Astrocytomas are primary intracranial tumors derived from astrocytes cells of the brain. They may arise in the cerebral hemispheres, in the posterior fossa, in the optic nerve, and rarely, the spinal cord. Astrocytomas are a type of neoplasm of the brain. They originate in a particular kind of glial cells, star-shaped brain cells in the cerebrum called astrocytes. This type of tumor does not usually spread outside the brain and spinal cord and it does not usually affect other organs.

Astrocytoma was the first glioma tumor to be described. It was first explained as glioma duram by Virchow in 1840 and then as spider cell glioma by T.Simon in 1874 and astroma by M von Lenhossek in 1895. Histological description of astrocytoma was first given by Bergstrand in 1932.

Astrocytoma may be classified according to its histology into 4 grades: pilocytic astrocytoma, diffuse astrocytoma, anaplastic astrocytoma and glioblastoma multiforme.

The exact pathogenesis of astrocytoma is not completely understood but it is believed that this tumor has a close association with genetic mutations. Microscopic pathologic findings in pilocytic astrocytoma include normal cells with slow growth rate, biphasic pattern (dense fibrillar tissue within loose myxoid tissue), Calcification, Vascular hyalinization and Nested fibrotic pattern. In diffuse astrocytoma we may see atypical cells, relatively slow mitosis rate, diffusely infiltrate neuropil and poorly defined cytoplasm. In anaplastic astrocytoma we may see pleomorphic and malignant cells, High mitosis rate, hyperchromatosis and prominent small vessels. In glioblastoma multiform we may see Pleomorphic cells, Naked nuclei, Multi-focal necrosis, Pseudopalisading pattern, Scattered pyknotic nuclear debris in the center, Micro-vascular proliferation and Vascular thrombi.

The exact cause of astrocytoma is not known but it seems that Genetic mutation has a strong association with this tumor.

Astrocytoma must be differentiated from other space occupying CNS lesions that cause neurological symptoms such as subependymal nodule, central neurocytoma, oligodendroglioma, intraventricular meningioma, intraventricular metastasis, medulloblastoma, sarcoma, primitive neuroectodermal tumor, choroid plexus carcinoma and glioblastoma multiforme.

The incidence of astrocytoma is 0.23 per 100,000 and the number of new cases is 700 per year. In 2012, there were an estimated 148,818 people living with brain and other nervous system cancer in the United States. The number of deaths was 4.3 per 100,000 men and women per year based on 2008-2012 deaths. The low-grade type is more often found in children or young adults, while the high-grade type is more prevalent in adults. Pilocytic astrocytoma is more common in men, who account for 62% of all cases. The male-to-female ratio of diffuse astrocytoma is 1.5:1 and for anaplastic astrocytoma is 1.8:1. Astrocytoma is more common in caucasian race.

Common risk factors in the development of astrocytoma include environmental factors such as: Vinyl chloride, Phenols, organic solvents, pesticides, Formaldehyde, lubricating fluids, polycyclic aromatic hydrocarbons and past radiation therapy to the brain and genetic diseases such as: Neurofibromatosis, Tuberous sclerosis, Li-Fraumeni syndrome, Nevoid basal cell carcinoma syndrome, Turcot syndrome and Melanoma-astrocytoma syndrome. Less common risk factors include: Blood group A, previous head trauma, history of meningitis, history of epilepsy.

If left untreated, eventually 100% of patients with low grade astrocytomas will growth rapidly similar to high grade astrocytoma tumors and 100% of patients with high grade astrocytoma will become symptomatic and deteriorate. Astrocytoma being a space occupying lesion can have following complications depending on the location of the tumor: Increased intracranial pressure, cognitive dysfunction, emotional disturbances, behavioral complications, visual defects and Muscle weakness. Low-grade astrocytomas (grade I [pilocytic] and grade II) have a relatively favorable prognosis, particularly for circumscribed, grade I lesions where complete excision may be possible. High-grade astrocytomas generally carry a poor prognosis in younger patients.

