Oligodendroglioma overview: Difference between revisions
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==Differentiating Oligodendroglioma from other diseases== | ==Differentiating Oligodendroglioma from other diseases== | ||
Oligodendroglioma must be differentiated from [[pilocytic astrocytoma]], [[Adult brain tumors classification|central neurocytoma]], [[ependymoma]], [[dysembryoplastic neuroepithelial tumor]], and [[meningioma]]. | Oligodendroglioma must be differentiated from [[pilocytic astrocytoma]], [[Adult brain tumors classification|central neurocytoma]], [[ependymoma]], [[dysembryoplastic neuroepithelial tumor]], and [[meningioma]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Revision as of 22:49, 7 May 2019
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Oligodendroglioma Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]Sujit Routray, M.D. [3]
Overview
Oligodendrogliomas are a type of glioma that are believed to originate from the tripotential glial precursor cells and not from the bipotential oligodendrocytes. The term "oligodendroglioma" was first coined by Bailey and Cushing in 1926 following the observation that the tumor cells are morphologically similar to oligodendrocytes. Oligodendroglioma may be classified according to the WHO classification of the central nervous system tumors into five subtypes: oligodendroglioma (OII), anaplastic oligodendroglioma (OIII), oligoastrocytoma (OAII), anaplastic oligoastrocytoma (OAIII), and glioblastoma with oligodendroglioma component (GBMo). Genes associated with the pathogenesis of oligodendroglioma include t(1;19)(q10;p10), NJDS, IDH1, IDH2, CIC, FUBP1, p53, Leu-7, TCF-12, MGMT, TP73, EGFR, and PTEN. On gross pathology, oligodendroglioma is characterized by a well-circumscribed, gelatinous, calcified, gray mass which may expand a gyrus and remodel the skull. On microscopic histopathological analysis, oligodendroglioma is characterized by diffuse growth pattern of highly cellular lesion with rounded nucleus with atypia and perinuclear halo resembling fried eggs, distinct cell borders, clear cytoplasm, and abundant calcification. Common causes of oligodendroglioma include genetic mutations. Oligodendroglioma must be differentiated from pilocytic astrocytoma, central neurocytoma, ependymoma, dysembryoplastic neuroepithelial tumor, and meningioma. Oligodendroglioma is a disease that tends to affect the middle-aged adult population. Oligodendroglioma most commonly occurs in the 4th and 5th decade of life. Males are more commonly affected with oligodendroglioma than females. The male to female ratio is approximately 2 to 1. Oligodendroglioma usually affects individuals of the Caucasian race. African American, Latin American, and Asian individuals are less likely to develop oligodendroglioma. The most potent risk factor in the development of oligodendroglioma is family history of brain tumors. If left untreated, patients with oligodendroglioma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death. When evaluating a patient for oligodendroglioma, you should take a detailed history of the presenting symptom (onset, duration, and progression), other associated symptoms, and a thorough past medical history review. Other specific areas of focus when obtaining the history include review of common risk factors such as family history of brain tumors. Symptoms associated with oligodendroglioma include seizure, headache, nausea, vomiting, vertigo, visual loss, diplopia, strabismus, muscle weakness, numbness, speech difficulties, mood disturbances, and personality changes. Common physical examination findings of oligodendroglioma include nystagmus, papilledema, esotropia, visual field loss, altered mental status, aphasia, ataxia, hemiparesis, tremors, and focal neurological deficits. Findings on CT scan suggestive of oligodendroglioma are round or oval, marginated, hypo- to isodense mass with hemorrhage, calcification, and ill-defined enhancement following intravenous contrast administration. On brain MRI, oligodendroglioma is characterized by a mass which is typically hypointense on T1-weighted images and hyperintense on T2-weighted images. Calcification is observed on T2* decay component of MRI. Other imaging studies for oligodendroglioma include MR spectroscopy (dominant N-acetyl aspartate peak, increased choline levels and decreased NAA levels with a myo-inositol peak), MR perfusion (increased "chicken wire" network of vascularity, which results in elevated relative cerebral blood volume), PET scan (to differentiate between oligodendroglioma from anaplastic oligodendroglioma and tumor recurrence from tumor necrosis), and bone scan (bone metastasis). The predominant therapy for oligodendroglioma is surgical resection. Adjunctive chemotherapy and radiation are required. Supportive therapy for oligodendroglioma includes anticonvulsants and corticosteroids.
