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Background: Currently, the gadolinium retention in the brain after the use of contrast agents is studied by T1‐weighted magnetic resonance imaging (MRI) (T1w) and T1 mapping. The former does not provide easily quantifiable data and the latter requires prolonged scanning and is sensitive to motion. T2 mapping may provide an alternative approach. Animal studies of gadolinium retention are complicated by repeated intravenous (IV) dosing, whereas intraperitoneal (IP) injections might be sufficient. Hypothesis: T2 mapping will detect the changes in the rat brain due to gadolinium retention, and IP administration is equivalent to IV for long‐term studies. Study Type: Prospective longitudinal. Animal Model: A total of 31 Sprague–Dawley rats administered gadodiamide IV (N = 8) or IP (N = 8), or saline IV (N = 6) or IP (N = 9) 4 days per week for 5 weeks. Field strength/sequences: A 7 T, T1w, and T2 mapping. Assessment: T2 relaxation and image intensities in the deep cerebellar nuclei were measured pre‐treatment and weekly for 5 weeks. Then brains were assessed for neuropathology (N = 4) or gadolinium content using inductively coupled plasma mass spectrometry (ICP‐MS, N = 12). Statistical tests: Repeated measures analysis of variance with post hoc Student–Newman–Keuls tests and Hedges' effect size. Results: Gadolinium was detected by both approaches; however, T2 mapping was more sensitive (effect size 2.32 for T2 vs. 0.95 for T1w), and earlier detection (week 3 for T2 vs. week 4 for T1w). ICP‐MS confirmed the presence of gadolinium (3.076 ± 0.909 nmol/g in the IV group and 3.948 ± 0.806 nmol/g in the IP group). There was no significant difference between IP and IV groups (ICP‐MS, P = 0.109; MRI, P = 0.696). No histopathological abnormalities were detected in any studied animal. Conclusion: T2 relaxometry detects gadolinium retention in the rat brain after multiple doses of gadodiamide irrespective of the route of administration. Evidence Level 1 Technical Efficacy: Stage 1 [ABSTRACT FROM AUTHOR]

Purpose: To measure the reproducibility of T2 relaxation and to determine the statistical power of T2 mapping in the rat brain as a characteristic of the baseline performance of the T2 relaxation as a potential biomarker of neurotoxicity.Materials and Methods: Multislice multiecho spin-echo imaging was utilized to obtain the quantitative T2 maps in 138 naïve rats at 7T. Images were skull-stripped and coregistered to the common anatomical reference. A full anatomical segmentation mask, which included all major brain structures, was created using the same reference T2 map. The overall variability map was also calculated from all T2 maps and the areas with arbitrarily high variability (coefficient of variation >25%) were excluded from the full segmentation mask to produce a trimmed mask. T2 maps were segmented using both these masks and statistical power analysis was conducted in all segmented areas.Results: The coefficient of variation of T2 relaxation in different brain areas varied from 5.4% (cerebrospinal fluid) to 1.2% (cortex) when using a full segmentation mask. The use of a trimmed segmentation mask decreased the coefficient of variation in many areas, which ranged between 3.2% (inferior colliculi) and 1.2% (cortex) in this case. As revealed by statistical power analysis to detect 5% change with power of 0.8, the minimum number of observations needed for different areas ranged from 3 (cortex) to 8 (inferior colliculi) in the case of use of a trimmed segmentation mask.Conclusion: T2 relaxation is a very reproducible MRI parameter of the rat brain with high statistical power, which allows detecting very small changes in groups consisting of a minimal number of experimental animals.Level Of Evidence: 1 J. Magn. Reson. Imaging 2017;45:700-709. [ABSTRACT FROM AUTHOR]

The aim of this study was to assess quantitative changes in T2 relaxation using magnetic resonance imaging approaches in rats exposed to kainic acid to assess the utility of such endpoints as biomarkers of neurotoxicity. Quantitative T2 mapping was performed in 21 rats before and 2, 24, and 48h after a single ip injection of 10 mg/kg of kainic acid. Three methods of quantifying T2 changes were explored: (1) Thresholding: all voxels exhibiting T2<=72ms were designated normal tissue, whereas voxels exhibiting T2>72ms were designated as lesioned tissue; (2) Statistical mapping: T2 maps obtained after treatment were statistically compared with averaged "baseline" maps, voxel-by-voxel; (3) Within-subject difference from baseline: for each individual the baseline T2 map was subtracted from the T2 map obtained after treatment. Based on the follow-up histopathological response there were 9 responders, 7 nonresponders, and 5 animals were not classified due to early sacrifice at 2 h which was too soon after treatment to detect any morphological evidence. The "thresholding" method (1) detected differences between groups only at the later time point of 48 h, the "statistical mapping" approach (2) detected differences 24 and 48h after treatment, and the "within-subject difference from baseline" method (3) detected statistically significant differences between groups at each time point (2, 24, and 48 h). T2 mapping provides an easily quantifiable biomarker and the quantification method employing the use of the same animal as its own control provides the most sensitive metrics. [ABSTRACT FROM AUTHOR]