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Seasonal variation in incidence of cerebellar medulloblastoma
creased 0.76 and 0.56 in the frontal and occipital lobes, respectively, in comparison with that (1.61) in the frontal lobe of the control. However, in the white matter, there was no difference in the total level of lipid-bound sialic acid or the ratio of GDla/GM I among the FCMD, DMD and control cases . Discussion
4. Dawson RMC. A hydrolytic procedure for the identification and estimation of individual phospholipids in biological samples. Biochem J 1960; 75:45-53 . 5. Abramson MB , Norton WT, Katzman R: Study of ionic structures in phospholipids by infrared spectra. J Biol Chem 1965;240:2389-95. 6. Suzuki K, Chen GC. Brain ceramide hexosides in Tay-Sachs disease and generalized gangliosidosis (GM1-gangliosidosis). J Lipid Res 1967 ;8:10513 . 7. Skipski VP, Peterson RF, Barclay M. Quantitative analysis of phospholipid by thin-layer chromatography. Biochem J 1964;90:374-78 . 8. Ando S, Chang NC, Yu RK. High-performance thin-layer chromatography and densitom etric determination of brain ganglioside. Analyt Biochem 1978;89:437-50. 9. Suzuki K. A simple and accurate microm ethod for quantitative determination of ganglioside patterns. Life Sci 1964;3:1227-33. 10. Fukuyama Y. Myopathies in infants and children (in Japanese). Rynsho Shinkei (Tokyo) 1961;1 : 409-16 .
The pathogenic mechanism underlying FCMD is unkown, although there are several theories. A genetic factor may be more important, judging from the high incidence of consanguineous marriage and sibling reccurrence. Fukuyama [ 10] proposed an autosomal ressesive pattern of inheritance. Cerebral malformation may be secondary to an Underlying, genetically determined biochemical abnormality arising from the dystrophic process or occurring in connection with the dystrophic process. However, the lipid analysis of the brain has not been reported . In this study, the lipid abnormality was restricted to gangliosides in the gray matter of the brain. The water and lipid content of the cerebral white matter were nearly normal Seasonal Variation in Incidence compared to those in the patients with DMD of Cerebellar Medulloblastoma and the normal control. These results do not suggest that there are abnormal lipid compositions in the cerebral white matter of cases with FCMD. Although the ganglioside pattern of normal Jean·Pierre Manshande, MD, Jan Van Tornout, MD, adult brains differs from that of normal chilMarleen Coppens, Cand Med and dren, the level of GDla is higher than that of Paul Casaer, MD GMI even in adult. According to Suzuki [9], it is undoubtful that GDla is the most predominant component of gangliosides in the gray The incidence of 16 cerebellar medulloblastoma matter in children. Therefore, it is seemed that admitted to the University Hospital of Leuven during the ganglioside pattern in the cerebral gray the last 8 years shows a seasonal peak between Sepmatter examined in our case with FCMD was tember and December. abnormal. Since only one patient with FCMD Manshande J-P, Van Tornout J, Coppens M, was analyzed, however, the problem remains in Casaer P. Seasonal variation in incidence the future whether the abnormal ganglioside of cerebellar medulloblastoma. pattern examined in this study exists commonBrain Dev 1985; 7:525-6 ly in patients with FCMD. References 1. Takada K, Nakamura H, Tanaka J. Cortical dysplasia in congenital muscular dystrophy with central nervous system involvement (Fukuyama type). J Neuropathol Neural 1984;43:395-407. 2. Folch J, Lees M, Sloane-Stanley GH. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem 1957; 226 :497-507 . 3. Zak B. Simple rapid micro technic for serum total cholesterol. Am J Clin Pathol1957 ;27:583-8.
From the Department of Pediatrics, D.Z. Gasthuisberg, Leuven. Received for publication: June 26, 1985. Accepted for publication: July 16, 1985 .
Key words: Medulloblastoma, season, incidence. Correspondence address: Prof. Paul Casaer, Department of Pediatrics, V.Z. Gasthuisberg, 49 3000 Belgium.
