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Brain Tumor, Pediatric


Basics


Description


A primary neoplasm arising in the CNS  

Epidemiology


  • Most common solid neoplasm of childhood (2nd to leukemia in overall incidence)
  • Slight male predominance
  • Majority arise infratentorially (within cerebellum or brainstem) in children 1-11 years of age.
  • Majority arise supratentorially in children <1 year of age.

Incidence
  • Incidence rising (>3,000 new cases/year)
  • 4.5 cases/100,000 children/year
  • Peak incidence in children ≤7 years of age

Risk Factors


Genetics
  • Not a heritable condition
  • Primary CNS tumors are associated with several familial syndromes:
    • Neurofibromatosis with optic pathway gliomas (NF1) and meningiomas (NF2)
    • Tuberous sclerosis with gliomas and rarely ependymomas
    • Li-Fraumeni syndrome with astrocytomas
    • Von Hippel-Lindau with cerebellar hemangioblastoma
    • Turcot syndrome with primitive neuroectodermal tumor

Pathophysiology


The majority of tumors are classified based on their histology. The most common are the following:  
  • Glioma
    • Arises from glial cells (e.g., astrocytes most common)
    • >50% of childhood CNS tumors
    • Ranges from low-grade (often in the cerebellum or optic pathway) to high-grade (grade III-IV; in the cerebrum or brainstem)
    • Locally recurrent and invasive when high-grade
  • Primitive neuroectodermal tumor/medulloblastoma
    • Malignant embryonal tumor arising from unknown cell type
    • Comprises ~20% of childhood CNS tumors
    • Most common malignant brain tumor in children
    • Majority arise in the midline of the cerebellum (referred to as medulloblastoma).
    • Predisposition for leptomeningeal dissemination
  • Ependymoma
    • Arises from ependymal cells that line the ventricular system
    • 8-10% of childhood CNS tumors
    • Most commonly occurs in the 4th ventricle; may arise in the spinal cord
    • Locally recurrent and invasive; spinal metastases rare at initial diagnosis
  • Germ cell tumor
    • Derived from totipotent germ cells
    • 3-5% of childhood CNS tumors
    • Majority are located in the pineal or suprasellar region.
  • Atypical teratoid/rhabdoid tumor
    • Rare embryonal tumor arising from unknown cell type; often misdiagnosed as primitive neuroectodermal tumor
    • <3% of childhood CNS tumors
    • Majority arise in children <5 years of age.
    • Propensity to arise in the posterior fossa with frequent leptomeningeal dissemination; reported in association with malignant rhabdoid tumors of the kidney
  • Craniopharyngioma: 6-9% of childhood CNS tumors
  • Choroid plexus tumors (papilloma and carcinoma)
  • Ganglioglioma
  • Meningioma and hemangioblastoma, rare in children

Etiology


  • No specific causative agents are known, but there is an association with radiation, chemical exposure, other malignancies, familial/heritable diseases, immunosuppression/immunodeficiency (CNS lymphoma).
  • Molecular markers and variants of individual tumor types are being identified.

Diagnosis


Tumor location dictates symptoms and signs.  

History


  • Headache and vomiting (particularly in the morning), irritability, and lethargy are associated with increased intracranial pressure.
  • Difficulty swallowing, slurred speech, and diplopia may indicate brainstem tumor.
  • Visual field deficits (bumps into things) could indicate optic pathway lesion.
  • Focal weakness hints at pyramidal tract lesion.
  • Ataxia may be a sign of cerebellar lesion.
  • Changes in behavior or school performance, new-onset seizures, and weakness could be signs of supratentorial lesion.
  • Polyuria/polydipsia may indicate hypothalamic/pituitary lesion.
  • Failure to thrive, emaciation, euphoria, and increased appetite in an infant may indicate hypothalamic lesion (diencephalic syndrome).
  • Back pain, extremity weakness, and bowel/bladder dysfunction could signify spinal cord metastases (often seen with primitive neuroectodermal tumor/medulloblastoma and germ cell tumors).

