Online newspaper of professor Yasser Metwally

The author:Professor Yasser Metwally

http://yassermetwally.com

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INTRODUCTION

Most adult intracranial tumors, such as gliomas and metastases, occur in the supratentorial compartment. Glioblastoma multiforme (GBM), the most common adult brain tumor, is also the most malignant. Therefore, knowledge of specific histopathology of brain lesions is important for assessment of overall prognosis and course of treatment. The radiologist’s role, in addition to establishing the presence of a brain tumor, is to identify more subtle findings that may preclude total resection or pose problems during treatment. All of the structural and mechanical effects of brain tumors including potential consequences, such as transtentorial herniation, are easily evaluated by conventional computed tomography (CT) and magnetic resonance (MR) imaging. With the advent of MR techniques, such as functional MR imaging (MRI), it has become possible to identify involvement of areas of eloquent cortex in relation to nearby tumor. This regionally specific information is becoming important in the preoperative planning of surgical treatment and for intraoperative guidance. As more experience is gained from in vivo evaluation of a large number of different brain neoplasms, MR spectroscopy is another MR tool that is becoming useful in certain clinical settings.

GRADING OF CENTRAL NERVOUS SYSTEM TUMORS

The World Health Organization (WHO) classification for brain tumors was revised in 1993. 1 Previous designations of central nervous system (CNS) tumors as noninfiltrating (ie, pilocytic astrocytomas) and diffusely infiltrating neoplasms (ie, low-grade astrocytoma, anaplastic astrocytoma, and GBM) are replaced by WHO grades I to IV. Cytological atypia, mitotic activity, high cellularity, vascular proliferation, and necrosis are pathological features used to determine the grade of CNS tumors. Grade I lesions include pilocytic astrocytomas, which generally have low proliferative potential. Special variants, such as giant cell astrocytomas, gangliogliomas, and dysembroplastic neuroepithelial tumors (DNT), are also considered grade I. Well- differentiated low-grade astrocytomas, oligodendrogliomas, and ependymomas are typical examples of grade 11 lesions. Histological evidence of malignancy with mitotic activity and anaplasia are present in grade III lesions, such as anaplastic astrocytomas, anaplastic oligodendroglioma, and anaplastic ependymal tumors. GBMs are considered grade IV showing cellular atypia, mitoses, endothelial proliferation, and necrosis. Choroid plexus carcinomas and embryonal tumors are also in this category.

GLIOMAS

Although there are only three major tumor types recognized, corresponding to the three types of glial cells (astrocytes, oligodendrocytes, and ependymal cells), gliomas encompass a broad spectrum of histopathologic and imaging findings. The variation in the phenotype and biological behavior of gliomas likely reflects the nature of the transformation- associated genes involved in the development of neoplasia. 2 There have been numerous classification schemes and staging criteria proposed for glial neoplasms. The WHO classification is generally used as a reference. 3

Primary cerebral gliomas account for up to 45% of intracranial tumors, with peak incidence in the seventh decade of life. 4 In children, most (70% to 80%) of gliomas are infratentorial. In the adult, GBM accounts for more than half (55%) of all gliomas. The. remaining subtypes in decreasing order of frequency include astrocytoma (20.5%), ependymoma (6%), medulloblastoma (6%), oligodendroglioma (5%), and choroid plexus papilloma (2% to 3%). 4 Histopathology may range from benign or “low-grade” tumors to the highly malignant anaplastic astrocytoma and GBM. Glial neoplasms can be heterogeneous, with anaplasia developing focally This can limit the diagnostic accuracy of small surgical biopsies. Furthermore, there can be significant change in the degree of malignancy over time. 5,6 Morbidity and mortality of these lesions can also be significantly influenced by the location of the lesion, which may limit surgical accessibility. 7

All gliomas, particularly the diffusely infiltrating variety, have a tendency toward progression to more malignant forms. Genetic alterations that appear to be common across low-grade to higher-grade astrocytomas include p53 mutations. 2 Mutations in pl6 and CDK4 gene amplification are present in both anaplastic astrocytomas and glioblastomas, 2 whereas loss of heterozygosity of chromosome 10 and EGF-R gene amplification are almost exclusively found in glioblastomas. 8

Clinical presentation includes focal neurological signs or symptoms related to increased intracranial pressure (ICP). Signs and symptoms of increased ICP include headache (typically more severe in the morning), nausea, vomiting, and visual disturbances. In GBMs and anaplastic astrocytomas, these signs can develop rapidly and are progressive. Because many of these neoplasms tend to develop and grow in the deep white matter, they can be clinically silent until achieving relatively large sizes. Patients who present with focal neurological signs or seizures tend to have a more optimistic prognosis due to an earlier presentation.

