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Journal Article

A Study of Radiation Necrosis and Edema in the Canine Brain Using Positron Emission Tomography and Magnetic Resonance Imaging

Kathleen M. Brennan, Mark S. Roos, Thomas F. Budinger, Robert J. Higgins, Sam T. S. Wong and Kay S. Bristol
Vol. 134, No. 1 (Apr., 1993), pp. 43-53
DOI: 10.2307/3578500
Stable URL: http://www.jstor.org/stable/3578500
Page Count: 11

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Abstract

Radiation injury, a major hazard of central nervous system (CNS) radiotherapy, was investigated using sequential studies with positron emission tomography (PET) and magnetic resonance imaging (MRI) in beagle dogs with both helium and neon-ion hemibrain irradiation. All dogs receiving 7.5-11 Gy of neon showed no signs of radiation injury to 3 years after irradiation. Dogs receiving ≥13 Gy neon or helium succumbed to radiation necrosis and died 21-32 weeks after irradiation. The findings of imaging studies for all dogs who succumbed to radiation necrosis were normal until 3-6 weeks before death. Sequential studies were performed using 0.5 T MRI spin-echo and inversion recovery imaging sequences, and high-resolution (2-3 mm) PET with ${}^{18}{\rm F}$ deoxyglucose and ${}^{82}{\rm Rb}$. The same axial slices (within 1-2 mm) were imaged repeatedly (weekly) after irradiation until death. The earliest CNS changes were seen as decreased metabolic activity in the cortex of the irradiated hemisphere with PET or an increase in signal intensity in the periventricular white matter on $T_{2}\text{-weighted}$ spin-echo imaging on MRI. From the time this increase in signal intensity was first observed, T1 and T2 values increased steadily in both the gray and white matter until death. The changes in white matter were consistently greater than those in gray matter. The results of PET, MRI, and histopathological examinations support the theory that both cellular and vascular mechanisms are involved in radiation necrosis.

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