A positive history of Vinyl chloride, Phenols, organic solvents, pesticides, Formaldehyde, lubricating fluids, polycyclic aromatic hydrocarbons, past radiation therapy to the brain, Genetic disorders, blood group A, previous head trauma, Meningitis, Epilepsy, Headache, limb parasthesia or weakness, difficulty swallowing, Nausea, Diplopia, Lethargy, personality changes and Blurred vision is suggestive of astrocytoma. The most common symptoms of astrocytoma include morning headache or headache that goes away after vomiting, Nausea and vomiting, Vision, hearing, and speech problems, loss of balance and trouble walking, worsening handwriting or slow speech, Weakness or change in feeling on one side of the body, unusual sleepiness, Change in personality or behavior, Increase in the size of the head (in infants), Seizures, decreased memory, attention, and motor abilities, but unaffected intelligence, language, and academic skills. Less common symptoms of astrocytoma include Weight loss or weight gain for no known reason and more or less energy than usual.

Common physical examination findings of astrocytoma include gait disturbances, Tachycardia or bradycardia, Orthostatic hypotension, reduced hearing acuity, nystagmus, abnormal extra-ocular movement, nonreactive pupils, papilledema, blurry vision, head tilt, Altered mental status, Clonus , Hyperreflexia, Muscle rigidity, proximal/distal muscle weakness unilaterally or bilaterally, cranial nerve involvement , unilateral/bilateral sensory loss in the upper/lower extremity, positive Trendelenburg’s sign, unilateral/bilateral tremor and Dysmetria.

There are no diagnostic lab findings associated with astrocytoma.

Frontal astrocytomas can disturb autonomic pathways and cause prolonged QT syndrome.

There are no characteristic x-ray findings associated with astrocytomas.

There are no echocardiography/ultrasound findings associated with astrocytoma.

CT scan may be helpful in the diagnosis of astrocytoma. Findings on CT scan suggestive of astrocytoma include: Poorly demarcated mass, low density and no inhancement inside the tumor In low grade astrocytoma, poorly demarcated mass, low density and there are partial enhancement inside the tumor mas In high grade astrocytoma.

Findings on MRI suggestive of astrocytoma in Low grade astrocytoma (pilocytic and diffuse astrocytoma) include Decreased resonance in comparison to surrounding brain tissue in T1 and Increased resonance in comparison to surrounding brain tissue in T2. In anaplastic astrocytoma we have Hypointense T1, Hyperintense T2 and some contrast enhancement and edema. In glioblastoma multiform we have irregular ring-nodular enhancing lesions and central necrosis surrounding vasogenic edema.

PET/SPECT may be helpful in the differentiation of astrocytoma grading. Finding on PET/SPECT suggestive of low grade astrocytoma is hypometabolic mass and finding on PET/SPECT suggestive of high grade astrocytoma is hypermetabolic mass.

Biopsy is helpful in the diagnosis of astrocytomas. Findings suggestive diagnostic of astrocytoma include normal cells with slow growth rate, biphasic pattern (dense fibrillar tissue within loose myxoid tissue), Calcification, Vascular hyalinization and Nested fibrotic pattern in pilocytic astrocytoma, atypical cells, relatively slow mitosis rate, diffusely infiltrate neuropil and poorly defined cytoplasm in diffuse astrocytoma, pleomorphic and malignant cells, High mitosis rate, hyperchromatosis and prominent small vessels in anaplastic astrocytoma, Pleomorphic cells, Naked nuclei, Multi-focal necrosis, Pseudopalisading pattern, Scattered pyknotic nuclear debris in the center, Micro-vascular proliferation and Vascular thrombi in glioblastoma multiform.

The mainstay of treatment for low grade astrocytoma is wait and see approach, radiation therapy and chemotherapy. Treatment for anaplastic astrocytoma is radiotherapy with adjunctive chemotherapy, radiotherapy alone and chemotherapy alone. Treatment for glioblastoma multiform is chemotherapy and radiotherapy, Bevacizumab, alternating electric fields and Carmustine polymer wafers.