Physical Exam


  • Papilledema, impaired upgaze and/or lateral gaze, macrocephaly (infants), and bulging fontanelle are signs of increased intracranial pressure.
  • Focal deficit on neurologic exam helps localize the mass lesion:
    • Isolated cranial nerve VI and VII palsies may indicate brainstem tumor.
    • Ataxia and dysmetria could indicate cerebellar mass.
    • Decreased visual acuity, visual field deficit, absent pupillary light response, and strabismus may all be signs of optic pathway tumor.
    • Changes in cognitive function, mood, and affect could indicate supratentorial lesion.
    • Impaired upgaze, convergence nystagmus, and pupils responding to accommodation but poorly to light are signs of pineal lesion (Parinaud or dorsal midbrain syndrome).
  • Signs of neurocutaneous disease (e.g., caf © au lait spots, Lisch nodules) may indicate a syndrome such as neurofibromatosis type 1.

Diagnostic Tests & Interpretation


Imaging
  • MRI with and without gadolinium enhancement is the "gold standard"ť for identification, localization, and characterization of tumors.
  • CT can be used as an initial study, but if negative and a high index of suspicion, follow with MRI. Useful to evaluate for hydrocephalus and hemorrhage

Diagnostic Procedures/Other
Staging of tumor  
  • Postoperative head MRI within 24-48 hours to determine residual disease before postoperative inflammatory changes are prominent
  • Spine MRI and CSF cytology required for neuraxis staging of tumors with high risk of leptomeningeal dissemination
  • Elevated α-fetoprotein and quantitative β-human chorionic gonadotropin in CSF and serum are markers for germ cell tumors.

Differential Diagnosis


  • Infection: cerebral abscess
  • Tumors: metastatic tumor to brain, uncommon with childhood cancers
  • Trauma: hemorrhage unlikely to be confused with tumor
  • Congenital
    • Arteriovenous malformation
    • Hamartoma
    • Dysplastic brain
  • Psychosocial: Some patients with nausea, vomiting, or behavior changes are first diagnosed with psychiatric disorders, GI disorders, failure to thrive, or anorexia nervosa prior to discovery of a brain tumor.

Alert
New onset of psychoses should prompt imaging to rule out tumor.  

Treatment


Surgery/Other Procedures


  • Both for histology and to attempt maximal tumor debulking; should be performed by experienced pediatric neurosurgeon
  • Rarely indicated in intrinsic pontine (brainstem) glioma; although biopsy for molecular profiling increasingly in use
  • Ventriculoperitoneal shunt or endoscopic 3rd ventriculostomy when needed for obstructive hydrocephalus (risk of peritoneal seeding minimal)

Alert
Patient should be referred to a pediatric brain tumor/oncology center at diagnosis (preoperatively).  
Radiotherapy
  • Volume and dose vary depending on histology.
  • Radiation therapy to the tumor bed is used for most patients with brain tumors.
  • Medulloblastoma/primitive neuroectodermal tumor patients need craniospinal radiation therapy. The one exception is infants and young children (<3 years of age) in whom cognitive deficits from radiation therapy are devastating.
  • Duration of radiation therapy: usually 6 weeks
  • Newer approaches to limit exposure of normal brain include intensity-modulated and proton radiotherapy.

Medication


  • Dexamethasone to control increased intracranial pressure (0.5 mg/kg/24 h IV/PO divided q6h)
  • Chemotherapy
    • Drugs are most often used in combination:
      • Carboplatin, vincristine, or 6-thioguanine, procarbazine, CCNU, vincristine for low-grade glioma
      • Cisplatin, CCNU, vincristine, etoposide, and cyclophosphamide are active agents for primitive neuroectodermal tumor/medulloblastoma.
      • Temozolomide for high-grade glioma
    • New protocols currently being evaluated:
      • High-dose chemotherapy with autologous stem cell rescue for high-risk primitive neuroectodermal tumor/medulloblastoma
      • Targeted therapies, angiogenesis inhibitors
    • Duration of chemotherapy: 6 months to 2 years

Alert
Possible conflict with other treatments: Chemotherapy can alter anticonvulsant levels.  

