Oligoastrocytoma

• Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Oligoastrocytomas are extremely rare brain tumors that together with oligodendrogliomas account for approximately 10% of primary CNS tumors. They are a subtype of gliomas and account for 25% of all gliomas. These tumors are composed of astrocytoma and oligodendroglioma. Celli et al in 1994 gave the name of “oligoastrocytoma” to those oligodendroglial tumors where the astrocytes formed more than 20% of the tumor cells. Morphologic characteristics of oligoastrocytomas resemble those of pure oligodendrogliomas and astrocytomas. Oligoastrocytomas are primarily tumors of adulthood with peak incidence in 4th to 6th decade of life. Even though these tumors can arise anywhere within the the brain, but usually in the supratentorial region, especially frontal and temporal lobes are the most common sites. Based on WHO classification, oligoastrocytomas are devided into two classes: oligoastrocytoma corresponding to grade II and anaplastic oligoastrocytoma corresponding to grade III. Clinical manifestaions of oligoastrocytoma vary and can range from seizure and headaches to personality changes. Many risk fators seem to play a role in pathogenesis of oligoastrocytoma. The molecular changes can resemble those of oligodendrogliomas (loss of heterozygosity on 1p and 19q, in 30-70% of cases) or astrocytoma (TP53 mutation and loss of heterozygosity on 17p). Treatment is based on sugery, however the tumor is responsive to chemotherapy in most cases, when necessary.

The broad topic “oligodendroglial tumors”, of which oligoastrocytoma is a part of, was first described by Bailey and Cushing in 1926. They reported that gliomas were formed by transformation of glial cells.Celli et al in 1994 gave the name of “oligoastrocytoma” to those oligodendroglial tumors where the astrocytes formed more than 20% of the tumor cells.

Oligoastrocytoma may be classified according to the WHO classification of the central nervous system tumors into two subtypes: oligoastrocytoma (OAII) and anaplastic oligoastrocytoma (OAIII). OAII can evolve to OAIII overtime.

Oligoastrocytomas are mixed tumors that arise from the proliferation of both oligodendrocytes and astrocytes. Genes associated with the pathogenesis of oligoastrocytoma and anaplastic oligoastrocytoma include IDH1, p53, EGFR, ATRX, EGFR, PTEN, MGMT, CIC, and FUBP1. 30-70% of oligoastrocytomas show loss of heterozygosity (LOH) of 1p and 19q.

Common causes of oligoastrocytoma include genetic mutations and ionizing radiation. Common genetic mutations involved in the development of oligoastrocytoma can be found here. Genes associated with the pathogenesis of oligoastrocytoma and anaplastic oligoastrocytoma include IDH1, p53, EGFR, ATRX, EGFR, PTEN, MGMT, CIC, and FUBP1.

As clinical manifestation of oligoastrocytoma differ based on the site of the tumor, many disease and intracranial space occupying lesions can be named as its differential diagnosis: Astrocytoma, anaplastic astrocytoma, oligodendroglioma, pilocytic astrocytoma, central neurocytoma, ependymoma, dysembryoplastic neuroepithelial tumor, meningioma, cerebral metastasis, multiple sclerosis, and intracranial cysts.

Oligoastrocytoma is the third most common glioma. Oligoastrocytoma accounts for 1% of all brain tumors and 5–10% of all glial neoplasms. The incidence of oligoastrocytoma is approximately 0.03 per 100,000 individuals in the United States. Oligoastrocytoma is a disease that tends to affect the young and middle-aged adult population with peak incidence in 4th to 6th decades of life. The median age of diagnosis is 42 years. Males are more commonly affected with oligoastrocytoma than females. Oligoastrocytoma usually affects individuals of the Caucasian race. The incidence rate of oligoastrocytoma is higher in developed countries than in developing countries.

Common risk factors in the development of oligoastrocytoma include family history of brain tumors, ionizing radiation, and allergic diseases. However other risk factors such as viral infections and immune factors seem to play a role. Of these factors, only the association of ionizing radiation has been proven.

There is insufficient evidence to recommend routine screening for oligoastrocytoma.

