Meningioma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

Meningioma is a relatively common neoplasm of the central nervous system that arises from arachnoidal cells which are normally involved in the protection of the brain and spinal cord by forming a thick envelope of meninges around them. Meningioma is the most common benign tumors of the brain. About 90% of meningiomas are benign with about 2% being malignant. Meningioma was first discovered by Dr Felix Platter, a Swiss physician, in the 16th century. Meningioma may be classified according to the histological criteria of the WHO. It is classified into 3 groups: benign classic meningioma (WHO grade 1), atypical meningioma (WHO grade 2), and anaplastic malignant meningioma (WHO grade 3). Neurofibromatosis type II, cowden syndrome, and multiple endocrine neoplasia 1 are among a few conditions that are associated with meningioma. There are no established direct causes for meningioma. Meningioma must be differentiated from other diseases that cause similar presentation such as schwannoma, hemangiopericytoma, and solitary fibrous tumor. The incidence of meningioma is approximately 7.62 per 100,000 individuals in the United States. The prevalence of meningioma was estimated to be 97.5 cases per 100,000 individuals in the United States. Common risk factors in the development of meningioma are history of radiation treatment, increasing age, and female gender. There is insufficient evidence to recommend routine screening for meningioma. Meningioma could present with complications such as peritumoral brain edema, stroke, and increased intracranial pressure. The hallmark symptom of meningioma is headache. Other common symptoms of meningioma include visual impairment, hearing loss/tinnitus, focal neurological deficits, behavioral changes. Head CT scan may be diagnostic of meningioma. Some of the findings on CT scan suggestive of meningioma include edema, CSF attenuation cleft, round/elongated extraaxial mass, and hyperostosis of the adjacent skull. MRI with gadolinium is the investigation of choice for the diagnosis of meningioma. On MRI, meningioma is characterized by a homogeneous, well circumscribed, and extra-axial mass with a broad dural base. Other findings on MRI suggestive of meningioma include CSF vascular cleft sign, dural tail sign, and central necrosis or calcification that do not enhance. In asymptomatic meningiomas, the decision of surgical resection must be weighed against the possibility of conservative management according to the patient’s age, clinical presentation, and the anatomical location of the tumor. The predominant therapy for meningioma is surgical resection. Current data suggest that both external beam radiotherapy and radiosurgery play an important role in the management of grade II and III meningiomas.

Meningioma was first discovered by Dr Felix Platter, a Swiss physician, in the 16th century. He described the tumor as having the shape of an acorn, fleshy, and full of holes.

Meningioma may be classified according to the histological criteria of the WHO into 3 groups: benign classic meningioma (WHO grade 1) which is made up of nine variants, atypical meningioma (WHO grade 2) which is made up of three, and anaplastic malignant meningioma (WHO grade 3) made up of three variants.

Meningioma arises from the arachnoid “cap” cells, which are normally involved in the protection of the central nervous system by forming a thick envelope of meninges around the brain and spinal cord. Because of the abundance of arachnoid cap cells in the skull base and perivenous sinuses, meningiomas are commonly found in these sites. Some meningiomas may have progesterone receptors which could make the tumor grow in size during pregnancy and in the luteal phase of the menstrual cycle. Meningiomas could be found in various locations such as sphenoid ridge, olfactory grove, falx cerebri, cerebellopontine angle, foramen magnum, ventricles, etc. Though most meningiomas are benign in nature, some may be malignant and this characterization is usually based on brain invasion, frank anaplasia, and distant metastasis. NF2, MEG2, TERT, AKT1, and NDRG2 are some of the genes that may be involved in the pathogenesis of meningioma. Some conditions could be associated with meningioma, they include neurofibromatosis type 2, cowden syndrome, nevoid basal cell carcinoma, multiple endocrine neoplasia 1 (MEN1), etc. On gross pathology, a gray, well-circumscribed, dome-shaped mass is a characteristic finding of meningioma. On microscopic histopathological analysis, meningiomas may have different characeteristics, they include mitotic figures, interdigitating processes and intercellular junctions, prominent nucleoli, necrosis, and increased cellularity.

