AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

Background

Oligodendroglioma is a well-differentiated, diffusely infiltrating tumor of adults that is typically located in the cerebral hemispheres and is predominantly composed of cells that morphologically resemble oligodendroglia.

In 1900, Robertson first recognized oligodendroglial cells as the myelin-forming unit of the neuroglial portion of the central nervous system (CNS).

In 1924, Bailey and Hiller suggested that the oligodendrocyte may be a constituent of certain CNS tumors.¹

In 1926, Bailey and Cushing first described oligodendrogliomas in a histogenetic classification of gliomas.²

In 1929, Bailey and Bucy described 13 cases of oligodendroglioma, including the tumor's clinical and pathologic characteristics.³

For excellent patient education resources, visit eMedicine's Cancer and Tumors Center. Also, see eMedicine's patient education article Brain Cancer.

Pathophysiology

Oligodendrogliomas seem much more complex than their classic description suggests. Several systems have been used for the histologic grading of oligodendroglial tumors, including the Kernohan, Smith, Ringertz, and Saint Anne/Mayo (St. Anne-Mayo) (originally designed for astrocytic tumors) systems.

The classic method is the World Health Organization (WHO) grading system.⁴ Histologically, oligodendroglial tumors comprise a continuous spectrum of lesions, ranging from well-differentiated neoplasms to frankly malignant tumors. The WHO grading system recognizes 2 grades for oligodendroglial tumors: WHO grade II for well-differentiated tumors and WHO grade III for anaplastic oligodendroglioma.

Gross morphologic features

Macroscopically, oligodendrogliomas are usually solid, relatively well-defined, soft gray-pink tumors. Cases with extensive mucoid degeneration may appear gelatinous. The tumor is typically located in the cortex and white matter, and infiltration of the overlying leptomeninges may be seen. Calcification is frequent. Necrosis, cyst formation, and hemorrhage are possible.

Microscopic features

Well-differentiated oligodendrogliomas are composed of cells with uniform, round to oval nuclei and a fine chromatin pattern with small nucleoli. Perinuclear halos are characteristic and are a result of autolysis because of a delay in fixation. The tumor cells exhibit a clear, swollen cytoplasm that is surrounded by a well-defined membrane, which lends a fried-egg or honeycomb appearance, and the cells are associated with capillary-sized blood vessels that are arranged in an acutely branching or chicken-wire pattern.

The tumor cells are present in sheets and lobular groups between a prominent vascular network that is composed of branching capillaries. Infiltration of the tumor into the cerebral cortex results in perineuronal satellitosis and perivascular and subpial tumor cell aggregates. Circumscribed leptomeningeal infiltration may induce a marked desmoplastic reaction.

As the tumors become more anaplastic (WHO grade III), the oligodendrogliomas typically become more cellular, with increased nuclear pleomorphism, marked cytologic atypia, high mitotic activity, developing vascular proliferation, and areas of focal tumor necrosis. Whereas low-grade oligodendrogliomas lack astrocytic features, histologically malignant oligodendroglial tumors tend to develop certain astrocytic features.

Ultrastructural features

Oligodendroglial tumor cells contain variable amounts of cytoplasm that are often rich in organelles, including numerous microtubules, free ribosomes, and mitochondria. An associated prominent Golgi apparatus may be present. Usually, large compact bundles of glial filaments, as seen in astrocytomas, are absent.

Immunohistochemistry

No specific marker that is equivalent to astrocytomal glial filament acidic protein has been found to identify tumoral oligodendrocytes.

Catherine Daumas-Duport developed another approach to identifying oligodendrogliomas.^{5, 6} She concluded that these tumors are not monomorphous tumors as their classic description suggests and has distinguished 2 different growth patterns of gliomas. First, with solid tumor tissue, tumor cells are in contact with each other and are associated with newly formed microblood vessels.⁵ Second, with isolated tumor cells (ITCs), the tumor cells permeate largely intact brain parenchyma that is without neovascularity but has edema.

