C Zenobi1, J L Wisnowski2,3, B Tamrazi2,4, A M-C Wong5,6, R Chapman3, S Blüml2,7,4, T-W Wu8,3. 1. From the Los Angeles County+USC Medical Center (C.Z.). 2. Departments of Radiology and Pediatrics (J.L.W., B.T., S.B.). 3. Division of Neonatology (J.L.W., R.C., T.-W.W.), Fetal and Neonatal Institute. 4. Department of Radiology (B.T., S.B.), Children's Hospital Los Angeles, Los Angeles, California. 5. Department of Medical Imaging and Intervention (A.M.-C.W.), Chang Gung Memorial Hospital, Keelung/Linkou, Taiwan. 6. Department of Diagnostic Radiology (A.M.-C.W.), Chang Gung University, Taoyuan City, Taiwan. 7. Pediatrics (S.B., T.-W.W.), Keck School of Medicine of USC, Los Angeles, California. 8. Pediatrics (S.B., T.-W.W.), Keck School of Medicine of USC, Los Angeles, California twu@chla.usc.edu.
Abstract
BACKGROUND AND PURPOSE: ADC changes are useful in detecting ischemic brain injury, but mechanisms other than tissue pathology may affect the kinetic movement and diffusion of water molecules. We aimed to determine the effects of brain temperature on the corresponding ADC in infants undergoing therapeutic hypothermia. MATERIALS AND METHODS: Brain temperature and ADC values in the basal ganglia, thalamus, cortical GM, and WM were analyzed during and after therapeutic hypothermia. The study cohort was categorized as having no-injury or injury. Among infants without injury, the correlation between ADC values and temperature was analyzed using the Pearson correlation. Intrasubject comparison of ADC changes during and after therapeutic hypothermia were analyzed, excluding patients who had an MR image interval of >5 days to minimize the effects of injury evolution. RESULTS: Thirty-nine infants with hypoxic-ischemic encephalopathy were enrolled (23 no-injury; 16 injury). The median ADC was significantly lower during therapeutic hypothermia (837; interquartile range, 771-928, versus 906; interquartile range, 844-1032 ×10-6mm2/s; P < .001). There was no difference in the ADC between the no-injury and injury groups during therapeutic hypothermia (823; interquartile range, 782-868, versus 842; interquartile range, 770-1008 ×10-6mm2/s; P = .4). In the no-injury group, in which ADC is presumed least affected by the evolution of injury, the median ADC was significantly lower during therapeutic hypothermia (826; interquartile range, 771-866, versus 897; interquartile range, 846-936 ×10-6mm2/s; P < .001). There was a moderate correlation between temperature and ADC in the no-injury group (during therapeutic hypothermia: Spearman ρ, 0.48; P < .001; after therapeutic hypothermia: ρ, 0.4; P < .001). CONCLUSIONS: Aside from brain injury, reduced tissue temperature may also contribute to diffusion restriction on MR imaging in infants undergoing therapeutic hypothermia.
BACKGROUND AND PURPOSE: ADC changes are useful in detecting ischemic brain injury, but mechanisms other than tissue pathology may affect the kinetic movement and diffusion of water molecules. We aimed to determine the effects of brain temperature on the corresponding ADC in infants undergoing therapeutic hypothermia. MATERIALS AND METHODS: Brain temperature and ADC values in the basal ganglia, thalamus, cortical GM, and WM were analyzed during and after therapeutic hypothermia. The study cohort was categorized as having no-injury or injury. Among infants without injury, the correlation between ADC values and temperature was analyzed using the Pearson correlation. Intrasubject comparison of ADC changes during and after therapeutic hypothermia were analyzed, excluding patients who had an MR image interval of >5 days to minimize the effects of injury evolution. RESULTS: Thirty-nine infants with hypoxic-ischemic encephalopathy were enrolled (23 no-injury; 16 injury). The median ADC was significantly lower during therapeutic hypothermia (837; interquartile range, 771-928, versus 906; interquartile range, 844-1032 ×10-6mm2/s; P < .001). There was no difference in the ADC between the no-injury and injury groups during therapeutic hypothermia (823; interquartile range, 782-868, versus 842; interquartile range, 770-1008 ×10-6mm2/s; P = .4). In the no-injury group, in which ADC is presumed least affected by the evolution of injury, the median ADC was significantly lower during therapeutic hypothermia (826; interquartile range, 771-866, versus 897; interquartile range, 846-936 ×10-6mm2/s; P < .001). There was a moderate correlation between temperature and ADC in the no-injury group (during therapeutic hypothermia: Spearman ρ, 0.48; P < .001; after therapeutic hypothermia: ρ, 0.4; P < .001). CONCLUSIONS: Aside from brain injury, reduced tissue temperature may also contribute to diffusion restriction on MR imaging in infants undergoing therapeutic hypothermia.
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