NUMBER 01 _ _ _ _ _ _ _ _ _ _ _ _ _ _ _---, PAT I ENTS
4
3
2
OL....-....................J-...&..............
Jan Feb Mar Apr May Jun lui Aug Sep Oct Nov Dec
Fig 1 Incidence by month of cerebellar medulloblastoma in childhood.
The irregular pattern of admission of children with cerebellar medulloblastoma prompted us to review the 16 cases which were diagnosed during the last 8 years in our unit. In order to avoid a possible bias due to a seasonal influence on the time of diagnosis, we considered the date of onset of symptoms obtained by a careful history. There were 8 boys and 8 girls and median age at onset of symptoms was 5.7 years. The incidence by month (Fig I) shows a seasonal peak (Multinomial test, p < 0.001) [1] in onset of symptoms, occurring during the last 4 months of the year (September to December). Unlike a study from Japan [2] we could not distinguish a seasonal trend by month of birth in our own serie. Seasonal variation in incidence has been reported for leukemia and basal cell epithelioma in summer, Hodgkin disease in winter, Burkitt's lymphoma in the second half of the year [2], female breast cancer in spring [3] and testicular seminoma in winter [4] . However, as far as we know, it is the first time that such a phenomenon is observed for a brain tumor. Seasonality in incidence of neurotrope viral infections or a circannual rhythm in the functioning of the immune surveillance are attractive hypothetical etiologies but more research is needed in order to confirm our finding and before speculating on the causative factors. References 1. Carchon H. Multinomial test (unpublished).
526 Brain & Development, Vol 7, No 5, 1985
2. Yamakawa Y, Fukui M, Kinoshita K, Ohgami S, Kitamura K. Seasonal variations in incidence of cerebellar medulloblastoma by month of birth. Fukuoka Igaku Zasshi (Fukuoka) 1979 ;70 : 295-300. 3. Cohen P, Wax Y, Modan B. Seasonality in the occurrence of breast cancer. Cancer Res 1983; 43:892-6. 4. Hrushesky WIM , Hans E, Lakatua D, Vogelzang N, Kennedy Bl. Seasonality in testicular cell proliferation and seminoma incidence . Proe Am Soc CUn Oneal 1983;24 :18(C-561).
4. Dawson RMC. A hydrolytic procedure for the identification and estimation of individual phospholipids in biological samples. Biochem J 1960; 75:45-53 . 5. Abramson MB , Norton WT, Katzman R: Study of ionic structures in phospholipids by infrared spectra. J Biol Chem 1965;240:2389-95. 6. Suzuki K, Chen GC. Brain ceramide hexosides in Tay-Sachs disease and generalized gangliosidosis (GM1-gangliosidosis). J Lipid Res 1967 ;8:10513 . 7. Skipski VP, Peterson RF, Barclay M. Quantitative analysis of phospholipid by thin-layer chromatography. Biochem J 1964;90:374-78 . 8. Ando S, Chang NC, Yu RK. High-performance thin-layer chromatography and densitom etric determination of brain ganglioside. Analyt Biochem 1978;89:437-50. 9. Suzuki K. A simple and accurate microm ethod for quantitative determination of ganglioside patterns. Life Sci 1964;3:1227-33. 10. Fukuyama Y. Myopathies in infants and children (in Japanese). Rynsho Shinkei (Tokyo) 1961;1 : 409-16 .