• If left untreated, patients with oligoastrocytoma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death.^[1][2][3]
• Oligoastrocytomas are slow growing tumors.^[4]
• These tumors can evolve in terms of WHO classification from OAII to OAIII over time.
• Common complications associated with oligoastrocytoma include hydrocephalus, intracranial hemorrhage, coma, metastasis, venous thromboembolism, and side effects of chemotherapy and radiation.^{[2][5][6][1][7][3]}
• Depending on the extent and grade of the tumor at the time of diagnosis, the prognosis of oligoastrocytoma may vary. However, the prognosis is generally regarded as good.^[8]
• The prognosis of low-grade oligoastrocytoma is more favorable than that for anaplastic oligoastrocytoma because of the more indolent course and younger age at which most patients are diagnosed.^[2]
• The prognosis of oligoastrocytoma is better than that of astrocytoma and poorer than that of oligodendrogliomas.
• The 1, 5, and 10-year survival rates of patients with oligoastrocytoma are approximately 87%, 56.97%, and 45.80%, respectively.^[9]

• Histopathologic examination remains the gold standard for diagnosis of oligoastrocytoma.
• On gross pathology, oligoastrocytoma is characterized by a soft, well-defined, grey-tan, mucoid or hemorrhagic, calcified mass with or without necrosis, which may expand the gyrus and cause blurring of the grey-white junction.^[4]
• In histopathologic examination:
• Oligoastrocytoma is characterized by highly cellular lesions composed of both oligodendroglial and astrocytic components.^{[10][11][12][13][14]}
• In addition to the histological features of oligoastrocytoma, anaplastic oligoastrocytoma also has significant or brisk mitotic activity, marked cytologic and nuclear atypia, necrosis, apoptosis, and microvacular proliferation.^[10][11][12]
• Oligoastrocytoma is demonstrated by positivity to tumor markers such as MAP2, GFAP(due to presence of reactive astrocytes), IDH1, OLIG-1 protein, OLIG-2 protein, and Iba-2 protein.^{[15][16][8][2][4]}

There is no established system for the staging of oligoastrocytoma.^[1]

When evaluating a patient for oligoastrocytoma, 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 the history of any ionizing radiation, allergic diseases, and the family history for any brain tumors.^[17][18][1] Symptoms associated with oligoastrocytoma include seizure, headache, nausea, vomiting, loss of balance, vision loss, and changes in speech, mood, and personality.^{[19][11][20][21][6][22][1]}

Common physical examination findings of oligoastrocytoma include:

• nystagmus
• papilledema
• esotropia
• visual field loss
• altered mental status
• focal neurological deficits.^[21][1]

Some patients with oligoastrocytoma may have elevated protein and cell count with normal glucose and lactate on CSF analysis, which is usually suggestive of hydrocephalus.^[23][24]

Chest x-ray may be performed to detect metastases of anaplastic oligoastrocytoma to the lungs.^[25][7]

• Head CT scan may be helpful in the diagnosis of oligoastrocytoma, however it lacks the required specificity for definitive diagnosis.
• The findings on CT scan have unsharp edges and appear as patchy lesions.
• Tumors may show areas of calcification in CT scan.
• Findings on CT scan suggestive of oligoastrocytoma are intra-axial low-attenuation areas with mass effect and little to no associated edema.^[26]

• Brain MRI is helpful in the diagnosis of oligoastrocytoma.
• On brain MRI, oligoastrocytoma is characterized by a mass which is typically hypointense on T1-weighted images and hyperintense on T2-weighted images.
• No enhancement is observed on gadolinium enhanced T1-weighted images.^[27]

• Creatinine levels may be decreased.
• Choline-containing compumds may be incresed, however, in cases of necrosis in highly malignant tumors they may be decreased.
• Lactate levels may be increased.
• N-acetyl aspartate can be significantly decreased.
• MRS can help with classification of tumors as ratios of these compunds can help with classification of these malignacies.

There are no specific ultrasound findings associated with oligoastrocytoma.

Other imaging studies for oligoastrocytoma include PET scan (accumulation of [18F]-fluorodeoxyglucose) and bone scan (bone metastasis).^{[28][29][30][7]}

Other diagnostic studies for oligoastrocytoma include biopsy (“star-shaped” astrocytes with ovoid nucleus and homogeneous, compact oligodendrocytes with distinct borders, round nucleus, and clear cytoplasm surrounding a dense central nucleus and perinuclear halo, giving it the characteristic “fried egg” appearance) and fluorescent in-situ hybridization (FISH) technique (deletions of chromosome 1p and 19q).^[31][32]

• The predominant therapy for oligoastrocytoma is surgical resection.^[21][1]
• Adjunctive chemotherapy and radiation are required.^{[21][1][33][34][35][36][5]}
• Supportive therapy for oligoastrocytoma includes anticonvulsants and corticosteroids.^[33]
• Temozolomide can be effective for cases of recurrent anaplastic oligoastrocytoma.

