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Medulloblastoma Workup

  • Author: George I Jallo, MD; Chief Editor: Amy Kao, MD  more...
 
Updated: Oct 16, 2014
 

Laboratory Studies

No specific biochemical test exists for the presence of medulloblastoma, although several molecular studies have revealed that histologically identical medulloblastomas are composed of distinct subgroups with different prognosis. The expression of ErbB2 has been shown to be a negative predictor of outcome. Conversely, expression of TrkC or neurotophin-3 receptor is associated with a favorable outcome. However, these markers are not standard testing at this time.

Molecular markers such as chromosome 10q and chromosome 17 statuses can be used for molecular risk stratification of adult medulloblastoma, but only in a subgroup-specific context

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Imaging Studies

See the list below:

  • Computed tomographic scan
    • Because most patients present with headache, a noncontrast head CT scan usually is performed because of its easy availability. These tumors typically are located midline in the cerebellum and extend into and fill the fourth ventricle.
    • Prior to administration of intravenous (IV) contrast, the tumor is hyperdense to the brain as a result of its high cellularity as shown below. Preoperatively, high density on CT scan can help distinguish medulloblastoma from the hypodense appearance of a cerebellar astrocytoma. Medulloblastoma shows marked contrast enhancement. Surrounding hypodensity is indicative of vasogenic edema. Owing to compression of the fourth ventricle and outflow of CSF, marked hydrocephalus is the rule.
      CT scan demonstrates a hyperdense lesion within thCT scan demonstrates a hyperdense lesion within the posterior fossa of an 8-year-old boy who presented with nausea and vomiting.
    • Ependymoma is another hyperdense tumor that affects the posterior fossa of children. Unlike medulloblastoma, however, it often contains calcifications that can be recognized easily on CT scan. Choroid plexus papilloma usually arises in the trigone of the lateral ventricle in children; however, in adults it is most common in the fourth ventricle. Similar to ependymoma, choroid plexus papilloma commonly contains calcifications.
  • Magnetic resonance imaging
    • MRI with the administration of gadolinium DTPA is the diagnostic test of choice for medulloblastoma. Unlike CT scan, MRI can obtain multiplanar views without significant bony artifact in the posterior fossa.
    • Nevertheless, with any increased intracranial pressure, MRI of children must be considered carefully. Younger children usually require sedation for this study. Without careful monitoring, cerebral carbon dioxide levels may increase, further aggravating intracranial hypertension.
    • Tumor appears hypointense on pre-gadolinium T1-weighted images, usually seen expanding the fourth ventricle from its origin in the cerebellar vermis as depicted in the following images. Brain stem is compressed and shifted ventrally.
      T1-weighted sagittal MRI of an 8-year-old boy who T1-weighted sagittal MRI of an 8-year-old boy who presented with nausea and vomiting reveals an enhancing tumor within the fourth ventricle. The child underwent a suboccipital craniotomy and resection of his medulloblastoma.
      T1-weighted sagittal MRI of 4-year-old boy who preT1-weighted sagittal MRI of 4-year-old boy who presented with gait ataxia and precocious puberty. MRI shows a heterogenous enhancing tumor located within the fourth ventricle with marked hydrocephalus.
      T1-weighted axial MRI shows heterogeneous enhancemT1-weighted axial MRI shows heterogeneous enhancement of the medulloblastoma in a 4-year-old boy who presented with gait ataxia and precocious puberty.
      Coronal MRI confirms the presence of the tumor witCoronal MRI confirms the presence of the tumor within the fourth ventricle of a 4-year-old boy who presented with gait ataxia and precocious puberty.
    • Upon administration of gadolinium in children, homogeneous enhancement commonly occurs, whereas in adults, a more heterogeneous pattern usually is seen. Proton density and T2-weighted imaging displays a hyperintense mass with a surrounding area of edema.
    • If the tumor extends upward into the cerebral aqueduct and third ventricle, marked hydrocephalus with transependymal reabsorption of CSF may occur. Extension also can be inferior into the cervical canal.
    • Occasional areas of hemorrhage or cyst can be distinguished. Because calcifications are very rare, any area of signal loss must be considered a vascular flow void.
    • MRI can help differentiate medulloblastoma from ependymoma: the latter extends further into the lateral recess of the fourth ventricle or even further into the cerebellopontine angle.
    • MRI also can help distinguish between medulloblastoma and exophytic brainstem glioma (the latter having a broader attachment to the floor of the fourth ventricle).
    • Adults, more frequently than children, can have the desmoplastic variant of medulloblastoma. This form of the tumor is situated laterally in the hemisphere with indistinct borders and small cystic or necrotic areas.
    • Besides identifying the primary lesion, MRI is beneficial in detecting metastatic lesions. To rule out drop metastases, MRI of the spine is obligatory when medulloblastoma is either considered or diagnosed.
    • Imaging of the spine is best performed prior to surgery in order to avoid postoperative artifacts, which may be interpreted as tumor metastasis. Metastases can occur in the basal cisterns. Both recurrent lesions and metastases show sparse enhancement.
  • Myelography
    • In the past, myelography was the standard diagnostic test for medulloblastoma metastases to the spine.
    • Today, when MRI is contraindicated, myelography is utilized, accompanied by CT scan.
  • Skeletal imaging
    • Metastasis to the bone must be considered in any child with medulloblastoma and bone pain.
    • A skeletal survey helps elucidate lytic or sclerotic lesions.
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Other Tests

