Hippocampal damage and memory impairment in congenital cyanotic heart disease.

Mónica Muñoz‐López,Martin J Chadwick,Kling Chong,Tina Banks,Michelle De Haan,Mortimer Mishkin,Faraneh Vargha‐Khadem,Torsten Baldeweg,David G Gadian,Aparna Hoskote,Anna M Dzieciol

doi:10.1002/hipo.22700

Abstract

ABSTRACTNeonatal hypoxia can lead to hippocampal atrophy, which can lead, in turn, to memory impairment. To test the generalizability of this causal sequence, we examined a cohort of 41 children aged 8‐16, who, having received the arterial switch operation to correct for transposition of the great arteries, had sustained significant neonatal cyanosis but were otherwise neurodevelopmentally normal. As predicted, the cohort had significant bilateral reduction of hippocampal volumes relative to the volumes of 64 normal controls. They also had significant, yet selective, impairment of episodic memory as measured by standard tests of memory, despite relatively normal levels of intelligence, academic attainment, and verbal fluency. Across the cohort, degree of memory impairment was correlated with degree of hippocampal atrophy suggesting that even as early as neonatal life no other structure can fully compensate for hippocampal injury and its special role in serving episodic long term memory. © 2017 Wiley Periodicals, Inc.

Highlights

Because the children had been selected on the basis, not of memory impairment nor of hippocampal damage, but of the presumed precipitating event, the findings provided especially strong evidence of a causal sequence: hypoxia followed by hippocampal damage followed by memory deficiency
To determine whether this causal sequence was generalisable to a hypoxic-ischaemic event with a different aetiology, we undertook a study of another cohort of children, this one having been treated at birth for transposition of the great arteries (TGA)
The cohort of children born with transposition of the great arteries (TGA) and treated with the arterial switch operation (ASO), like the cohort studied earlier that had sustained acute hypoxaemic respiratory failure (AHRF), showed significant memory impairment in association with abnormally small hippocampal volumes

Summary

Introduction

The vulnerability of the hippocampus and, of memory, to hypoxia/ischaemia has been reported in adults (Volpe and Hirst, 1983; Volpe et al, 1986; Zola-Morgan et al, 1986; Press et al, 1989; Rempel-Clower et al, 1996; Caine and Watson, 2000; Yonelinas et al, 2004; Allen et al, 2006; Di Paola et al, 2008), and in children (Vargha-Khadem et al, 1997; Gadian et al, 2000; Isaacs et al, 2003; De Haan et al, 2006; Golan and Huleihel, 2006). Because the children had been selected on the basis, not of memory impairment nor of hippocampal damage, but of the presumed precipitating event, the findings provided especially strong evidence of a causal sequence: hypoxia followed by hippocampal damage followed by memory deficiency. To determine whether this causal sequence was generalisable to a hypoxic-ischaemic event with a different aetiology, we undertook a study of another cohort of children, this one having been treated at birth for transposition of the great arteries (TGA). With ASO having markedly improved the possibility of survival in cases with TGA, it has become important to assess the risk of brain damage and neuropsychological impairment (von Rhein et al, 2014), with their implications for the survivors’ quality of life (Tyagi et al, 2014)

Methods

Results

Conclusion