ in the facial cranial nerve V1 topography and by clinical manifestations such as seizures, hemiparesis and hemianopsia [51] (Fig. 13). The choroid plexus is usually enlarged and presents intense contrast enhancement that is related to angiomatosis or disturbance of the superficial cortical venous drainage with a resultant elevation of the deep venous pressure and drainage [51—53]. The associated lesions in SturgeWeber syndrome are pial angiomatosis with serpentine

Figure 12 Choroid plexus cryptococcoma. Coronal T2WI (A) and axial T1WI gadolinium (B). Engorged choroid plexus with an intermediate signal on T2WI and intense contrast enhancement related to choroid plexitis (white arrows). A thin linear ependymal enhancement of the occipital horns of the lateral ventricles (yellow arrows) and periventricular vasogenic edema are noted in the right peritrigonal region.

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Figure 13 STURGE-WEBER SYNDROME. Axial T1 gadolinium (A) and axial T2* (B). Engorged choroid plexus (white arrow) related to angiomatosis associated with gyral calcifications (red arrow) and contrast enhancement of pial vessels (yellow arrow).

leptomeningeal enhancement, ‘‘tram-track’’ gyriform cerebral calcifications, engorgement of deep veins, cerebral hemiatrophy and calvarial hemihypertrophy [51,54]. The cerebral abnormalities are homolateral to the facial nevus flammeus.

Histiocytosis Histiocytoses are a heterogeneous group of diseases characterized by tissue infiltration by histiocytes. The most common histiocytoses with CNS involvement are Langerhans cell histiocytosis, Erdheim-Chester and Rosai-Dorfman diseases. The diagnosis is confirmed by histopathology with special markers that allow differentiation between these entities. CNS involvement is rare. Hypointense T2 masses with homogeneous enhancement affecting the choroid plexus are rare [55], as is thin linear ependymal enhancement. Intracranial associated lesions may help to evoke the diagnosis of histiocytosis: masses of the pituitary axis, neurodegenerative lesions of dentate nuclei, dural thickening or masses with low signal on T2WI [55].

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Figure 14 Colloid cyst. Sagittal T1WI (A) and coronal T2WI (B). A well-defined round lesion in the anterosuperior portion of the third ventricle in the topography of the foramen of Monro that is hyperintense on T1WI and presents a nodule with a marked T2WI hyposignal inside (white arrow), compatible with a protein concretion. The cortical T1 hypointensity visualized in the occipital lobe (yellow arrow) is related to ischemic changes secondary to infratentorial herniation.

Cystic lesions Colloid cyst Colloid cysts are histologically benign, but they may obstruct the interventricular foramen of Monro, resulting in hydrocephalus with the risk of sudden death [2] (Fig. 14). They are attached to the anterosuperior third ventricle roof into the foramen of Monro in more than 99% of the cases [56]. The topography of the cyst is the most important feature for its diagnosis because the cyst density on CT and intensity in MRI may change, depending on the cyst content (amount of mucin, cholesterol and hemorrhage) and hydration state. Most frequently, colloid cysts are well demarcated, oval or rounded and hyperdense on CT scans, hyperintense on T1WI and isointense to the brain on T2WI, without contrast enhancement. Calcifications are rare [2]. Epidermoid cyst Epidermoid cysts are congenital inclusion cysts and represent 0.2—1.8% of primary intracranial neoplasms (Fig. 15). The cyst wall is composed of keratinized stratified squamous epithelium that produces keratin, water and cholesterol.

Figure 15 Epidermoid cyst. Axial FLAIR (A), coronal T2WI (B) and axial DWI (C). Intraventricular cyst hyperintense on T2WI, heterogeneous on FLAIR and with restricted diffusion.