Historical Perspective
The term "oligodendroglioma" was first coined by Bailey and Cushing in 1926 following the observation that the tumor cells are morphologically similar to oligodendrocytes. Oligodendroglioma was first described and published by W. E. Carnegie Dickson in 1926. In 2009, NJDS mutation was first identified in the pathogenesis of oligodendroglioma by Kevin Smith. Irradiation of pituitary adenoma was also discovered to be associated with oligodendroglioma by Kevin Smith et al.
Classification
Oligodendroglioma may be classified according to the WHO classification of the central nervous system tumors into five subtypes: oligodendroglioma (OII), anaplastic oligodendroglioma (OIII), oligoastrocytoma (OAII), anaplastic oligoastrocytoma (OAIII), and glioblastoma with oligodendroglioma component (GBMo).
Pathophysiology
Oligodendroglioma arises from the tripotential glial precursor cells and not from the bipotential oligodendrocytes. Genes associated with the pathogenesis of oligodendroglioma include t(1;19)(q10;p10), NJDS, IDH1, IDH2, CIC, FUBP1, p53, Leu-7, TCF-12, MGMT, TP73, EGFR, and PTEN. On gross pathology, oligodendroglioma is characterized by a well-circumscribed, gelatinous, calcified, gray mass which may expand a gyrus and remodel the skull. On microscopic histopathological analysis, oligodendroglioma is characterized by diffuse growth pattern of highly cellular lesion with rounded nucleus with atypia and perinuclear halo resembling fried eggs, distinct cell borders, clear cytoplasm, and abundant calcification. Oligodendroglioma is demonstrated by positivity to tumor markers such as MAP2, GFAP, S-100, EMA, IDH1-R132H, ATRX, Ki-67, NSE , Synaptophysin, OLIG1, and OLIG2.
Causes
Common causes of oligodendroglioma include genetic mutations. Common genetic mutations involved in the development of oligodendroglioma can be found here.
Differentiating Oligodendroglioma from other diseases
Oligodendroglioma must be differentiated from pilocytic astrocytoma, central neurocytoma, ependymoma, dysembryoplastic neuroepithelial tumor, and meningioma.
Epidemiology and Demographics
Oligodendroglioma, although rare, is the third most common glioma.[1] The incidence of oligodendroglioma and anaplastic oligodendroglioma is estimated to be 0.32 and 0.17 cases per 100,000 individuals in the United States, respectively.[2] Oligodendroglioma is a disease that tends to affect the middle-aged adult population.[1] Oligodendroglioma most commonly occurs in the 4th and 5th decade of life. Males are more commonly affected with oligodendroglioma than females. The male to female ratio is approximately 2 to 1.[3] Oligodendroglioma usually affects individuals of the Caucasian race. African American, Latin American, and Asian individuals are less likely to develop oligodendroglioma.[4]
Risk factors
The most potent risk factor in the development of oligodendroglioma is family history of brain tumors.[2]
Screening
There is insufficient evidence to recommend routine screening for oligodendroglioma.[5]
Natural History, Complications and Prognosis
If left untreated, patients with oligodendroglioma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death.[6] Common complications associated with oligodendroglioma include hydrocephalus, intracranial hemorrhage, coma, bone marrow metastasis, recurrence, venous thromboembolism, parkinsonism, and side effects of chemotherapy and radiotherapy.[3][7][8][9][10][11][12] Depending on the extent and grade of the tumor at the time of diagnosis, the prognosis of oligodendroglioma may vary. However, the prognosis is generally regarded as good. The median survival time for oligodendroglioma is 11.6 years for grade II and 3.5 years for grade III.[13]
Diagnosis
- CT or MRI scan is necessary to characterize the anatomy of oligodendroglial tumors such as:
- Tumor size
- Tumor location
- Heter/homogeneity
- However, the confirmation of final diagnosis is dependent on histopathologic examination of the biopsy specimen
Staging
There is no established system for the staging of oligodendroglioma.