Surgical intervention is the mainstay of treatment for astrocytomas. Extensive resection is preferred over partial resection. The relative contraindications of brain surgery are: Advanced age, sever cardiopulmonary dysfunction, inaccessible lesions and sever systemic illness such as sepsis.

Effective measures for the primary prevention of astrocytoma include eliminating environmental risk factors from happening such as: Exposure to Vinyl chloride, Phenols, Organic solvents, Pesticides, Formaldehyde, Lubricating fluids, Polycyclic aromatic hydrocarbons and Previous radiation to the brain.

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

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Astrocytoma was the first glioma tumor to be described. It was first explained as glioma duram by Virchow in 1840 and then as spider cell glioma by T.Simon in 1874 and astroma by M von Lenhossek in 1895. Histological description of astrocytoma was first given by Bergstrand in 1932.

• Astrocytoma was the first glioma tumor to be described.^[1]
• Astrocytoma was first explained as glioma duram by Virchow in 1840.
• Astrocytoma was decribed as spider cell glioma by T.Simon in 1874.
• Astrocytoma was also described as astroma by M. von Lenhossek in 1895.
• Earlier nomenclatures included:

• Amoebiod giant cell glioma in 1918 by O Lotmar
• Fibrillary, protoplasmic astrocytoma and astroblastoma in 1926 by Baley and Cushing
• Afibrillary and gigantocellular astrocytoma in 1932 by Roussy and Oberling
• Piloid, gemistocytic and diffuse astrocytoma in 1932 by Penfield

• Cerebellar astrocytoma was first described by Harvey Cushing in 1931.^[2]
• Histological description of astrocytoma was first given by Bergstrand in 1932.^[3]

• Prolific United States Republican Party political strategist Lee Atwater.^[4]

• U.S. Senator Ted Kennedy (D-MA) died of malignant glioma.^[5]

• 2001 World Rally Championship winner Richard.

• Composer George Gershwin had glioblastoma multiforme.

• University of Texas sniper Charles Whitman was diagnosed with astrocytoma post-mortem. ^[6]

• Mo Mowlam (Secretary of State for Northern Ireland May 1997 – October 1999) – had glioma.^[7]

• Dan Quisenberry (Major League pitcher) had grade IV astrocytoma.^[8]

Astrocytoma may be classified according to its histology into 4 grades: pilocytic astrocytoma, diffuse astrocytoma, anaplastic astrocytoma and glioblastoma multiforme.

• Astrocytoma may be classified according to its histology into 4 grades:^[1][2]

• Low-grade astrocytoma may be classified based on tumor spread into four subtypes including:

The exact pathogenesis of astrocytoma is not completely understood but it is believed that this tumor has a close association with genetic mutations. Microscopic pathologic findings in pilocytic astrocytoma include normal cells with slow growth rate, biphasic pattern (dense fibrillar tissue within loose myxoid tissue), calcification, vascular hyalinization, and nested fibrotic pattern. In diffuse astrocytoma, we may see atypical cells, relatively slow mitosis rate, diffusely infiltrate neuropil and poorly defined cytoplasm. In anaplastic astrocytoma, we may see pleomorphic and malignant cells, high mitosis rate, hyperchromatosis, and prominent small vessels. In glioblastoma multiform, we may see pleomorphic cells, naked nuclei, multi-focal necrosis, pseudopalisading pattern, scattered pyknotic nuclear debris in the center, micro-vascular proliferation, and vascular thrombi.

• The exact pathogenesis of astrocytoma is not completely understood but it is believed that this tumor has a close association with genetic mutations.^[1]
• The origin of this tumor is from neuroepithelial cells.

• There are no conditions associated with astrocytoma.