Surgery is the first-line treatment option for patients with oligoastrocytoma.^{[21][1][33][37]} CSF shunting is usually reserved for patients with hydrocephalus.^[24]

There are no primary preventive measures available for oligoastrocytoma.

Patients treated for oligoastrocytoma should follow-up for secondary prevention. Secondary prevention strategies following oligoastrocytoma include a clinical assessment of neurological function and corticosteroid usage, checking for signs of venous thromboembolism, regular laboratory tests, and routine imaging (MRI and Positron Emission Tomography) at scheduled intervals after treatment.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

The broad topic “oligodendroglial tumors”, of which oligoastrocytoma is a part of, was first described by Bailey and Cushing in 1926. They reported that gliomas were formed by transformation of glial cells. Celli et al in 1994 gave the name of “oligoastrocytoma” to those oligodendroglial tumors where the astrocytes formed more than 20% of the tumor cells.

• The broad topic “oligodendroglial tumors” was first described by Bailey and Cushing in 1926.^[1][2]
• The anaplastic nature of oligodendroglial tumors was described by Kernohan based on the features such as endotheliael proliferation, nuclear atypia, mitoses, and necrosis.
• The studies by Zulch, Kleihues et al, and Daumas-Duport system (St. Anne-Mayo schema) resulted in the formulation of the WHO classification of CNS tumors, where oligoastrocytoma and anaplastic oligoastrocytoma were graded as WHO grade II (low-grade) and WHO grade III (high-grade) tumor, respectively.^[3][4]
• Celli et al in 1994 gave the name of “oligoastrocytoma” to those oligodendroglial tumors where the astrocytes formed more than 20% of the tumor cells.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Oligoastrocytoma may be classified according to the WHO classification of the central nervous system tumors into two subtypes: oligoastrocytoma (OAII) and anaplastic oligoastrocytoma (OAIII).

Oligoastrocytoma may be classified according to the WHO classification of the central nervous system tumors into two subtypes:^[1]

WHO classification of tumors of CNS

WHO grade II

WHO grade III

Oligoastrocytoma (OAII)

Anaplastic oligoastrocytoma (OAIII)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Oligoastrocytomas are mixed tumors that arise from the proliferation of both oligodendrocytes and astrocytes. Genes associated with the pathogenesis of oligoastrocytoma and anaplastic oligoastrocytoma include IDH1, p53, EGFR, ATRX, EGFR, PTEN, MGMT, CIC, and FUBP1. 30-70% of oligoastrocytomas show loss of heterozygosity (LOH) of 1p and 19q. On gross pathology, oligoastrocytoma is characterized by a soft, well-defined, grey-tan, mucoid or hemorrhagic, calcified mass with or without necrosis, which may expand the gyrus and cause blurring of the grey-white junction. On microscopic histopathological analysis, oligoastrocytoma is characterized by highly cellular lesions composed of both oligodendroglial and astrocytic components. In addition to the histological features of oligoastrocytoma, anaplastic oligoastrocytoma also has significant or brisk mitotic activity, marked cytologic and nuclear atypia, necrosis, apoptosis, and microvacular proliferation. Oligoastrocytoma is demonstrated by positivity to tumor markers such as MAP2, GFAP, IDH1, OLIG-1 protein, OLIG-2 protein, and Iba-2 protein.

• Oligoastrocytomas are mixed tumors that arises from the proliferation of both oligodendrocytes and astrocytes.^[1]
• Oligoastrocytomas are low-grade (grade II) tumors and anaplastic oligoastrocytomas are high-grade (grade III) tumors that occur in the brain.^[2]

• Development of oligoastrocytoma is the result of multiple genetic mutations.
• Oligoastrocytomas are mixed tumors that have overlapping molecular genetics with both oligodendrogliomas and astrocytomas.^[3]
• 30-70% of oligoastrocytomas show loss of heterozygosity (LOH) of 1p and 19q.^[3][4][5]
• Genes associated with the pathogenesis of oligoastrocytoma and anaplastic oligoastrocytoma include:^{[3][6][7][8][9][10][11][4]}

