Abstract
The most severe radiation-induced brain damage is brain necrosis. Clinically, it is difficult to differentiate between brain necrosis and recurrent brain tumor1. Radiation brain necrosis is a terminal stage of the brain damage. However, it is not well known the mechanisms underlying the process that produce the brain necrosis after irradiation: i.e. how glucose metabolism and blood flow distribution change after irradiation. We studied the uptake of 18F-2-deoxy-D-glucose (FDG) and 99mTc-hexamethylpropylene amine oxine (HMPAO) in the irradiated brain of the mouse regarding glucose and blood flow distribution, respectively. This study is a feasible for positron emission tomography.
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References
G. Di Chiro et al. Cerebral necrosis after radiation therapy and/or intraarterial chemotherapy for brain tumors: PET and neurologic studies. AJNR 8: 1083–1091, 1987.
W. Calvo et al. Time and dose related changes in the white matter of the rat brain after single doses of X-rays. Brit. J. Radiol. 61: 1043–1052, 1988.
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© 1996 Springer Science+Business Media New York
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Abe, Y., Ono, S., Takahashi, J., Sato, T., Fukuda, H. (1996). Assessment of Radiation Induced Damage of Mouse Brain Using 18F-2-Deoxy-D-Glucose and 99mTc-Hexamethylpropylene Amine Oxine. In: Mishima, Y. (eds) Cancer Neutron Capture Therapy. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9567-7_83
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DOI: https://doi.org/10.1007/978-1-4757-9567-7_83
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-9569-1
Online ISBN: 978-1-4757-9567-7
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