eMedicine Specialties > Radiology > Brain/Spine

Juvenile Pilocytic Astrocytoma

Simon Lo, MBBS, Assistant Professor, Department of Radiation Oncology, Indiana University School of Medicine
Karl K Kish, MD, Chief, Section of Neuroradiology, Department of Radiology, Harper University Hospital; Eric L Chang, MD, Assistant Professor, Department of Radiation Oncology, University of Texas MD Anderson Cancer Center; Kenneth J Levin, MD, Assistant Professor, Karmanos Cancer Institute, Medical Advisor, Radiation Therapy Technology School, Department of Radiation Oncology, Wayne State University School of Medicine; Clinical Assistant Professor, Medical Laboratory Science, Oakland University School of Health Sciences; Medical Director, Department of Radiation Oncology, North Oakland lMedical Centers and Henry Ford Medical Center; Sameer R Keole, MD, Staff Physician, Department of Radiation Oncology, Gershenson Radiation Oncology Center, Karmanos Cancer Institute, Harper Hospital, Wayne State University School of Medicine; Andrew E Sloan, MD, Associate Professor of Neurosurgery and Radiation Oncology, Case Western Reserve University Medical School; James Fontanesi, MD, Chairman, Department of Radiation Oncology, Cedars-Sinai Medical Center

Updated: Sep 10, 2008

Introduction

Background

Juvenile pilocytic astrocytomas occur more often in children and young adults. They are the most common astrocytic tumors in children, accounting for 80-85% of cerebellar astrocytomas and 60% of optic gliomas.

Juvenile pilocytic astrocytomas usually arise in the cerebellum, brainstem, hypothalamic region, or optic pathways, but they may occur in any area where astrocytes are present, including the cerebral hemispheres and the spinal cord. The most common site of occurrence of juvenile pilocytic astrocytoma is the cerebellum.¹

These tumors are usually discrete, indolent lesions associated with cyst formation. The cysts may be unilocular or multilocular, with an associated tumor nodule.

The most common presenting symptoms are associated with increased intracranial pressure resulting from mass effect or hydrocephalus. Symptoms may include headache, nausea, vomiting, irritability, ataxia, and visual complaints, depending on the site of occurrence.^{1,2,3,4,5,6,7,8}

Pathophysiology

The etiologic factors of juvenile pilocytic astrocytomas are unknown. Transformation to a malignant high-grade tumor is rare.

Juvenile pilocytic astrocytoma is associated with neurofibromatosis type 1 (NF1), an autosomal-dominant disorder characterized by the development of benign tumors, as well as some malignant tumors. Optic gliomas, 60% of which are pilocytic astrocytomas, are common tumors in patients with this disorder. Patients with optic pilocytic astrocytomas associated with NF1 usually have better outcomes than other patients with juvenile pilocytic astrocytomas because optic pilocytic astrocytomas are more likely to be confined to the optic nerve. Bilateral optic gliomas are more common in patients with NF1.

Macroscopically, an astrocytoma is a well-circumscribed mass that commonly has a large cyst and a focal mural nodule. The tumor may also be solid, with or without cystic degeneration. Microscopically, juvenile pilocytic astrocytoma demonstrates well-differentiated pilocytes with hairlike glial processes associated with microcysts that contain mucopolysaccharide material. The pilocytes are mixed with Rosenthal fibers , eosinophilic rod-shaped bodies, and granular eosinophilic bodies, which are commonly found in indolent neoplasms. Capillary formation is usually present.

Juvenile pilocytic astrocytomas are not graded histopathologically. The 4 morphologic criteria of the Daumas-Duport system — nuclear atypia, mitoses, endothelial proliferation, and necrosis — may sometimes be found in pilocytic astrocytomas, but they have no known prognostic significance.

Frequency

United States

Tumors of the optic pathway account for 3.6-6% of pediatric brain tumors, 60% of which are juvenile pilocytic astrocytomas. Astrocytomas account for 50% of pediatric primary central nervous system tumors. About 80-85% of cerebellar astrocytomas are juvenile pilocytic astrocytomas.

Mortality/Morbidity

Patients with juvenile pilocytic astrocytoma have a better prognosis than patients with most other types of astrocytomas. If gross total resection is possible, the 10-year survival rate is as high as 90%. After subtotal resection or biopsy, the 10-year survival rate is as high as 45%. Morbidity is related to the location of the tumor and to the associated complications of tumor resection.

Sex

The incidence of juvenile pilocytic astrocytomas is the same for males and females.