• IDH1
• p53
• EGFR
• ATRX
• EGFR
• PTEN
• MGMT
• CIC
• FUBP1

• On gross pathology, oligoastrocytoma is characterized by a soft, well-defined, grey-tan, mucoid or hemorrhagic, calcified mass with or without necrosis, which may expand the gyrus and cause blurring of the grey-white matter junction.^[4]
• Oligoastrocytomas are commonly found in the supratentorial region.
• Common intracranial sites associated with oligoastrocytoma include:^{[12][13][14][3]}
  • Frontal lobe (most common)
  • Temporal lobe
  • Parietal lobe
  • Occipital lobe
  • Insula
  • Diencephalon
  • Spinal cord

On microscopic histopathological analysis, oligoastrocytoma is characterized by:^{[15][16][17][18][19]}

• Highly cellular lesions composed of both oligodendroglial and astrocytic components
• Two types of pattern: biphasic and diffuse
  • Biphasic pattern demonstrates oligodendroglial and astrocytic differentiation, whereas diffuse pattern demonstrates intermingling of both the components
• Oligodendrocytes
  • Fried-egg shaped cells
  • Composed of minigemistocytes
  • Round nucleus
  • Distinct cell borders
  • Moderate-to-marked nuclear atypia with speckled “salt-and-pepper” chromatin pattern and perinuclear halo
  • Focal microcalcification
• Astrocytes
  • Star-shaped cells
  • Composed of gemistocytes
  • Multinucleated giant cells
  • Ovoid nucleus
  • Nuclear atypia

On microscopic histopathological analysis, anaplastic oligoastrocytoma is characterized by:^[15][16][17]

• Significant or brisk mitotic activity (≥ 6 mitoses per 10 high power field)
• Marked cytologic and nuclear atypia
• Necrosis
• Apoptotic cells
• Microvacular proliferation
  • ‘Glomeruloid’ vessels or endothelial hyperplasia

• 
  _{Biopsy specimen of an oligoastrocytoma (HE stain).^[20]}

Oligoastrocytoma is demonstrated by positivity to tumor markers such as:^{[21][22][11][23][4]}

• MAP2
• GFAP
• IDH1
• OLIG-1 protein
• OLIG-2 protein
• Iba-2 protein
• ID4 protein
• Ki-67
• Vimentin
• Synaptophysin

• 
  _{Histology of oligoastrocytoma cells demonstrating positivity to tumor marker GFAP.^[24]}
• 
  _{Histology of oligoastrocytoma cells demonstrating positivity to tumor marker Ki-67.^[25]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Common causes of oligoastrocytoma include genetic mutations. Common genetic mutations involved in the development of oligoastrocytoma can be found here.

Common causes of oligoastrocytoma include genetic mutations. The genes associated with the etiology of oligoastrocytoma include:^{[1][2][3][4][5][6]}

• IDH1
• t(1;19)(q10;p10)
• p53
• ATRX
• EGFR
• PTEN
• MGMT
• CIC
• FUBP1

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Oligoastrocytoma must be differentiated from astrocytoma, anaplastic astrocytoma, oligodendroglioma, pilocytic astrocytoma, central neurocytoma, ependymoma, dysembryoplastic neuroepithelial tumor, meningioma, and cerebral metastasis.

Oligoastrocytoma must be differentiated from:^[1][2][3][4]

• Astrocytoma
• Anaplastic astrocytoma
• Oligodendroglioma
• Pilocytic astrocytoma
• Central neurocytoma
• Ependymoma
• Dysembryoplastic neuroepithelial tumor
• Meningioma
• Cerebral metastasis
• Brain abscess
• Tuberculoma
• Sarcoidosis
• Neurocysticercosis
• Multiple myeloma
• Primary CNS lymphoma
• Cerebral toxoplasmosis
• Germ cell tumor
• Ganglioglioma
• Pleomorphic xanthoastrocytoma
• Herpes simplex encephalitis
• Stroke
• Cerebral arteriovenous malformation
• Epilepsy