In the absence of contraindications’ such as pacemakers, ferromagnetic aneurysm clips, metallic foreign bodies in the eye, or cochlear implants, contrast-enhanced MR imaging is the modality of choice for the diagnosis and follow-up of brain neoplasms. MR imaging is more sensitive than CT in the detection of gliomas, in the assessment of tumor extent, and for identification of potential complications (ie, herniation syndromes, venous thrombosis, leptomeningeal and ependymal spread). Functional MR imaging can be added to the preoperative assessment of patients for identification of critical motor and language areas. 9 This assessment is facilitated by the use of high field strength units (1.5 T) with echo-planar imaging capabilities. In addition, intraoperative interactive navigational workstations can be used to review combined functional and anatomic information during biopsy and surgical resection of tumors. 10

Despite the exquisite sensitivity of MR imaging for identifying alterations in water content, it lacks specificity in the determination of histological grade. In general, the presence of contrast enhancement and hemorrhage correlate with increasing grade of tumor.”-” However, the presence or pattern of contrast enhancement or degree of T2-prolongation cannot be used to grade these lesions. In addition, it has been well recognized that regions of “normal- appearing brain” in patients with infiltrative or anaplastic astrocytomas and GBMs can harbor malignancy. 1,15

MR spectroscopy has long held the promise of in vivo histopathologic specificity Preliminary work indicates that N-acetylaspartate (NAA) and gamma-amino butyric acid are decreased in brain tumors, whereas choline is elevated. Lactate levels may correlate with histologic grade, and alanine may be associated with benign tumors. 16-18 NAA is found primarily in neuronal cells. Any process that either replaces normal neurons, or causes neuronal loss, can be expected to decrease the NAA level. For example, meningiomas are reported to have low NAA, low creatine, a prominent choline peak, and a mild elevation in lactate. 19 The H spectrum of gliomas appears to be dependent on the grade of the tumor, with higher grade lesions having lower levels of creatine and more significant elevations of lactate and choline. 19,20 Currently, MR spectroscopy may be useful in distinguishing tumor from other lesions that may mimic a neoplasm, such as encephalitis. However, the histopathologic specificity has been predominantly anecdotal, and its clinical usefulness has been limited by long imaging times and limited voxel resolutions. This may change with improvements in imaging hardware and novel imaging pulse sequences.

• Astrocytomas

Astrocytomas are tumors predominantly composed of astrocytes. Unless otherwise indicated, the term usually applies to diffusely infiltrating neoplasms (WHO grades 11 through IV). The pilocytic astrocytoma (WHO grade 1), pleomorphic xanthoastrocytoma, and giant cell astrocytomas have distinctly different biological, genetic, and phenotypic features. 2,3 This distinction should be kept in mind during the discussion of astrocytomas.

• Glioblastoma Multiforme

Glioblastoma multiforme is the most common adult supratentorial neoplasm. It is the most malignant of the glial tumors with a median survival of 6 months. It represents the bulk of brain gliomas and up to 20% of all intracranial neoplasms. GBM is rare in patients less than 30 years old, with most presenting between 45 and 55 years of age. There is a slight male predominance of 3:2. Most lesions occur in the frontal lobe (which is statistically the favored site of many neoplasms because of lobar volume considerations). These lesions characteristically cross the corpus callosum resulting in a butterfly distribution with bihemispheric involvement. Tumor can spread along the leptomeningeal and dura, the subarachnoid space, across white matter pathways, and along the ependyma. These neoplasms rarely metastasize beyond the CNS.

The histopathology demonstrates diverse cell forms with areas of marked cellularity and necrosis. 4 There is vascular endothelial proliferation within and adjacent to the tumor. Microscopically, no clear margin between normal brain and tumor cells, edema, or reactive gliosis is identified. GBM can develop de novo, or by progression from low-grade or anaplastic astrocytomas. These cannot be reliably distinguished histopathologically, although genetic distinctions have been suggested involving p53 mutations, EGF-R amplification, and loss of heterozygosity on chromosomes 10 and 17p. 21,22

Gliosarcoma is a variant of GBM containing a neoplastic mesenchymal (sarcomatous) component. Immunohistochemical and genetic analyses suggest a common origin from neoplastic glial cells. 23,24 Gliosarcomas have a greater tendency toward dural invasion, cerebrospinal fluid (CSF) seeding, and distant metastases.