Age

The peak incidence is in patients 5-14 years of age. Age affects the clinical course of optic nerve gliomas. Of children younger than 5 years, the mortality rate is comparable to that of patients aged 5-20 years.^6,9,8

Anatomy

Juvenile pilocytic astrocytomas usually arise in the cerebellum, brainstem, hypothalamic region, or optic pathways, but they may occur in any area where astrocytes are present, including the cerebral hemispheres and spinal cord.

Presentation

The presenting signs and symptoms of juvenile pilocytic astrocytoma depend on the location of the tumor. The most common symptoms are the result of increased intracranial pressure, caused by a mass effect, or hydrocephalus. Such symptoms include nausea, vomiting, headache, ataxia, and visual effects.

Astrocytic tumors are categorized into pilocytic and ordinary subtypes. The ordinary subtypes include fibrillary, protoplasmic, and gemistocytic tumors. Ordinary astrocytomas are associated with a worse overall prognosis because of their more aggressive behavior and their potential to undergo malignant transformation.

The classic juvenile pilocytic astrocytoma arises in a cerebellar hemisphere; it is easily seen on CT scans and MRIs as a well-circumscribed lesion with an associated macrocyst. The nodular portion of the lesion usually demonstrates homogeneous contrast enhancement. Calcification is present in 10% of juvenile pilocytic astrocytomas. Other low-grade gliomas are typically hypoattenuating or hypointense, poorly defined, nonenhancing lesions on CT scans and MRIs.

Preferred Examination

The preferred examination is MRI (see Images 1-5).^10,11,12,13

Pilocytic astrocytomas are typically treated with surgery; MRIs are useful in outlining the contrast-enhancing tumor. The tumor should be completely resected whenever possible. Cyst wall enhancement may be seen on MRIs; when such enhancement is present, resection of the entire cyst is indicated.^{14,15,16,17,18}

Limitations of Techniques

Use of radiologic findings alone to identify low-grade gliomas results in an incorrect diagnosis in as many as 50% of cases.

Differential Diagnoses

Brain, Metastases
Medulloblastoma
Oligodendroglioma

Other Problems to Be Considered

Supratentorial juvenile pilocytic astrocytoma

Grade 2 astrocytoma
Oligodendroglioma
High-grade glioma
Ependymoma
Brain metastasis

Optic nerve and optic chiasm hypothalamic gliomas

Craniopharyngioma
Meningioma
Hamartoma
Germinoma
Histiocytosis
Sarcoidosis

Posterior fossa juvenile pilocytic astrocytoma

Grade 2 common astrocytoma
Oligodendroglioma
High-grade glioma
Ependymoma
Medulloblastoma
Brain metastasis

Computed Tomography

Findings

Supratentorial juvenile pilocytic astrocytomas

Juvenile pilocytic astrocytomas may occur anywhere in the central nervous system. On CT scans, these astrocytomas cannot be reliably differentiated from other more diffuse or aggressive tumors on the basis of imaging characteristics alone. CT may show hypoattenuating areas, isoattenuating areas, or both. Enhancement varies from none to extensive, with varying degrees of necrosis and cyst formation.

Supratentorial malignant glioma, ependymoma, and oligodendroglioma may have similar appearances. Lower-grade tumors tend to be homogeneous and well circumscribed. Peritumoral edema is mild, and no hemorrhage is present. Higher-grade tumors have more surrounding edema, are more heterogeneous in density, and may have areas of hemorrhage.

Optic nerve and optic chiasm hypothalamic juvenile pilocytic astrocytomas

A subset of astrocytic tumors occurs in patients with NF1. These tumors may involve the optic nerves, the optic chiasm, and the optic tracts. Most are juvenile pilocytic astrocytomas, but their imaging characteristics are not specific with regard to their histologic features. Varying degrees of cystic change and enhancement are demonstrated. These tumors may appear smooth, fusiform, eccentric, or lobulated. CT demonstrates the intraorbital optic nerves and is sensitive in the detection of the tumors. About 20% of juvenile pilocytic astrocytomas have microscopic calcifications; these calcifications are less frequently seen on CT scans than on other types of images.

Posterior fossa juvenile pilocytic astrocytomas

Among pediatric tumors of the posterior fossa, astrocytomas are second in frequency only to medulloblastoma. Approximately 75% of cerebellar astrocytomas are of the pilocytic type; imaging does not help in predicting their histologic features because fibrillary forms may have similar appearances.

Imaging characteristics are most typical for cerebellar tumors during the first decade of life. The typical presentation of a juvenile pilocytic astrocytoma is of a large cerebellar hemispheric or vermian mass that is predominantly cystic in a child younger than 10 years. Nonenhanced CT scans show hypoattenuation or isoattenuation. Tumor contrast enhancement is homogeneous or heterogeneous, depending on the extent of the cystic necrotic changes.