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10 Cysts tend to grow in a racemose pattern and insinuate within CSF spaces, surrounding and encasing adjacent vessels and nerves. In approximately 40—50% of cases, they are located within the cerebellopontine angle cistern [57]. The fourth ventricle is the second most common intracranial location. [58]. On imaging, epidermoid cysts appear as CSF-like masses, hypodense on CT scans, slightly hyperintense to CSF on T1WI and isointense to CSF on T2WI. They are hyperintense to CSF on FLAIR sequences, and DWI demonstrates areas with high signals and low ADC values. Calcifications may be observed in 10-25% of cases. The margin of the cyst may be enhanced. MRS shows a peak of lactates [59]. Ruptured dermoid cyst The dermoid cyst is a midline tumor, usually in the posterior fossa and parasellar region, with a typical fatty component. It is hypodense on CT scans and has high signal intensity on T1WI and T2WI, with signal suppression in the fat-suppressed sequences. When it has ruptured, the fatty droplets may be localized inside the ventricular system and cisterns, floating on the superior part of these structures. Extensive enhancement of the meninges is possible, secondary to chemical meningitis [60,61]. Ependymal cyst The ependymal cyst, also known as a neuroepithelial cyst or glioependymal cyst, is a congenital benign ependymallined cyst. The main location is intraventricular, normally in the third ventricle. Intraparenchymal or subarachnoid locations are less common. Ependymal cysts appear as smooth, thin-walled cysts with a density on CT and an intensity on MRI similar to those of the CSF. There is no enhancement or diffusion restriction [57,62]. Choroid plexus cyst Choroid plexus cysts, also known as choroid plexus xanthogranulomas [63], occur when lipids accumulate in the choroid plexus from degenerating and/or desquamating choroid epithelium. Choroid plexus cysts are benign lesions, usually bilateral, and are located in the glomus of the lateral ventricles [57]. Most are smaller than 1 cm. On CT scans, the cysts are iso- to slightly hyperdense compared with the CSF. Peripheral calcifications are common.

L. Vandesteen et al. On MRI, the signal intensity is variable, with most being hypo- or hyperintense on T1WI and hyperintense on T2WI, with no suppression of the liquid signal on the FLAIR sequences. Two-thirds of these cysts show a DWI hypersignal [64]. After the administration of contrast media, the cysts show rim or nodular enhancement [57]. Neurocysticercosis Neurocysticercosis, the most frequent parasitic disease involving the human CNS, is caused by the encysted larvae of the tapeworm Taenia solium, acquired through fecal-oral contamination [65—68]. Neurocysticercosis develops according to four pathologic stages: vesicular, colloidal vesicular, granular nodular and nodular calcified stages. The most common locations are subarachnoid spaces, cisterns and parenchyma. Intraventricular neurocysticercosis is infrequent, occurring in the fourth ventricle (50%), followed by the lateral ventricles (35%), third ventricle (10%) and cerebral aqueduct (5%) [65]. It often leads to obstructive hydrocephalus and ventriculitis or adhesions due to prior ventricular infestation [69]. Isolated intraventricular neurocysticercosis has been reported in one-third of cases. The imaging findings depend on the pathologic stage. On CT scans, the cyst may be very difficult to distinguish from the CSF. It may be calcified. On MRI, the signal intensity may differ slightly from the CSF on T1WI and T2WI. In some cases, the cyst may be isointense compared with the CSF in all MRI conventional sequences. In such cases, alternative sequences, such as three-dimensional balanced steady-state free precession or contrast-enhanced MR cisternography, might be useful in the visualization of the membrane and/or content of the cyst [70].

Miscellaneous lesions Cavernous malformation Cavernous malformations are typically observed in the subcortical brain parenchyma, deep cerebral white-matter and basal ganglia, and their intraventricular location is very rare [71]. Most intraventricular cavernous malformations are located in the third ventricle (44%) [72] (Fig. 16).

Figure 16 Cavernous malformation. Coronal T2 (A) and axial T2* (B). Nodular lesion into the third ventricle with a hypointense halo on T2 and very hypointense on T2*.

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Figure 17 Hamartoma. Sagittal T1WI (A) and coronal T2WI (B). Small round lesion into the floor of the third ventricle with a signal intensity similar to that of the gray matter.

They have CT and MR characteristics similar to those of intraparenchymal cavernous malformations. On CT scans, they are hyperdense with possible speckled calcifications. On MRI, they are described as ‘‘popcorn-like’’ lesions on T1WI and T2WI, with usually hyperintense foci on T1WI representing methemoglobin. On T2WI, a hypointense rim related to the paramagnetic effect of hemosiderin can be seen. A marked hyposignal on T2 GRE is essential to demonstrate this paramagnetic effect of hemosiderin [73]. After intravenous contrast administration, there is usually no or mild enhancement, except when an associated venous angioma is present. Intraventricular cavernous malformations tend to be more voluminous than intraparenchymal malformations. It has been hypothesized that the CSF does not restrict the growth as does the brain parenchyma [74]. The growth of cavernous malformations is suggested to arise from repetitive intralesional hemorrhages [71].

Glial tumors The detection of ependymal dissemination is important because it usually indicates advanced disease with an even poorer prognosis that requires intrathecal chemotherapy to improve the survival [78] (Fig. 18). The MRI evaluation of these patients is very important because CSF cytological studies frequently yield false negative results [79]. Ependymal enhancement due to glial ventriculitis is often secondary to contiguity dissemination of a high-grade glioma. It usually presents as a thick enhancement on T1WI after contrast administration, associated with a hypersignal on the FLAIR sequences of the ventricular wall and subjacent periventricular white-matter that is likely related to edema.