CT and MR imaging of GBMs demonstrate heterogeneous masses, reflecting the presence of hemorrhage, necrosis, and varying cellularity. Flow voids may be identified indicating the hypervascular nature of these tumors, whereas calcification is rare. These tumors are associated with significant mass effect with extensive surrounding edema. Areas of abnormal signal on T2-weighted images may represent the presence of tumor or edema. In addition, regions of “normal-appearing brain” on MR images may be infiltrated by tumor cells on pathological evaluation. Thus, tumor margins cannot be accurately defined by imaging.

Figure 1. Glioblastoma multiforme. A, Axial FLAIR and T2-weighted images demonstrate a large right temporal lobe mass with extensive signal abnormality extending across the splenium of the corpus callosum. There is also significant mass effect with right uncal herniation. The right temporal horn is trapped (white arrow). B, Axial and coronal enhanced Tl-weighted images show thick irregular enhancement. (Click to magnify figure)

Enhancement patterns of GBMs are heterogeneous and can be nodular, ringlike, diffuse, or irregular with necrotic areas. The appearance can be similar to metastases, as well as radiation necrosis. GBMs are reported to be multifocal in 5% of cases. 4 These likely represent diffuse infiltration by tumor rather than synchronous development of separate lesions. Contrast enhancement can be useful in guiding surgical biopsy, as well as identifying the presence of subependymal or subarachnoid seeding. Postoperative imaging is typically performed within 2 days to distinguish postsurgical change and scar from enhancing residual tumor. Necrosis can develop following radiotherapy, and the appearance may be difficult to distinguish from recurrent tumor. SPECT imaging and MR cerebral perfusion imaging may be of value in this setting. Recurrent tumor should be hypervascular, whereas areas of radiation necrosis appear avascular.

Figure 2. Multifocal glioblastoma multiforme (GB). A, B,C,D Axial T2 and FLAIR images demonstrate multiple regions of increased signal abnormality including the right cerebellum, right temporal lobe, and left frontal lobe. Despite diffuse involvement, white matter signal abnormality cannot be traced to connect all the lesions. E,F, Axial enhanced Tl -weighted images show multiple discrete ring-enhancing masses. Imaging findings are indistinguishable from metastatic disease. (Click to magnify figure)

• Infiltrating Astrocytomas.

Astrocytomas account for 25% to 30% of all hemispheric gliomas with a peak incidence between 20 and 50 years of age. 4,25 Low-grade astrocytomas (WHO grade II) are slow-growing tumors without significant necrosis or vascular proliferation. Most of these lesions will progress to a higher pathological grade. Fibrillary astrocytoma is the most frequent variant of astrocytoma with low to moderate cell density and consistent expression of glial fibrillary acidic protein (GFAP). Gemistocytic astrocytomas are predominantly composed of gemistocytic astrocytes, which have plump, glassy, eosinophilic cell bodies. This variant has a propensity for progression to anaplastic astrocytoma. 2

Figure 3. GBM in a 49-year-old man. A, Axial T2-weighted image demonstrates a large right heterogeneous hemorrhagic mass with areas of necrosis (black arrow). B, Axial susceptibility gradient echo image demonstrates variable low signal intensity within the tumor, which confirms the presence of the blood products (white arrow) C, Axial enhanced Tl-weighted image. Note second right frontal lobe-enhancing lesion representing multifocal involvement (open arrow). (Click to magnify figure)

Anaplastic astrocytomas (WHO grade 111) demonstrate focal or diffuse areas of anaplasia with mitotic activity They may arise from low- grade astrocytomas, but are also frequently found at initial presentation. These tumors have a rapid tendency to progress toward GBM.