See the list below:

  • Cerebrospinal fluid
    • Cytology of CSF is important for the staging of medulloblastoma; however, no standardized method has been agreed upon for how and when to obtain CSF.
    • Lumbar puncture is the most common method for obtaining CSF; however, this can precipitate cerebellar tonsillar herniation (coning) in a patient with increased intracranial pressure.
    • Although safer, lumbar puncture performed shortly after surgery can have misleading results; the fluid may contain clinically insignificant cells that have been disturbed during surgery. This may be performed 2 weeks following surgery.
    • If a ventricular drain is placed, it can be used to obtain CSF for cytologic testing; however, ventricular samples of CSF will contain malignant cells less commonly than a sample obtained from the thecal sac.
    • Some authors suggest obtaining CSF at the time of surgery from the cisterna magna for cytologic analysis.
  • Tumor genetics
    • To date, use of cytogenetic studies has been controversial.
    • Some original reports found a correlation between aneuploid DNA content and a better prognosis. Interestingly, DNA content of most medulloblastoma cells is diploid, signifying a poorer outcome. More recent studies, however, have failed to reproduce this relationship between ploidy and outcome.
    • The most common genetic abnormality found in medulloblastoma, 17qi, is an isochromosome on the long arm of chromosome 17. Found in one third to two thirds of medulloblastomas, it is common in other tumors, including leukemias.
    • Accompanying the isochromosome 17qi is the loss of genetic material from the short arm of chromosome 17, where the tumor-suppressor gene p53 is located.
    • Studies have shown that loss or damage to the p53 site is rare in medulloblastoma. Theories now implicate another focus on the short arm of chromosome 17, which is either a tumor-suppressor gene in itself or a modulator for the function of p53.
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Procedures

See the list below:

  • Lumbar puncture: To obtain CSF, a lumbar puncture may be necessary. Consider this very carefully since obstructive hydrocephalus, common in medulloblastoma, is an absolute contraindication.
  • Ventriculostomy: If the patient is symptomatic from obstructive hydrocephalus, placement of an external ventricular drain may be a lifesaving procedure. Some centers also advocate an endoscopic third ventriculostomy to bypass the obstruction. This may also obviate the need for a shunt in the future following surgical removal of the tumor.
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Histologic Findings

See the list below:

