Detection of Cerebral Hypoxia in Arteriovenous Malformation (AVM) by [F-18]Fluorodeoxyglucose (FMISO)

R.S. Liu, S.H. Yeh, W.Y. Guo, D.H.C. Pan, L.S. Lee, L.S. Chu, C.P. Chang, J.K. Wang, and L.C. Wu


Introduction

Cerebral ischemia occurs commonly in the lesion of AVM and the surrounding brain tissue. Cerebral oxygen extraction fraction and cerebral oxygen metabolism of AVM's has been studied using PET (Stroke 1989; 20:890-8). However, hypoxia in the affected regions has not well been demonstrated. In this study, [F-18]FMISO was used to detect the cerebral hypoxia caused by AVM and compared with the disturbance of cerebral glucose metabolism.

Methods and Patients

Eight patients (pts) with AVM's less than 6 cm in size in 3 and greater than 6 cm in size in 5 pts were studied. Cerebral angiography, MRI, [F-18]fluorodeoxyglucose (FDG) PET scan and FMISO-PET scan were performed for anatomical and functional evaluation of the AVM's. PET images were obtained at 2 hr after intravenous injection of 10 mCi (370 MBq) of [F-18]FMISO. The FDG and FMISO-PET images were analysed by visual inspection first, and then a standard uptake value (SUV) of FMISO was used to assess the tissue hypoxia in the AVM and/or its surrounding areas and the normal brain tissue.

Results

In 3 pts with AVM's less than 6 cm in size, FDG-PET scan showed a hypometabolic region larger than the lesion seen on MRI. The regions of hypoxia were equal to hypometabolism in 1 pt, greater in 1 and smaller in 1. Five pts with AVM's larger than 6 cm in size revealed more extensive involvement of hypoxia in the surrounding brain tissue than the AVM's less than 6 cm. The hypoxic region was larger than hypometabolic region in 3 pts and equal in 2 pts. SUV's of FMISO obtained from the AVM's were 0.041± 0.005 (mean± s.d.), which is significantly higher than the SUV's of 0.027± 0.003 of normal brain tissue (p<0.05, Wilcoxon signed-ranks test).

Conclusion

In summary, FMISO-PET scan may provide a useful means to detect the tissue hypoxia in AVM's. The larger the size of AVM is the more extensive the involvement of hypoxia will be. Cerebral hypoxia caused by the stealing effect of AVM may not completely couple with the changes of cerebral glucose metabolism.

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Figure 1. Lager cerebellar AVM on the left. A. T1-weighted MRI. The AVM is characterized by the signal void but flow-induced variations in signals. B. FDG-PET scan shows glucose hypometabolism in both cerebellar hemispheres. C. FMISO-PET scan detects a wider area of hypoxia than the area of hypometabolism in cerebellum.

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