Figure 4. World Health Organization (WHO)Grade II infiltrating astrocytoma. Axial T2-weighted, FLAIR, and enhanced Tl -weighted images. There is a high signal intensity mass in the left frontal lobe. No significant edema or enhancement is identified. (Click to magnify figure)

The infiltrating astrocytomas may appear as well-defined masses on CT or MR images with little edema or associated mass effect. However, this belies the infiltrating nature of gliomas, with tumor cells extending beyond the areas of signal abnormality identified on imaging. 12 These lesions can be difficult to distinguish from non-neoplastic processes, such as an infarct, cerebritis, or focal demyelination. Calcification is rarely present in gliosis, whereas it can be present in 15% of the infiltrating astrocytomas. 26 A malignant astrocytoma that has diffusely infiltrated large portions of the brain produces the condition of gliomatosis cerebri. The CT characteristics of gliomatosis can be subtle, reflecting only mild hypodensity or mass effect. MR imaging typically demonstrates a large area of hemispheric T2 signal abnormality involving white and gray matter, reflecting the infiltrative nature of this lesion with mild mass effect. Enhancement in gliomatosis may be subtle or absent. The lesion can radiographically resemble infarct and cerebritis. Diffusion imaging can be helpful in distinguishing tumor from an acute infarct as there will be no corresponding decrease in apparent diffusion coefficient (ADC), which is diagnostic for acute infarction.

Figure 5. Anaplastic astrocytoma. Axial T2-weighted and enhanced Tl -weighted images demonstrate a large right temporal mass with prominent enhancement and extensive surrounding infiltration. Differential diagnosis includes lymphoma. (Click to magnify figure)

Figure 6. Anaplastic astrocytoma. Axial T2-weighted, FLAIR, and gradient echo images demonstrate a left frontal opercular mass with a minimal amount of edema. Appearance might suggest low-grade glioma; however, the presence of hemorrhage (white arrow) suggests higher grade. (Click to magnify figure)

Figure 7. Gliomatosis cerebri. Coronal FLAIR images show diffuse infiltration of the left temporal lobe with gray and white matter involvement (arrowhead). Note the relative lack of mass effect for the degree of infiltration. The white matter infiltration extends across the corpus callosum (white arrow) and involves bilateral deep white matter tracts (double arrow). (Click to magnify figure)

Figure 8. Gliomatosis cerebri in a 74-year-old woman. A, Axial T2-weighted, FLAIR, and enhanced Tl -weighted images demonstrate high signal intensity in the right temporal lobe involving white matter and cortex. The acute clinical presentation suggested infarct. B, Diffusion weighted image and TRACE apparent diffusion coefficient (ADC) map demonstrate increased water diffusion in the lesion (slightly higher values on ADC map, outlined by arrowheads), excluding acute infarction. Note that encephalitis may have a similar MR appearance and diffusion characteristics. (Click to magnify figure)

• Oligodendroglioma

Oligodendrogliomas (WHO grade 11) are slow-growing tumors comprising less than 10% of all intracranial gliomas. 26,27 The peak incidence is in the 4th to 5th decades of life, with a frontal and frontotemporal predominance.

Pathologically, these lesions are solid lesions with poorly defined borders, and infiltration similar to astrocytomas. Nearly 50% of these lesions are of mixed type, containing both oligodendrocytic and astrocytic cellular elements. 4 The astrocytic component of the tumor is more likely to dedifferentiate to a higher grade. They frequently demonstrate focal calcifications, particularly in the peripheral zone of infiltration. The common markers for oligodendroglial cells (myelin basic protein, myelin-associated glycoprotein, myelin proteolipid proteins) are not expressed to a significant extent. 2,28 More than 80% show loss of heterozygosity for loci in chromosome 1, suggesting the presence of a tumor-suppressor gene. 2, 29,30

Radiologically, these are typically well- defined masses with slight or no edema, and mild contrast enhancement. Cystic-appearing areas and areas of hemorrhage may be present. 7 Nodular or linear tumoral calcification can be seen in 50% to 90% of these lesions on CT. 31 The calcification is typically clumped and dystrophic. Although these lesions calcify much more frequently than astrocytomas, a calcified brain tumor is still more likely to be an astrocytoma owing to the much higher incidence of astrocytomas. 32 Oligodendrogliomas have a tendency to diffusely infiltrate the cortex and are more likely than astrocytomas to involve the arachnoid, dura, and skull. 15 Overlying calvarial change suggesting long-standing mass can be helpful in the differential.