There are no established direct causes for meningioma.

Meningioma must be differentiated from other diseases that have similar presentation such as schwannoma, oligodendroglioma, pituitary adenoma, hemangioblastoma, etc

The prevalence of meningioma was estimated to be 97.5 cases per 100,000 individuals in the United States. The incidence of meningioma is approximately 7.62 per 100,000 individuals in the United States. Meningiomas may appear at any age, but occur most commonly among patients between 40 to 60 years. Females are more commonly affected with meningiomas than males, with the ratio being 2:1. Meningioma usually affects individuals of the African American race. Caucasian and Latin American individuals are less likely to develop meningioma.

Common risk factors in the development of meningioma are history of radiation treatment, increasing age, and female gender.

There is insufficient evidence to recommend routine screening for meningioma.

The median age at diagnosis of meningioma is about 65 years, with incidence increasing with advancing age. A higher annual growth rate may be seen in patients with an initial tumor diameter of greater than 25mm, MR imaging T2 signal hyperintensity, patients presenting with symptoms and edema, and male patients. Most meningiomas are single with about 1-10% being multiple. Common complications of meningioma include increased intracranial pressure, cranial nerve palsies, and hydrocephalus. Prognosis is generally good, and the survival rate of patients with meningioma mainly depends on the histological grade of the tumor and the extent of resection during surgery. A poorer survival rate may be seen in patients of advanced age, male patients, black race, malignant tumors, and patients with no initial treatment.

MRI is the gold standard test for the diagnosis of meningioma but CT is more widely available and better in urgent settings.

The hallmark symptom of meningioma is headache. Other common symptoms of meningioma include weakness, focal neurological deficits, visual impairement, hearing loss, and confusion. However, the specific clinical presentation of meningioma is determined by the exact anatomical location of the tumor.

Common physical examination findings of meningioma include decreased visual acuity, hearing loss, ataxia, muscle weakness, focal neurological deficits, and more. Patients with meningioma present with different signs depending on the location of the tumor, its character, and the structures it may compress. Some patients are asymptomatic and may have not present with sign on physical examination.

There are no diagnostic lab findings associated with meningioma.

There are no ECG findings associated with meningioma.

Plain radiography no longer has a role in the diagnosis or management of meningioma.

There are no echocardiography/ultrasound findings associated with meningioma.

Head CT scan may be diagnostic of meningioma. Some of the findings on CT scan suggestive of meningioma include edema, CSF attenuation cleft, round/elongated extraaxial mass, and hyperostosis of the adjacent skull. Although MRI is the diagnostic study of choice, CT is easier to use and may be used in cases where there is a contraindication to the use of an MRI.

MRI with gadolinium is the investigation of choice for the diagnosis of meningioma. On MRI, meningioma is characterized by a homogeneous, well circumscribed, and extra-axial mass with a broad dural base. Other findings on MRI suggestive of meningioma include CSF vascular cleft sign, dural tail sign, and central necrosis or calcification that do not enhance. Meningiomas may appear different on T1 and T2-weighted sequence but with a few similarities.

Other imaging studies that may be helpful in the diagnosis of meningioma include magnetic resonance (MR) spectroscopy, perfusion MRI, and diffusion MRI. With MR spectroscopy, elevated levels of alanine, choline, and/or lactate could be seen. MR perfusion study could demonstrate an elevated value of relative cerebral blood volume (rCBV).

Bromodeoxyuridine labeling study may be helpful in the diagnosis of meningioma. An elevated bromodeoxyuridine labeling index is suggestive of a rapid growth rate of meningioma and a greater incidence of recurrence following surgical resection.

In asymptomatic meningiomas, the decision of surgical resection must be weighed against the possibility of conservative management according to the patient’s age, clinical presentation, and the anatomical location of the tumor.^[1][2] Current data suggest that both external beam radiotherapy and radiosurgery play an important role in the management of grade II and III meningiomas.^[3][4] Chemotherapeutic agents are generally not effective against meningioma.^[2]

Asymptomatic meningiomas found incidentally are usually treated expectantly. In cases with tissue edema and vascular compromise, another approach can be taken. Radiotherapy is pursued depending on the patient factor and location of the tumor. It can be done after surgery with little advantage over radiotherapy alone.

