eMedicine Specialties > Pediatrics: General Medicine > Oncology

Medulloblastoma: Treatment & Medication

Author: Tobey MacDonald, MD, Clinical Director of Neuro-Oncology, Children's Hospital National Medical Center; Associate Professor, Department of Pediatric Hematology-Oncology, George Washington University
Coauthor(s): Roger J Packer, MD, Executive Director, Neuroscience and Behavioral Medicine, Director, Brain Tumor Institute, Children's National Medical Center; Professor of Neurology and Pediatrics, The George Washington University
Contributor Information and Disclosures

Updated: Feb 12, 2009

Treatment

Medical Care

Standard therapy for medulloblastoma consists of aggressive surgery followed by radiation to the entire craniospinal axis with boost to both the primary tumor site and focal CNS metastatic sites. Recently, adjuvant chemotherapy has also been shown to be beneficial.

  • Radiation therapy
    • Average-risk disease
      • Reducing the amount of craniospinal radiation in an attempt to decrease morbidity without jeopardizing survival appears to be successful in this group. In a report by the International Society of Pediatric Oncology, children with average-risk medulloblastoma randomly received either the standard 36 Gy or a reduced dose of 24 Gy to the neuraxis.3 It was found that no statistical difference in progression-free survival rates was demonstrated between the groups as long as the initiation of radiotherapy was not delayed by the administration of chemotherapy before radiation.
      • The dose for average-risk medulloblastoma patients enrolled on Children's Oncology Group (COG) last completed trial was 23.4 Gy to the craniospinal axis followed by 32.4 Gy boost directly to the primary tumor site.4 In both the poor-risk and average-risk groups, the total radiation dose to sites of known disease is 55.8 Gy. An ongoing study is investigating further reduction of the craniospinal dose to 18 Gy in a subset of children with average-risk disease.
    • Poor-risk disease
      • The current recommendation is 36 Gy to the craniospinal axis, followed by a boost of 19.8 Gy to the primary tumor site and an additional 19.8 Gy to focal metastatic sites. The amount of boost that can be given is limited by the presence of the optic nerves within the radiation field or if more than two thirds of the supratentorial compartment volume is within the radiation field.
      • Spinal disease that is visible after 30.6 Gy of the prescribed 36 Gy to the craniospinal axis receives an additional boost up to a total of 45 Gy if the tumor is located above the termination of the spinal cord and as much as 50.4 Gy if the tumor is located below the termination of the cord.
    • Infants
      • Radiotherapy for patients younger than 3 years, the poorest risk group, remains controversial. Because the effects of radiotherapy on intellectual development are most severe in this age group, attempts have been made to delay or omit radiation by using chemotherapy. However, in the most recent COG study, infants receiving chemotherapy alone had a 29% 3-year progression-free survival rate for those without dissemination and only 11% for those with metastasis. The Pediatric Oncology Group (POG) reported that, in infants with medulloblastoma treated initially with chemotherapy followed by delayed radiation, the 2-year progression-free survival rate was 34%.5
      • Trials are currently underway to avoid or delay radiotherapy in this population by using cycles of high-dose chemotherapy followed by autologous stem cell rescue. Initial reports have indicated a good response rate to chemotherapy, and, although overall survival (30-40%) is comparable to prior studies, most patients who survived in the latest trials did not receive radiotherapy. Infants with desmoplastic tumor treated with chemotherapy fare better than those with classic tumors because 70% or more can be successfully treated without radiotherapy.
  • Chemotherapy
    • Average-risk disease
      • The most encouraging results with adjuvant chemotherapy have been reported in children with nondisseminated medulloblastoma receiving 8 cycles of lomustine (CCNU), vincristine, and cisplatin chemotherapy for approximately 1 year following conventional dose radiotherapy and concomitant vincristine.
      • Latest trials indicate that children aged 3-10 years who received this regimen with reduced-dose craniospinal radiation have a superior survival rate compared to those who received standard radiation alone. The current 3-year progression-free survival rate for those receiving adjuvant chemotherapy is approximately 80%.
    • Poor-risk disease
      • Chemotherapeutic agents that have been found to be most effective for this disease are cisplatin, carboplatin, cyclophosphamide, and vincristine.
      • To improve survival rates in this group, current trials are investigating the use of high-dose chemotherapy (most commonly using carboplatinum and thiotepa-containing regimens) and autologous stem cell rescue after a course of conventional craniospinal radiotherapy and chemotherapy.
      • Studies using chemotherapy (carboplatin and vincristine) concurrent with radiotherapy are also underway.
      • Retinoic acid as a maturation agent following radiation is under investigation in a randomized trial.
    • Infants
      • In children younger than 3 years, evidence suggests that some do respond, at least partially, to chemotherapy. In patients with minimal residual postoperative disease, this response may be long-lasting.
      • Ongoing trials are investigating high-dose chemotherapy (carboplatin and thiotepa) and stem cell rescue, following induction with chemotherapeutic agents similar to those used in the treatment for older children with poor-risk disease. Whether radiotherapy can be safely delayed or omitted altogether in certain subgroups has not yet been determined.
      • Methotrexate, both intrathecally and intravenously, is being added to more conventional chemotherapy in some studies; primarily for infants with partially resected and/or disseminated tumors.
    • Relapsed disease: Current studies investigating the use of biologic agents that specifically target the most common molecular alterations described in this disease, such as tyrosine kinase inhibitors that block the function of EBB2, are ongoing.