Figure 9. Oligodendroglioma in an 81-year-old man. A, Axial CT image shows a calcified left frontal lobe mass (white arrowhead). B, Axial T2-weighted image demonstrates heterogeneous T2 signal reflecting the presence of calcifications and some surrounding edema. C, Postcontrast coronal Tl -weighted image shows mild enhancement (long white arrow). Statistically, a calcified mass is still more likely to represent low-grade astrocytoma. (Click to magnify figure)

• Ependymoma

Ependymomas (WHO grade 11) arise from the ependymal or subependymal cells surrounding the ventricles. There are also ependymal cells surrounding the central canal of the spinal cord, as well as clusters in the filum terminate. Clinically, patients present with symptoms of increased ICP from blockage of the CSF pathways. Histologically, these demonstrate perivascular pseudorosettes and ependymal rosettes. 2 Brisk mitotic activity indicates the more aggressive anaplastic ependymoma (WHO grade 111). In adults, ependymomas most frequently arise in the fourth ventricle. They expand the fourth ventricle and have a tendency to extrude through the outlet foramina of Magendie and Luschka. 15 They are usually isodense on CT with heterogeneous enhancement and signal patterns on MR imaging. Calcification is common, and hemorrhage may be present. The supratentorial ependymomas are typically large, calcified, cystic parenchymal masses found more commonly in children and young adults. 33

Subependymomas are slow-growing benign tumors (WHO grade 1), which arise as firm nodules attached to the walls of the fourth or lateral ventricle (predominately frontal horns). 1 They are usually asymptomatic and detected at autopsy; however, they may obstruct CSF pathways. Histopathologically, the formation of microcysts and calcification is common, with clusters of ependymal cells. 33 Familial clustering of some cases suggests a genetic basis. 33,34 Supratentorial subependymomas are solid intraventricular masses, which are usually smaller than ependymomas, and present in the fourth to fifth decade of life. 33

• Glial-Neuronal Neoplasms

There are several tumors that demonstrate mixed glial and neuronal features. Gangliogliomas (WHO grade 1) are benign and slow- growing lesions of young adults and children, with a female predominance. They are composed of neoplastic astrocytes and differentiated ganglion cells. 2 These benign lesions grow slowly and only rarely undergo anaplastic transformation. Growth is related to the gliomatous portion of the tumor. They demonstrate variable MR imaging appearance resulting from cyst formation and calcification. Fifty percent have mild enhancement. 15,32

Dysembryoplastic neuroepithelial tumor (WHO grade I) is a relatively new entity that typically affects children and young adults. 36,37 Presentation is related to partial complex seizures. This is a benign lesion, located in the cerebral cortex. There is frequently some associated adjacent cortical dysplasia, which may be responsible for the clinical presentation. 2 Pathologically, these lesions are composed of oligodendroglial-like cells that are arranged in a nodular fashion, as well as loose extranodular components containing “floating neurons”. 36,37 On MR images, they can resemble benign cysts and may demonstrate associated cortical dysplasia. They are hypointense on Tl-weighted images, hyperintense on T2-weighted sequences, and can demonstrate enhancement. 38 Thinning of the overlying calvarium may be present. 39

PRIMITIVE NEUROECTODERMAL TUMORS

The nomenclature of embryonal tumors (WHO grade IV), which originate from primitive, undifferentiated neuroepithelial cells, is still controversial among neuropathologists. The prototype of primitive neuroectodermal tumors (PNETS) is the cerebellar medulloblastoma. PNETs of the cerebral hemispheres or “cerebral neuroblastomas” are rare and are usually seen in children younger than 5 years of age. Occasionally, these bulky heterogeneous lesions can present in patients up to 35 years of age. Supratentorial PNETs are usually well-defined solid tumors with frequent calcification, hemorrhage, and cystic necrosis. 40,41 Evaluation of the entire neural axis is imperative as these tumors have a propensity for seeding the CSF.

Figure 10. Primitive neuroectodermal tumor (PNET). A, Axial T2-weighted image demonstrates a large hemispheric heterogeneous signal mass with areas of cyst formation (white arrow). Note iso-intense signal of the mass on T2-weighted image reflecting high cellularity. B, Axial Tl -weighted image demonstrates presence of hemorrhage (arrowhead). C, Axial postcontrast Tl -weighted images shows heterogeneous enhancement pattern. (Click to magnify figure)

