Ependymoma 

  • Author: Jeffrey N Bruce, MD; Chief Editor: Jules E Harris, MD   more...
 
Updated: Jan 13, 2012
 

Background

Ependymomas are glial tumors that arise from ependymal cells within the central nervous system (CNS). They were first described by Bailey in 1924. The World Health Organization (WHO) classification scheme for these tumors includes 4 divisions based on histologic appearance: WHO grade I, myxopapillary ependymoma and subependymoma; WHO grade II, ependymoma (with cellular, papillary, and clear cell variants); WHO grade III, anaplastic ependymoma. Myxopapillary ependymomas are considered a biologically and morphologically distinct variant of ependymoma, occurring almost exclusively in the region of the cauda equina and behaving in a more benign fashion than grade II ependymoma. Subependymomas are uncommon lesions that share the benign features of myxopapillary ependymomas. Ependymoblastomas are now considered a primitive neuroectodermal tumor (PNET) and are distinct from ependymoma.

See the image below.

Gross surgical specimen of a fourth ventricle epenGross surgical specimen of a fourth ventricle ependymoma.

Intracranial ependymomas present as intraventricular masses with frequent extension into the subarachnoid space,[1] while spinal ependymomas present as intramedullary masses arising from the central canal or exophytic masses at the conus and cauda equina.

The anatomic distinction between intracranial and spinal locations has an epidemiologic and clinical correlate. In children, approximately 90% of ependymomas are intracranial, with the majority of these usually arising from the roof of the fourth ventricle (infratentorial). In adults and adolescents, 75% of ependymomas arise within the spinal canal, with a significant minority occurring intracranially in the supratentorial compartment.[2]

Treatment of patients with ependymomas depends upon neurosurgical intervention to facilitate definitive diagnosis and to decrease tumor burden. Postoperative adjuvant therapy can include brain or spine radiation, chemotherapy, and radiosurgery.[3, 4, 5, 6]

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Pathophysiology

Ependymomas are traditionally thought to arise from oncogenetic events that transform normal ependymal cells into tumor phenotypes. The precise nature and order of these genetic events are unknown; however, significant progress has been made toward delineating mutations that segregate with various tumor phenotypes. Some evidence now suggests that radial glia may be the cells of origin.[7, 8]

In 1988, Dal Chin and colleagues described cytogenetic studies on a supratentorial ependymoma from a 3-year-old girl that showed a t(10;11;15)(p12.2;q13.1;p12) and loss of one X chromosome.[9] This relatively simple karyotypic change was not observed in the analysis of 4 ependymomas published 1 year later. In 1 of the 4 ependymomas studied, translocations involving chromosomes 9, 17, and 22 were observed together with loss of the normal chromosome 17. A second ependymoma had many chromosomal alterations that included a translocation between chromosomes 1 and 2 and rearrangements involving chromosome 17. Consistent genetic alterations were not detected in the remaining 2 cases.

These initial studies underscore the molecular heterogeneity that can exist among histologically identical tumors. Subsequent studies have identified more consistent genetic defects as follows: a loss of loci on chromosome 22, a mutation of p53 in malignant ependymoma,[10] a recurring breakpoint at band 11q13,[11] abnormal karyotypes with frequent involvement of chromosome 6 and/or 16,[12] and NF2 mutations. Clustering of ependymomas has been reported in some families, with segregation analysis in one family suggesting the presence of an ependymoma tumor suppressor gene in the region of the chromosome 22 locus loss (22pter-22q11.2).[13, 14, 15, 16, 17, 18]

The ultimate goal of genetic studies is to demonstrate a causal relationship between specific mutations and tumor progression. Current efforts in the field are directed toward identifying another tumor suppressor gene on chromosome 22.

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Epidemiology

Frequency

United States

Frequency of ependymomas is similar to that in other parts of the world.

International

Intracranial ependymomas represent 6-9% of primary CNS neoplasms and account for 30% of primary CNS neoplasms in children younger than 3 years.[19]

Mortality/Morbidity

Depending on the patient population, the reported 10-year overall survival rate for ependymoma can vary from 45-55%. The current 5-year survival rate for patients with intracranial ependymomas is approximately 50%, when rates from children and adults are combined.[20] Stratification based on age reveals 5-year survival rates of 76% in adults and 14% in children.

