Abstracts

Delayed abnormalities in diffusion following perinatal hypoxia-ischaemia to the brain: a marker for secondary injury and a late therapeutic window?

Presented at the Neonatal Society 2003 Autumn Meeting.

Rutherford MA1, Counsell SJ1, Allsop JM1, Boardman JM2, Kapellou O2, Edwards D2, Cowan FM2

Robert Steiner MR Unit, Imaging Sciences Department, Hammersmith Hospital, Du Cane Road London W12 OHS, UK
Division of Paediatrics, Obstetrics & Gynaecology, Imperial College, Hammersmith Hospital, Du Cane Road London W12 OHS, UK

Introduction: Following severe perinatal hypoxia-ischaemia at term the most common pattern of brain injury seen on magnetic resonance imaging (MRI) is bilateral damage to the basal ganglia and thalami (BGT), which is associated with later motor impairment. However even if initial white matter (WM) images are normal, infants with BGT lesions often develop WM atrophy, which relates to additional cognitive impairment. We postulate that this atrophy occurs consequent on injury to the central grey matter.

Aim: This study used diffusion weighted MR imaging (DWI) to address the question: is there evidence of delayed onset microstructural abnormality in WM of infants with BGT injury and initially normal WM after perinatal hypoxia-ischaemia at term?

Methods: Ethical approval for this study was obtained from the Hammersmith Hospitals Trust Research Ethics Committee. MR imaging was performed using a 1.5 Tesla Philips Eclipse Scanner. Images were obtained with conventional T1 and T2 weighted sequences. DWI was acquired using single shot echo planar imaging (EPI) at multiple levels. Fifteen slices of 5mm thickness were obtained (TR 6000ms, TE 110ms, FOV 24cm, b values of 0 and 1000 s/mm²) in three orthogonal directions. The total acquisition time was 37 seconds. Analysis of the DWI was undertaken using in house software, and apparent diffusion coefficients (ADC) were measured using the diffusion trace maps.

Results: 17 infants with BGT lesions following perinatal asphyxia and 15 term born control infants were studied. WM was normal on MR imaging during the first week, and in patients with BGT lesions ADC values in WM during the first week were similar to controls. In scans performed after the first week ADC values in WM were significantly higher than both those imaged during the first week and those in all the controls in all WM brain regions studied.

Delayed abnormalities in diffusion following perinatal hypoxia-ischaemia to the brain: a marker for secondary injury and a late therapeutic window?


Table 1. ADC x10ˉ³ mm²/sec values in the white matter of controls and patients *p<0.05

Discussion: ADC values normally decrease after normal delivery, but were found to increase >7 days following perinatal hypoxia-ischaemia, consistent with a delayed injury effecting axons and/or oligodendrocytes. This secondary injury may be amenable to interventions in the first week following perinatal hypoxia-ischaemia.

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