Degree of Confidence

See Findings above.

Magnetic Resonance Imaging

Findings

Supratentorial juvenile pilocytic astrocytomas

On T1-weighted images, the signal intensity is generally low; on T2-weighted images, the signal intensity is increased. Enhancement patterns are similar to those depicted on CT scans.

Optic nerve and optic chiasm hypothalamic juvenile pilocytic astrocytomas

Optic chiasm hypothalamic gliomas cannot be distinguished on the basis of their site of origin and are considered to be a single entity. On T1-weighted images, the signal intensity is low. On T2-weighted images, the signal intensity is generally increased. The increase in T2-weighted signal intensity may extend as far as the optic radiations, but such findings do not correlate directly with the presence of tumor. Enhancement is similar to that seen on CT scans. Use of fat-saturated T1-weighted postcontrast MRI of the intraorbital optic nerves is a sensitive method for demonstrating the tumor.

Posterior fossa juvenile pilocytic astrocytomas

The signal intensity is low with T1-weighted sequences and high with T2-weighted sequences. Enhancement patterns are similar to those seen on CT scans. MRI is less sensitive to calcium than is CT.

Vermian tumors are often associated with hydrocephalus. Three general tumor patterns are found:

1. Less than 10% are solid. These tumors may enhance in a homogeneous or a heterogeneous fashion.
2. Approximately 50% are simple cysts with a single mural nodule. On both CT scans and MRIs, the nodule enhances homogeneously, but the associated cyst wall usually does not. Likewise, no histologic evidence of tumor is present in the cyst wall. For this kind of tumor, removal of the mural nodule may be sufficient for treatment.
3. About 40-45% consist of multilocular cysts. These are actually necrotic tumors; they have a cystlike appearance. The periphery or cyst wall enhances. Histologic evidence of tumor is present in the cyst wall. Cure requires resection of the entire wall. Imaging shows clear-cut enhancement of the non-necrotic portions of the tumor.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. 

NSF/NFD has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Specific findings on MRI may be suggestive of juvenile pilocytic astrocytomas, but they are not diagnostic for this disease. Metastatic disease, neoplasm, and high-grade glioma cannot be excluded on the basis of radiographic findings. With regard to tumors of the posterior fossa, the most common possibilities in the differential diagnosis are medulloblastoma and ependymoma. Metastases are rare in childhood. Medulloblastomas are typically isoattenuating to hyperattenuating on nonenhanced CT scans.

Ependymomas may extend laterally or inferiorly to the foramina of Luschka or Magendie; extension is to the cerebellopontine angle or through the foramen magnum, respectively. They are isoattenuating to hyperattenuating on nonenhanced CT. About 50% of ependymomas exhibit small multifocal calcifications on CT scans. The major differential diagnostic consideration for optic chiasm/hypothalamic glioma is craniopharyngioma.

Angiography

Findings

Angiography is usually not useful in the diagnosis of juvenile pilocytic astrocytoma except to exclude an aneurysm in the presence of a suprasellar tumor mass.

Intervention

The primary therapy for juvenile pilocytic astrocytomas is complete surgical resection. In cerebellar lesions, gross total resection is possible in more than 70% of cases. With completely resected tumors, no adjuvant therapy is needed.

In patients in whom tumor resection is incomplete, the clinical course is often benign; postoperative stabilization of the disease is achieved, despite positive findings of tumor in surgical margins. For this reason, postoperative radiation therapy in these patients is controversial. Frequent follow-up with MRI is helpful.

To patients in whom a juvenile pilocytic astrocytoma that is limited to 1 orbit causes proptosis and significant visual loss, surgical resection is offered. Patients with NF1, those with tumors located in the posterior optic pathway, and those with juvenile pilocytic astrocytomas that do not appreciably affect vision are treated symptomatically. Shunts are placed to treat hydrocephalus. Endocrine dysfunction is treated as indicated. Patients with juvenile pilocytic astrocytomas in the posterior optic pathway who experience visual deterioration or progressive neurologic deficits but who do not have NF1 are treated surgically.

Multimedia

Media file 1: Juvenile pilocytic astrocytoma (JPA). Axial T1-weighted MRI without intravenous gadolinium contrast enhancement shows a cystic JPA in the right cerebellar hemisphere (same patient and tumor as in Images 2-3).

Media file 2: Juvenile pilocytic astrocytoma (JPA). Axial T2-weighted MRI shows a cystic JPA in the right cerebellar hemisphere. The fluid in the cyst has a higher signal intensity than that of the solid component. Peritumoral vasogenic edema is present. (Same patient and tumor as in Images 1 and 3.)