• Genomic alterations involving BRAF activation are very common in sporadic cases of pilocytic astrocytoma, resulting in activation of the ERK/MAPK pathway.^[2][3][4][5]
• BRAF activation in pilocytic astrocytoma occurs most commonly through a KIAA1549–BRAF gene fusion, producing a fusion protein that lacks the BRAF regulatory domain.
• This fusion is seen in most infratentorial and midline pilocytic astrocytomas, but is present at lower frequency in supratentorial (hemispheric) tumors.^{[6][7][8][9][10]}
• Presence of the BRAF–KIAA1549 fusion predicted for better clinical outcome (progression-free survival [PFS] and overall survival) in one report that described children with incompletely resected low-grade gliomas.^[11]
• Other factors such as p16 deletion and tumor location may modify the impact of BRAF mutation on outcome.
• Progression to high-grade glioma is rare for pediatric low-grade glioma with the BRAF–KIAA1549 fusion.^[12]
• BRAF activation through the KIAA1549–BRAF fusion has also been described in other pediatric low-grade gliomas (e.g.,pilomyxoid astrocytoma).
• Other genomic alterations in pilocytic astrocytomas that may also activate the ERK/MAPK pathway (e.g., alternative BRAF gene fusions, RAF1 rearrangements, RAS mutations, and BRAF V600E point mutations) are less commonly observed.^[13]
• BRAF V600E point mutations are observed in nonpilocytic pediatric low-grade gliomas as well, including approximately two-thirds of pleomorphic xanthoastrocytoma patients and in ganglioglioma and desmoplastic infantile ganglioglioma patients.
• A retrospective study of 53 children with gangliogliomas demonstrated BRAF V600E staining in approximately 40% of tumors.
• Five-year recurrence-free survival was worse in the V600E-mutated tumors (about 60%) than in the tumors that did not stain for V600E (about 80%).
• The frequency of the BRAF V600E mutation was significantly higher in pediatric low-grade glioma that transformed to high-grade glioma (8 of 18 cases) compared to the frequency of the mutation in cases that did not transform (10 of 167 cases).^[14]
• As expected, given the role of NF1 deficiency in activating the ERK/MAPK pathway, activating BRAF genomic alterations are uncommon in pilocytic astrocytoma associated with NF1.
• Activating mutations in FGFR1 and PTPN11, as well as NTRK2 fusion genes, have also been identified in non-cerebellar pilocytic astrocytomas. In pediatric grade II diffuse astrocytomas, the most common alterations reported are rearrangements in the MYB family of transcription factors in up to 53% of tumors.^[15]