History and Symptoms
When evaluating a patient for oligodendroglioma, you should take a detailed history of the presenting symptom (onset, duration, and progression), other associated symptoms, and a thorough past medical history review. Other specific areas of focus when obtaining the history include review of common risk factors such as family history of brain tumors.[2] Symptoms associated with oligodendroglioma include seizure, headache, nausea, vomiting, vertigo, visual loss, diplopia, strabismus, muscle weakness, numbness, speech difficulties, mood disturbances, and personality changes.[14][15][16][17]
Physical examination
Common physical examination findings of oligodendroglioma include nystagmus, papilledema, esotropia, visual field loss, altered mental status, and focal neurological deficits.[17][14][18][19][12]
Laboratory Findings
Some patients with oligodendroglioma may have elevated protein and cell count with normal glucose and lactate on CSF analysis, which is usually suggestive of hydrocephalus.[20]
Chest X Ray
Chest x-ray may be performed to detect metastases of anaplastic oligodendroglioma to the lungs.[21]
CT
Head CT scan may be helpful in the diagnosis of oligodendroglioma. Findings on CT scan suggestive of oligodendroglioma are round or oval, marginated, hypo- to isodense mass with hemorrhage, calcification, and ill-defined enhancement following intravenous contrast administration.[22][20]
MRI
Brain MRI is helpful in the diagnosis of oligodendroglioma. On brain MRI, oligodendroglioma is characterized by a mass which is typically hypointense on T1-weighted images and hyperintense on T2-weighted images. Calcification is observed on T2* decay component of MRI.[23][20]
Ultrasound
There are no ultrasound findings associated with oligodendroglioma.
Other Imaging Findings
Other imaging studies for oligodendroglioma include MR spectroscopy (dominant N-acetyl aspartate peak, increased choline levels and decreased NAA levels with a myo-inositol peak), MR perfusion (increased "chicken wire" network of vascularity, which results in elevated relative cerebral blood volume), PET scan (to differentiate between oligodendroglioma from anaplastic oligodendroglioma and tumor recurrence from tumor necrosis), and bone scan (bone metastasis).[18][24][25][26][27][28][29][30][31]
Other Diagnostic Studies
Other diagnostic studies for oligodendroglioma include biopsy (homogeneous, compact, rounded cells with distinct borders and clear cytoplasm surrounding a dense central nucleus and perinuclear halo) and fluorescent in-situ hybridization (FISH) technique (deletions of chromosome 1p and 19q).[32][18][33]
Treatment
Medical Therapy
The predominant therapy for oligodendroglioma is surgical resection. Adjunctive chemotherapy and radiation are required.[34][35][36] Supportive therapy for oligodendroglioma includes anticonvulsants and corticosteroids.[34]
Surgery
Surgery is the first-line treatment option for patients with oligodendroglioma.[34] CSF shunting is usually reserved for patients with hydrocephalus.[20]
Primary Prevention
There is no established method for prevention of oligodendroglioma.
Secondary Prevention
There are no secondary preventive measures available for oligodendroglioma.
References
- ↑ 1.0 1.1 Epidemiology of oligodendroglioma. Dr Henry Knipe and Dr. Frank Gaillard et al. http://radiopaedia.org/articles/oligodendroglioma
- ↑ 2.0 2.1 2.2 McCarthy BJ, Rankin KM, Aldape K, Bondy ML, Brännström T, Broholm H; et al. (2011). "Risk factors for oligodendroglial tumors: a pooled international study". Neuro Oncol. 13 (2): 242–50. doi:10.1093/neuonc/noq173. PMC 3064625. PMID 21149253.
- ↑ 3.0 3.1 Simonetti G, Gaviani P, Botturi A, Innocenti A, Lamperti E, Silvani A (2015). "Clinical management of grade III oligodendroglioma". Cancer Manag Res. 7: 213–23. doi:10.2147/CMAR.S56975. PMC 4524382. PMID 26251628.