Diseases	Clinical manifestations					Para-clinical findings			Gold standard	Additional findings
	Symptoms				Physical examination
						Lab Findings	MRI	Immunohistopathology
	Head- ache	Seizure	Visual disturbance	Constitutional	Focal neurological deficit
Adult primary brain tumors
Oligoastrocytoma[1][2][3][4]	+	+/−	+/−	−	+	−	No contrast enhancement with gadollonium Hypointense lesion at T1 Hyperintense lesion at T2	Oligodendrocytes and astrocytes origin soft, well-defined, grey-tan, mucoid or hemorrhagic, calcified mass with or without necrosis supratentorial region Highly cellular lesions Round or oviod nucleus Nuclear atypia Significant or brisk mitotic activity (≥ 6 mitoses per 10 high power field)	Biopsy	Commonly diagnosed late in the term of the disease
Glioblastoma multiforme [5][6][7]	+	+/−	+/−	−	+	−	Supratentorial Irregular ring-nodular enhancing lesions Central necrosis Surrounding vasogenic edema Cross corpus callosum (butterfly glioma)	Astrocyte origin Pleomorphic cell Pseudopalisading appearance GFAP + Necrosis + Hemorrhage + Vascular prolifration +	Biopsy	Highest incidence in fifth and sixth decades of life Most of the time, focal neurological deficit is the presenting sign.
Oligodendroglioma [8][9][10]	+	+	+/−	−	+	−	Almost always in cerebral hemisphers (frontal lobes) Hypointense on T1 Hyperintense on T2 Calcification Chicken wire capillary pattern	Oligodendrocyte origin Calcification + Fried egg cell appearance	Biopsy	Highest incidence is between 40 and 50 years of age. Most of the time, epileptic seizure is the presenting sign.
Meningioma [11][12][13]	+	+/−	+/−	−	+	−	Well circumscribed Extra-axial mass Dural attachment CSF vascular cleft sign Sunburst appearance of the vessels	Arachnoid origin Psammoma bodies Whorled spindle cell pattern	Biopsy	Highest incidence is between 40 and 50 years of age. Most of the time, focal neurological deficit and epileptic seizure are the presenting signs. May be associated with NF-2
Hemangioblastoma [14][15][16][17]	+	+/−	+/−	−	+	−	Infratentorial Cystic lesion with a solid enhancing mural nodule	Blood vessel origin Capillaries with thin walls	Biopsy	Might secret erythropoietin and cause polycythemia May be associated with von hippel-lindau syndrome
Pituitary adenoma [18][19][7]	−	−	+ Bitemporal hemianopia	−	−	Endocrine abnormalities as a result of functional adenomas or pressure effect of non-functional adenomas	Isointense to normal pituitary gland in T1	Endocrine cell hyperplasia	Biopsy	It is associated with MEN1 disease. Initialy presents with upper bitemporal quadrantanopsia followed by bitemporal hemianopsia (pressure on optic chiasma from below)
Schwannoma [20][21][22][23]	−	−	−	−	+	−	Split-fat sign Fascicular sign Often have areas of hemosiderin	Schwann cell origin S100+	Biopsy	It causes hearing loss and tinnitus May be associated with NF-2 (bilateral schwannomas)
Primary CNS lymphoma [24][25]	+	+/−	+/−	−	+	−	Usually deep in the white matter Single mass with ring enhancement	B cell origin Similar to non hodgkin lymphoma (diffuse large B cell)	Biopsy	Usually in young immunocompromised patients (HIV) or old immunocompetent person.
Childhood primary brain tumors
Pilocytic astrocytoma [26][27][28]	+	+/−	+/−	−	+	−	Infratentorial Solid and cystic component Mostly in posterior fossa Usually in cerebellar hemisphers and vermis	Glial cell origin Solid and cystic component GFAP +	Biopsy	Most of the time, cerebellar dysfunction is the presenting signs.
Medulloblastoma [29][30][31]	+	+/−	+/−	−	+	−	Infratentorial Mostly in cerebellum Non communicating hydrocephalus	Neuroectoderm origin Homer wright rosettes	Biopsy	Drop metastasis (metastasis through CSF)
Ependymoma [32][7]	+	+/−	+/−	−	+	−	Infratentorial Usually found in 4th ventricle Mixed cystic/solid lesion Hydrocephalus	Ependymal cell origin Perivascular pseudorosette	Biopsy	Causes an unusually persistent, continuous headache in children.
Craniopharyngioma [33][34][35][7]	+	+/−	+ Bitemporal hemianopia	−	+	Hypopituitarism as a result of pressure effect on pituitary gland	Calcification Lobulated contour Motor-oil like fluid within tumor	Ectodermal origin (Rathkes pouch) Calcification +	Biopsy	Initialy presents with lower bitemporal quadrantanopsia followed by bitemporal hemianopsia (pressure on optic chiasma from above)