• Pediatric high-grade gliomas, especially glioblastoma multiforme, are biologically distinct from those arising in adults.^{[16][17][18][19]}
• Pediatric high-grade gliomas, compared with adult tumors, are more frequently associated with PDGF/PDGFR genomic alterations and mutations in histone H3.3genes and less frequently with PTEN and EGFR genomic alterations.
• Although, it was believed that pediatric glioblastoma multiforme tumors were more closely related to adult secondary glioblastoma multiforme tumors in which there is step-wise transformation from lower-grade into higher-grade gliomas with tumors having IDH1 and IDH2 mutations, the latter mutations are rarely observed in childhood glioblastoma multiforme tumors.^[20][21]
• Based on epigenetic patterns (DNA methylation), pediatric glioblastoma multiforme tumors are separated into relatively distinct subgroups with distinctive chromosome copy number gains/losses and gene mutations.^[22]
• Two subgroups have identifiable recurrent H3F3A mutations, suggesting disrupted epigenetic regulatory mechanisms, with one subgroup having mutations at K27 (lysine 27) and the other group having mutations at G34 (glycine 34). The subgroups are the following:
  • H3F3A mutation at K27: The K27 cluster occurs predominately in mid-childhood (median age, approximately 10 years), is mainly midline (thalamus, brainstem, and spinal cord), and carries a very poor prognosis. These tumors also frequently have TP53 mutations. Thalamic high-grade gliomas in older adolescents and young adults also show a high rate of H3F3A K27 mutations.
  • H3F3A mutation at G34: The second H3F3A mutation tumor cluster, the G34 grouping, is found in older children and young adults (median age, 18 years), arises exclusively in the cerebral cortex, and carries a better prognosis. The G34 clusters also have TP53 mutations and widespread hypomethylation across the whole genome.
• The H3F3A K27 and G34 mutations appear to be unique to high-grade gliomas and have not been observed in other pediatric brain tumors.^[23] Both mutations induce distinctive DNA methylation patterns compared with the patterns observed in IDH-mutated tumors, which occur in young adults.^[24]
• Other pediatric glioblastoma multiforme subgroups include the RTK PDGFRA and mesenchymal clusters, both of which occur over a wide age range, affecting both children and adults.
• The RTK PDGFRA and mesenchymal subtypes are comprised predominantly of cortical tumors, with cerebellar glioblastoma multiforme tumors being rarely observed; they both carry a poor prognosis.
• Childhood secondary high-grade glioma (high-grade glioma that is preceded by a low-grade glioma) is uncommon (2.9% in a study of 886 patients).
• No pediatric low-grade gliomas with the BRAF–KIAA1549 fusion transformed to a high-grade glioma, whereas low-grade gliomas with the BRAF V600E mutations were associated with increased risk of transformation.
• Approximately 40% of patients (7 of 18) with secondary high-grade glioma had BRAF V600E mutations, with CDKN2A alterations present in 57% of cases (8 of 14).

Astrocytoma causes regional effects by compression, invasion, and destruction of brain parenchyma, arterial and venous hypoxia, competition for nutrients, release of metabolic end products (e.g., free radicals, altered electrolytes, neurotransmitters), and release and recruitment of cellular mediators e.g., cytokines) that disrupt normal parenchymal function. Secondary clinical sequel may be caused by elevated intracranial pressure (ICP) attributable to direct mass effect, increased blood volume, or increased cerebrospinal fluid (CSF) volume.[25]

Pathological findings diagnostic of astrocytoma include:^{[26][27][28][29]}

Pilocytic Cells appearance is normal and growth rate is slow. Biphasic pattern (dense fibrillar tissue within loose myxoid tissue) Calcification Vascular hyalinization Nested fibrotic pattern
Diffuse There might be some atypical cells inside tumor Mitosis rate is relatively slow Diffusely infiltrate neuropil Poorly defined cytoplasm
Anaplastic: Tumor cells are pleomorphic and malignant High mitosis rate Hyperchromatosis Prominent small vessels
Glioblastoma Pleomorphic cells Naked nuclei Multi-focal necrosis Pseudopalisading pattern Scattered pyknotic nuclear debris in the center Micro-vascular proliferation Vascular thrombi

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The exact cause of astrocytoma is not known but it seems that genetic mutation has a strong association with this tumor.

The exact cause of astrocytoma is not known but it seems that genetic mutation has a strong association with this tumor.^[1][2]

On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from oligodendroglioma, meningioma, 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, astrocytoma must be differentiated from oligodendroglioma, meningioma, 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.

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

The incidence of astrocytoma is 0.23 per 100,000 and the number of new cases is 700 per year. In 2012, there were an estimated 148,818 people living with brain and other nervous system cancer in the United States. The number of deaths was 4.3 per 100,000 individuals per year based on 2008-2012 mortality records. The low-grade type is often found in children or young adults, while the high-grade type is more prevalent in adults. Pilocytic astrocytoma is more common in men, who account for 62% of all cases. The male-to-female ratio of diffuse astrocytoma is 1.5:1 and for anaplastic astrocytoma is 1.8:1. Astrocytoma is more common in caucasian race.

