DOI: 10.1148/rg.256055137
RadioGraphics 2005;25:1669-1688
From the Archives of the AFIP
Oligodendroglioma and Its Variants: Radiologic-Pathologic Correlation1
Kelly K. Koeller, CAPT, MC, USN and
Elisabeth J. Rushing, COL, MC, USA
1 From the Departments of Radiologic Pathology (K.K.K.) and Neuropathology (E.J.R.), Armed Forces Institute of Pathology, Washington, DC; the Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences, Bethesda, Md (K.K.K.); and the Department of Pathology, George Washington University, Washington, DC (E.J.R.). Received June 30, 2005; accepted August 30. Both authors have no financial relationships to disclose.
Address correspondence to K.K.K., Department of Radiology, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (e-mail: koeller.kelly{at}mayo.edu).
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Abstract
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Oligodendroglioma is the third most common glial neoplasm and most commonly arises in the frontal lobe. It occurs in males more frequently, and the peak manifestation is during the 5th and 6th decades. Children are affected much less commonly. The clinical presentation is often of several years duration with most patients presenting with seizures, reflecting the strong predilection of this tumor to involve the cortical gray matter. Current histopathologic classification schemes recognize two main types of tumors: well-differentiated oligodendroglioma and its anaplastic variant. Less commonly, neoplastic mixtures of both oligodendroglial and astrocytic components occur and are termed oligoastrocytomas, with both well-differentiated and anaplastic forms. Surgical resection is the mainstay of initial treatment, and many patients experience a long progression-free period. Recent genotyping has revealed chromosomal loss of 1p and 19q as a genetic signature in most oligodendrogliomas, and these tumors respond favorably to chemotherapy. Hence, radiation therapy is now generally reserved for partially resected tumors and cases that failed to benefit from chemotherapy. At cross-sectional imaging, the tumor characteristically involves the cortical gray matter and frequently contains calcification. Robust enhancement is not a common feature and suggests transformation to a higher histologic grade. Advanced magnetic resonance imaging techniques and metabolic imaging play increasingly important roles in both pre- and postoperative assessment of these complex neoplasms.
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LEARNING OBJECTIVES FOR TEST 6
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After reading this article and taking the test, the reader will be able to:
- Identify the distinguishing imaging features of oligodendroglioma and its variant forms.
- Describe the gross pathologic and histologic appearances of oligodendroglioma and its variants and the direct correlation with the imaging appearances.
- Discuss the importance of genotyping in establishing the diagnosis of these tumors and the correlation with imaging features.
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Historical Perspective and Nomenclature
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The oligodendrocyte, as recognized by Robertson in 1900, is part of the neuroglial family of cells and is found predominantly in the white matter of the central nervous system (1). This is not a surprise as its primary function is the production and replenishment of myelin, which it spins off to form a bilaminar layer around axons. As with other glial cells, neoplastic transformation of the oligodendrocyte may occur, eventually resulting in a true neoplasm known as an oligodendroglioma. As described in their famous treatise on brain tumors, Bailey and Cushing (2) were the first to recognize this tumor as a distinct entity in 1926. Three years later, Bailey and Bucy (3) provided the classic description of 13 cases of the tumor and, through the early and middle portion of the 20th century, other reports accumulated of this fairly uncommon brain neoplasm (1,4).
These early investigators noted that this tumor had unusual characteristics compared to other glial tumors, particularly concerning its quite variable biologic behavior. In general, it was not as biologically aggressive as astrocytic gliomas of similar histologic grade. Yet, occasionally, it could show clinical and pathologic features much more consistent with the most highly malignant glial neoplasms (1,4).
As one might surmise, these seemingly unpredictable tumors have defied mutually agreeable histologic classification among neuropathologists despite many schemes being implemented over the years, from four-tiered systems originally employed by Kernohan, St Anne–Mayo, and the Armed Forces Institute of Pathology (AFIP) (4–6), to three-tiered schemes such as that used by Ringertz (7), and finally to today’s two-tiered systems such as the World Health Organization (WHO) system and others (8–10). In this classification scheme, oligodendrogliomas are divided into two forms: the well-differentiated oligodendroglioma and the less common anaplastic oligodendroglioma. In addition, oligodendrogliomas may occasionally contain clear evidence of neoplastic astrocytes and may then be considered "mixed gliomas," most commonly as oligoastrocytomas (11). These tumors are also divided into two groups: the better differentiated oligoastrocytoma and the anaplastic oligoastrocytoma.