The pathogenic mechanism underlying FCMD is unkown, although there are several theories. A genetic factor may be more important, judging from the high incidence of consanguineous marriage and sibling reccurrence. Fukuyama [ 10] proposed an autosomal ressesive pattern of inheritance. Cerebral malformation may be secondary to an Underlying, genetically determined biochemical abnormality arising from the dystrophic process or occurring in connection with the dystrophic process. However, the lipid analysis of the brain has not been reported . In this study, the lipid abnormality was restricted to gangliosides in the gray matter of the brain. The water and lipid content of the cerebral white matter were nearly normal Seasonal Variation in Incidence compared to those in the patients with DMD of Cerebellar Medulloblastoma and the normal control. These results do not suggest that there are abnormal lipid compositions in the cerebral white matter of cases with FCMD. Although the ganglioside pattern of normal Jean·Pierre Manshande, MD, Jan Van Tornout, MD, adult brains differs from that of normal chilMarleen Coppens, Cand Med and dren, the level of GDla is higher than that of Paul Casaer, MD GMI even in adult. According to Suzuki [9], it is undoubtful that GDla is the most predominant component of gangliosides in the gray The incidence of 16 cerebellar medulloblastoma matter in children. Therefore, it is seemed that admitted to the University Hospital of Leuven during the ganglioside pattern in the cerebral gray the last 8 years shows a seasonal peak between Sepmatter examined in our case with FCMD was tember and December. abnormal. Since only one patient with FCMD Manshande J-P, Van Tornout J, Coppens M, was analyzed, however, the problem remains in Casaer P. Seasonal variation in incidence the future whether the abnormal ganglioside of cerebellar medulloblastoma. pattern examined in this study exists commonBrain Dev 1985; 7:525-6 ly in patients with FCMD. References 1. Takada K, Nakamura H, Tanaka J. Cortical dysplasia in congenital muscular dystrophy with central nervous system involvement (Fukuyama type). J Neuropathol Neural 1984;43:395-407. 2. Folch J, Lees M, Sloane-Stanley GH. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem 1957; 226 :497-507 . 3. Zak B. Simple rapid micro technic for serum total cholesterol. Am J Clin Pathol1957 ;27:583-8.
From the Department of Pediatrics, D.Z. Gasthuisberg, Leuven. Received for publication: June 26, 1985. Accepted for publication: July 16, 1985 .
Key words: Medulloblastoma, season, incidence. Correspondence address: Prof. Paul Casaer, Department of Pediatrics, V.Z. Gasthuisberg, 49 3000 Belgium.
NUMBER 01 _ _ _ _ _ _ _ _ _ _ _ _ _ _ _---, PAT I ENTS
4
3
2
OL....-....................J-...&..............
Jan Feb Mar Apr May Jun lui Aug Sep Oct Nov Dec
Fig 1 Incidence by month of cerebellar medulloblastoma in childhood.
The irregular pattern of admission of children with cerebellar medulloblastoma prompted us to review the 16 cases which were diagnosed during the last 8 years in our unit. In order to avoid a possible bias due to a seasonal influence on the time of diagnosis, we considered the date of onset of symptoms obtained by a careful history. There were 8 boys and 8 girls and median age at onset of symptoms was 5.7 years. The incidence by month (Fig I) shows a seasonal peak (Multinomial test, p < 0.001) [1] in onset of symptoms, occurring during the last 4 months of the year (September to December). Unlike a study from Japan [2] we could not distinguish a seasonal trend by month of birth in our own serie. Seasonal variation in incidence has been reported for leukemia and basal cell epithelioma in summer, Hodgkin disease in winter, Burkitt's lymphoma in the second half of the year [2], female breast cancer in spring [3] and testicular seminoma in winter [4] . However, as far as we know, it is the first time that such a phenomenon is observed for a brain tumor. Seasonality in incidence of neurotrope viral infections or a circannual rhythm in the functioning of the immune surveillance are attractive hypothetical etiologies but more research is needed in order to confirm our finding and before speculating on the causative factors. References 1. Carchon H. Multinomial test (unpublished).
526 Brain & Development, Vol 7, No 5, 1985
2. Yamakawa Y, Fukui M, Kinoshita K, Ohgami S, Kitamura K. Seasonal variations in incidence of cerebellar medulloblastoma by month of birth. Fukuoka Igaku Zasshi (Fukuoka) 1979 ;70 : 295-300. 3. Cohen P, Wax Y, Modan B. Seasonality in the occurrence of breast cancer. Cancer Res 1983; 43:892-6. 4. Hrushesky WIM , Hans E, Lakatua D, Vogelzang N, Kennedy Bl. Seasonality in testicular cell proliferation and seminoma incidence . Proe Am Soc CUn Oneal 1983;24 :18(C-561).