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.[1][2][3][4][5][6] Supportive therapy for gliomatosis cerebri includes anticonvulsants and corticosteroids.[7]
Medical Therapy
The predominant therapy for gliomatosis cerebri is surgical resection. Adjunctive chemotherapy and radiation may be required.[1][2][3][4][5][6] Supportive therapy for gliomatosis cerebri includes anticonvulsants and corticosteroids.[7]
1. Radiotherapy
- Post-operative radiotherapy is recommended among all patients who develop gliomatosis cerebri.[1]
- Radiotherapy may not cure the cancer but can control the tumor, delay recurrence, and increase survival.
- Radiation therapy is associated with temporary improvement of clinical symptoms.[7]
- External beam radiation therapy is preferred to whole brain radiotherapy.[2]
- The median dose of radiation is 60 Gy (range: 50-72 Gy).[1]
2. Chemotherapy
- Chemotherapy is indicated as adjuvant therapy for gliomatosis cerebri.
- Temozolomide (Temodar) is the preferred drug for the treatment of high-grade gliomatosis cerebri.[3]
- PCV 3 combination chemotherapy is the preferred drug regimen for slow growing, low-grade gliomatosis cerebri.[4]
- 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.[6]
- Other chemotherapeutic drugs that may be used for the treatment of gliomatosis cerebri include:[5][8]
- Hydroxyurea
- 6-thioguanine
3. Supportive treatment
- Supportive therapy for gliomatosis cerebri includes anticonvulsants and corticosteroids, which focuses on relieving symptoms and improving the patient’s neurologic function.[7]
- Anticonvulsants are administered to the patients who have a seizure. 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
- ↑ 1.0 1.1 1.2 1.3 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.
- ↑ 2.0 2.1 2.2 Hejazi N, Witzmann A, Hergan K (2001). "Gliomatosis cerebri: intra vitam stereotactic determination in two cases and review of the literature". Br J Neurosurg. 15 (5): 396–401. PMID 11708542.
- ↑ 3.0 3.1 3.2 Levin N, Gomori JM, Siegal T (2004). "Chemotherapy as initial treatment in gliomatosis cerebri: results with temozolomide". Neurology. 63 (2): 354–6. PMID 15277636.
- ↑ 4.0 4.1 4.2 Sanson M, Napolitano M, Cartalat-Carel S, Taillibert S (2005). "[Gliomatosis cerebri]". Rev Neurol (Paris). 161 (2): 173–81. PMID 15798516.
- ↑ 5.0 5.1 5.2 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.
- ↑ 6.0 6.1 6.2 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.
- ↑ 7.0 7.1 7.2 7.3 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.
- ↑ Qaddoumi I, Kocak M, Pai Panandiker AS, Armstrong GT, Wetmore C, Crawford JR; et al. (2014). "Phase II Trial of Erlotinib during and after Radiotherapy in Children with Newly Diagnosed High-Grade Gliomas". Front Oncol. 4: 67. doi:10.3389/fonc.2014.00067. PMC 3978340. PMID 24744992.