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NEONATAL SOCIETY ABSTRACTS

Cerebral glucose metabolism measured by positron emission tomography (PET), magnetic resonance imaging (MRI), diffusion weighted imaging (DWI) and ¹H spectroscopy (MRS) in term newborn infants with hypoxic ischemic encephalopathy (HIE) after birth asphyxia

Presented at the Neonatal Society 2004 Summer Meeting (programme).

Thorngren-Jerneck K1, Burtscher I2, Geijer B2, Ohlsson T3, Sandell A3, Strand S-E3, Holtås S2

1 Department of Pediatrics, University Hospital, Lund, Sweden
2
Department of Neuroradiology, University Hospital, Lund, Sweden
3 Department of Radiation Physics, University Hospital, Lund, Sweden

Background: Severe birth asphyxia in term newborn infants is an important cause of cerebral palsy.

Aim: To investigate early changes in MRI, 1H-MRS, DWI in relation to cerebral metabolic rate of glucose (CMRgl) measured by PET, and outcome in terms of cerebral palsy, in term newborn infants with HIE after birth asphyxia.

Method: Six term infants (35-42 weeks) with HIE were studied with MRI, DWI and MRS (1.5 T MR unit; patient in sedation) at a postnatal age of 1-5 days. MR spectra were analysed for N-acetylaspartat (NAA), cholin, creatine and lactate. Four patients were studied with 2-18FDG-PET (2-[18F]fluoro-2-deoxy-D-glucose-PET, Scanditronic PC 384-7 PET-camera with a spatial resolution of 7 mm; no sedation) at postnatal age 7-11 days. HIE was classified according to Sarnat (mild, moderate or severe).

Results: All infants had signs of perinatal distress (first artery pH 6.88-7.09; base excess -25 to -16; low 5-minute Apgar score (< 4). Four infants developed moderate HIE and two severe HIE. Two infants with severe HIE died, two infants with moderate HIE developed cerebral palsy, one infant is healthy at 18 months follow up and one infant at present age of 7 month is not yet conclusive concerning outcome. On conventional MRI (T1 and T2) pathological signs were detectable at 1-5 days postnatal age in the ventral part of thalamus and posterior part of putamen. Increased signal on DWI was detectable in the thalamus in all infants with CP and both infants who died. In one infant with CP also parasagittal cortical changes were detectable. All but one child with moderate HIE and CP showed detectable lactate levels. Lactate levels were higher in cases with severe HIE compared to those with moderate HIE. In the two cases with severe HIE, creatine levels were lower compared to NAA levels than in cases with moderate HIE. All patients showed higher choline/NAA ratios than normal controls presented in the literature. In all four infants studied with PET, the most metabolically active brain areas were the deep subcortical parts, thalamus and basal ganglia. In two infants with CP after moderate HIE, quantitative values were measured with CMRglc 25,6 and 27,6 μmol/100g/min respectively.

Conclusion: This is the first study presenting MRI, DWI, MRS and CMRglc in infants with HIE.
MRI and DWI show pathologic alterations in patients with HIE. MRS might be useful in the prediction of clinical outcome in infants with perinatal asphyxia based on detectable lactate levels, decreased total creatine and decreased NAA levels, in patients with HIE. Infants who develop CP after HIE, have low cerebral glucose metabolism, when measured in the subacute phase after perinatal asphyxia.

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