The predominant therapy for meningioma is surgical resection. Adjunctive radiation therapy may be required among certain patients.^[2] The Simpson criteria for meningioma correlates the degree of surgical resection completeness with the probability of post-surgical tumor recurrence.^[2][5][6] Surgical resection is not recommended among patients with asymptomatic stable meningioma.^[2]

There are no established measures for the primary prevention of meningioma.

There are no established measures for the secondary prevention of meningioma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

Meningioma was first discovered by Dr. Felix Platter, a Swiss physician, in the 16th century. He described it as being round, fleshy and full of holes. Dr. Antonie Louis is known to be the first to attempt naming a meningioma.

• In 1614, the first case of meningioma was described by Dr. Felix Platter.^[1]
• He described the tumor as being round with a shape like an acorn. He said it was as large as a medium-sized apple, fleshy, and full of holes.
• The tumor had no connection with the brain matters, was covered with its own membrane, and a cavity was left behind after its removal.
• In 1774, Antonie Louis was acknowledged to have had the first major attempt at naming meningioma with his scientific treatise devoted to meningioma: “Sur les tumeurs fongueuses de la dure-mère” meaning “fungoid tumors of the dura mater” when translated to English.
• This was published in the Memoires of the ARC (académie royale de chirurgie).^[2]
• In 1910, a very large meningioma was successfully removed from the brain of General Leonard Wood by Dr. Harvey Cushing.
• General Leonard Wood was a physician and also the Chief of Staff of the US Army.^[3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

Meningioma has been classified into 3 groups by the WHO: benign classic meningioma (WHO grade 1), atypical meningioma (WHO grade 2), and anaplastic malignant meningioma (WHO grade 3). The WHO grade 1 group grow very slowly and consists of about 9 variants. About 3 variants correspond to WHO grade II, their association with malignancy is not clear but they grow faster than benign meningiomas. About 2 variants correspond to WHO grade III.

• WHO has classified meningiomas into histological and cytomorphological variants. Nine variants correspond to WHO grade I which are the benign classic meningiomas, three correspond to WHO grade II which are atypical meningiomas, and three in WHO grade III and are anaplastic malignant meningiomas.^[1]

• The table below lists the subtypes of meningioma according to the WHO grades:^[1][2]

WHO Grade	Subtypes
Benign classic meningioma (WHO grade 1)	Meningothelial, fibrous, transitional, psammomatous, angiomatous, micrcystic, secretory, lymphoplasmacyte-rich, and metaplastic meningioma They are low-grade tumors that grow very slowly and rarely invade the surrounding tissues
Atypical meningioma (WHO grade 2)	Chordoid, clear cell, and atypical meningioma. These are not clearly malignant, but grow faster than benign meningiomas 4 or more mitotic cells per hpf and/or 3 or more of the following features: small cells, increased cellularity, necrosis, prominent nucleoli, sheeting, &/or brain invasion in an otherwise Grade I tumor
Anaplastic malignant meningioma (WHO grade 3)	Rhabdoid, papillary, and anaplastic meningioma 20 or more mitoses per 10 hpf and/or possess cytological characteristics of an obvious malignancy such that the tumor cell resembles carcinoma, sarcoma, or melanoma.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

Meningioma arises from the arachnoid “cap” cells, which are normally involved in the protection of the central nervous system by forming a thick envelope of meninges around the brain and spinal cord. The majority of meningiomas are benign. They can be found anywhere in the central nervous system but are most commonly seen in the parasagittal, convexity and turbeculum sellae areas. There may be genetic mutations involved in the development of a meningioma, some of the genes involved includes NF2, MEG3, NDRG2, and SMARCE1. Multiple endocrine neoplasia 1, cowden syndrome, werner syndrome and neurofibromatosis 2 are some of the conditions that may be associated with meningioma. On microscopic pathology, some of the characteristic findings of a meningioma include mitotic figures, necrosis, interdigitating processes, and brain invasion. Most meningiomas are positive for vimentin and negative for cytokeratin.