- ↑ Patterns by Gender for Selected Histologies CBTRUS Statistical Report: NPCR and SEER Data from 2004-2006. CBTRUS.org 2015. http://www.cbtrus.org/2010-NPCR-SEER/CBTRUS-WEBREPORT-Final-3-2-10.pdf
- ↑ Early detection, diagnosis, and staging of brain tumors. American cancer society. http://www.cancer.org/cancer/braincnstumorsinadults/detailedguide/brain-and-spinal-cord-tumors-in-adults-detection
- ↑ Manousaki M, Papadaki H, Papavdi A, Kranioti EF, Mylonakis P, Varakis J; et al. (2011). "Sudden unexpected death from oligodendroglioma: a case report and review of the literature". Am J Forensic Med Pathol. 32 (4): 336–40. doi:10.1097/PAF.0b013e3181d3dc86. PMID 20375839.
- ↑ Guppy KH, Akins PT, Moes GS, Prados MD (2009). "Spinal cord oligodendroglioma with 1p and 19q deletions presenting with cerebral oligodendrogliomatosis". J Neurosurg Spine. 10 (6): 557–63. doi:10.3171/2009.2.SPINE08853. PMID 19558288.
- ↑ Sharma A, Agarwal A, Sharma MC, Anand M, Agarwal S, Raina V (2003). "Bone marrow metastasis in anaplastic oligodendroglioma". Int J Clin Pract. 57 (4): 351–2. PMID 12800473.
- ↑ Solitare GB, Robinson F, Lamarche JB (1967). "Oligodendroglioma: recurrence following an exceptionally long postoperative symptom-free interval". Can Med Assoc J. 97 (14): 862–5. PMC 1923454. PMID 6051252.
- ↑ Harada K, Kiya K, Matsumura S, Mori S, Uozumi T (1982). "Spontaneous intracranial hemorrhage caused by oligodendroglioma--a case report and review of the literature". Neurol Med Chir (Tokyo). 22 (1): 81–4. PMID 6176898.
- ↑ Hentschel S, Toyota B (2003). "Intracranial malignant glioma presenting as subarachnoid hemorrhage". Can J Neurol Sci. 30 (1): 63–6. PMID 12619787.
- ↑ 12.0 12.1 Krauss JK, Paduch T, Mundinger F, Seeger W (1995). "Parkinsonism and rest tremor secondary to supratentorial tumours sparing the basal ganglia". Acta Neurochir (Wien). 133 (1–2): 22–9. PMID 8561031.
- ↑ Ohgaki H, Kleihues P (2005). "Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas". J Neuropathol Exp Neurol. 64 (6): 479–89. PMID 15977639.
- ↑ 14.0 14.1 Douay X, Daems-Monpeurt C, Labalette P, Blond S, Petit H (1997). "[Bilateral 3rd cranial nerve palsy disclosing oligodendroglioma]". Rev Neurol (Paris). 153 (6–7): 430–2. PMID 9684012.
- ↑ Hata N, Shono T, Mizoguchi M, Matsumoto K, Guan Y, Nagata S; et al. (2007). "Loss of heterozygosity analysis in an anaplastic oligodendroglioma arising after radiation therapy". Neurol Res. 29 (7): 723–6. doi:10.1179/016164107X208068. PMID 17553214.
- ↑ Ogasawara H, Kiya K, Uozumi T, Sugiyama K, Kawamoto K, Ohta M (1990). "Multiple oligodendroglioma--case report". Neurol Med Chir (Tokyo). 30 (2): 127–31. PMID 1695334.
- ↑ 17.0 17.1 Raciti-Daurio C, Caruso J (1990). "Oligodendroglioma--a case presentation". Optom Vis Sci. 67 (1): 56–8. PMID 2308753.
- ↑ 18.0 18.1 18.2 Eskandar EN, Loeffler JS, O'Neill AM, Hunter GJ, Louis DN (2004). "Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 33-2004. A 34-year-old man with a seizure and a frontal-lobe brain lesion". N Engl J Med. 351 (18): 1875–82. doi:10.1056/NEJMcpc049025. PMID 15509821.
- ↑ Mittelbronn M, Wolff M, Bültmann E, Nägele T, Capper D, Beck R; et al. (2005). "Disseminating anaplastic brainstem oligodendroglioma associated with allelic loss in the tumor suppressor candidate region D19S246 of chromosome 19 mimicking an inflammatory central nervous system disease in a 9-year-old boy". Hum Pathol. 36 (7): 854–7. doi:10.1016/j.humpath.2005.05.017. PMID 16084959.