NONGLIAL NEOPLASMS

• Lymphoma

Primary CNS lymphoma is more common than secondary lymphomas. 42 Most primary CNS lymphomas are high-grade non-Hodgkin’s B-cell lymphomas. 4 The site of origin is controversial because the CNS does not have endogenous lymphoid tissue or lymphatic circulation. 7 The incidence is increasing in both immunocompromised and immunocompetent individuals. Lesions can be multiple in up to 50% of cases, involving the basal ganglia, periventricular white matter, and corpus callosum. The lesions are very radiosensitive but frequently recur. The masses demonstrate high cellularity, with 90% isodense to hyperdense on CT, and isodense to hypointense to brain signal intensity on T2-weighted imaging. In immunocompetent individuals, there is prominent enhancement that tends to be solid and homogeneous. In these patients, lymphomas do not calcify, and hemorrhage is uncommon. 43 Up to 75% of these masses are in contact with the ependyma or meninges. 43 The imaging appearance is more heterogeneous in AIDS owing to hemorrhage and necrosis. 44 Enhancement patterns in immunocompromised individuals may be irregular and heterogeneous, often with a ring pattern. 42 In the AIDS population, CT and MR imaging cannot reliably distinguish between lymphoma and toxoplasmosis. SPECT imaging may be helpful in this setting.

Figure 11. Lymphoma. A, Axial T2-weighted image shows relatively low signal intensity of the mass indicating high cellularity (black arrow) with surrounding edema high signal intensity B, Postcontrast Tl-weighted image demonstrates marked enhancement of the mass in the right centrum semiovale with surrounding edema. (Click to magnify figure)

Secondary CNS lymphoma occurs from spread of systemic disease to the CNS (non- Hodgkin’s more common than Hodgkin’s). Secondary lymphomas typically involve the leptomeninges, and CSF with parenchymal involvement is much less common. MR imaging findings include leptomeningeal/dural enhancement and hydrocephalus. 7

• Meningioma

Meningioma is the most common nonglial primary intracranial tumor, with a female preponderance, occurring most commonly in the 40- to 60-year-old age range. 4 Most arise from arachnoid cap cells in arachnoid granulations, and 90% are supratentorial. Common locations include the parasagittal dura, the convexities, along the sphenoid wing, the cerebellopontine angle, the olfactory groove, and the planum sphenoidale. In approximately 8% of cases meningiomas are multiple, and the multiplicity is usually sporadic but may be familial or associated with neurofibromatosis type 11. Other causes of meningiomas include prior cranial irradiation and previous head trauma. 45 There is an increased incidence of meningioma with breast carcinoma and pregnancy, 46,47 suggesting a hormonal influence.

Figure 12. Meningioma in a 27-year-old woman who presented with new-onset seizure. A, Axial unenhanced CT image demonstrates a large hyperdense extra-axial mass in the left temporal region with associated central calcification (black arrow) and surrounding edema. B, Axial enhanced CT demonstrates intense homogeneous enhancement. Distinction of intra- versus extra-axial mass by CT can be difficult. C, Axial T2-weighted MR image clearly demonstrates a CSF cleft around the circumference of the tumor (arrowhead) indicating this to be an extra-axial mass. D, Sagittal postcontrast Tl -weighted image demonstrates a dural tail anteriorly and posteriorly along the tentorium (white arrows). (Click to magnify figure)

Meningiomas can be divided into three histological groups: (1) classic, (2) angioblastic, and (3) malignant. There are histological subtypes for each of these groupings as well. The classic type of meningioma includes syncytial, transitional, and fibroblastic subtypes. Most intracranial meningiomas are of the syncytial or; transitional subtype. The angioblastic group includes hemangioblastic and hemangiopericytic subtypes. The angioblastic meningioma is a rapidly growing aggressive variant with extensive thin-walled vascular spaces. Although meningiomas tend to invade venous sinuses, distant metastasis is rare, with an incidence of 0.1%. 48 The angioblastic type is the most frequent type to metastasize. 4

Figure 13. Cystic meningioma. A, Axial postcontrast Tl -weighted image reveals a cystic mass lesion involving the left frontal lobe with peripheral enhancement, as well as enhancement around a trapped CSF intensity collection laterally (white arrow). B, Axial postcontrast Tl -weighted image near vertex of the head demonstrates the extra-axial nature of the mass with associated dural attachment (white arrow). (Click to magnify figure)