• Meningiomas are the most common benign tumors of the brain. They are also the most common nonglial brain tumors.^[1]
• Meningioma arises from the arachnoid “cap” cells, which are normally involved in the protection of the central nervous system by forming a thick envelope of meninges around the brain and spinal cord.^[2]
• Meningiomas are commonly found in the base of the skull and perivenous sinuses due to the abundance of arachnoid cap cells in these sites. They are usually non-infilterative.^[1]
• The majority of meningiomas are benign (90%), about 6% are atypical, and 2% are malignant.^[1]
• Some meningiomas may be positive for progesterone receptors on histological examination. This can lead to increased tumor size and symptom burden during pregnancy and the luteal phase of the menstural cycle.^[1]
• Meningiomas may possess receptors for platelet derived growth factor, vascular endothelial growth factor (VEGF), glucocorticoid, and epidermal growth factor.^[1]
• Meningiomas can be found anywhere in the central nervous system, with its most frequent distribution as follows: parasagittal (20.8%), then convexity (15.2%), and tuberculum sellae (12.8%).^[3]
• The symptoms of meningioma can be flared by water retention, engorgement of blood vessels, and the presence of sex hormone receptors on tumor cells.^[1]
• A meningioma can be localized in the following areas: sphenoid ridge, olfactory groove, falx, lateral ventriculi, tentorium, the middle fossa, the orbit, the spinal channel, the Sylvian fissure, extracalvarial, multiple localization, the pontocerebral angle, the sphenoidal plane, and the foramen magnum.^[3]
• The characteristics of a meningioma can be determined based on histopathological variables like tumor gradient, histological subtype, proliferative index, and invasiveness of a tumor to the brain.^[3]
• The characterization of a meningioma being malignant is based on one or more of the following criteria: brain invasion, frank anaplasia, and distant metastasis^[4]

Genes involved in the pathogenesis of meningioma include:^{[5][4][6][7][8][9][10][11]}

• Neurofibromatosis 2 (NF2) gene on chromosome 22
• MEG3 (maternally expressed gene 3): Loss of expression, genomic DNA deletion, and promoter methylation on chromosome 14q32.
• NDRG2 (N-Myc downstream-regulated gene 2): Down regulation of this gene expression at the mRNA level is associated with the malignant progression and predisposition to recurrence of meningiomas.
• SMARCE1 (SWI/SNF chromatin-remodeling complex subunit gene): Heterozygous loss-of-function mutation. Its is commonly seen in meningiomas with clear cell histology and those located in the spine.
• SMARCB1: Predisposes to multiple meningiomas preferentially in the falx cerebri.
• TERT promoter mutation: Seen in meningiomas undergoing malignant histological progression.
• TRAF7
• AKT1
• KLF4
• SMO
• PIK3CA

Conditions associated with meningioma include:^[12]

• Neurofibromatosis type 2
• Nevoid basal cell carcinoma syndrome
• Multiple endocrine neoplasia 1 (MEN1)
• Cowden syndrome
• Werner syndrome
• BAP1 tumor predisposition syndrome
• Rubinstein-Taybi syndrome
• Familial meningiomatosis

• On gross pathology, a gray, well-circumscribed, dome-shaped mass is a characteristic finding of meningioma.^[13]

• On microscopic pathology, characteristic findings of meningioma include:^[4][14]

• Interdigitating processes and intercellular junctions
• Small foci of necrosis surrounded by pseudopalisading tumor cells in nonembolized atypical meningiomas
• Necrosis occurring in large geographic areas with a quick line demarcating it from viable tissues in embolized menigiomas
• Prominent macronucleoli in the perinecrotic areas in embolized meningiomas
• Mitotic figures (low in benign cases and high in malignant and atypical cases)
• Brain invasion histologically seen as a finger-like, a tongue-like, or a knobby protrusion into the tissue
• Small cells with a high nuclear:cytoplasmic ratio
• Prominent nucleoli
• Uninterrupted patternless or sheet-like growth
• Increased cellularity

• The following immunohistochemistry profile can be used to support the diagnosis of meningioma:^[4]

• Positive for vimentin
• Negative for cytokeratin
• Weak or negative staining for S 100 protein
• Focal membranous positivity for EMA

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

There are no established direct causes for meningioma.