Media file 3: Juvenile pilocytic astrocytoma (JPA). Axial T1-weighted MRI obtained with intravenous gadolinium-based contrast agent shows a cystic JPA with an enhancing component in the cyst in the right cerebellar hemisphere (same patient and tumor as in Images 1-2).

Media file 4: Juvenile pilocytic astrocytoma (JPA). Sagittal T1-weighted MRI obtained with intravenous gadolinium-based contrast agent shows a JPA with enhancement in the hypothalamic area.

Media file 5: Juvenile pilocytic astrocytoma (JPA). Axial CT scan obtained with intravenous contrast material shows a contrast-enhancing JPA with cystic components in the cerebellum.

References

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17. Hirai T, Murakami R, Nakamura H, Kitajima M, Fukuoka H, Sasao A, et al. Prognostic Value of Perfusion MR Imaging of High-Grade Astrocytomas: Long-Term Follow-Up Study. AJNR Am J Neuroradiol. Jun 12 2008;[Medline].

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Keywords

juvenile pilocytic astrocytoma, astrocytoma, brain tumor, brain astrocytoma, JPA, astrocytic tumor, pilocytic astrocytoma, piloid tumors, astrocytoma WHO 1, cerebellar astrocytoma, low-grade astrocytoma, optic glioma, neurofibromatosis type 1, NF1, Daumas-Duport system

Contributor Information and Disclosures

Author

Simon Lo, MBBS, Assistant Professor, Department of Radiation Oncology, Indiana University School of Medicine
Simon Lo, MBBS is a member of the following medical societies: American College of Radiology, American Medical Association, American Society for Therapeutic Radiology and Oncology, and Radiological Society of North America
Disclosure: Nothing to disclose.

Coauthor(s)

Karl K Kish, MD, Chief, Section of Neuroradiology, Department of Radiology, Harper University Hospital
Karl K Kish, MD is a member of the following medical societies: Radiological Society of North America
Disclosure: Nothing to disclose.

Eric L Chang, MD, Assistant Professor, Department of Radiation Oncology, University of Texas MD Anderson Cancer Center
Eric L Chang, MD is a member of the following medical societies: American Society for Therapeutic Radiology and Oncology
Disclosure: Nothing to disclose.

Kenneth J Levin, MD, Assistant Professor, Karmanos Cancer Institute, Medical Advisor, Radiation Therapy Technology School, Department of Radiation Oncology, Wayne State University School of Medicine; Clinical Assistant Professor, Medical Laboratory Science, Oakland University School of Health Sciences; Medical Director, Department of Radiation Oncology, North Oakland lMedical Centers and Henry Ford Medical Center
Kenneth J Levin, MD is a member of the following medical societies: American Medical Association, American Society for Therapeutic Radiology and Oncology, Michigan State Medical Society, Oakland County Medical Society, and Society for Neuro-Oncology
Disclosure: Nothing to disclose.

Sameer R Keole, MD, Staff Physician, Department of Radiation Oncology, Gershenson Radiation Oncology Center, Karmanos Cancer Institute, Harper Hospital, Wayne State University School of Medicine
Sameer R Keole, MD is a member of the following medical societies: American Society for Therapeutic Radiology and Oncology
Disclosure: Nothing to disclose.

Andrew E Sloan, MD, Associate Professor of Neurosurgery and Radiation Oncology, Case Western Reserve University Medical School
Andrew E Sloan, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Neurological Surgeons, American College of Surgeons, American Society for Therapeutic Radiology and Oncology, and Congress of Neurological Surgeons
Disclosure: Nothing to disclose.

James Fontanesi, MD, Chairman, Department of Radiation Oncology, Cedars-Sinai Medical Center
James Fontanesi, MD is a member of the following medical societies: American Medical Group Association, American Radium Society, American Society for Therapeutic Radiology and Oncology, Children's Oncology Group, Radiological Society of North America, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Hugh J F Robertson, MD, DMR, FRCPC, FRCR, FACR, Professor Emeritus of Radiology, Professor of Clinical Radiology, Louisiana State University Health Sciences Center, New Orleans; Clinical Professor of Radiology, Tulane University School of Medicine; Active Staff, Department of Radiology, University Hospital
Hugh J F Robertson, MD, DMR, FRCPC, FRCR, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Neuroradiology, American Society of Spine Radiology, Louisiana State Medical Society, Orleans Parish Medical Society, Radiological Society of North America, Royal College of Physicians and Surgeons of Canada, Royal College of Radiologists, and Royal Society of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences
James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, American Society of Head and Neck Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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