Surgical Care

  • Suboccipital craniotomy
    • Because the tumor is often friable, gentle suction is used. Microdissection is used to remove adherent portions.
    • Modern neurosurgical techniques permit complete or near-complete resection with little or no significant increase in morbidity and mortality rates compared with more conservative surgery.
    • Because surgical estimates of the extent of resection may not be reliable, postoperative MRI evaluation for residual disease is required within several days of the procedure.
    • As many as 40% of patients have some degree of new neurologic dysfunction postoperatively. One ill-defined syndrome is posterior fossa syndrome, characterized by mutism, cerebellar dysfunction, supranuclear cranial nerve palsy, and hemiparesis that occurs 12-48 hours after surgery. As many as 50% of patients have residual deficits.
  • Ventriculoperitoneal shunt: Approximately 50% of patients require placement of a ventriculoperitoneal shunt at the time of operation (or shortly thereafter) because of unresolving obstructive hydrocephaly. Third ventriculostomy is increasingly used to avoid the placement of a permanent ventricular shunt.

Consultations

  • As a direct result of the tumor and/or therapy, many patients are referred to occupational, physical, hearing, and speech therapists for rehabilitation of common neurologic dysfunction. Neurophthalmologists may also be consulted after successful treatment to evaluate persistent gaze palsies that may effect visual development.
  • Team members for the care of all patients should include specialists from each of the following:
    • Neurosurgery
    • Pediatric oncology and/or neuro-oncology
    • Radiation oncology
    • Neurology
    • Neuropsychology
    • Endocrinology

Diet

  • No specific dietary restrictions or requirements are indicated.
  • Patients who develop severe anorexia or weight loss as a result of therapy may need supplemental nutrition to maintain daily requirements. Most patients can tolerate enteral supplementation, but some may need parenteral support.

Activity

  • Most patients have no restrictions on activity other than limitations from neurologic deficits caused by the tumor and treatment.
  • Patients with ventriculoperitoneal shunts may be restricted from performing high-impact sports (eg, diving).
  • School performance needs to be carefully monitored, as most children, especially those younger than 7 years at diagnosis, require added support at school.

Medication

Chemotherapeutic agents are continually evolving. Historically, the most active drugs have been DNA alkylators. These agents cause DNA damage and disrupt DNA replication. The agents with the longest clinical history in the treatment of medulloblastoma are vincristine, lomustine (CCNU), and cisplatin.

Antineoplastic agents

These agents disrupt DNA replication, which inhibits tumor growth and promotes tumor cell death.


Vincristine (Oncovin)

Plant-derived vinca alkaloid used during radiotherapy and in combination with other chemotherapeutic agents. Acts as a mitotic inhibitor by binding tubulin.

Adult

Pediatric

<10 kg or BSA <1 m2: 0.05 mg/kg/dose IV push; not to exceed 2 mg/dose
>10 kg or BSA >1 m2: 1-1.5 mg/m2/dose IV push; not to exceed 2 mg/dose

Acute pulmonary reaction may occur when taken concurrently with mitomycin-C; asparaginase, CYP450 3A4 inhibitors (eg, itraconazole, quinupristin/dalfopristin, sertraline, ritonavir), GM-CSF (eg, sargramostim, filgrastim), or nifedipine increase toxicity; CYP450 3A4 inducers (eg, carbamazepine, phenytoin, phenobarbital, rifampin) may decrease effects

Documented hypersensitivity; demyelinating form of Charcot-Marie-Tooth syndrome, universally fatal if delivered intrathecally

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Dosage modification required with impaired hepatic function, coadministration with other neurotoxic drugs, or preexisting neuromuscular disease; use extravasation precautions; caution in severe cardiopulmonary disease


Lomustine (CeeNU)

DNA alkylator used in combination with other chemotherapeutic agents. Causes interstrand and intrastrand DNA-DNA crosslinks resulting in damage to the DNA template and inhibition of DNA replication.