- ↑ 20.0 20.1 20.2 20.3 Stark AM, Hugo HH, Mehdorn HM, Knerlich-Lukoschus F (2009). "Acute Hydrocephalus due to Secondary Leptomeningeal Dissemination of an Anaplastic Oligodendroglioma". Case Rep Med. 2009: 370901. doi:10.1155/2009/370901. PMC 2797365. PMID 20052406.
- ↑ Han SR, Yoon SW, Yee GT, Choi CY, Lee DJ, Sohn MJ; et al. (2008). "Extraneural metastases of anaplastic oligodendroglioma". J Clin Neurosci. 15 (8): 946–9. doi:10.1016/j.jocn.2006.09.013. PMID 18280737.
- ↑ Radiographic features of oligodendroglioma. Dr Henry Knipe and Dr Frank Gaillard et al. http://radiopaedia.org/articles/oligodendroglioma
- ↑ Radiographic features of oligodendroglioma. Dr Henry Knipe and Dr Frank Gaillard et al. http://radiopaedia.org/articles/oligodendroglioma
- ↑ Nikaido K, Nihira H, Wakai S, Honmo O, Tsuzuki A (2003). "[A case of oligodendroglioma with temporal lobe epilepsy initially suspected as having paroxymal tachycardia]". No To Hattatsu. 35 (5): 401–5. PMID 13677949.
- ↑ Axial MRS of oligodendroglioma. Dr. Bruno Di Muzio. Radiopaedia 2015. http://radiopaedia.org/cases/oligodendroglioma-14
- ↑ Rijpkema M, Schuuring J, van der Meulen Y, van der Graaf M, Bernsen H, Boerman R; et al. (2003). "Characterization of oligodendrogliomas using short echo time 1H MR spectroscopic imaging". NMR Biomed. 16 (1): 12–8. doi:10.1002/nbm.807. PMID 12577293.
- ↑ Radiographic features of oligodendroglioma. Dr. Henry Knipe and Dr. Frank Gaillard et al. http://radiopaedia.org/articles/oligodendroglioma
- ↑ Ceyssens S, Van Laere K, de Groot T, Goffin J, Bormans G, Mortelmans L (2006). "[11C]methionine PET, histopathology, and survival in primary brain tumors and recurrence". AJNR Am J Neuroradiol. 27 (7): 1432–7. PMID 16908552.
- ↑ Beauchesne P (2011). "Extra-neural metastases of malignant gliomas: myth or reality?". Cancers (Basel). 3 (1): 461–77. doi:10.3390/cancers3010461. PMC 3756372. PMID 24212625.
- ↑ Al-Ali F, Hendon AJ, Liepman MK, Wisniewski JL, Krinock MJ, Beckman K (2005). "Oligodendroglioma metastatic to bone marrow". AJNR Am J Neuroradiol. 26 (9): 2410–4. PMID 16219856.
- ↑ Gerrard GE, Bond MG, Jack AS (1995). "Bone marrow infiltration by a parietal lobe grade III oligodendroglioma". Clin Oncol (R Coll Radiol). 7 (5): 321–2. PMID 8580060.
- ↑ Wesseling P, van den Bent M, Perry A (2015). "Oligodendroglioma: pathology, molecular mechanisms and markers". Acta Neuropathol. 129 (6): 809–27. doi:10.1007/s00401-015-1424-1. PMC 4436696. PMID 25943885.
- ↑ Ersen, Ayca (2008), Pathology of malignant gliomas: Challenges of everyday practice and the WHO 2007, Turkish Journal of Pathology, retrieved 9 October, 2015 Check date values in:
|accessdate=(help) - ↑ 34.0 34.1 34.2 Treatment of oligodendroglioma. Canadian Cancer Society 2015. http://www.cancer.ca/en/cancer-information/cancer-type/brain-spinal/brain-and-spinal-tumours/oligodendroglioma/?region=on
- ↑ Cairncross JG, Macdonald DR (1988). "Successful chemotherapy for recurrent malignant oligodendroglioma". Ann Neurol. 23 (4): 360–4. doi:10.1002/ana.410230408. PMID 3382171.
- ↑ Chemotherapeutic drugs in malignant gliomas. Canadian Cancer Society 2015. http://www.cancer.ca/en/cancer-information/cancer-type/brain-spinal/treatment/chemotherapy/?region=on