Daumas-Duport classified gliomas as follows: structure type I, which is solid tumor tissue only; structure type II, which is tumor tissue and ITCs; and structure type III, which are ITCs only.⁵ Oligodendrogliomas exhibit a structure type II or III growth pattern, but these tumors never adopt a structure type I pattern. According to Daumas-Duport, the "diffuse fibrillary astrocytomas" are composed of isolated tumoral oligodendrocytes, which induce chronic fibrillary astrogliosis in the infiltrated white matter.⁵

Oligodendrogliomas reveal a variable appearance according to their pattern of growth. The classic morphologic features, a honeycomb appearance, and a rich capillary network with a chicken-wire pattern are seen in the tumor tissue, whereas ITC components usually exhibit the morphologic appearance of the diffuse fibrillary astrocytomas. Therefore, oligodendrogliomas occur much more frequently than previously believed and probably account for one third of gliomas.⁵ The tumor tissue destroys the brain parenchyma and exhibits newly formed microblood vessels, whereas ITCs do not destroy brain parenchyma and are not accompanied by microangiogenesis.

Furthermore, delayed angiogenesis is a crucial event in the tumor's progression toward more aggressive behavior. Endothelial hyperplasia and contrast enhancement are powerful negative prognostic factors (contrast enhancement is strongly related to the degree of microvascularity). Daumas-Duport suggested the following new grading system based on morphologic and imaging criteria: grade A, which is the absence of endothelial hyperplasia and contrast enhancement, and grade B, which is the presence of endothelial hyperplasia and/or contrast enhancement.⁶

The median survival in Daumas-Duport's series was 11 years for patients classified with grade A oligodendrogliomas and 3.5 years for those with grade B. This classification requires close cooperation between the neuroradiologist and pathologist.

The problem of mixed oligodendrogliomas remains a matter of debate. (Note the lack of interobserver reproducibility concerning pathologic diagnosis in this field). The distinction between an oligoastrocytoma and astrocytoma is more than simply academic interest, because there is a marked difference in response to chemotherapy with procarbazine, lomustine, and vincristine (PCV).

Frequency

United States

In 2005, the US Central Brain Tumor Registry reported an annual incidence of oligodendroglial tumors of 0.35 cases per 100,000 individuals.⁷

International

According to conventional histologic classifications, oligodendrogliomas are uncommon neoplasms, accounting for 2-4% of primary brain tumors or 5-18% of cerebral gliomas. Their frequency is probably underestimated; some authors believe they account for approximately 30% of gliomas.

Oligodendroglioma may be the second most common glioma in adults after glioblastoma multiforme.⁷

Mortality/Morbidity

Median postoperative survival times ranging from 3 to 5 years have been reported in patients with oligodendrogliomas of all histologic grades. Median survival time is less than 2 years for patients with anaplastic oligodendrogliomas and approximately 10 years for persons with low-grade oligodendrogliomas.

According to several studies, survival is not correlated with tumor location or surgical removal. Rather, survival seems to be primarily correlated with the histologic features, clinical findings (age at onset, epilepsy vs deficit), and radiologic criteria (especially contrast enhancement).^{8, 9, 10, 11} Retrospective studies have shown that the deletions of chromosome 1p and 19q may predict a good response to chemotherapy and a better prognosis.^{9, 10}

• Oligodendrogliomas generally recur locally.
• Malignant progression with recurrence is not uncommon, although this is considered less frequent with oligodendrogliomas than with diffuse astrocytomas.
• Concerning anaplastic oligodendrogliomas, patients may develop metastases via the cerebrospinal fluid (CSF) or even systemic metastases (the skeletal system, lymph nodes, lung and pleura, and liver are the most commonly reported extraneural sites).