Ongoing Care


  • Neurologic deficits can take months to improve or stabilize with permanent deficit.
  • Any worsening or relapse of symptoms must be evaluated for tumor recurrence.
  • MRI every 3 months the 1st year, every 6 months for the next 2 years, and annually thereafter. Benefit of routine surveillance imaging is controversial.

Prognosis


  • Dependent on histology of tumor, location, and extent of initial resection
  • Glioma
    • Low-grade: ≥90% 5-year progression-free survival (PFS) following gross total resection; 45-65% for subtotal resection
    • High-grade: median survival 8-31 months; depends on grade and extent of resection
    • Intrinsic pontine: median overall survival of 9-13 months from diagnosis
  • Medulloblastoma
    • 79-83% PFS at 5 years if localized, gross total resection achieved, and >3 years old at diagnosis
    • <50% PFS if disseminated
  • Ependymoma
    • 50-70% survival at 5 years with total resection
    • <30% survival with subtotal resection
  • Infants overall have a worse prognosis, possibly due to the limitations of therapy and/or the aggressiveness of the tumor.

Alert
Even benign tumors may be life threatening if their location precludes resection.  

Complications


  • Secondary to disease
    • Increased intracranial pressure
      • Obstruction of CSF flow
      • Requires immediate neurosurgical evaluation
  • Secondary to radiotherapy
    • Neurocognitive sequelae (age- and dose-related)
    • Endocrinopathy (growth hormone deficiency, hypothyroidism, gonadal dysfunction)
    • Risk of second malignancies (meningioma, glioma, sarcoma)
    • Increased risk of stroke
  • Secondary to chemotherapy
    • Risks associated with bone marrow suppression (infection, bleeding, anemia)
    • Hearing loss
    • Risk of secondary leukemia

Additional Reading


  • Abdullah  S, Qaddoumi  I, Bouffet  E. Advances in the management of pediatric central nervous system tumors. Ann N Y Acad Sci.  2008;1138:22-31.  [View Abstract]
  • Blaney  SM, Haas-Kogan  D, Poussaint  TY, et al. Gliomas, ependymomas, and other nonembryonal tumors. In: Pizzo  PA, Poplack  DG, eds. Principles and Practice of Pediatric Oncology. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2010:717-824.
  • Ostrom  QT, Gittleman  H, Liao  P, et al. CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2007-2011. Neuro Oncol.  2014;16(Suppl 4):iv1-iv63.  [View Abstract]
  • Packer  RJ. Brain tumors in children. Arch Neurol.  1999;56(4):421-425.  [View Abstract]
  • Phillips  PC, Grotzer  MA. Brain tumors in children. In: Asbury  AK, McKhann  GM, McDonald  WI, et al, eds. Diseases of the Nervous System: Clinical Neuroscience and Therapeutic Principles. 3rd ed. Cambridge, United Kingdom: Cambridge University Press; 2002:1448-1461.
  • Sievert  AJ, Fisher  MJ. Pediatric low-grade gliomas. J Child Neurol.  2009;24(11):1397-1408.  [View Abstract]

Codes


ICD09


  • 239.6 Neoplasm of unspecified nature of brain
  • 191.9 Malignant neoplasm of brain, unspecified
  • 225.0 Benign neoplasm of brain
  • 225.2 Benign neoplasm of cerebral meninges

ICD10


  • D49.6 Neoplasm of unspecified behavior of brain
  • C71.9 Malignant neoplasm of brain, unspecified
  • D33.2 Benign neoplasm of brain, unspecified
  • D32.9 Benign neoplasm of meninges, unspecified

SNOMED


  • 126952004 Neoplasm of brain (disorder)
  • 428061005 malignant neoplasm of brain (disorder)
  • 92030004 benign neoplasm of brain (disorder)
  • 126960003 Neoplasm of cerebellum (disorder)
  • 302820008 Intracranial meningioma
  • 126961004 Neoplasm of brain stem (disorder)

FAQ


  • Q: Are my other children at risk for getting a brain tumor?
  • A: No (except in rare cases of certain familial syndromes).
  • Q: Did something I do caused this?
  • A: No. In addition, the claims made about high-power lines and cellular phones causing brain tumors or cancer are unproven.
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