Using case material from the Thompson Archives of the Department of Radiologic Pathology at the AFIP, this review highlights the epidemiologic, clinical, neuropathologic, and neuroimaging manifestations of these four tumor types and presents information that facilitates the recognition of these tumors at neuroimaging. Therapy, recurrence and metastasis, and prognosis and survival rates are also discussed.
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Epidemiology
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Oligodendroglioma is the third most common glioma overall, accounting for 2%–5% of primary brain tumors and 5%–18% of all glial neoplasms (8,12–14). The tumor accounts for less than 1% of pediatric central nervous system neoplasms (15). According to the Central Brain Tumor Registry of the United States, oligodendrogliomas have an annual incidence of 0.3 per 100,000 people, while the tumor composed 4.2% of all primary brain tumors over a 25-year period in the Norwegian Cancer Registry (14,16).
The actual prevalence of the other oligodendroglial tumors is difficult to determine, primarily because of a lack of uniformity regarding the morphologic criteria at histopathologic analysis and the lack of a defining immunohistochemical or molecular marker that would facilitate the diagnosis. The prevalence of anaplastic oligodendrogliomas varies from 3.5% of all malignant gliomas to 20%–54% of all oligodendroglial tumors in reported series (16–20). Mixed oligoastrocytomas accounted for about 9% of all glial tumors in the Norwegian Cancer Registry, while they composed only 1.8% of all brain tumors in the Central Brain Tumor Registry of the United States (21,22).
In recent years, the number of reported oligodendrogliomas has substantially increased, in part because of implementation of superior cross-sectional imaging techniques (23). Most important, recognition of the significant differences in prognosis between oligodendrogliomas and astrocytomas of similar histologic grade has influenced recent changes in accepted histopathologic criteria and is believed to have contributed to a dramatic increase in the number of oligodendrogliomas being diagnosed by neuropathologists. With use of these criteria modifications, up to 25% of gliomas may be considered oligodendrogliomas (24).
Most oligodendrogliomas manifest in the adult age groups with a peak incidence in the fourth and fifth decades (5,14,25). Patients with anaplastic tumors are usually slightly older (peak age, sixth and seventh decades) than those with well-differentiated oligodendrogliomas (17,25). Patients with oligoastrocytomas have a median age of 35–45 years (11,22). A small percentage (about 6%) arise in children, accounting for a second smaller age peak at 6–12 years (13,14,26–28). The tumor may rarely manifest as a fetal tumor (29).
Males are more commonly affected, up to 2:1 in some series, among patients with oligodendrogliomas (1,5,13). This male gender predilection is also noted in the other oligodendroglial tumors (11,17,22). While no definite inheritance pattern or known genetic risk factors have been documented, occasional familial groupings of oligodendroglioma and oligoastrocytoma have been reported (30–32).
The vast majority of all oligodendroglial tumors occur in the supratentorial brain with the frontal lobe the most common site overall (50%–65%) (5,11–14,18,33–35). The temporal lobe (47%) is the second most common location, with the parietal lobe (7%–20%) and occipital lobe (1%–4%) being less frequent sites of involvement (34,35). Multiple lobar involvement is possible (34). Other sites for primary tumors include the cerebellum (3%), brainstem, spinal cord (1%), leptomeninges (so-called "oligodendrogliomatosis"), cerebellopontine angle, cerebral ventricles, retina, and optic nerve (1,8,12,15,35–41). Primary leptomeningeal tumors are speculated to arise from glial heterotopias in this location (42).
Interesting observations of oligodendrogliomas coexisting with other intracranial neoplasms and diseases have been noted. Meningioma, sarcoma, lymphoma, pilocytic astrocytoma, and pleomorphic xanthoastrocytoma in association with oligodendrogliomas have been reported in the literature (43–49). Several reports of oligodendroglioma with arteriovenous malformation, some presenting with subarachnoid hemorrhage, and with multiple sclerosis have also been added (50–56).
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Clinical Features
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In accordance with its slow growth, oligodendroglioma typically demonstrates a long clinical presentation, frequently 5 years or more (6,13,14, 18,57). Patients with anaplastic oligoastrocytomas typically have a shorter clinical presentation (11). Seizure activity (35%–85%) is the most common symptom overall (5,13,14,19,34,35,58–60). It is believed that the high incidence of seizure activity is likely related to the tendency of the tumor to involve the cortical gray matter (8). Headache is the second most common symptom, followed by mental status changes, vertigo or nausea, visual complaints, and weakness (13, 14,57). Patients with intraventricular oligodendrogliomas tend to present with headaches as a consequence of increased intracranial pressure and usually have a shorter duration of symptoms without focal neurologic deficits compared to those whose tumors arise within the brain parenchyma (61). Among 323 patients from an AFIP series, the most common clinical signs were paralysis (50%), visual loss (49%), papilledema (47%), ataxia (39%), abnormal reflexes (37%), and meningismus (10%) (6).