Sex

The incidence of oligodendrogliomas is reportedly equal between men and women, although some authors report a higher male preponderance.⁹

Age

Most oligodendrogliomas arise in adults, with a peak incidence in the fourth or fifth decades of life.⁹ Approximately 6% of oligodendrogliomas arise during infancy and childhood.⁹

Anatomy

The tumor is supratentorial in 92% of patients. In adults, oligodendrogliomas arise within the cortex and further extend into the white matter of the cerebral hemispheres in rough proportion to the mass of each lobe (frontal, parietal, temporal, and occipital). The lesion is predominantly peripheral, rarely affecting median structures. In tumors that are adjacent to the ventricular system or the subarachnoid spaces, seeding of the CSF pathways may occur. On occasion, frontal lobe tumors may extend through the corpus callosum.

Infratentorial locations are possible but uncommon. Packer et al reported 4 oligodendrogliomas of the posterior fossa in children and suggested that these tumors may behave aggressively in this location.¹² Intramedullary oligodendrogliomas have been reported in rare cases, with exceptional case reports describing holocord localization. Primary leptomeningeal oligodendrogliomas have also been reported.

Clinical Details

Because of the typically slow growth of oligodendrogliomas, the elapsed time between the initial symptoms and clinical diagnosis may vary from 1 week to 12 years. However, with easy access to magnetic resonance imaging (MRI), this interval has been greatly reduced.

Seizures are the most common presenting symptom of oligodendrogliomas. The frequency of seizures reported in the literature ranges from 24-100%. The high incidence of seizures may be related to the tendency of these tumors to diffusely infiltrate the cerebral cortex. Although generalized convulsions occur at a higher rate, various types of seizures may occur in relation to tumoral localization. For many years, epilepsy may be the only manifestation of intracerebral tumors that behave in a relatively benign manner. In this instance, epilepsy is a clinically favorable prognostic factor.

Headache is another frequent symptom. The remainder of the symptoms vary and include intracranial hypertension and focal neurologic deficit. The neurologic deficits often occur secondarily in patients who at first present with seizures only. Some authors report the negative prognostic implication of presentation with a focal neurologic deficit.

Preferred Examination

Computed tomography (CT) scanning and MRI are complementary exploratory techniques that are suitable for imaging oligodendrogliomas.¹³ However, tumor calcification is better defined on CT scans than on MRI.

DIFFERENTIALS

Section 3 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Central neurocytoma
Dysembryoplastic neuroepithelial tumor

CT SCAN

Section 4 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

Findings

Oligodendrogliomas are the brain tumors with the highest frequency of calcification. CT scanning must be performed before and after the injection of contrast material to avoid missing the presence of calcifications. Typically, a round or oval, well-limited, and fairly large peripheral lesion is revealed. The tumor matrix is either hypoattenuating or isoattenuating and occasionally hyperattenuating because of tumoral hemorrhage or calcification.

Calvarial erosion in association with slow-growing, peripherally located oligodendrogliomas is occasionally noted. Calvarial erosion also appears to be independent of the tumor grade. Contrast enhancement is sometimes difficult to visualize because of the presence of calcification.

Degree of Confidence

Tumoral calcification, seen in approximately 40% of patients, is better defined on CT scans than on MRIs. It seems to have no direct correlation with the tumor grade.

MRI

Section 5 of 9  

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• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

Findings

Oligodendrogliomas do not behave specifically; they are usually heterogeneous but have a relatively low intensity on T1-weighted sequences and a high intensity on T2-weighted sequences. Peritumoral edema is nicely depicted with T2-weighted sequences and with fluid-attenuated inversion recovery sequences, which are sensitive, but surrounding vasogenic edema is not common in oligodendrogliomas. Perifocal edema is less often observed in low-grade oligodendrogliomas. Small cystic-appearing regions and hemorrhage are commonly found in the mass.