There are no established direct causes for meningioma.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

On the basis of seizure, visual disturbance, and constitutional symptoms, meningioma must be differentiated from oligodendroglioma, astrocytoma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

On the basis of seizure, visual disturbance, and constitutional symptoms, meningioma must be differentiated from oligodendroglioma, astrocytoma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

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
Meningioma [1][2][3]	+	+/−	+/−	−	+	−	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
Glioblastoma multiforme [4][5][6]	+	+/−	+/−	−	+	−	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 [7][8][9]	+	+	+/−	−	+	−	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.
Hemangioblastoma [10][11][12][13]	+	+/−	+/−	−	+	−	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 [14][15][6]	−	−	+ 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 [16][17][18][19]	−	−	−	−	+	−	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 [20][21]	+	+/−	+/−	−	+	−	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 [22][23][24]	+	+/−	+/−	−	+	−	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 [25][26][27]	+	+/−	+/−	−	+	−	Infratentorial Mostly in cerebellum Non communicating hydrocephalus	Neuroectoderm origin Homer wright rosettes	Biopsy	Drop metastasis (metastasis through CSF)
Ependymoma [28][6]	+	+/−	+/−	−	+	−	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 [29][30][31][6]	+	+/−	+ 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 [32][33][34]	+	+/−	+/−	−	+ 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 [35][36][6]	+	+	+/−	−	+/−	−	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 [37][38][39][40][41]	+	+/−	+/−	−	+/−	−	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 [42][43]	+	+/−	+/−	+	+	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 [44][6][45]	+	+/−	+/−	+	+	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 [46][47]	+	+/−	+/−	−	+	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 [48][6]	+	+/−	+/−	+/−	+	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 [49]	+	+/−	+/−	+	+	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 [50]	+	+/−	+/−	+	+	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 [51][6]	+	+/−	+/−	+	+	−	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: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

The prevalence of meningioma is estimated to be 97.5 cases per 100,000 individuals in the United States. The incidence of meningioma is approximately 7.62 per 100,000 individuals in the United States. Meningiomas may appear at any age, but are most commonly noticed among patients older than 50 years of age. Females are more commonly affected with meningiomas than males, with a ratio of about 2:1. Meningioma usually affects individuals of the African American race. Caucasian and Latin American individuals are less likely to develop meningioma.

• The prevalence of meningioma is estimated to be 97.5 cases per 100,000 individuals in the United States. There are over 170,000 diagnosed cases in the United States.^[1]
• It was the most reported primary brain and central nervous system tumor in the Unites States between 2002 and 2006. It accounted for about 33.8% of the tumors reported, making it the most frequently diagnosed brain tumor.^[1]
• Meningioma is the second most common primary brain tumor worldwide.^[2]

• The incidence of meningiomas annually is approximately 7.62 per 100,000 individuals in the United States. The incidence of benign meningiomas is about 7.18, about 0.32 for borderline malignant meningiomas, and about 0.12 for malignant meningiomas.^[3]

• Meningiomas can occur at any age but is mostly seen with advancing age. ^[3]
• It is commonly seen between the ages of 40 to 60 and is more common in postmenopausal women.^[4]
• In childhood and adolescence, meningiomas account for about 1.5% of brain tumors.^[5]

• Females are more commonly affected with meningiomas than males.^[1]
• The female to male ratio is approximately 2 to 1.
• The incidence of meningioma among females is approximately 8.36 per 100,000 individuals in the United States, with that of males being 3.61 per 100,000 individuals.^[1]
• The female to male ratio of meningiomas may be inverted among affected patients who are younger than 15 years of age.^[1]
• Atypical and malignant meningiomas have a slight male predominace.^[1]

• Meningioma usually affects individuals of the black race. Caucasian and Latin American individuals are less likely to develop meningioma.^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

Common risk factors in the development of meningioma are history of radiation treatment, female gender, hormones, and some genetic disorders.