  • Upon gross examination, medulloblastoma appears as a pinkish-gray mass usually arising from the cerebellar vermis in children. Cysts, areas of necrosis, or calcification are rare.
  • On microscopic examination, cells are small and poorly differentiated, with scant cytoplasm and little stroma (see the image below). A high mitotic index is common. Classic Homer-Wright rosettes can be seen in one fifth of cases. Elongated cells surrounding eosinophilic circular zones devoid of lamina and blood vessels form these pseudorosettes. Differentiation can be seen along astrocytic, neuronal, ependymal, or even mesenchymal lines.
    High-power magnification hematoxylin and eosin (H&High-power magnification hematoxylin and eosin (H&E) section of a typical medulloblastoma
  • Rorke classified this tumor with other primitive neuroectodermal tumors, which include pineoblastoma, ependymoblastoma, retinoblastoma, central neuroblastoma, and peripheral neuroblastoma.[3] This classification system is not accepted universally.
  • Desmoplastic medulloblastoma is a variant more often seen in adults and more common in the cerebellar hemisphere. In addition to containing all microscopic characteristics of childhood medulloblastoma, the desmoplastic type contains a dense reticulin network; cells are arranged in a biphasic pattern with areas of high and low cellularity. Cells in this variant may assemble along reticulin fibers.
  • Histologic subtypes
    • Three other histologic subtypes exist: Medullomyoblastoma, melanotic medulloblastoma, and large cell medulloblastoma.
      • Medullomyoblastoma: Striated and smooth muscle cells are the hallmark of medullomyoblastoma. The tumor can contain cells that show elements of neuronal and glial differentiation. If the presumptive medullomyoblastoma contains elements of ectodermal, mesodermal, and endodermal differentiation, the tumor must be considered a teratoma.
      • Melanotic medulloblastoma: Small, undifferentiated cells containing melanin are characteristic of the very rare melanotic medulloblastoma.
      • Large-cell medulloblastoma: This subtype has large vesicular nuclei with prominent nucleoli. Cells of the large-cell medulloblastoma are remarkable in their immunoreactivity for synaptophysin. This particular tumor is associated with a poorer clinical outcome.
    • Although large-cell medulloblastoma is associated with a more aggressive course, medullomyoblastoma has a clinical course similar to that of ordinary medulloblastoma. However, the desmoplastic variant has a more favorable outcome.
  • Aside from these findings, associating histologic findings with outcome has been very difficult. As in other tumors, vascularity and endothelial hyperplasia do not seem to influence recurrence rates. In some studies, however, the presence of necrosis (or a high mitotic index) has been associated with a shorter relapse-free interval.
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Contributor Information and Disclosures
Author

George I Jallo, MD Professor of Neurosurgery, Pediatrics, and Oncology, Director, Clinical Pediatric Neurosurgery, Department of Neurosurgery, Johns Hopkins University School of Medicine

George I Jallo, MD is a member of the following medical societies: American Association of Neurological Surgeons, American Medical Association, American Society of Pediatric Neurosurgeons

Disclosure: Received grant/research funds from Codman (Johnson & Johnson) for consulting; Received grant/research funds from Medtronic for consulting.

Coauthor(s)

David A Chesler, MD, PhD Clinical and Research Fellow, Division of Pediatric Neurosurgery, Johns Hopkins University School of Medicine

David A Chesler, MD, PhD is a member of the following medical societies: American Association of Neurological Surgeons, American Medical Association, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Faisal A Almayman, MBBS Post Doctorate Research Fellow, Department of Neurosurgery, Johns Hopkins University School of Medicine

Faisal A Almayman, MBBS is a member of the following medical societies: American Association of Neurological Surgeons, Saudi Stroke Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Kenneth J Mack, MD, PhD Senior Associate Consultant, Department of Child and Adolescent Neurology, Mayo Clinic

Kenneth J Mack, MD, PhD is a member of the following medical societies: American Academy of Neurology, Child Neurology Society, Phi Beta Kappa, Society for Neuroscience

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.

Additional Contributors

Raj D Sheth, MD Chief, Division of Pediatric Neurology, Nemours Children's Clinic; Professor of Neurology, Mayo College of Medicine; Professor of Pediatrics, University of Florida College of Medicine

Raj D Sheth, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, American Neurological Association, Child Neurology Society

Disclosure: Nothing to disclose.

Acknowledgements

Alvin Marcovici, MD Consulting Staff, Southcoast Neurosurgery

Alvin Marcovici, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, and Phi Beta Kappa

Disclosure: Nothing to disclose.

References
  1. Bailey P, Cushing H. A common type of midcerebellar glioma of childhood. Arch Neurol Psychiatr. 1925. 14:192-224.

  2. Salaroli R, Ronchi A, Buttarelli FR, Cortesi F, Marchese V, Bella ED, et al. Wnt activation affects proliferation, invasiveness and radiosensitivity in medulloblastoma. J Neurooncol. 2014 Sep 28. [Medline].