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Pathologic Features
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At gross inspection, oligodendrogliomas are usually soft, fleshy, grayish-pink masses, frequently extending to the pial margin of the cerebral hemispheres, most commonly in the frontal lobe (8,38,62). Occasionally, mucoid degeneration and leptomeningeal infiltration are seen (8). Calcification is a common feature and may be detected at surgical resection by a hard "gritty" sensation (8).
Histopathologic evaluation of oligodendroglioma reveals a moderately cellular neoplasm with a typically monotonous pattern of uniformly rounded hyperchromatic nuclei surrounded by prominent clear cytoplasm ("perinuclear halo"). This frequently results in a classic "fried-egg" appearance at hematoxylin-eosin staining (8). This manifestation is actually an artifact of delayed fixation of the tissue and will not be seen in frozen section specimens (8). A delicate branching network of capillaries is characteristic, often producing a "honeycomb" or "chicken-wire" pattern (Fig 1) (8).
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Figure 1. Well-differentiated oligodendroglioma. Photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows uniform round cells that are interrupted by a dense network of branching capillaries, a few of which are indicated by arrows.
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Microcalcifications are seen in 90% of tumors, making oligodendroglioma the most common glial tumor to have this feature (63). Mucoid or cystic degeneration is also frequently noted (8). In accordance with its low-level proliferative ability, little or no mitotic activity is noted. Reactive gemistocytic astrocytes are seen occasionally (8). Rarely, an oligodendroglioma may be predominantly composed of signet-ring cells ("signet-cell oligodendroglioma") or in combination with giant cells ("polymorphous oligodendroglioma") (30,64).
While low levels of angiogenesis-promoting epidermal growth factor and vascular endothelial growth factor have been noted in most oligodendrogliomas, endothelial proliferation and necrosis are not characteristic features (8,65). Accordingly, the WHO classifies well-differentiated oligodendroglioma as a WHO grade II lesion (8).
Involvement of the cortical gray matter is a highly distinctive feature of this tumor (63). In this area, perineuronal satellitosis, perivascular aggregations of tumor cells, and subpial accumulations may be noted and provide valuable ancillary clues to the diagnosis (8,63). Normal neuronal cells of the cortex are often "overrun" by the infiltrating neoplastic oligodendroglial cells (63). This infiltration also gives rise to the typical "diffuse" appearance seen both histologically and at neuroimaging (63). Occasionally, the tumor may have an abrupt and well-defined margin (63).
Unfortunately, there is no specific immunohistochemical marker to substantiate the diagnosis of an oligodendroglioma (8). However, recent molecular investigations have revealed a propensity for loss of heterozygosity on the long arm of chromosome 19 (19q) in 50%–80% of oligodendrogliomas and on the short arm of chromosome 1 (1p) in 40%–92%, and virtually all oligodendrogliomas with loss of heterozygosity on 1p also have loss on 19q (8). This consistent finding is now being recognized as a signature genetic feature of an oligodendroglioma and is strongly affiliated with the classic histopathologic findings seen in well-differentiated (WHO grade II) oligodendrogliomas (66–68). In contrast, those oligodendroglial tumors that do not possess these chromosomal losses are associated with more variable and atypical histopathologic features (68). Losses of genetic material from other chromosomes (4, 6, 9, 10, 11p, 14, and 22q) have also been identified (8). It is becoming clear that genotyping of oligodendroglial tumors is important to the diagnosis of these tumors, perhaps even surpassing the importance of the histopathologic features (68).
The anaplastic oligodendroglioma, arising either de novo or from an existing well-differentiated oligodendroglioma, is noted for its increased cellularity, marked atypia, and increased mitotic activity. Endothelial proliferation, resulting from amplification of epidermal growth factor, and necrosis are also common (Fig 2) (69–71). Not surprisingly, these tumors are regarded as grade III neoplasms in the WHO classification scheme (17).
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Figure 2. Anaplastic oligodendroglioma. Photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows florid microvascular proliferation (arrows) within a typical oligodendroglial morphology.