Pinealoma [36][37][38]	+	+/−	+/−	−	+ vertical gaze palsy	B-hCG rise leads to precocious puberty in males	Hydrocephalus (compression of cerebral aqueduct)	Similar to testicular seminoma	Biopsy	May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
Vascular
AV malformation [39][40][7]	+	+	+/−	−	+/−	−	Supratentorial: ~85% Flow voids on T2 weighted images	We do not perform biopsy for AVM	Angiography	We may see bag of worms appearance in CT angiography
Brain aneurysm [41][42][43][44][45]	+	+/−	+/−	−	+/−	−	In magnetic resonance angiography, we may see aneurysm mostly in anterior circulation (~85%)	We do not perform biopsy for brain aneurysm	MRA and CTA	It is associated with autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome, pseudoxanthoma elasticum and Bicuspid aortic valve (Angiography is reserved for patients who have negative MRA and CTA)
Infectious
Bacterial brain abscess [46][47]	+	+/−	+/−	+	+	Leukocytosis Elevated ESR Blood culture may be positive for underlying organism	Central hypodense signal and surrounding ring-enhancement in T1 Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2	We do not perform biopsy for brain abscess	History/ imaging	The most common causes of brain abscess are Streptococcus and Staphylococcus.
Tuberculosis [48][7][49]	+	+/−	+/−	+	+	Positive acid-fast bacilli (AFB) smear in CSF specimen Positive CSF nucleic acid amplification testing Hyponatremia (inappropriate secretion of antidiuretic hormone) Mild anemia Leukocytosis	Hydrocephalus combined with marked basilar meningeal enhancement	We do not perform biopsy for brain tuberculosis	Lab data/ Imaging	It is associated with HIV infection
Toxoplasmosis [50][51]	+	+/−	+/−	−	+	Normal CSF	Multifocal masses with ring enhancement Mostly in basal ganglia, thalami, and corticomedullary junction.	We do not perform biopsy for brain toxoplasmosis	History/ imaging	It is associated with HIV infection
Hydatid cyst [52][7]	+	+/−	+/−	+/−	+	Positive serology (Antibody detection for E. granulosus)	Honeycomb appearance Necrotic area	We do not perform biopsy for hydatid cysts	Imaging	Brain, eye, and splenic cysts may not produce detectable amount of antibodies
CNS cryptococcosis [53]	+	+/−	+/−	+	+	Positive CSF antigen testing (coccidioidomycosis) CSF lymphocytic pleocytosis Elevated CSF proteins and lactate Low CSF glucose	Dilated perivascular spaces Basal ganglia pseudocysts Soap bubble brain lesions (cryptococcus neoformans)	We may see numerous acutely branching septate hyphae	Lab data/ Imaging	It is the most common brain fungal infection It is associated with HIV, immunosuppressive therapies, and organ transplants In may happen in immunocompetent patients undergoing invasive procedures ( neurosurgery) or exposed to contaminated devices or drugs Since brain biopsies are highly invasive and may may cause neurological deficits, we diagnose CNS fungal infections based on laboratory and imaging findings
CNS aspergillosis [54]	+	+/−	+/−	+	+	Positive galactomannan antigen testing (aspergillosis) CSF lymphocytic pleocytosis Elevated CSF proteins and lactate Low CSF glucose	Multiple abscesses Ring enhancement Peripheral low signal intensity on T2	We may see numerous acutely branching septate hyphae	Lab data/ Imaging	It is associated with HIV, immunosuppressive therapies, and organ transplants In may happen in immunocompetent patients undergoing invasive procedures ( neurosurgery) or exposed to contaminated devices or drugs Since brain biopsies are highly invasive and may may cause neurological deficits, we diagnose CNS fungal infections based on laboratory and imaging findings
Other
Brain metastasis [55][7]	+	+/−	+/−	+	+	−	Multiple lesions Vasogenic edema	Based on the primary cancer type we may have different immunohistopathology findings.	History/ imaging	Most common primary tumors that metastasis to brain: Lung cancer Renal cell carcinoma Breast cancer Melanoma Gastrointestinal tract If there is any uncertainty about etiology, biopsy should be performed

