J B De Vis1, E T Petersen2, T Alderliesten3, F Groenendaal4, L S de Vries5, F van Bel6, M J N L Benders7, J Hendrikse8. 1. Department of Radiology, University Medical Centre Utrecht, HP E 01.132, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: j.devis-2@umcutrecht.nl. 2. Department of Radiology, University Medical Centre Utrecht, HP E 01.132, P.O. Box 85500, 3508GA Utrecht, The Netherlands; Department of Radiotherapy, University Medical Centre Utrecht, HP Q 00.118, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: e.petersen-5@umcutrecht.nl. 3. Department of Neonatology, University Medical Centre Utrecht, HP KE 04.123.1, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: t.alderliesten-2@umcutrecht.nl. 4. Department of Neonatology, University Medical Centre Utrecht, HP KE 04.123.1, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: f.groenendaal@umcutrecht.nl. 5. Department of Neonatology, University Medical Centre Utrecht, HP KE 04.123.1, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: l.s.devries@umcutrecht.nl. 6. Department of Neonatology, University Medical Centre Utrecht, HP KE 04.123.1, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: f.vanbel@umcutrecht.nl. 7. Department of Neonatology, University Medical Centre Utrecht, HP KE 04.123.1, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: m.benders@umcutrecht.nl. 8. Department of Radiology, University Medical Centre Utrecht, HP E 01.132, P.O. Box 85500, 3508GA Utrecht, The Netherlands. Electronic address: j.hendrikse@umcutrecht.nl.
Abstract
BACKGROUND AND PURPOSE: Brain oxygen consumption reflects neuronal activity and can therefore be used to investigate brain development or neuronal injury in neonates. In this paper we present the first results of a non-invasive MRI method to evaluate whole brain oxygen consumption in neonates. MATERIALS AND METHODS: For this study 51 neonates were included. The T1 and T2 of blood in the sagittal sinus were fitted using the 'T2 prepared tissue relaxation inversion recovery' pulse sequence (T2-TRIR). From the T1 and the T2 of blood, the venous oxygenation and the oxygen extraction fraction (OEF) were calculated. The cerebral metabolic rate of oxygen (CMRO2) was the resultant of the venous oxygenation and arterial spin labeling whole brain cerebral blood flow (CBF) measurements. RESULTS: Venous oxygenation was 59±14% (mean±sd), OEF was 40±14%, CBF was 14±5ml/100g/min and CMRO2 was 30±12μmol/100g/min. The OEF in preterms at term-equivalent age was higher than in the preterms and in the infants with hypoxic-ischemic encephalopathy (p<0.01). The OEF, CBF and CMRO2 increased (p<0.01, <0.05 and <0.01, respectively) with postnatal age. CONCLUSION: We presented an MRI technique to evaluate whole-brain oxygen consumption in neonates non-invasively. The measured values are in line with reference values found by invasive measurement techniques. Preterms and infants with HIE demonstrated significant lower oxygen extraction fraction than the preterms at term-equivalent age. This could be due to decreased neuronal activity as a reflection of brain development or as a result of tissue damage, increased cerebral blood flow due to immature or impaired autoregulation, or could be caused by differences in postnatal age.
BACKGROUND AND PURPOSE: Brain oxygen consumption reflects neuronal activity and can therefore be used to investigate brain development or neuronal injury in neonates. In this paper we present the first results of a non-invasive MRI method to evaluate whole brain oxygen consumption in neonates. MATERIALS AND METHODS: For this study 51 neonates were included. The T1 and T2 of blood in the sagittal sinus were fitted using the 'T2 prepared tissue relaxation inversion recovery' pulse sequence (T2-TRIR). From the T1 and the T2 of blood, the venous oxygenation and the oxygen extraction fraction (OEF) were calculated. The cerebral metabolic rate of oxygen (CMRO2) was the resultant of the venous oxygenation and arterial spin labeling whole brain cerebral blood flow (CBF) measurements. RESULTS: Venous oxygenation was 59±14% (mean±sd), OEF was 40±14%, CBF was 14±5ml/100g/min and CMRO2 was 30±12μmol/100g/min. The OEF in preterms at term-equivalent age was higher than in the preterms and in the infants with hypoxic-ischemicencephalopathy (p<0.01). The OEF, CBF and CMRO2 increased (p<0.01, <0.05 and <0.01, respectively) with postnatal age. CONCLUSION: We presented an MRI technique to evaluate whole-brain oxygen consumption in neonates non-invasively. The measured values are in line with reference values found by invasive measurement techniques. Preterms and infants with HIE demonstrated significant lower oxygen extraction fraction than the preterms at term-equivalent age. This could be due to decreased neuronal activity as a reflection of brain development or as a result of tissue damage, increased cerebral blood flow due to immature or impaired autoregulation, or could be caused by differences in postnatal age.
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