Preterm cranial ultrasound scanning is both feasible and effective in a middle-income country

© 2016 Foundation Acta Pædiatrica. Published by John Wiley & Sons Ltd.Aim Cranial ultrasound is seldom used in middle-income countries, and the burden of preterm brain injury and its relationship to perinatal data is unknown. We assessed cranial ultrasound abnormalities in very low-birthweight (VLBW) infants and correlated the findings with perinatal data. Methods VLBW Armenian infants receiving neonatal intensive care in 2012 were scanned from birth to term-equivalent age (TEA). Clinical data were collected prospectively. Results We studied 100 VLBW infants with a median gestation of 30 weeks. Periventricular white matter echogenicity (PVE) lasting more than two weeks was seen in 34 infants, grade III intraventricular haemorrhage (IVH) in 10, haemorrhagic parenchymal infarction (HPI) in seven and cystic periventricular leukomalacia in two. Caudothalamic notch echogenicity appeared in 36 infants after two to three weeks, with cystic transformation in 22. At TEA, 17 infants had persisting PVEs and 55 had increased basal ganglia/thalamic (BGT) echogenicity. Lack of antenatal steroids was significantly associated with IVH and HPI and intubation at birth with IVH. Late BGT echogenicity was generally seen in infants without perinatal problems. Conclusion Our study demonstrated that cranial ultrasound can be used effectively in a middle-income country to identify high-risk infants and monitor quality of care

Disruption of raphe serotonergic neural projections to the cortex: a potential pathway contributing to remote loss of brainstem neurons following neonatal hypoxic-ischemic brain injury

Neuronal injury is a key feature of neonatal hypoxicischemic (HI) brain injury. However, the mechanisms underpinning neuronal losses, such as in the brainstem, are poorly understood. One possibility is that disrupted neural connections between the cortex and brainstem may compromise the survival of neuronal cell bodies in the brainstem. We investigated whether brainstem raphe serotonergic neurons that project to the cortex are lost after HI. We also tested if neuroinflammation has a role in disrupting brainstem raphe projections. Postnatal day 3 (P3) rats underwent unilateral carotid artery ligation followed by hypoxia (6% oxygen for 30 min). A retrograde tracer, choleratoxin b, was deposited in the motor cortex on P38. On P45 we found that retrogradely labelled neurons in the dorsal raphe dorsal, ventrolateral, interfascicular, caudal and ventral nuclei were lost after P3 HI. All retrogradely labelled neurons in the raphe nuclei were serotonergic. Numbers of retrogradely labelled neurons were also reduced in the ventromedial thalamus and basolateral amygdala. Minocycline treatment (45 mg/kg 2 h post-HI, 22.5 mg/kg daily P4P9) attenuated losses of retrogradely labelled neurons in the dorsal raphe ventrolateral, interfascicular and ventral raphe nuclei, and the ventromedial thalamus. These results indicate that raphe neurons projecting to the cortex constitute a population of serotonergic neurons that are lost after P3 HI. Furthermore, neuroinflammation has a role in the disruption of raphe and thalamic neural projections. Future studies investigating the cellular mechanisms of axonal degeneration may reveal new targets for interventions to prevent neuronal losses after neonatal HI