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While similar to oligodendrogliomas with common deletions of 1p and 19q alleles, anaplastic oligodendrogliomas also show even more chromosomal deletions overall and an increased rate of deletions involving 9p and on chromosome 10 (17). In addition, a subgroup of anaplastic oligodendrogliomas is suspected because loss of chromosome 10 and gain of chromosome 7 is usually linked with absence of 1p and 19q deletions (17). Such tumors show more aggressive biologic behavior and may be genetically related to glioblastoma multiforme (17). About 25% of anaplastic oligodendrogliomas have deletion of a tumor suppressor gene, CDKN2A, located on the short arm of chromosome 9 (69).
As its name implies, the diagnosis of oligoastrocytoma rests on the detection of two different but definitely neoplastic glial components, one oligodendroglial and the other astrocytic (Fig 3) (22). Similar to oligodendroglioma, the tumor is moderately cellular, may contain microcalcifications or cystic degeneration, and demonstrates little or no mitotic activity and no necrosis or endothelial proliferation (22). The tumor may be either biphasic, with the two components clearly adjacent to each other, or intermingled, with the components diffusely intertwined. Many oligoastrocytomas (30%–50%) contain deletions of 1p and 19q alleles, while about 30% carry genetic changes (ie, mutation of the TP53 tumor suppressor gene and loss of heterozygosity of chromosome 10) typically seen in astrocytomas, supporting the hypothesis that oligoastrocytomas may be composed of two different subsets (72, 73). The tumor is considered a WHO grade II lesion (22).
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Figure 3. Oligoastrocytoma. Photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows unequivocal neoplastic astrocytic (a) and oligodendroglial components combined in this field. Arrowheads = representative oligodendrocytes with the typical "fried-egg" appearance.
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While the terminology is simple, it has been difficult to establish a uniform criterion regarding exactly what percentage of astrocytic component—recommendations have ranged from 1% to 50%—is required before one labels the tumor an oligoastrocytoma instead of an oligodendroglioma (22,63,68). Hence, the tumor remains a nosologically controversial entity. The distinction between an oligoastrocytoma and astrocytoma is of more than simply academic interest, as there is a marked difference in response to chemotherapy with procarbazine, lomustine, and vincristine (PCV) and hence in prognosis for patients with the anaplastic forms of these tumors (74–76).
The anaplastic oligoastrocytoma is an even more heterogeneous tumor histopathologically and contains the additional features of nuclear atypia, pleomorphism, increased cellularity, and high mitotic activity. Therefore, it is considered a WHO grade III tumor (11). Many chromosomal alterations similar to those found in the other oligodendroglial neoplasms have been reported (11).
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Histogenesis
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To date, definitive proof that oligodendrogliomas arise from oligodendroglial cells is lacking. The perception that these tumors are oligodendroglial in nature rests primarily on the morphologic similarities of the tumor cells to normal oligodendrocytes at histopathologic analysis. On the basis of animal models, it may be that the cell of origin is a bipotential progenitor cell that can differentiate into either oligodendrocytes or astrocytes (8). This may also explain the origin of the mixed oligoastrocytoma, which is suspected to arise from a single precursor cell (22,77). The recent finding of neuron-related genes being expressed in oligodendrogliomas with the 1p loss raises the intriguing possibility that perhaps some of these tumors may have a neuronal heritage (78).
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Imaging Features
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Oligodendrogliomas typically manifest as a round or oval sharply marginated mass involving the cortex or subcortical white matter at cross-sectional neuroimaging (79). Occasionally, the tumor margins are not well-defined, as it appears to blend imperceptibly into the normal adjacent brain parenchyma. At computed tomography (CT), about 60% are hypoattenuating while 23% are isoattenuating and about 6% are hyperattenuating (Fig 4) (79). Calcification, usually coarse in morphology, is noted in 20%–91% of cases (Fig 5) (34,79,80). Occasionally, cystic degeneration and hemorrhage may be seen (79). When the mass is sufficiently exophytic, calvarial erosion may be noted (Fig 6) (79). Subtle ill-defined enhancement following intravenous contrast material administration is seen in 15%–20% of oligodendrogliomas and is associated with higher-grade tumors (34,79,80). Calcification, vasogenic edema, and enhancement are less commonly noted in children with oligodendrogliomas than in adults (26). The tumor may not be visualized on CT images (34).
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Figure 4a. Oligodendroglioma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the cortex and subcortical white matter of the right frontal lobe. (b) Axial T1-weighted magnetic resonance (MR) image shows low signal intensity of the mass, which spares the extreme perimeter of the cortical gray matter. (c) Axial T2-weighted MR image shows high signal intensity of the mass. (d) Axial apparent diffusion coefficient (ADC) MR image shows mild high signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (e) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass, a finding typical of this tumor. (f ) Photograph of the gross specimen shows expanded gyri, which are a result of neoplastic involvement. Scale is in centimeters.