Tuber cinereum hamartoma Hamartoma is a non-neoplastic congenital heterotopia of the gray matter located in the tuber cinereum region. On occasion, this lesion may protrude into the third ventricle, which looks similar to a primary intraventricular lesion. Hamartoma is usually diagnosed in children, and the classic clinical presentation is precocious puberty and/or gelastic seizures [75,76] (Fig. 17). The lesion is usually small and round, with a density and intensity similar to those of gray matter or presenting with a T2WI hypersignal as a result of gliosis, dysplastic neurons or balloon cells [76]. There is no contrast enhancement. On MRS, the NAA/Cr ratio is low, and the myo-inositol peak is elevated [76,77].

Ependymal dissemination An ependymal spread with the typical aspect of ventriculitis on imaging findings may occur in patients with systemic and infectious diseases or with tumors, such as germinomas, high grade gliomas and lymphomas.

Figure 18 Glial ventriculitis. Axial T1WI gadolinium pre- (A) and post-surgical resection (B). (A) Typical high grade glial tumor in the right frontal lobe with intense heterogeneous enhancement and glial ventriculitis related to the extension by contiguity of this lesion (white arrow). (B) Control MRI 1 year after the surgical resection: increased of the ependymal dissemination with diffuse ependymal enhancement (yellow arrows).

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L. Vandesteen et al.

Figure 19 Primary CNS lymphoma. Axial FLAIR (A), axial T1WI gadolinium (B), ADC map (C) and perfusion curve (D). Periventricular lymphoma with ependymal enhancement around the lateral ventricles (B). The most cellular portion of the lesion is visualized in the splenium of the corpus callosum with an intermediate signal on FLAIR (A) and restricted diffusion — blue on the ADC map (C). Adjacent perilesional vasogenic edema with FLAIR hypersignal is observed in (A). On MR perfusion imaging, lymphomas demonstrate a characteristic pattern of blood-brain barrier rupture (curve crossing above the baseline) (D).

Primary CNS lymphoma Most primary CNS lymphomas are of the non-Hodgkin’s Bcell type [80] and frequently occur around the ventricles, in the periventricular white-matter and within the basal ganglia. Subependymal spread with ependymal enhancement is characteristic (Fig. 19). These lymphomas may present as isolated or multiple mass lesions or as a periventricular infiltration with moderate perilesional edema [81]. The imaging findings reflect the high cellularity and high nucleus/cytoplasm ratio of the lymphoma and disruption of the blood-brain barrier. On CT images, the lesion is mainly hyperdense compared with the brain parenchyma. On MRI, the lesion is typically hypointense on T2WI and hyperintense on DWI, with low ADC values [80,81]. After intravenous contrast administration, the enhancement is intense and homogeneous for immunocompetent patients and heterogeneous in immunocompromised patients. The enhancement may disseminate along the perivascular spaces of Virchow Robin, which is very specific for lymphoma [81]. Calcification

and hemorrhage are rare. On CT or MR perfusion imaging, these lymphomas demonstrate a characteristic pattern of blood-brain barrier rupture (curve crossing above the baseline) [82]. On MRS, lipid peaks are observed, associated with a high Cho/Cr ratio [81].

Germinoma Germinoma represents the most frequent germ cell tumor, and 90% of patients with germinoma are less than 20 years old [83] (Fig. 20). The majority (50 to 65%) of these lesions occur in the pineal region, and 25-35% are located in the suprasellar region [84]. Dissemination via the CSF and infiltration of the adjacent brain parenchyma commonly occur. On CT scan, the lesion is hyperdense due to a high nucleus/cytoplasm ratio, and it engulfs pineal calcifications. On MRI, germinomas are iso- to hyperintense compared with the gray matter on T1 and T2WI, and they demonstrate avid, homogeneous enhancement after contrast administration.

Figure 20 Germinoma. Sagittal T2WI (A) and axial T1WI gadolinium (B). Suprasellar heterogeneous lesion with an intermediate signal in T2 (yellow arrow) related to a germinoma. Thick and nodular (white arrow) enhancement of the ventricle walls related to ependymal spread is visualized.