Most meningiomas are hyperdense relative to adjacent brain on CT (70%) with calcification in 20% to 25% 49 and intense uniform enhancement. Cystic meningiomas are uncommon, occurring in less than I0% of cases. Cysts may be intratumoral, intraparenchymal, or may represent trapped CSF. Hemorrhagic meningiomas are uncommon. There is a rare lipoblastic or xanthomatous type of meningioma, which can show negative CT numbers. Diagnosis of meningiomas using MR imaging is made by demonstrating the extra-axial nature of the mass. Several key MR imaging signs aid in this distinction including: (1) the CSF cleft sign (a cleft of CSF between the lesion and the brain); (2) direct visualization of displaced or involved dura; (3) demonstration of displaced pial vessels, which lie between the brain and the extra-axial mass; and (4) buckling of the gray-white matter junction. 7,32 Most demonstrate a dural tail; however, this does not necessarily represent neoplastic infiltration and may instead reflect reactive fibrovascular proliferation. Meningiomas encase and narrow vessels. They are vascular tumors, which parasitize pial vessels. Bone changes can be hyperostotic 50 or, less commonly, osteolytic. These changes can result from hypervascularity of the periosteum or from tumor infiltration. Involvement of the outer table makes tumor invasion more likely.

METASTASES

Metastases are among the most common adult supratentorial mass, representing 40% of intracranial neoplasms. The most common primary tumors are breast and lung, followed by melanoma and renal carcinomas. They are usually multiple but can be solitary in 30% to 50% (more commonly lung and breast). 4,51,52 Metastases may be intra-axial, extra-axial, or dural. Metastatic disease can also involve the subarachnoid space or the skull. Ten percent of metastases may be hemorrhagic, especially melanoma, thyroid, renal cell carcinoma, and choriocarcinoma. Although lung and breast metastases are less commonly hemorrhagic, a hemorrhagic metastasis is still more likely to be associated with one of these primary tumors because of their higher prevalence.

Metastases are typically well-defined enhancing masses with moderate edema located at the gray-white junction. Vasogenic edema is out of proportion to the size of the lesion. However, in cortical metastases, edema may be minimal or absent so that no abnormality may be present on T2-weighted images, making contrast imaging essential. Magnetization transfer imaging with gadolinium improves sensitivity as does high-dose gadolinium and delayed contrast imaging.

Epidural metastatic disease usually develops from bone metastases and commonly demonstrates involvement of the overlying calvarium. Subdural tumor involvement likely results from direct hematogenous seeding, rather than invasion of the dura from epidural disease. Both epidural and subdural involvement may appear similar (unlike in the case of fluid collections), with a biconvex configuration. The involvement of the overlvin calvarium in epidural disease can be helpful in making the distinction. 7

Leptomeningeal carcinomatosis is the result of leptomeningeal spread of tumor. Leptomeningeal disease can occur with primary CNS malignancies, adenocarcinomas (lung and breast), leukemia, or lymphoma. Clinical presentation is frequently related to cranial nerve palsies and ataxia, due to infiltration of the subarachnoid space and the basal cisterns. Although contrast MR imaging will detect many of these cases, 56,57 CSF sampling is more sensitive, and the absence of MR enhancement does not exclude leptomeningeal disease. In a patient with hydrocephalus and a known malignancy, leptomeningeal carcinomatosis should be considered.

Figure 14. Metastatic breast carcinoma. A, Axial FLAIR images demonstrate a solitary mass with extensive surrounding edema in the left subinsular region. B, Axial and coronal enhanced Tl -weighted images show ring enhancement. Although the differential for a solitary mass lesion includes primary neoplasms and infectious etiologies, the peripheral location of this lesion, and the disproportionate amount of edema incited by the mass suggest metastatic disease. (Click to magnify figure)

Figure 15. Intraventricular metastases from lung carcinoma. Axial enhanced Tl-weighted images demonstrate an enhancing mass within the atrium and occipital horn of the right lateral ventricle. Note attachment to the pedicle of the choroid plexus (arrow). (Click to magnify figure)

SUMMARY

Magnetic resonance imaging plays a critical role in the diagnosis, management, and follow-up of adult supratentorial neoplasms. However, there is considerable overlap in the imaging findings of these lesions. New imaging methods, such as functional MR imaging, diffusion imaging, and spectroscopy may further improve diagnostic specificity and surgical management. Knowledge of the pathogenesis of these tumors, imaging characteristics, and available novel imaging tools will aid the radiologist in making meaningful contributions in the evaluation and treatment of these lesions.

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