Contrast enhancement is better seen with MRI than with CT scanning,^{14, 15, 16} especially with magnetization-transfer, T1-weighted spin-echo MRI sequences after gadolinium enhancement. The importance of contrast enhancement for the prognosis of these tumors has been emphasized (see Pathophysiology – Immunohistochemistry), as it seems to be the strongest negative factor affecting survival. Because the detection of contrast enhancement is of paramount importance, postcontrast MRI should always be performed; however, it appears that the presence or absence of contrast enhancement is not a specific finding for simply discriminating low-grade from anaplastic oligodendrogliomas.¹⁵

MR spectroscopy is a new technique to the field that provides spatially encoded chemical information for normal and tumoral tissue in selected regions of the brain. This technique is a safe, noninvasive means of performing biochemical analyses in vivo.

MR diffusion imaging can also be contributive: lower apparent diffusion coefficient (ADC) values that are indicative of water restriction are noted in high-grade tumors compared with the higher ADC values that are seen in low-grade tumors.

MR perfusion imaging is a noninvasive method of assessing the tumor microvasculature.
Such perfusion imaging has been used to calculate the perfusion parameters in gliomas, guide biopsies, provide prognostic information, and demonstrate differences in the vascularity of low-grade astrocytomas and oligodendrogliomas.

Increased vascular density is apparently seen in both low-grade and high-grade oligodendrogliomas. That pattern is in contrast to the pattern noted in fibrillary astrocytomas, for which microvascular proliferation is seen in only the higher-grade tumors.

Perfusion MR results (regional cerebral blood volume [rCBV] measurements) correlate with histologic differences in the tumor vasculature between low-grade oligodendrogliomas and astrocytomas. Low-grade oligodendrogliomas are more vascular than astrocytomas on both histologic evaluation and perfusion MR. Thus, perfusion MR is useful for improving the specificity of the diagnosis of grade II oligodendrogliomas and grade II astrocytomas.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving  or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

The oligodendroglioma anatomic situation and tumoral limits are better defined on MRI than on CT scanning. A large proportion of oligodendrogliomas is peripherally situated, and the tumor usually involves the whole thickness of the cortex. MRI is particularly reliable for appreciating cortical involvement. The frontal lobes are most often involved, followed by the temporal, parietal, and occipital lobes.

Occasionally, stereotactic biopsy is performed outside of the area of contrast enhancement, leading to a falsely reassuring diagnosis (ie, low-grade oligodendroglioma). The visualization of such a contrast enhancement on MRI modifies the grading of the tumor, which becomes anaplastic. Gradient-echo sequences are highly sensitive to calcification and therefore are a useful adjunct.

False Positives/Negatives

High-grade oligodendrogliomas may be difficult to differentiate from the more frequent glioblastoma multiforme. However, the presence of tumor calcification, a peripheral location, and the sometimes associated calvarial erosion may indicate an oligodendroglioma.

The most difficult lesion to differentiate is the astrocytoma that appears as a hypoattenuating, nonenhancing mass on CT scans. However, these astrocytic tumors tend to be deeper in location, extend along the fiber tracts, and usually lack calcification.

Two other conditions that must be considered in the differential diagnosis are (1) dysembryoplastic neuroepithelial tumor (partial seizures beginning before age 20 y, nonneurologic deficit, cortical tumoral topography on MRI) and (2) central neurocytoma (midline tumor). Immunomarkers and electron microscopy may help in the definitive diagnosis.

ANGIOGRAPHY

Section 6 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

Findings

The most frequent finding with angiography is a vascular void (see Image 22). A slight hypervascularization that is suggestive of malignant transformation is seldom seen.

INTERVENTION

Section 7 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

The optimum management of patients with low-grade glioma remains largely undefined.

The standard treatment of high-grade oligodendroglial tumors is based on surgery, radiotherapy, and chemotherapy. The benefit of the extent of surgical resection is a controversial issue. The efficacy of radiotherapy on overall survival is demonstrated, but the optimal timing is unknown. Although immediate postoperative radiation therapy is indicated for incompletely resected higher-grade oligodendrogliomas, its use for partially resected low-grade tumors is controversial.