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Figure 21 Non-Langerhans cell histiocytosis: Rosai-Dorfman disease. Coronal T2WI (A) and axial T1WI gadolinium (B). Hypointense T2 nodules in the frontal horns of the lateral ventricles (yellow arrows) with intense contrast enhancement (white arrows) and peripheral vasogenic edema. An associated subcortical enhancing micronodular lesion is visualized (red arrow).

Restricted diffusion may be observed, indicating high cellularity. The lesion has a tendency to infiltrate the posterior wall of the third ventricle when located in the pineal region and to infiltrate the third ventricular floor when located in the suprasellar region. When there is ependymal dissemination, linear and/or nodular ependymal enhancement are observed.

Metastatic ependymal dissemination Metastatic ependymal dissemination in the context of primary CNS tumors is usually secondary to a high-grade glioma, PNET, ependymoma or germinoma, which have been described in the sections above. The metastatic ependymal dissemination of extra CNS tumors is rare. Rarely, it can occur without associated intraparenchymal lesions. This isolated ependymal metastatic involvement has been described for small cell lung cancer and melanomas [85—87]. The supposed mechanism of ependymal involvement is the hematogenous dissemination of tumor cells. The imaging findings are nonspecific and comprise periventricular enhancement, which may be regular or nodular in aspect [88].

Systemic diseases Sarcoidosis can involve any part of the CNS and its meningeal layers. Linear or nodular ependymal enhancement may occur in neurosarcoidosis, frequently associated with hydrocephalus [87]. Micronodular leptomeningeal enhancement is often associated with this aspect of granulomatous ventriculitis. The presence of other associated lesions, such as pituitary stalk or hypothalamic masses, pachymeningeal thickening, cranial nerve enhancement and enhancing brain parenchymal lesions, may help suggest the diagnosis [55,89]. Thin linear ependymal enhancement and periventricular nodules (Fig. 21) are rare manifestations of histiocytosis. The possible intracranial associated lesions are cited above.

Infectious diseases Viral diseases, pyogenic diseases, tuberculosis or toxoplasmosis may cause infectious ependymitis. The most common viral infection involving the ependyma is the cytomegalovirus (CMV) and, less frequently, the varicella zoster virus (VZV) by hematogenous dissemination. CMV encephalitis is an opportunistic infection, usually occurring in HIV patients with a CD4+ count of less than 50 cells/␮L. The most characteristic imaging finding is the presence of a diffuse isolated thin subependymal contrast enhancement associated with T2 hyperintensity that is best visualized on FLAIR sequences corresponding to necrotizing ependymitis [49,88]. Other CNS involvement, such as myelitis, polyradiculitis and retinitis, may provide an additional clue for the diagnosis. The CSF analysis has a high sensitivity and specificity with the demonstration of the viral genome via the polymerase chain reaction technique [88]. The imaging findings in VZV ventriculitis are similar to those of CMV and present associated findings related to vasculitis, such as basal ganglia infarcts secondary to inflammatory involvement of the lenticulostriate arteries. Pyogenic ependymitis is more frequently secondary to surgical intervention or ruptured periventricular abscess. The well-formed capsule of the pyogenic abscess is normally more thickened toward the more vascularized cortex. The thinner capsule abutting the white-matter helps explain the propensity for intraventricular rupture and subsequent ventriculitis/ependymitis. Ventriculitis secondary to abscess rupture increases mortality to 80% [49]. The imaging findings of intraventricular abscess rupture are characterized by the regular thickening of the ventricular wall with T2WI hypersignal and enhancement after contrast administration. The ventricular system may contain pus with dependent areas of bright hypersignal on DWI and low ADC values. Ependymal dissemination secondary to meningitis is rare [88]. On MRI, there is diffuse ependymal enhancement associated with periventricular edema. A choroid plexitis may be present, and the diagnosis can be confirmed by CSF analysis.

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14 Ventriculitis due to tuberculosis is rare. The intraventricular rupture of a granuloma or the hematogenous dissemination of this disease may result in ependymal spread [88,90,91]. Ependymal enhancement is often associated with other classical imaging findings described above (basal leptomeningitis, basal ganglia infarction and parenchymal tuberculomas). Ventriculitis due to toxoplasmosis is also very rare and usually associated with basal ganglia granulomas [88,92,93].

Conclusion Intraventricular and ependymal lesions are relatively rare and comprise a wide spectrum of tumoral, cystic, vascular, infectious and inflammatory disorders. Knowledge of the imaging characteristics, topography in the ventricular system, age and associated findings help the radiologist to narrow the diagnostic possibilities and to evoke the correct diagnosis in typical cases. We expect that our approach of intraventricular focal masses and ependymal enhancement will be useful in this workup.

Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.

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