American Journal of Neuroradiology 27:2137-2140, November-December 2006
© 2006 American Society of Neuroradiology
BRAIN
Whole-Brain N-Acetylaspartate Spectroscopy and Diffusion Tensor Imaging in Patients with Newly Diagnosed Gliomas: A Preliminary Study
a From the Department of Radiology, New York University School of Medicine, NY
Please address correspondence to Oded Gonen, PhD, Department of Radiology, New York University School of Medicine, 650 First Ave, 6th Floor, New York, New York 10016; e-mail: oded.gonen{at}med.nyu.edu
BACKGROUND AND PURPOSE:Glial cancer cells can be found well beyond the MR imaging T2 signal-intensity hyperintensity. To quantify the extent of the diffuse microstructural tissue damage possibly due to the presence of these satellite tumor cells, we investigated the relationships between global metabolic and microstructural abnormalities in the normal-appearing brain regions of patients with newly diagnosed glioma.
MATERIAL AND METHODS:Ten patients (6 men, 4 women) with radiologically suspected untreated supratentorial glial tumors and 9 healthy controls (5 men, 4 women) were studied with T1- and T2-weighted MR imaging, diffusion-weighted echo-planar MR imaging, and whole-brain N-acetylaspartate (WBNAA) proton MR spectroscopy. The relationship between the WBNAA concentration, the mean diffusivity (MD), and fractional anisotropy (FA) values in a large contralateral normal-appearing white matter (NAWM) brain region was investigated with the Spearman rank correlation test.
RESULTS:WBNAA values were significantly lower (P < .001) in patients (9.7 ± 1.7 mmol/L) than controls (13.1 ± 1.1 mmol/L). MD values were higher (P = .0001) in patients (0.95 ± 0.07 mm2s1) than in controls (0.61 ± 0.04 mm2s1). FA values did not differ between patients (0.42 ± 0.08) and controls (0.43 ± 0.041). A strong inverse correlation between WBNAA and MD (r = 0.88, P = .0008) was found in the patients but not in controls (r = 0.012, P = .975).
CONCLUSION:The correlation between the WBNAA and MD in the contralateral NAWM suggests that the microstructural damage possibly related to the presence of infiltrative tumor cells contributes to WBNAA decline in these patients.
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