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Figure 4b. Oligodendroglioma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the cortex and subcortical white matter of the right frontal lobe. (b) Axial T1-weighted magnetic resonance (MR) image shows low signal intensity of the mass, which spares the extreme perimeter of the cortical gray matter. (c) Axial T2-weighted MR image shows high signal intensity of the mass. (d) Axial apparent diffusion coefficient (ADC) MR image shows mild high signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (e) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass, a finding typical of this tumor. (f ) Photograph of the gross specimen shows expanded gyri, which are a result of neoplastic involvement. Scale is in centimeters.
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Figure 4c. Oligodendroglioma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the cortex and subcortical white matter of the right frontal lobe. (b) Axial T1-weighted magnetic resonance (MR) image shows low signal intensity of the mass, which spares the extreme perimeter of the cortical gray matter. (c) Axial T2-weighted MR image shows high signal intensity of the mass. (d) Axial apparent diffusion coefficient (ADC) MR image shows mild high signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (e) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass, a finding typical of this tumor. (f ) Photograph of the gross specimen shows expanded gyri, which are a result of neoplastic involvement. Scale is in centimeters.
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Figure 4d. Oligodendroglioma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the cortex and subcortical white matter of the right frontal lobe. (b) Axial T1-weighted magnetic resonance (MR) image shows low signal intensity of the mass, which spares the extreme perimeter of the cortical gray matter. (c) Axial T2-weighted MR image shows high signal intensity of the mass. (d) Axial apparent diffusion coefficient (ADC) MR image shows mild high signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (e) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass, a finding typical of this tumor. (f ) Photograph of the gross specimen shows expanded gyri, which are a result of neoplastic involvement. Scale is in centimeters.
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Figure 4e. Oligodendroglioma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the cortex and subcortical white matter of the right frontal lobe. (b) Axial T1-weighted magnetic resonance (MR) image shows low signal intensity of the mass, which spares the extreme perimeter of the cortical gray matter. (c) Axial T2-weighted MR image shows high signal intensity of the mass. (d) Axial apparent diffusion coefficient (ADC) MR image shows mild high signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (e) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass, a finding typical of this tumor. (f ) Photograph of the gross specimen shows expanded gyri, which are a result of neoplastic involvement. Scale is in centimeters.
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Figure 4f. Oligodendroglioma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the cortex and subcortical white matter of the right frontal lobe. (b) Axial T1-weighted magnetic resonance (MR) image shows low signal intensity of the mass, which spares the extreme perimeter of the cortical gray matter. (c) Axial T2-weighted MR image shows high signal intensity of the mass. (d) Axial apparent diffusion coefficient (ADC) MR image shows mild high signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (e) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass, a finding typical of this tumor. (f ) Photograph of the gross specimen shows expanded gyri, which are a result of neoplastic involvement. Scale is in centimeters.
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Figure 6a. Oligodendroglioma. (a) Axial CT image shows a peripheral, ill-defined, hypoattenuating mass (arrow) in the posterior portion of the right temporal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Coronal contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 6b. Oligodendroglioma. (a) Axial CT image shows a peripheral, ill-defined, hypoattenuating mass (arrow) in the posterior portion of the right temporal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Coronal contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 6c. Oligodendroglioma. (a) Axial CT image shows a peripheral, ill-defined, hypoattenuating mass (arrow) in the posterior portion of the right temporal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Coronal contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 6d. Oligodendroglioma. (a) Axial CT image shows a peripheral, ill-defined, hypoattenuating mass (arrow) in the posterior portion of the right temporal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Coronal contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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MR imaging is superior to CT in defining the full extent of tumor involvement (81). The tumor is usually hypointense compared to gray matter on T1-weighted images and hyperintense compared to gray matter on T2-weighted images (Figs 4, 6, 7) (79). Heterogeneity of this signal intensity is the rule. Less commonly, a large cyst-like pattern may be seen (82). Surrounding vasogenic edema is not common (79). On occasion, frontal lobe tumors may extend through the corpus callosum to produce a "butterfly glioma" pattern. Advanced MR imaging with the apparent diffusion coefficient (ADC) shows a characteristic but not pathognomonic difference between low-grade and high-grade glial neoplasms. Lower ADC values, indicative of water restriction and likely reflective of lowered extracellular hyaluronic acid, are noted in high-grade tumors compared to the higher ADC values seen in low-grade tumors (Figs 4, 7) (83).
