Kim Annink

95 The long-term effect of perinatal asphyxia on hippocampal volumes INTRODUCTION The prevalence of hypoxic-ischemic encephalopathy (HIE) after perinatal asphyxia is 1.5 per 1000 live-born term neonates (1). Despite the introduction of hypothermia, the current standard of care, still around 45% of the infants with HIE die or have neurological deficits, such as cerebral palsy (CP), epilepsy or cognitive impairment (2). This risk is especially increased in infants with moderate and severe HIE according to the Sarnat criteria (3). In the past, it was considered unlikely that cognitive deficits in the absence of CP could be due to HIE, but nowadays, it is widely accepted that infants with HIE can develop isolated cognitive deficits (4). The first landmark paper looking at long-term cognitive outcome following HIE, found that survivors of moderate HIE who did not develop CP had similar receptive vocabulary and perceptual motor skill outcomes as controls, but showed marked delays in reading, spelling and arithmetic (5). Several studies confirmed these findings and it became more accepted that survivors of HIE are at increased risk of cognitive impairment, even in the absence of motor deficits (4,6–9). In addition, several studies have now shown that even children with mild HIE experience more memory problems than controls, as well as behavioral and attention problems (10–13). We have shown in a previous publication using the same cohort, that HIE especially affects long-term episodic memory, verbal working memory and learning which are all associated with the degree of HIE (10). Several studies, in different populations, have shown that (episodic) memory impairment might be related to smaller hippocampal volumes (14,15). The hippocampus is a specific brain structure that is specifically vulnerable to hypoxia. In addition, some small sample-sized studies suggested smaller hippocampal volumes in HIE compared to controls (6,8,16). However, these groups were heterogeneous and the relation between the hippocampus and memory functioning following HIE has not been fully elucidated. The primary aim of this study is to evaluate the effect of neonatal HIE on hippocampal volumes in 9- to 10-year-old children. The secondary aim is to investigate whether these hippocampal volumes are associated with the previously found impaired memory and cognitive functions in HIE in the current cohort (10). 5

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