• The incidence of astrocytoma is 0.23 per 100,000 and the number of new cases is 700 per year.^[1]
• Diffuse astrocytoma has an incidence of 0.1 per 100,000, with 1500 to 1800 new cases per year in North America.
• Anaplastic astrocytoma has an incidence of 0.49 per 100,000 per year.
• Glioblastoma has an incidence of 5 per 100,000 per year.
• Pilocytic astrocytoma accounts for 0.6 – 5.1% of all intracranial neoplasms (1.7-7% of all glial tumors) and are the most common primary brain tumor of childhood, accounting for 70-85% of all cerebellar astrocytomas.^[2]

• In 2012, there were an estimated 148,818 people living with brain and other nervous system cancer in the United States.

• The number of deaths was 4.3 per 100,000 individuals per year based on 2008-2012 mortality records.^[3][4]

• People may develop astrocytoma at any age.
• The low-grade type is often found in children or young adults, while the high-grade type is more prevalent in adults.
• Subependymal giant cell tumors are a well known manifestation of tuberous sclerosis (TS), affecting 5-15% of patients with the condition. They are principally diagnosed in patients under 20 years of age, but are occasionally found in older patients as well.^[5]
• Anaplastic astrocytomas occur in adulthood with peak incidence between 40 and 50 years of age, which is older than low grade astrocytomas and younger than glioblastoma.^[6]
• Pilocytic astrocytomas are tumors of young people, with 75% occurring in the first two decades of life, typically 9-10 years of age. The mean age of presentation is 17 years.^[5]
• The median age of diffuse astrocytoma at the time of the diagnosis is 35 years, with a bimodel age distribution at 6 to 12 years and 26 to 46 years.
• Diffuse low grade gliomas of the cerebral hemispheres are typically diagnosed in young adults between 20-45 years old (mean 35 years of age).^[7][8]
• Pleomorphic xanthoastrocytoma has a median age of 22 years at initial presentation.
• Mean age at the time of diagnosis of anaplastic astrocytoma is 40 years.
• The peak incidence of glioblastoma is at ages 65 to 74 years.

• Pilocytic astrocytoma is more common in men, who account for 62% of all the cases.
• The male-to-female ratio of diffuse astrocytoma is 1.5:1.
• The male-to-female ratio of anaplastic astrocytoma is 1.8:1.

• Astrocytoma is more common in Caucasian race.^[4]

Common risk factors in the development of astrocytoma include environmental factors such as vinyl chloride, phenols, organic solvents, pesticides, formaldehyde, lubricating fluids, polycyclic aromatic hydrocarbons, and past radiation therapy to the brain and genetic diseases such as neurofibromatosis, tuberous sclerosis, Li-Fraumeni syndrome, nevoid basal cell carcinoma syndrome, Turcot syndrome and melanoma-astrocytoma syndrome. Less common risk factors include blood group A, previous head trauma, history of meningitis, history of epilepsy.

• Environmental risk factors:
  • Exposure to:^[1]
    1. Vinyl chloride
    2. Phenols
    3. Organic solvents
    4. Pesticides
    5. Formaldehyde
    6. Lubricating fluids
    7. Polycyclic aromatic hydrocarbons
  • Past radiation therapy to the brain^[2]
• Genetic risk factors:^[3][4][5]
  • Neurofibromatosis
  • Tuberous sclerosis
  • Li-Fraumeni syndrome
  • Nevoid basal cell carcinoma syndrome
  • Turcot syndrome
  • Melanoma-astrocytoma syndrome

• Blood group A^[6][7]
• Previous head trauma^[8]
• History of meningitis
• History of epilepsy^[7]

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If left untreated, all of patients with low grade astrocytomas will have a rapid growth of the tumor similar to high grade astrocytoma and all of the patients with high grade astrocytoma will become symptomatic and deteriorate. Astrocytoma being a space occupying lesion may have following complications depending on the location of the tumor including increased intracranial pressure, cognitive dysfunction, emotional disturbances, behavioral complications, visual defects and muscle weakness. Low-grade astrocytomas (grade I [pilocytic] and grade II) have a relatively favorable prognosis, particularly for circumscribed, grade I lesions where complete excision may be possible. High-grade astrocytomas generally carry a poor prognosis in younger patients.

