Abstracts

White matter injury can lead to cognitive deficits without major motor deficits following perinatal asphyxia and early encephalopathy

Presented at the Neonatal Society 2003 Spring Meeting.

Cowan F, Dubowitz L, Mercuri E, Counsell S, Rutherford M

Department of Paediatrics, Imperial College, Hammersmith Hospital, London, UK

Purpose: to assess the outcome of term born infants with perinatal asphyxia and neonatal encephalopathy whose early brain MRI scans showed abnormality in the white matter (WM) without involvement of the central grey matter (basal ganglia and thalami).

Experimental design: From 1991 – 2000, all inborn and referred term infants, with evidence for fetal distress (abnormal CTG and/or meconium), Apgar scores = 6 at 5 min, cord pH < 7.0 and BE > -15 mmol, the need for resuscitation and an early encephalopathic illness had a neonatal brain MRI scan. The WM was scored for mild, moderate or severe abnormality, based on tissue T1 and T2. Eighteen infants who fulfilled the entry criteria but had normal scans were studied for comparison. No infant had evidence for congenital, metabolic or infective disease. Neurodevelopmental status at a minimum of 2 years was obtained in all children and all had follow up scans.

Results: Forty-four infants (16% of the total studied) had WM abnormality (19 mild, 13 moderate and 12 severe) without abnormality in the central grey matter. Infants with normal scans and mild WM abnormality were normal at follow up bar 3 with mild language delay. Follow up scans were normal or had very mild long T2 in the WM.

Of the 13 children with moderate WM abnormality 12 were independently mobile. Six had DQs < 85, 5 became microcephalic, 3 had seizures and 6 behavioural problems. Two had feeding difficulties, 8 concerns about hearing and/or language and two strabismus. Follow up MRI scans showed some gliosis and reduction in WM volume +/- ventricular dilatation and a thinned posterior corpus callosum.

Of the 12 children with severe WM abnormality 6 had a diplegic pattern of cerebral palsy but all could be independently mobile. Eight had DQs of < 85 with learning and/or behavioural difficulties. Eight became microcephalic, 7 had seizures, 6 feeding difficulties, most had delay in language and hearing difficulties, 8 had strabismus and 3 other visual difficulties. For most infants follow up scans showed a marked reduction in WM volume, gliosis, widened sulci, ventricular dilatation and thinning of the corpus callosum. Three infants had scans with the appearance of periventricular leucomalacia.

Conclusions: These data show that significant cognitive deficits often with microcephaly, seizures, strabismus, and behavioural problems but unaccompanied by severe motor deficits occur in a small number of infants following term perinatal asphyxia.

References
1. Cowan F. Outcome after intrapartum asphyxia in term infants. Seminars in Neonatology. 2000; 5: 127-140.
2. Rutherford M et al. Hypoxic-ischaemic encephalopathy: early and late magnetic resonance imaging findings in relation to outcome. Arch Dis Child 1996;75:F145-151

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