Race

Grade II and III ependymoma are more common in black Americans than white Americans.[21]

Sex

The incidence of ependymoma is approximately equal in males and females.

Age

Ependymomas generally present in young children with a mean age of diagnosis of 4 years, yet 25-40% of patients are younger than 2 years. Spinal ependymomas are most common in patients aged 15-40 years, most of which are of a myxopapillary subtype. Intracranial tumors are seen more often in children, particularly in the infratentorial compartment.

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Contributor Information and Disclosures
Author

Jeffrey N Bruce, MD  Edgar M Housepian Professor of Neurological Surgery Research, Vice-Chairman and Professor of Neurological Surgery, Director of Brain Tumor Tissue Bank, Director of Bartoli Brain Tumor Laboratory, Department of Neurosurgery, Columbia University College of Physicians and Surgeons

Jeffrey N Bruce, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Neurological Surgeons, American Society of Clinical Oncology, Congress of Neurological Surgeons, New York Academy of Sciences, North American Skull Base Society, Pituitary Society, Society for Neuro-Oncology, and Society of Neurological Surgeons

Disclosure: NIH Grant/research funds Other

Coauthor(s)

David J Fusco, MD  Resident Physician in Neurological Surgery, Barrow Neurosurgical Institute, St Joseph's Hospital and Medical Center

David J Fusco, MD is a member of the following medical societies: American Association of Neurological Surgeons, American Medical Association, Congress of Neurological Surgeons, and North American Spine Society

Disclosure: Nothing to disclose.

Neil A Feldstein, MD  Director of Pediatric Neurosurgery, Department of Neurosurgery, Babies and Children's Hospital of New York, Assistant Professor, Departments of Clinical Neurosurgery and Pediatrics, Columbia-Presbyterian Medical Center, Columbia University

Neil A Feldstein, MD is a member of the following medical societies: American Association of Neurological Surgeons, American Cleft Palate/Craniofacial Association, American College of Surgeons, American Medical Association, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

Benjamin Kennedy  Columbia University College of Physicians and Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert C Shepard, MD, FACP  Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International

Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physician Executives, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Medical Association, American Medical Informatics Association, American Society of Hematology, Association of Clinical Research Professionals, Eastern Cooperative Oncology Group, European Society for Medical Oncology, Massachusetts Medical Society, and Society for Biological Therapy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rajalaxmi McKenna, MD, FACP  Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems

Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis

Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD  Clinical Professor of Medicine, Section of Hematology/Oncology, University of Arizona College of Medicine, Arizona Cancer Center

Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research

Disclosure: GlobeImmune Salary Consulting

Additional Contributors

We wish to acknowledge previous contributions to this article by Paul C McCormick, MD, and Allen Waziri, MD.

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CT scan without contrast. Fourth ventricle ependymoma.
CT scan without contrast. Fourth ventricle ependymoma. Note blood in the fourth ventricle.
CT scan without contrast in the patient with fourth ventricle ependymoma. Blood has refluxed into the third and lateral ventricles.
CT scan without contrast in the patient with fourth ventricle ependymoma. Note blood traversing foramina.
T1-weighted MRI. Rare case of a fourth ventricle ependymoma presenting as an intraventricular bleed.
T1-weighted MRI without contrast demonstrating ependymoma located in the fourth ventricle.
T2-weighted MRI demonstrating ependymoma in the fourth ventricle.
Coronal T1-weighted MRI with contrast demonstrating ependymoma of the fourth ventricle.
Gross surgical specimen of a fourth ventricle ependymoma.
Histologic study of a classic ependymoma. Note the characteristic perivascular pseudorosettes.
Cellular ependymoma. Cells with a high nuclear-cytoplasmic ratio. Few pseudorosettes or paucicellular areas are present.
Myxopapillary ependymoma. Clusters of loosely arranged cuboidal cells separated by pools of mucin.
Clear cell ependymoma. Round cells with cytoplasmic clearing. This may mimic an oligodendroglioma.
 
 
 
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