Oligodendroglial tumors exhibit a particular therapeutic chemosensitivity that is different from that of astrocytic tumors, particularly glioblastoma multiforme. Responses of these tumors to a variety of drugs have been observed, principally with alkylating agents, but combination PCV chemotherapy has emerged as the treatment of choice.

Approximately two thirds of anaplastic oligodendrogliomas and oligoastrocytomas respond to a combination of surgery, radiation, and PCV chemotherapy. The place of chemotherapy, either in the adjuvant setting or at recurrence, remains a matter of debate.

Objective responses to such first-line therapy are observed in 60-80% of patients with newly diagnosed aggressive pure or mixed oligodendrogliomas, with complete response and partial response in 20-60% of patients and a time to progression of 14-48 months. Despite the success of front-line therapy, most patients with malignant gliomas experience tumor recurrence. Response rates to second-line chemotherapy vary from 10-40%, with a progression-free survival of 6-9 months. Studies of temozolomide given after PCV failure have shown encouraging results, with an objective response rate of approximately 40%, including a complete response rate of approximately 20%. Furthermore, a good correlation exists between quality of response and progression-free survival.

In newly diagnosed low-grade oligodendroglial tumors, however, the benefit of surgical resection and postoperative radiotherapy on survival has not been clearly demonstrated. The standard treatment is based on surgery and radiotherapy in cases in which the resection is partial. The usefulness and timing of chemotherapy remain under investigation.

The heterogeneous responses of anaplastic oligodendrogliomas and oligoastrocytomas to chemotherapy may be the result of the unique genetic alteration in these tumors. The combined loss of chromosome arms 1p and 19q that is known to occur in 50-70% of anaplastic oligodendrogliomas could represent a significant predictor of chemotherapeutic response and survival in anaplastic oligodendrogliomas.^{9, 10} On diffusion-weighted and perfusion-weighted MRIs, tumors with these deletions demonstrate better chemosensitivity in focal areas of lower ADC and higher relative cerebral rCBV. Oligodendrogliomas with 1p and 19q deletions appear to have a better biologic behavior and are more likely to respond to PCV chemotherapy.

MULTIMEDIA

Section 8 of 9  

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Classic histologic image of oligodendroglioma. This image shows monomorphous tumoral proliferation that consists of round, regular cells with a small, central, hyperchromatic nucleus surrounded by clear cytoplasm. Few calcifications are present.
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Media type:  Histology

Media file 2:  Smear preparation of well-differentiated oligodendroglioma. This image reveals isolated tumoral cells with regular, round nuclei.
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Media type:  Histology

Media file 3:  Paraffin section of well-differentiated oligodendroglioma (same case as in Image 2). This image shows tumoral cells, some reactional astrocytes, and an absence of vascular proliferation.
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Media type:  Histology

Media file 4:  Smear preparation of anaplastic oligodendroglioma. This image reveals increased nuclear pleomorphism and vascular proliferation.
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Media type:  Histology

Media file 5:  Paraffin section of anaplastic oligodendroglioma (same case as in Image 4). This image shows dense tumoral proliferation with round nuclei, perinuclear halos, calcification, and endothelial hyperplasia.
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Media type:  Histology

Media file 6:  Lateral radiograph of the skull in a 44-year-old man with a 3-year history of epileptic seizures. This radiograph shows a left frontal oligodendroglioma. Note the vermicular calcifications that are projecting on the frontal lobe.
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Media type:  X-RAY

Media file 7:  Contrast-enhanced computed tomography scan in a 44-year-old man with a 3-year history of epileptic seizures (same patient as in Image 6). This image reveals a calcified hypoattenuating lesion that is invading the corpus callosum.
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Media type:  CT

Media file 8:  Contrast-enhanced computed tomography scan in a 50-year-old man. This image reveals recurrence of a frontal oligodendroglioma in the right basal ganglia that was excised 6 years earlier.
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Media type:  CT

Media file 9:  Computed tomography scan of a low-grade oligodendroglioma. This image reveals a well-demarcated, left frontal hypoattenuating lesion with a small calcification.
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Media type:  CT

