Abstracts

Rationale: Brain insults like status epilepticus (SE) may lead to the development of chronic epilepsy and distinct neurodegeneration. MR relaxometry with T2 relaxation time mapping can be used to determine numeric T2 values of brain tissues, which is not only useful in scientific research, but also helpful as a sensitive diagnostic tool to examine microstructural alterations in the brain. Previous data have mainly been obtained at low field strengths. As MR systems with higher field strengths (> 3 T) become more common in research and clinical use, a reliable and practicable method for T2 mapping at such higher field strengths is needed. Methods: To generate reference data, three na ve female adult Sprague-Dawley rats underwent four consecutive MR examinations on a 7 Tesla animal scanner (Bruker Pharmascan 70/16). The protocol included a T1-MDEFT sequence for imaging anatomic structures and two MSME-T2-map sequences containing different echoes, i.e. three versus 16 echoes, to find out the influence of echo numbers on T2 determination. T2 maps were obtained on a voxel-by-voxel basis using nonlinear least-squares fit. Quantitative T2 values of the grey and white matter were measured in exemplary regions of interest. Following baseline scans, rats were scanned immediately after a pilocarpine-induced SE which lasted 90 minutes. During the next two days two animals died. The remaining rat was examined 48 hours, seven days and one, three, six and eight months later. Finally, we compared SE-induced alterations detected by MR with histological alterations in immunostained brain sections. Results: In na ve rats, T2 values of about 49 ms for cortex and 40 ms for white matter were determined. No significant differences were found between the T2 values obtained from data of 16 echoes and those of three echoes (p < 0.01), although the signal-to-noise ratio was better by using the former. There was also no difference between values deduced from the repeated four MR examinations. Following SE, we observed dynamic brain alterations. Maximum cellular edema and swelling occurred 48 hours after SE, with visible lesions in temporal cortex, hippocampus, substantia nigra and thalamus. Interestingly, the hippocampal lesions showed a clear lamellar necrosis, indicating different vulnerability of the cellular structures. One week later, lesions were reduced, but global brain atrophy occurred and was still in progress until six months after SE. The measured T2 values confirmed these observations. First spontaneous seizures were detected about six weeks after SE. Conclusions: This preliminary study shows that the T2 relaxation time measurements complement the morphological findings in the brain after SE. T1- and T2-weighted images sufficiently characterize changes in brain morphology after SE without inacceptable timeslots needed for longitudinal studies in larger animal groups.