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Figure 7a. Oligodendroglioma. (a) Axial T2-weighted MR image shows a heterogeneous hyperintense mass (arrows) in the left frontal lobe with extension to the cortex and through the genu of the corpus callosum into the right frontal lobe. (b) Axial fluid-attenuated inversion-recovery MR image shows low signal intensity in more cystlike regions (arrowheads) of the mass. (c) Axial diffusion-weighted MR image shows low signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (d) Axial contrast-enhanced T1-weighted MR image shows minimal enhancement of the mass.
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Figure 7b. Oligodendroglioma. (a) Axial T2-weighted MR image shows a heterogeneous hyperintense mass (arrows) in the left frontal lobe with extension to the cortex and through the genu of the corpus callosum into the right frontal lobe. (b) Axial fluid-attenuated inversion-recovery MR image shows low signal intensity in more cystlike regions (arrowheads) of the mass. (c) Axial diffusion-weighted MR image shows low signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (d) Axial contrast-enhanced T1-weighted MR image shows minimal enhancement of the mass.
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Figure 7c. Oligodendroglioma. (a) Axial T2-weighted MR image shows a heterogeneous hyperintense mass (arrows) in the left frontal lobe with extension to the cortex and through the genu of the corpus callosum into the right frontal lobe. (b) Axial fluid-attenuated inversion-recovery MR image shows low signal intensity in more cystlike regions (arrowheads) of the mass. (c) Axial diffusion-weighted MR image shows low signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (d) Axial contrast-enhanced T1-weighted MR image shows minimal enhancement of the mass.
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Figure 7d. Oligodendroglioma. (a) Axial T2-weighted MR image shows a heterogeneous hyperintense mass (arrows) in the left frontal lobe with extension to the cortex and through the genu of the corpus callosum into the right frontal lobe. (b) Axial fluid-attenuated inversion-recovery MR image shows low signal intensity in more cystlike regions (arrowheads) of the mass. (c) Axial diffusion-weighted MR image shows low signal intensity of the mass, a finding that indicates absence of restricted water diffusion. (d) Axial contrast-enhanced T1-weighted MR image shows minimal enhancement of the mass.
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The pattern of contrast enhancement seen at CT is also noted at MR imaging. "Dot-like" lacy enhancement is commonly seen, but many tumors may not enhance at all (82). The presence or absence of enhancement has even been utilized to some extent in the grading of these neoplasms by Daumas-Duport and colleagues (10). While the presence of enhancement tends to be noted more commonly in more aggressive oligodendrogliomas, the reader is cautioned that this feature is not a fail-safe finding for that diagnosis. Conversely, the absence of enhancement does not inherently indicate a low-grade tumor. Histologic confirmation is always desired (84,85).
Evaluation with thallium 201 single photon emission CT (SPECT) reveals that the overall metabolic rate of oligodendrogliomas and mixed oligoastrocytomas correlates with the histologic grade and the presence of contrast enhancement. In their study using the amino acid tracer carbon 11 L-methylmethionine for positron emission tomography (PET), Derlon et al (86) reported that all oligodendrogliomas were hypermetabolic compared to the more variable activity seen in low-grade astrocytomas. A follow-up study that used the same tracer showed highly significant differences between low-grade and high-grade oligodendrogliomas (87). They also noted that PET studies with fluorine 18 fluorodeoxyglucose recorded less variance between these types of tumors (87). Another study showed that many low-grade oligodendrogliomas, including those with allelic loss of 1p and 19q, contain hypermetabolic regions (88). Metabolic imaging is useful in identifying tissue regions of potentially greater interest based on their hypermetabolism, helping establish the need for open surgical resection instead of biopsy, and determining the presence of residual disease (87).
Tumors with 1p and 19q deletions have noteworthy imaging features. They are also more likely to have ill-defined margins on T1-weighted MR images and to have calcification (89). They are more likely to be found in the frontal lobe and extend across the midline more often compared to tumors that lack these deletions, which are more common in the temporal lobe, insula, and midbrain (90).
