Gliomatosis cerebri medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sujit Routray, M.D. [2]
Overview
The predominant therapy for gliomatosis cerebri is surgical resection. Adjunctive chemotherapy and radiation may be required. Supportive therapy for gliomatosis cerebri includes anticonvulsants and corticosteroids.
Medical Therapy
The predominant therapy for gliomatosis cerebri is surgical resection. Adjunctive chemotherapy and radiation may be required. Supportive therapy for gliomatosis cerebri includes anticonvulsants and corticosteroids.
Radiotherapy
- Post-operative radiotherapy is recommended among all patients who develop gliomatosis cerebri.
- Radiotherapy may not cure the cancer, but can control the tumor and delay recurrence.
- Targeted three-dimensional conformal radiotherapy is preferred to whole brain radiotherapy.
- The median dose of radiation is 60 Gy (range: 50-72 Gy).[1]
Chemotherapy
- Chemotherapy is indicated as adjuvant therapy for gliomatosis cerebri.
- Temozolomide (Temodar) is the preferred drug for the treatment of high-grade gliomatosis cerebri.
- Procarbazine-CCNU-Vincristine is the preferred drug regimen for slow growing, low-grade gliomatosis cerebri.[2]
- CCNU is administered on day 1, procarbazine is administered daily for 14 days beginning on day 8, and vincristine is administered on days 8 and 29 of each 6-week cycle of therapy.[3]
- Other chemotherapeutic drugs that may be used for the treatment of gliomatosis cerebri include:[4]
Supportive treatment
- Supportive therapy for gliomatosis cerebri includes anticonvulsants and corticosteroids, which focuses on relieving symptoms and improving the patient’s neurologic function.[5]
- Anticonvulsants are administered to the patients who have a seizure.[5] Phenytoin given concurrently with radiation may have serious skin reactions such as erythema multiforme and Stevens-Johnson syndrome.
- Corticosteroids, usually dexamethasone given 4-10 mg every 4-6 h, can reduce peritumoral edema, diminish mass effect, and lower intracranial pressure with a decrease in headache or drowsiness.
References
- ↑ Inoue T, Kumabe T, Kanamori M, Sonoda Y, Watanabe M, Tominaga T (2010). "Prognostic factors for patients with gliomatosis cerebri: retrospective analysis of 17 consecutive cases". Neurosurg Rev. 34 (2): 197–208. doi:10.1007/s10143-010-0306-1. PMID 21301914.
- ↑ Sanson M, Napolitano M, Cartalat-Carel S, Taillibert S (2005). "[Gliomatosis cerebri]". Rev Neurol (Paris). 161 (2): 173–81. PMID 15798516.
- ↑ Levin VA, Edwards MS, Wright DC, Seager ML, Schimberg TP, Townsend JJ; et al. (1980). "Modified procarbazine, CCNU, and vincristine (PCV 3) combination chemotherapy in the treatment of malignant brain tumors". Cancer Treat Rep. 64 (2–3): 237–44. PMID 7407756.
- ↑ Herrlinger U, Felsberg J, Küker W, Bornemann A, Plasswilm L, Knobbe CB; et al. (2002). "Gliomatosis cerebri: molecular pathology and clinical course". Ann Neurol. 52 (4): 390–9. doi:10.1002/ana.10297. PMID 12325066.
- ↑ 5.0 5.1 Rajz GG, Nass D, Talianski E, Pfeffer R, Spiegelmann R, Cohen ZR (2012). "Presentation patterns and outcome of gliomatosis cerebri". Oncol Lett. 3 (1): 209–213. doi:10.3892/ol.2011.445. PMC 3362440. PMID 22740882.