ABBREVIATIONS

CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli, MRA=Magnetic resonance angiography, CTA=CT angiography

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Oligoastrocytoma is the third most common glioma. Oligoastrocytoma accounts for 1% of all brain tumors and 5–10% of all glial neoplasms. The incidence of oligoastrocytoma is approximately 0.03 per 100,000 individuals in the United States. Oligoastrocytoma is a disease that tends to affect the young and middle-aged adult population. The median age of diagnosis is 42 years. Males are more commonly affected with oligoastrocytoma than females. Oligoastrocytoma usually affects individuals of the Caucasian race. The incidence rate of oligoastrocytoma is higher in developed countries than in developing countries.

• Oligoastrocytoma is the third most common glioma.^[1]
• Oligoastrocytoma accounts for 1000 out of 100,000 of all brain tumors and 5000-10,000 out of 100,000 of all glial neoplasms.^[2]

• The incidence of oligoastrocytoma is approximately 3 per 100,000 individuals in the United States.^[3]

• Oligoastrocytoma is a disease that tends to affect the young and middle-aged adult population.^[2]
• Oligoastrocytoma most commonly occurs in between 30-50 years of age.
• The median age of diagnosis is 42 years.^[4]

• Males are more commonly affected with oligoastrocytoma than females. The male to female ratio is approximately 1.43 to 1.^[5]

• Oligoastrocytoma usually affects individuals of the Caucasian race. African American, Latin American, and Asian individuals are less likely to develop oligoastrocytoma.^[6]

• The incidence rate of oligoastrocytoma is higher in developed countries than in developing countries.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

Common risk factors in the development of oligoastrocytoma include family history of brain tumors, ionizing radiation, and allergic diseases.

Common risk factors in the development of oligoastrocytoma include:^[1]

• Family history of brain tumors
• Ionizing radiation
• Allergic diseases

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

There is insufficient evidence to recommend routine screening for oligoastrocytoma.

There is insufficient evidence to recommend routine screening for oligoastrocytoma.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]

If left untreated, patients with oligoastrocytoma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death. Oligoastrocytomas are slow growing tumors. Common complications associated with oligoastrocytoma include hydrocephalus, intracranial hemorrhage, coma, metastasis, venous thromboembolism, and side effects of chemotherapy and radiation. Depending on the extent and grade of the tumor at the time of diagnosis, the prognosis of oligoastrocytoma may vary. However, the prognosis is generally regarded as good. The prognosis of low-grade oligoastrocytoma is more favorable than that for anaplastic oligoastrocytoma because of the more indolent course and younger age at which most patients are diagnosed. The 1, 5, and 10-year survival rates of patients with oligoastrocytoma are approximately 87%, 56.97%, and 45.80%, respectively.

• Oligoastrocytomas are slow growing tumors.^[1] The tumors may be present for many years before they are diagnosed.^[2]
• If left untreated, patients with oligoastrocytoma may progress to develop seizures, focal neurological deficits, hydrocephalus, brain herniation, intracranial hemorrhage, and ultimately death.^[3][4][5]
• The mixed gliomas with a 1p/19q loss would behave in an indolent or chemo-responsive fashion as expected of an oligodendroglioma, whereas those without this profile act biologically like astrocytic tumors, i.e. more aggressively and more prone to high grade transformation.^[6]

Common complications associated with oligoastrocytoma include:^{[4][7][8][3][9][5]}

• Hydrocephalus
• Intracranial hemorrhage
• Coma
• Metastasis
• Recurrence
• Venous thromboembolism
• Side effects of chemotherapy
• Side effects of radiotherapy

• Depending on the extent and grade of the tumor at the time of diagnosis, the prognosis of oligoastrocytoma may vary. However, the prognosis is generally regarded as good.^[10]
• The prognosis of oligoastrocytoma is more favorable than that of anaplastic oligoastrocytoma because of the more indolent course and younger age at which most patients are diagnosed.^[4]
• The 1, 5, and 10-year survival rates of patients with oligoastrocytoma are approximately 87%, 56.97%, and 45.80%, respectively.^[11]
• Favorable prognostic factors for oligoastrocytoma include:^{[12][13][7][14][15][3]}

• Presence of 1p19q codeletion
• Age at presentation < 40 years
• Lower grade of tumor
• Absence of tumor necrosis
• Seizure as presenting symptom
• Presence of MGMT gene promoter hypermethylation
• Extent of surgical resection
• Good performance status
• Intact neurological function

• Presence of microvascular proliferation and necrosis are poor prognostic factors for oligoastrocytoma.^[16]

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