Intraventricular oligodendrogliomas are rare (Fig 8). Only six (3%) of 208 oligodendrogliomas from the Norwegian Cancer Registry were located within the ventricular system (14), while up to 14 (8%) of 165 oligodendrogliomas involved the ventricular system in the series of Earnest et al (1). Reports in the literature from the 1980s and early 1990s of such lesions note that many of these tumors have different imaging characteristics compared to those oligodendrogliomas arising in the brain parenchyma (91–96). The lesions were usually hyperattenuating at CT compared to normal brain parenchyma. Almost all of the tumors enhanced on postcontrast images, and a tumor blush was seen at angiography in a higher percentage compared to the parenchymal oligodendrogliomas. Attachment to the ventricular wall, a site not known to harbor any oligodendroglial cells, was noted in many cases. Together, these findings raise the distinct possibility that some of these tumors were actually central neurocytomas, a tumor that bears a striking resemblance to oligodendrogliomas not only at cross-sectional imaging but also at histopathologic examination with its "fried-egg" appearance (97). Interestingly, Lee et al (82) reported just such an occurrence in four tumors originally believed to be "intraventricular oligodendrogliomas" that were later reclassified as central neurocytomas following further analysis.
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Figure 8a. Intraventricular oligodendroglioma. (a) Axial CT image shows a heterogeneous mass (arrows) within the right lateral ventricle. (b) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (c) Axial contrast-enhanced T1-weighted MR image shows focal areas of enhancement in the mass. Findings at electron microscopy confirmed that the mass was an oligodendroglioma and not a central neurocytoma.
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Figure 8b. Intraventricular oligodendroglioma. (a) Axial CT image shows a heterogeneous mass (arrows) within the right lateral ventricle. (b) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (c) Axial contrast-enhanced T1-weighted MR image shows focal areas of enhancement in the mass. Findings at electron microscopy confirmed that the mass was an oligodendroglioma and not a central neurocytoma.
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Figure 8c. Intraventricular oligodendroglioma. (a) Axial CT image shows a heterogeneous mass (arrows) within the right lateral ventricle. (b) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (c) Axial contrast-enhanced T1-weighted MR image shows focal areas of enhancement in the mass. Findings at electron microscopy confirmed that the mass was an oligodendroglioma and not a central neurocytoma.
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Diffuse involvement of the cisternal and subarachnoid spaces characterizes the imaging appearance of diffuse leptomeningeal oligodendroglioma (39,42,98). Meningeal calcification has been noted at CT in one case of primary leptomeningeal oligodendroglioma (39).
Reflecting the presence of necrosis, cystic degeneration, and hemorrhage at histopathologic analysis, the usual imaging appearance of an anaplastic oligodendroglioma is more variable compared to that of an oligodendroglioma (69). On occasion, a ringlike contrast enhancement pattern may be seen and the overall appearance may mimic that classically associated with glioblastoma multiforme (Figs 9, 10) (17,69). While tumors with high mitochondrial activity accumulate technetium 99m methoxyisobutylisonitrile (MIBI), there is at least one report of a recurrent high-grade oligodendroglioma that was not detected in a SPECT study with this radiopharmaceutical (99). Perfusion imaging commonly shows increased relative cerebral blood volume (rCBV) in high-grade glial tumors and is useful to assess their response to therapy (100).
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Figure 9a. Anaplastic oligodendroglioma. (a) Axial CT image shows a heterogeneous mass with both cyst-like and calcified components (arrows). Extension through the corpus callosum with involvement of both frontal lobes is seen. (b) Axial contrast-enhanced CT image shows ringlike enhancement of the cystlike portion (arrowheads).
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Figure 9b. Anaplastic oligodendroglioma. (a) Axial CT image shows a heterogeneous mass with both cyst-like and calcified components (arrows). Extension through the corpus callosum with involvement of both frontal lobes is seen. (b) Axial contrast-enhanced CT image shows ringlike enhancement of the cystlike portion (arrowheads).
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Figure 10a. Anaplastic oligodendroglioma. (a) Axial T1-weighted MR image shows a mass in the right temporal lobe (arrows) with both soft-tissue and cystlike components. (b) Axial T2-weighted MR image shows heterogeneity of the mass and minimal surrounding vasogenic edema. (c) Axial contrast-enhanced MR image shows irregular ring-like enhancement of the mass (arrowheads). This appearance mimics that of a glioblastoma multiforme.
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Figure 10b. Anaplastic oligodendroglioma. (a) Axial T1-weighted MR image shows a mass in the right temporal lobe (arrows) with both soft-tissue and cystlike components. (b) Axial T2-weighted MR image shows heterogeneity of the mass and minimal surrounding vasogenic edema. (c) Axial contrast-enhanced MR image shows irregular ring-like enhancement of the mass (arrowheads). This appearance mimics that of a glioblastoma multiforme.