Media file 10:  Axial fluid-attenuated inversion recovery magnetic resonance of a low-grade oligodendroglioma (same patient as in Images 9, 11-12). This image shows heterogeneous high signal intensity in the left frontal lobe.
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Media type:  MRI

Media file 11:  Axial T1-weighted magnetic resonance image of a low-grade oligodendroglioma (same patient as in Images 9-10, 12). This image shows heterogeneous low signal intensity in the left frontal lobe that involves the cortex and white matter. Note the mass effect on the cortical sulci.
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Media type:  MRI

Media file 12:  Sagittal gadolinium-enhanced T1-weighted magnetic resonance image of a low-grade oligodendroglioma (same patient as in Images 9-11). This image demonstrates no contrast enhancement.
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Media type:  MRI

Media file 13:  Computed tomography scan of a low-grade oligodendroglioma. This image shows left frontal hypoattenuation that mainly involves the white matter.
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Media type:  CT

Media file 14:  Sagittal T1-weighted sequence magnetic resonance of a low-grade oligodendroglioma (same patient as in Images 13 and 15-18). This image shows heterogeneous low signal intensity involving the frontal lobe. Note the involvement of the corpus callosum.
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Media type:  MRI

Media file 15:  Sagittal gadolinium-enhanced T1-weighted magnetic resonance image of a low-grade oligodendroglioma (same patient as in Images 13-14, 16-18). This image shows a huge infiltrative lesion in the frontal lobe, no contrast enhancement, and a mass effect on the cortical sulci.
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Media type:  MRI

Media file 16:  Axial T2-weighted sequence magnetic resonance image of a low-grade oligodendroglioma (same patient as in Images 13-15, 17-18). This image shows heterogeneous high signal intensity in the left frontal lobe and low signal intensity in the white matter of the right parietal lobe that corresponds to a cavernous hemangioma.
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Media type:  MRI

Media file 17:  Axial gadolinium-enhanced T1-weighted magnetic resonance image of anaplastic transformation of a low-grade oligodendroglioma, 4 years later (same patient as in Images 13-16, 18). This image depicts local recurrence after surgery, with contrast enhancement in the left frontal lobe.
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Media type:  MRI

Media file 18:  Axial gadolinium-enhanced T1-weighted magnetic resonance image of anaplastic transformation of a low-grade oligodendroglioma, 4 years later (same patient as in Images 13-17). This image shows multifocal recurrence. A contrast-enhanced tumoral nodule is seen in the right temporal lobe. Note the left retro-ocular cavernous hemangioma.
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Media type:  MRI

Media file 19:  Axial gadolinium-enhanced T1-weighted magnetic resonance image of an anaplastic oligodendroglioma. This image shows heterogeneous contrast enhancement in the medial part of the left parieto-rolandic region.
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Media type:  MRI

Media file 20:  Axial T1-weighted gadolinium-enhanced magnetic resonance image of an anaplastic oligodendroglioma, 2 months after chemotherapy (same patient as in Image 19). This image shows disappearance of the contrast enhancement.
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Media type:  MRI

Media file 21:  Computed tomography scan of a low-grade oligodendroglioma. This image shows hypoattenuation of the left frontal lobe without contrast enhancement.
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Media type:  CT

Media file 22:  Lateral carotid angiograph of a low-grade oligodendroglioma (same patient as in Image 21). This images shows a vascular void due to the tumor.
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Media type:  Angiogram

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Differentials
• CT SCAN
• MRI
• Angiography
• Intervention
• Multimedia
• References

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22. Cairncross JG, Ueki K, Zlatescu MC, et al. Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst. Oct 7 1998;90(19):1473-9. [Medline].
23. Celli P, Nofrone I, Palma L, Cantore G, Fortuna A. Cerebral oligodendroglioma: prognostic factors and life history. Neurosurgery. Dec 1994;35(6):1018-34; discussion 1034-5. [Medline].
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Article Last Updated: Jul 13, 2007