  3. Rorke LB. The cerebellar medulloblastoma and its relationship to primitive neuroectodermal tumors. J Neuropathol Exp Neurol. 1983 Jan. 42(1):1-15. [Medline].

  4. Bode U, Zimmermann M, Moser O, Rutkowski S, Warmuth-Metz M, Pietsch T, et al. Treatment of recurrent primitive neuroectodermal tumors (PNET) in children and adolescents with high-dose chemotherapy (HDC) and stem cell support: results of the HITREZ 97 multicentre trial. J Neurooncol. 2014 Sep 2. [Medline].

  5. Yamada A, Moritake H, Kamimura S, Yamashita S, Takeshima H, Nunoi H. Proposed strategy for the use of high-dose chemotherapy with stem cell rescue and intrathecal topotecan without whole-brain irradiation for infantile classic medulloblastoma. Pediatr Blood Cancer. 2014 Aug 30. [Medline].

  6. Rieken S, Mohr A, Habermehl D, Welzel T, Lindel K, Witt O, et al. Outcome and prognostic factors of radiation therapy for medulloblastoma. Int J Radiat Oncol Biol Phys. 2011 Nov 1. 81(3):e7-e13. [Medline].

  7. Gupta T, Jalali R, Goswami S, Nair V, Moiyadi A, Epari S, et al. Early Clinical Outcomes Demonstrate Preserved Cognitive Function in Children with Average-Risk Medulloblastoma When Treated with Hyperfractionated Radiation Therapy. Int J Radiat Oncol Biol Phys. 2012 Feb 16. [Medline].

  8. Haddy N, Mousannif A, Tukenova M, et al. Relationship between the brain radiation dose for the treatment of childhood cancer and the risk of long-term cerebrovascular mortality. Brain. 2011 May. 134:1362-72. [Medline].

  9. Martin AM, Raabe E, Eberhart C, Cohen KJ. Management of Pediatric and Adult Patients with Medulloblastoma. Curr Treat Options Oncol. 2014 Sep 7. [Medline].

  10. Adamski J, Ramaswamy V, Huang A, Bouffet E. Advances in managing medulloblastoma and intracranial primitive neuro-ectodermal tumors. F1000Prime Rep. 2014. 6:56. [Medline]. [Full Text].

  11. Albright AL, Wisoff JH, Zeltzer PM, Boyett JM, Rorke LB, Stanley P. Effects of medulloblastoma resections on outcome in children: a report from the Children's Cancer Group. Neurosurgery. 1996 Feb. 38(2):265-71. [Medline].

  12. Allen JC, Epstein F. Medulloblastoma and other primary malignant neuroectodermal tumors of the CNS. The effect of patients' age and extent of disease on prognosis. J Neurosurg. 1982 Oct. 57(4):446-51. [Medline].

  13. Ater JL, van Eys J, Woo SY, et al. MOPP chemotherapy without irradiation as primary postsurgical therapy for brain tumors in infants and young children. J Neurooncol. 1997 May. 32(3):243-52. [Medline].

  14. Bailey CC, Gnekow A, Wellek S, et al. Prospective randomised trial of chemotherapy given before radiotherapy in childhood medulloblastoma. International Society of Paediatric Oncology (SIOP) and the (German) Society of Paediatric Oncology (GPO): SIOP II. Med Pediatr Oncol. 1995 Sep. 25(3):166-78. [Medline].

  15. Balter-Seri J, Mor C, Shuper A, et al. Cure of recurrent medulloblastoma: the contribution of surgical resection at relapse. Cancer. 1997 Mar 15. 79(6):1241-7. [Medline].

  16. Blaser SI, Harwood-Nash DC. Neuroradiology of pediatric posterior fossa medulloblastoma. J Neurooncol. 1996 Jul. 29(1):23-34. [Medline].

  17. Carrie C, Muracciole X, Gomez F, et al. Conformal radiotherapy, reduced boost volume, hyperfractionated radiotherapy, and online quality control in standard-risk medulloblastoma without chemotherapy: results of the French M-SFOP 98 protocol. Int J Radiat Oncol Biol Phys. 2005 Nov 1. 63(3):711-6. [Medline].

