BACKGROUND AND PURPOSE: To evaluate whether breath-holding (BH) blood oxygenation level-dependent (BOLD) fMRI can quantify differences in vascular reactivity (VR), as there is a need for improved contrast mechanisms in gliomas. METHODS: 16 patients (gliomas, grade II = 5, III = 2, IV = 9) were evaluated using the BH paradigm: 4-second single deep breath followed by 16 seconds of BH and 40 seconds of regular breathing for five cycles. VR was defined as the difference in BOLD signal between the minimal signal seen at the end of the deep breath and maximal signal seen at the end of BH (peak-to-trough). VR was measured for every voxel and compared for gray versus white matter and tumor versus normal contralateral brain. VR maps were compared to the areas of enhancement and FLAIR/T2 abnormality. RESULTS: VR was significantly lower in normal white matter than gray matter (P < .05) and in tumors compared to the normal, contralateral brain (P < 0.002). The area of abnormal VR (1103 ± 659 mm²) was significantly greater (P = .019) than the enhancement (543 ± 530 mm²), but significantly smaller (P = .0011) than the FLAIR abnormality (2363 ± 1232 mm²). However, the variability in the areas of gadolinium contrast enhancement versus VR abnormality indicates that the contrast mechanism elicited by BH (caused by abnormal arteriolar smooth muscles) appears to be fundamentally different from the contrast mechanism of gadolinium enhancement (caused by the presence of "leaky" gap junctions). CONCLUSIONS: BH maps based on peak-to-trough can be used to characterize VR in brain tumors. VR maps in brain tumor patients appear to be caused by a different mechanism than gadolinium enhancement.
BACKGROUND AND PURPOSE: To evaluate whether breath-holding (BH) blood oxygenation level-dependent (BOLD) fMRI can quantify differences in vascular reactivity (VR), as there is a need for improved contrast mechanisms in gliomas. METHODS: 16 patients (gliomas, grade II = 5, III = 2, IV = 9) were evaluated using the BH paradigm: 4-second single deep breath followed by 16 seconds of BH and 40 seconds of regular breathing for five cycles. VR was defined as the difference in BOLD signal between the minimal signal seen at the end of the deep breath and maximal signal seen at the end of BH (peak-to-trough). VR was measured for every voxel and compared for gray versus white matter and tumor versus normal contralateral brain. VR maps were compared to the areas of enhancement and FLAIR/T2 abnormality. RESULTS: VR was significantly lower in normal white matter than gray matter (P < .05) and in tumors compared to the normal, contralateral brain (P < 0.002). The area of abnormal VR (1103 ± 659 mm²) was significantly greater (P = .019) than the enhancement (543 ± 530 mm²), but significantly smaller (P = .0011) than the FLAIR abnormality (2363 ± 1232 mm²). However, the variability in the areas of gadolinium contrast enhancement versus VR abnormality indicates that the contrast mechanism elicited by BH (caused by abnormal arteriolar smooth muscles) appears to be fundamentally different from the contrast mechanism of gadolinium enhancement (caused by the presence of "leaky" gap junctions). CONCLUSIONS: BH maps based on peak-to-trough can be used to characterize VR in brain tumors. VR maps in brain tumorpatients appear to be caused by a different mechanism than gadolinium enhancement.
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