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Figure 10c. Anaplastic oligodendroglioma. (a) Axial T1-weighted MR image shows a mass in the right temporal lobe (arrows) with both soft-tissue and cystlike components. (b) Axial T2-weighted MR image shows heterogeneity of the mass and minimal surrounding vasogenic edema. (c) Axial contrast-enhanced MR image shows irregular ring-like enhancement of the mass (arrowheads). This appearance mimics that of a glioblastoma multiforme.
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There are no unique features at cross-sectional neuroimaging that allow distinction of a mixed oligoastrocytoma from an oligodendroglioma (Figs 11–14) (82). While calcification is not as common (14%) as seen in pure oligodendrogliomas, enhancement following intravenous contrast material administration (50%) is more common (58,79).
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Figure 11a. Oligoastrocytoma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the left frontal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass with mild exophytic extension beyond the normal cortical margin. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Axial contrast-enhanced MR image shows only a small focal region of enhancement (arrowhead) in the mass. (e) Intraoperative photograph shows the mass protruding beyond the normal cortical margin of the brain.
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Figure 11b. Oligoastrocytoma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the left frontal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass with mild exophytic extension beyond the normal cortical margin. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Axial contrast-enhanced MR image shows only a small focal region of enhancement (arrowhead) in the mass. (e) Intraoperative photograph shows the mass protruding beyond the normal cortical margin of the brain.
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Figure 11c. Oligoastrocytoma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the left frontal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass with mild exophytic extension beyond the normal cortical margin. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Axial contrast-enhanced MR image shows only a small focal region of enhancement (arrowhead) in the mass. (e) Intraoperative photograph shows the mass protruding beyond the normal cortical margin of the brain.
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Figure 11d. Oligoastrocytoma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the left frontal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass with mild exophytic extension beyond the normal cortical margin. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Axial contrast-enhanced MR image shows only a small focal region of enhancement (arrowhead) in the mass. (e) Intraoperative photograph shows the mass protruding beyond the normal cortical margin of the brain.
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Figure 11e. Oligoastrocytoma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the left frontal lobe. (b) Axial T1-weighted MR image shows low signal intensity of the mass with mild exophytic extension beyond the normal cortical margin. (c) Axial T2-weighted MR image shows heterogeneous high signal intensity of the mass. (d) Axial contrast-enhanced MR image shows only a small focal region of enhancement (arrowhead) in the mass. (e) Intraoperative photograph shows the mass protruding beyond the normal cortical margin of the brain.
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Figure 12a. Oligoastrocytoma. (a) Axial T1-weighted MR image shows a hypointense mass (arrow) in the right frontal lobe. (b) Axial T2-weighted MR image shows heterogeneity of the mass with exophytic extension. (c) Axial diffusion-weighted MR image shows that the mass is predominantly isointense relative to the adjacent gray matter. (d) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 12b. Oligoastrocytoma. (a) Axial T1-weighted MR image shows a hypointense mass (arrow) in the right frontal lobe. (b) Axial T2-weighted MR image shows heterogeneity of the mass with exophytic extension. (c) Axial diffusion-weighted MR image shows that the mass is predominantly isointense relative to the adjacent gray matter. (d) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 12c. Oligoastrocytoma. (a) Axial T1-weighted MR image shows a hypointense mass (arrow) in the right frontal lobe. (b) Axial T2-weighted MR image shows heterogeneity of the mass with exophytic extension. (c) Axial diffusion-weighted MR image shows that the mass is predominantly isointense relative to the adjacent gray matter. (d) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 12d. Oligoastrocytoma. (a) Axial T1-weighted MR image shows a hypointense mass (arrow) in the right frontal lobe. (b) Axial T2-weighted MR image shows heterogeneity of the mass with exophytic extension. (c) Axial diffusion-weighted MR image shows that the mass is predominantly isointense relative to the adjacent gray matter. (d) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass.
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Figure 13a. Anaplastic oligoastrocytoma. (a) Axial CT image shows a hypoattenuating mass (arrow) in the posterior portion of the right temporal lobe. The mass produces mild calvarial erosion. (b) Axial T1-weighted MR image shows low signal intensity of the mass. (c) Axial T2-weighted MR image shows mild heterogeneity of the mass. (d) Axial contrast-enhanced T1-weighted MR image shows no enhancement of the mass. (e) Intraoperative photograph shows exophytic extension of the mass beyond the normal cortical margin.
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Abstract
LEARNING OBJECTIVES FOR TEST...