  18. Chang CH, Housepian EM, Herbert C. An operative staging system and a megavoltage radiotherapeutic technic for cerebellar medulloblastomas. Radiology. 1969 Dec. 93(6):1351-9. [Medline].

  19. Cohen BH, Packer RJ. Chemotherapy for medulloblastomas and primitive neuroectodermal tumors. J Neurooncol. 1996 Jul. 29(1):55-68. [Medline].

  20. Dennis M, Spiegler BJ, Hetherington CR, et al. Neuropsychological sequelae of the treatment of children with medulloblastoma. J Neurooncol. 1996 Jul. 29(1):91-101. [Medline].

  21. Dufour C1, Kieffer V, Varlet P, Raquin MA, Dhermain F, Puget S, et al. Tandem high-dose chemotherapy and autologous stem cell rescue in children with newly diagnosed high-risk medulloblastoma or supratentorial primitive neuro-ectodermic tumors. [Full Text].

  22. Dunkel IJ, Boyett JM, Yates A, Rosenblum M, Garvin JH Jr, Bostrom BC, et al. High-dose carboplatin, thiotepa, and etoposide with autologous stem-cell rescue for patients with recurrent medulloblastoma. Children's Cancer Group. J Clin Oncol. 1998 Jan. 16(1):222-8. [Medline].

  23. Friedberg MH, David O, Adelman LS. Recurrence of medulloblastoma: violation of Collins' law after two decades. Surg Neurol. 1997 Jun. 47(6):571-4. [Medline].

  24. Giordana MT, Cavalla P, Dutto A, et al. Is medulloblastoma the same tumor in children and adults?. J Neurooncol. 1997 Nov. 35(2):169-76. [Medline].

  25. Giordana MT, Migheli A, Pavanelli E. Isochromosome 17q is a constant finding in medulloblastoma. An interphase cytogenetic study on tissue sections. Neuropathol Appl Neurobiol. 1998 Jun. 24(3):233-8. [Medline].

  26. Giordana MT, Schiffer P, Schiffer D. Prognostic factors in medulloblastoma. Childs Nerv Syst. 1998 Jun. 14(6):256-62. [Medline].

  27. Giralt J, Sánchez de Toledo J, Moraga F, et al. Improving survival of medulloblastoma: results in two groups of patients. Oncology. 1996 Jan-Feb. 53(1):38-42. [Medline].

  28. Hutzen B, Bid HK, Houghton PJ, Pierson CR, Powell K, Bratasz A, et al. Treatment of medulloblastoma with oncolytic measles viruses expressing the angiogenesis inhibitors endostatin and angiostatin. March,19,2014. [Full Text].

  29. Hye Sook Min,* Ji Yeoun Lee,† Seung-Ki Kim,† and Sung-Hye Park*‡. Genetic Grouping of Medulloblastomas by Representative Markers in Pathologic Diagnosis1. [Full Text].

  30. Jenkin D. The radiation treatment of medulloblastoma. J Neurooncol. 1996 Jul. 29(1):45-54. [Medline].

  31. Kiltie AE, Lashford LS, Gattamaneni HR. Survival and late effects in medulloblastoma patients treated with craniospinal irradiation under three years old. Med Pediatr Oncol. 1997 May. 28(5):348-54. [Medline].

  32. Kool M1, Korshunov A, Pfister SM. Update on molecular and genetic alterations in adult medulloblastoma. Sep 5,2012. [Full Text].

  33. Miralbell R, Bieri S, Huguenin P, et al. Prognostic value of cerebrospinal fluid cytology in pediatric medulloblastoma. Swiss Pediatric Oncology Group. Ann Oncol. 1999 Feb. 10(2):239-41. [Medline].

  34. Parsons DW1, Li M, Zhang X, Jones S, Leary RJ, Lin JC, et al. The genetic landscape of the childhood cancer medulloblastoma. [Full Text].

  35. Pollack IF, Polinko P, Albright AL, et al. Mutism and pseudobulbar symptoms after resection of posterior fossa tumors in children: incidence and pathophysiology. Neurosurgery. 1995 Nov. 37(5):885-93. [Medline].