• Common risk factors in the development of meningioma include:^[1][2][3]

• Ionizing radiation: This is seen with both high and low dose levels.
• Hormones: Some meningiomas have receptors for progesterone and estrogen and can increase in size during pregnancy and the luteal phase of the menstrual cycle.
• Obesity in women
• Increasing age
• Neurofibromatosis type 2
• Female gender

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

There is insufficient evidence to recommend routine screening for meningioma.

There is insufficient evidence to recommend routine screening for meningioma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

The incidence of meningioma increases with advancing age, with the median age of diagnosis being about 65 years. There are some factors associated with faster progression of the tumor, they include absence of calcification, age 60 or younger, and intial tumor diameter greater than 25mm. Meningiomas can grow in a linear or volumetric fashion. They can grow anywhere in the central nervous system containing arachnoid membrane. If left untreated, patients with meningioma may progress to developing morning headaches, focal neurological deficits, edema surrounding the tumor, cranial nerve palsies, and more. Prognosis is generally good, and the survival rate of patients with meningioma mainly depends on the grade and the extent of resection of the tumor.

• The median age at diagnosis of meningioma is about 65 years, with incidence increasing with advancing age.^[1]
• Absence of calcification, age 60 or younger, and initial tumor diameter of greater than 25 mm are among the factors associated with a short time to progression.^[2]
• Linear growth may be seen in 44% of the patients, while volumetric growth may be seen in 74%.^[2]
• A higher annual growth rate may be seen in patients with an initial tumor diameter of greater than 25 mm, MR imaging T2 signal hyperintensity, patients presenting with symptoms and edema, and male patients.^[2]
• Meningomas are usually single but can be multiple in about 1 – 10% of the patients. Multiple meningiomas are usually seen in patients with neurofibromatosis.^[3][4]
• The rate of growth in patients with multiple meningiomas is similar to those with solitary meningiomas.
• Meningiomas can grow anywhere in the central nervous system containing arachnoid membrane. For example, between the brain and the cranium, in the ventricles, down the spinal canal.^[5]

• Common complications of meningioma include:^[6][7]

• Increased intracranial pressure
• Cranial nerve palsies
• Hydrocephalus
• Peritumoral brain edema
• Stroke: Due to occlusion of the internal carotid artery. This can be seen in meningiomas located at the skull base

• The prognosis of meningioma is usually determined by 2 of the most important factors which are the extent of the resection and the histological grade of the tumor.^[8]
• The 5 year estimated survival for benign tumors is 85.6%, 82.3% for borderline malignant tumors, and 66% for malignant tumors. A poorer survival rate may be seen in patients of advanced age, male patients, black race, malignant tumors, and patients with no initial treatment.^[1]
• Patients with atypical meningioma have a higher overall recurrence-free survival rate than those with anaplastic meningioma.^[9]
• The prognostic factors in patients with anaplastic meningioma include brain invasion, adjuvant radiotherapy, malignant progression, p53 over expression, and extent of resection.^[9]
• There may be a chance of recurrence of higher grade meningiomas even if they received gross-total resection or not.^[8]
• Grade 1 meningioma is associated with a median survival of approximately 10 years.^[10]
• Grade 3 meningioma is associated with a median survival of approximately 2.7 years.
• For classic tumors, the 5 year recurrence rate is about 12%, and they are not associated with a decreased overall length of survival. Unlike atypical tumors which have a 41% recurrence rate and decreased overall length of survival.^[8]
• Progesterone positive tumors tend to have lower proliferation indices resulting in a better prognosis than those that are progesterone receptor negative.^[8]
• The tumors that are positive for estrogen receptors and those negative for both estrogen and progesterone receptors have an increased potential for aggressive clinical behavior, progression and recurrence.^[11]

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