Eva Bültmann1, Loukia M Spineli2, Hans Hartmann3, Heinrich Lanfermann4. 1. Institute of Diagnostic and Interventional Neuroradiology, Hannover Medical School, Hannover, Germany. Electronic address: bueltmann.eva@mh-hannover.de. 2. Institute for Biostatistics, Hannover Medical School, Hannover, Germany. 3. Department of Pediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School, Hannover, Germany. 4. Institute of Diagnostic and Interventional Neuroradiology, Hannover Medical School, Hannover, Germany.
Abstract
OBJECTIVE: To examine age-related changes in T2 relaxation times during infancy and childhood in order to assess T2 values obtained from routine MRI as a biomarker. METHODS: From our pool of clinical pediatric MRI examinations at 3T all patients with normal conventional MRI scans were retrospectively selected. Depending on their clinical findings the identified 99 patients (0-199months) were divided into 43 healthy controls and 56 diseased children with various clinical abnormalities (developmental delay, epilepsy, prematurity, and deafness). T2 maps based on routinely performed triple echo turbo spin echo sequences were created. T2 values were measured in 22 brain regions to determine age-related changes. We also investigated whether such changes differ between healthy and diseased children. RESULTS: Age significantly reduced T2 relaxation times across all regions (p<0.05), but health status had no impact. With increasing age, T2 values decreased continuously, with declines faster over the first 10months and slower thereafter. Early rapid and later slow decline was similar in healthy and diseased groups. CONCLUSIONS: Using T2 maps based on clinical MRI data we could determine age-related T2 relaxation times in 22 brain regions during infancy and childhood. Our data have relevance for future investigator independent T2 relaxation time measurements in determining whether T2 values are within the normal range or should be considered as potentially pathologic.
OBJECTIVE: To examine age-related changes in T2 relaxation times during infancy and childhood in order to assess T2 values obtained from routine MRI as a biomarker. METHODS: From our pool of clinical pediatric MRI examinations at 3T all patients with normal conventional MRI scans were retrospectively selected. Depending on their clinical findings the identified 99 patients (0-199months) were divided into 43 healthy controls and 56 diseased children with various clinical abnormalities (developmental delay, epilepsy, prematurity, and deafness). T2 maps based on routinely performed triple echo turbo spin echo sequences were created. T2 values were measured in 22 brain regions to determine age-related changes. We also investigated whether such changes differ between healthy and diseased children. RESULTS: Age significantly reduced T2 relaxation times across all regions (p<0.05), but health status had no impact. With increasing age, T2 values decreased continuously, with declines faster over the first 10months and slower thereafter. Early rapid and later slow decline was similar in healthy and diseased groups. CONCLUSIONS: Using T2 maps based on clinical MRI data we could determine age-related T2 relaxation times in 22 brain regions during infancy and childhood. Our data have relevance for future investigator independent T2 relaxation time measurements in determining whether T2 values are within the normal range or should be considered as potentially pathologic.