  36. Rajurkar M1, Huang H, Cotton JL, Brooks JK, Sicklick J, McMahon AP, et al. Distinct cellular origin and genetic requirement of Hedgehog-Gli in postnatal rhabdomyosarcoma genesis. [Full Text].

  37. Rossi A, Caracciolo V, Russo G, Reiss K, Giordano A. Medulloblastoma: from molecular pathology to therapy. Clin Cancer Res. 2008 Feb 15. 14(4):971-6. [Medline].

  38. Rutka JT, Hoffman HJ. Medulloblastoma: a historical perspective and overview. J Neurooncol. 1996 Jul. 29(1):1-7. [Medline].

  39. Saran FH, Driever PH, Thilmann C, et al. Survival of very young children with medulloblastoma (primitive neuroectodermal tumor of the posterior fossa) treated with craniospinal irradiation. Int J Radiat Oncol Biol Phys. 1998 Dec 1. 42(5):959-67. [Medline].

  40. Schmandt S, Kuhl J. Chemotherapy as prophylaxis and treatment of meningosis in children less than 3 years of age with medulloblastoma. J Neurooncol. 1998 Jun-Jul. 38(2-3):187-92. [Medline].

  41. Sure U, Berghorn WJ, Bertalanffy H. Collins' law. Prediction of recurrence or cure in childhood medulloblastoma?. Clin Neurol Neurosurg. 1997 May. 99(2):113-6. [Medline].

  42. Sutton LN, Phillips PC, Molloy PT. Surgical management of medulloblastoma. J Neurooncol. 1996 Jul. 29(1):9-21. [Medline].

  43. Tomita T. Medulloblastomas. Youmans JR, ed. Neurolgical Surgery. 5th ed. Philadelphia: WB Saunders; 1996. Vol 4: 2570-92.

  44. Weil MD, Lamborn K, Edwards MS, Wara WM. Influence of a child's sex on medulloblastoma outcome. JAMA. 1998 May 13. 279(18):1474-6. [Medline].

  45. Weitman DM, Cogen PH. Contemporary management of medulloblastoma. Contemporary Neurosurgery. 1998. 20(2):1-8.

  46. Whelan HT, Krouwer HG, Schmidt MH, et al. Current therapy and new perspectives in the treatment of medulloblastoma. Pediatr Neurol. 1998 Feb. 18(2):103-15. [Medline].

  47. Whittier KL1, Boese EA, Gibson-Corley KN, Kirby PA, Darbro BW, Qian Q, et al. G-protein coupled receptor expression patterns delineate medulloblastoma subgroups. Oct,10,2013. [Full Text].

  48. Yang SY, Wang KC, Cho BK, et al. Radiation-induced cerebellar glioblastoma at the site of a treated medulloblastoma: case report. J Neurosurg. 2005 May. 102(4 Suppl):417-22. [Medline].

  49. Zeltzer PM, Boyett JM, Finlay JL, Albright AL, Rorke LB, Milstein JM, et al. Metastasis stage, adjuvant treatment, and residual tumor are prognostic factors for medulloblastoma in children: conclusions from the Children's Cancer Group 921 randomized phase III study. J Clin Oncol. 1999 Mar. 17(3):832-45. [Medline].

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CT scan demonstrates a hyperdense lesion within the posterior fossa of an 8-year-old boy who presented with nausea and vomiting.
T1-weighted sagittal MRI of an 8-year-old boy who presented with nausea and vomiting reveals an enhancing tumor within the fourth ventricle. The child underwent a suboccipital craniotomy and resection of his medulloblastoma.
T1-weighted sagittal MRI of 4-year-old boy who presented with gait ataxia and precocious puberty. MRI shows a heterogenous enhancing tumor located within the fourth ventricle with marked hydrocephalus.
T1-weighted axial MRI shows heterogeneous enhancement of the medulloblastoma in a 4-year-old boy who presented with gait ataxia and precocious puberty.
Coronal MRI confirms the presence of the tumor within the fourth ventricle of a 4-year-old boy who presented with gait ataxia and precocious puberty.
High-power magnification hematoxylin and eosin (H&E) section of a typical medulloblastoma
 
 
 
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