Magnetic resonance (MR) imaging studies have demonstrated reduced global and regional brain volumes in infants with congenital heart disease (CHD). This study aimed to provide a more detailed evaluation of altered structural brain development in newborn infants with CHD compared to healthy controls using tensor-based morphometry (TBM). We compared brain development in 64 infants with CHD to 192 age- and sex-matched healthy controls. T2-weighted MR images obtained prior to surgery were analysed to compare voxel-wise differences in structure across the whole brain between groups. Cerebral oxygen delivery (CDO2) was measured in infants with CHD (n = 49) using phase contrast MR imaging and the relationship between CDO2 and voxel-wise brain structure was assessed using TBM. After correcting for global scaling differences, clusters of significant volume reduction in infants with CHD were demonstrated bilaterally within the basal ganglia, thalami, corpus callosum, occipital, temporal, parietal and frontal lobes, and right hippocampus (p < 0.025 after family-wise error correction). Clusters of significant volume expansion in infants with CHD were identified in cerebrospinal fluid spaces (p < 0.025). After correcting for global brain size, there was no significant association between voxel-wise brain structure and CDO2. This study localizes abnormal brain development in infants with CHD, identifying areas of particular vulnerability.

ObjectiveThresholds of cerebral hypoxia through monitoring of near-infrared spectroscopy tissue oxygenation index (TOI) were used to investigate the relationship between intraventricular haemorrhage (IVH) and indices of hypoxia.DesignProspective observational study.SettingA single-centre neonatal intensive care unit.PatientsInfants <28 weeks’ gestation with an umbilical artery catheter.MethodsThresholds of hypoxia were determined from mean values of TOI using sequential Χ2 tests and used alongside thresholds from existing literature to calculate percentage of time in hypoxia and burden of hypoxia below each threshold. These indices were then compared between IVH groups.Results44 infants were studied for a median of 18.5 (range 6–21) hours in the first 24 hours of life. Sequential Χ2 analysis yielded a TOI threshold of 71% to differentiate between IVH (16 infants) and no IVH (28 infants). Percentage of time in hypoxia was significantly higher in infants with IVH than those without, using thresholds of 60%–67%. Burden of hypoxia was significantly higher in infants with IVH than without, using thresholds of 62%–80%. With the threshold of 71%, percentage of time in hypoxia was lower by 12.2% with a 95% CI of (−25.7 to 1.2) (p=0.073), and the burden of hypoxia was lower by 29.2% hour (%h) (95% CI −55.2 to −3.1)%h (p=0.012) in infants without IVH than those with IVH.ConclusionsUsing defined TOI thresholds, infants with IVH spent higher percentage of time in hypoxia with higher burden of cerebral hypoxia than those without, in the first 24 hours of life.

Congenital heart disease (CHD) is the most frequent congenital abnormality. Most infants born with CHD now survive. However, survivors of CHD are at increased risk of neurodevelopmental impairment, which may be due to impaired brain development in the fetal and neonatal period. Magnetic resonance imaging (MRI) provides objective measures of brain volume and growth. Here, we review MRI studies assessing brain volume and growth in individuals with CHD from the fetus to adolescence. Smaller brain volumes compared to healthy controls are evident from around 30 weeks gestation in fetuses with CHD and are accompanied by increased extracerebral cerebrospinal fluid. This impaired brain growth persists after birth and throughout childhood to adolescence. Risk factors for impaired brain growth include reduced cerebral oxygen delivery in utero, longer time to surgery and increased hospital stay. There is increasing evidence that smaller total and regional brain volumes in this group are associated with adverse neurodevelopmental outcome. However, to date, few studies have assessed the association between early measures of cerebral volume and neurodevelopmental outcome in later childhood. Large prospective multicentre studies are required to better characterise the relationship between brain volume and growth, clinical risk factors and subsequent cognitive, motor, and behavioural impairments in this at-risk population.

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Cortical spreading depolarisation (CSD) is an emerging mode of secondary neuronal damage in acute brain injury (ABI). Subsequent repolarisation is a metabolic process requiring glucose. Instances of CSD and glucose derangement are both linked to poor neurological outcome, but their causal interrelationship is not fully defined. This systematic review seeks to evaluate the available human evidence studying CSD and glucose to further understand their dynamic relationship. We conducted a systematic review of studies examining CSD through electrocorticography and cerebral/systemic glucose concentrations in ABI, excluding animal studies. The search yielded 478 articles, of which 13 were eligible. Across 10 manuscripts, 125 patients received simultaneous monitoring, with 1,987 CSD episodes observed. 8/10 studies observed correlation between CSD and glucose change. 7/8 studies observed possible cumulative effect of recurrent CSD on glucose derangement and two identified correlation between glycopenia and incidence of CSD. These findings confirm a relationship between CSD and glucose, and suggest it may be cyclical, where CSD causes local glycopenia, which may potentiate further CSD. Positive observations were not common to all studies, likely due to differing methodology or heterogeneity in CSD propensity. Further study is required to delineate the utility of the clinical modulation of serum and cerebral glucose to alter the propensity for CSD following brain injury.

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