Adult

Pediatric

75-150 mg/m2/dose PO initially; adjust subsequent doses according to platelet and leukocyte count

Coadministration with cimetidine decreases effect; increased toxicity when coadministered with phenobarbital

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use with caution in patients with depressed platelet, leukocyte, or erythrocyte counts, adjust dose accordingly; advise patient to administer on empty stomach with fluids, do not eat or drink for 2 h following dose


Cisplatin (Platinol)

A heavy metal coordination complex that exerts its cytotoxic effect by platination of DNA. A mechanism analogous to alkylation, leading to interstrand and intrastrand DNA crosslinks and inhibition of DNA replication. Used in combination with other chemotherapeutic agents.

Adult

Pediatric

50-100 mg/m2/dose IV infusion; usually administered over 6 h for intermittent dosing q21-28d

Coadministration with aminoglycosides or amphotericin B causes increased risk of nephrotoxicity; coadministration with loop diuretics or aminoglycosides may potentiate ototoxicity

Documented hypersensitivity; hypersensitivity to cisplatin or platinum-containing agents; preexisting renal impairment; hearing impairment; myelosuppression

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Adequately hydrate before and for 24 hours after administration with a sodium chloride–containing solution to promote chloruresis, may administer mannitol and/or furosemide to ensure good urine output and decrease the chance of nephrotoxicity; reduce dosage in renal impairment and in infants; myelosuppression, ototoxicity, nausea and vomiting, may occur

More on Medulloblastoma

Overview: Medulloblastoma
Differential Diagnoses & Workup: Medulloblastoma
Treatment & Medication: Medulloblastoma
Follow-up: Medulloblastoma
Multimedia: Medulloblastoma
References
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References

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Further Reading

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Keywords

medulloblastoma, posterior fossa primitive neuroectodermal tumor, PNET, brain tumor, hypertension, bradycardia, hypoventilation, Cushing triad, facial weakness, tinnitus, hearing loss, head tilt, papilledema, optic pallor, stiff neck, gaze palsy, Turcot syndrome, ataxia-telangiectasia, Gorlin syndrome, nevoid basal cell carcinoma syndrome

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Contributor Information and Disclosures

Author

Tobey MacDonald, MD, Clinical Director of Neuro-Oncology, Children's Hospital National Medical Center; Associate Professor, Department of Pediatric Hematology-Oncology, George Washington University
Tobey MacDonald, MD is a member of the following medical societies: American Association for Cancer Research, Children's Oncology Group, Pediatric Brain Tumor Consortium, and Society for Neuro-Oncology
Disclosure: Nothing to disclose.

Coauthor(s)

Roger J Packer, MD, Executive Director, Neuroscience and Behavioral Medicine, Director, Brain Tumor Institute, Children's National Medical Center; Professor of Neurology and Pediatrics, The George Washington University
Roger J Packer, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Pediatric Society, Child Neurology Society, Children's Oncology Group, Neurofibromatosis Clinical Trials Consortium, Pediatric Brain Tumor Consortium, and Society for Neuro-Oncology
Disclosure: Nothing to disclose.

Medical Editor

Kathleen M Sakamoto, MD, PhD, Professor and Chief, Division of Hematology-Oncology, Vice-Chair of Research, Mattel Children's Hospital at UCLA; Department of Pathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA and California Nanosystems Institute and Molecular Biology, UCLA
Kathleen M Sakamoto, MD, PhD is a member of the following medical societies: American Society of Hematology, American Society of Pediatric Hematology/Oncology, New York Academy of Sciences, Society for Pediatric Research, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Steven K Bergstrom, MD, Assistant to the Chairman, Department of Pediatrics, Division of Hematology-Oncology, Kaiser Permanente Medical Center of Oakland
Steven K Bergstrom, MD is a member of the following medical societies: Alpha Omega Alpha, American Society of Clinical Oncology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, and International Society for Experimental Hematology
Disclosure: Nothing to disclose.

CME Editor

Samuel Gross, MD, Professor Emeritus, Department of Pediatrics, University of Florida; Clinical Professor, Department of Pediatrics, University of North Carolina; Adjunct Professor, Department of Pediatrics, Duke University
Samuel Gross, MD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Clinical Oncology, American Society of Hematology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Max J Coppes, MD, PhD, MBA, Executive Director, Center for Cancer and Blood Disorders, Children's National Medical Center; Professor of Medicine, Oncology, and Pediatrics, Georgetown University
Max J Coppes, MD, PhD, MBA is a member of the following medical societies: American Association for Cancer Research, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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