• Low grade astrocytoma:^[1][2][3][4]
  • The natural history of all low grade astrocytomas is not the same.
  • Most of the patients experience almost no progression of symptoms for initial 5 to 7 years.
  • If left untreated, all the patients with low grade astrocytomas will have rapid growth of tumor similar to high grade astrocytoma.
• High grade astrocytoma:
  • If left untreated, all of the patients become symptomatic and deteriorate.
  • Recurrence is more common in high grade astrocytoma compared to low grade astrocytoma.^[5]

• Astrocytoma being a space occupying lesion may have following complications depending on the location of the tumor:^[6][7][8]

• Increased intracranial pressure
• Cognitive dysfunction
• Emotional disturbances
• Behavioral complications
• Visual defects
• Muscle weakness
• Local neurological deficit

• Low-grade astrocytomas (grade I [pilocytic] and grade II) have a relatively favorable prognosis, particularly for circumscribed, grade I lesions where complete excision is possible.^{[9][10][11][12]}
• Tumor spread, when it occurs, is usually by contiguous extension; dissemination to other CNS sites may occur, although uncommon.^[13][14]
• Although, metastasis is uncommon, tumors may be of multi-focal origin, especially when associated with neurofibromatosis 1 (NF1).
• Unfavorable prognostic features for childhood low-grade astrocytomas include:^[15][16]

• Young age
• Fibrillary histology
• Inability to obtain a complete resection

• In patients with pilocytic astrocytoma, elevated MIB-1 labeling index, a marker of cellular activity, is associated with reduced progression-free survival.^[17][18]
• A BRAF-KIAA fusion, found in pilocytic tumors, confers a better clinical outcome.
• Children with isolated optic nerve tumors have a better prognosis than those with lesions that involve the chiasm or that extend along the optic pathway.^[19][20]
• Children with NF1 also have a better prognosis, especially when the tumor is found in asymptomatic patients at the time of screening.
• Grade 2 astrocytomas are defined as being invasive gliomas, meaning that the tumor cells penetrate into the surrounding normal brain.
• People with oligodendrogliomas (which might share common cells of origin) have better prognosis than those with mixed oligoastrocytomas, who in turn have better prognosis than patients with (pure) low-grade astrocytomas.
• Individuals with grade 2 astrocytoma have a 5-year survival rate of about 34% without treatment and about 70% with radiation therapy. The median survival time is 4 years.^[21]

• Biologic markers, such as p53 overexpression and mutation status, may be useful predictors of outcome in patients with high-grade gliomas.
  • MIB-1 labeling index is predictive of outcome in childhood malignant brain tumors.^[22]
  • Both histologic classification and proliferative activity evaluation have been shown to be independently associated with survival.^[23]
• Although, high-grade astrocytomas generally carry a poor prognosis in younger patients, those with anaplastic astrocytomas in whom a gross-total resection is possible may fare better.
• For low grade astrocytomas, removal of the tumor will generally allow functional survival for many years.
• In some reports, the five-year survival has been over 90% with well resected tumors.
• To date, complete resection of high grade astrocytomas is impossible because of the diffuse infiltration of tumor cells.
• Radiation therapy has been shown to prolong survival and is a standard component of treatment of anaplastic astrocytoma.
• Individuals with grade 3 astrocytoma have a median survival time of 18 months without treatment (radiation and chemotherapy).
• Although radiotherapy rarely cures glioblastoma multiforme, studies show that it doubles the median survival of patients, compared to supportive care alone.
• The prognosis is worst for these grade 4 gliomas.^[24][25][26]
  • Few patients survive beyond 3 years.
  • Individuals with grade 4 astrocytoma have a median survival time of:
    • 17 weeks without treatment,
    • 30 weeks with radiation
    • 37 weeks with surgical removal of most of the tumors.