Abstract

Background: The pathogenesis and clinical significance of lenticulostriate vasculopathy (LSV) are unclear. Our study aimed to determine the prevalence, presentation, and evolution of LSV, and the perinatal risk factors associated with LSV among very-low-birth-weight (VLBW) preterm infants. Methods: One-hundred-and-thirty VLBW preterm infants were retrospectively enrolled in this study. Serial cranial ultrasound examinations were performed regularly from birth until a corrected age of 1 year. Infants with LSV were assigned to early-onset (≤10 postnatal days) and late-onset (>10 postnatal days) groups. Data describing the infants’ perinatal characteristics, placental histopathology, and neonatal morbidities were collected, and the groups were compared. Results: Of the VLBW infants, 39.2% had LSV before they were 1 year old. Linear-type LSV was the most common presentation, and >50% of the infants had bilateral involvement. LSV was first detected at 112 ± 83 postnatal days, and its detection timing correlated negatively with gestational age (GA) (R2 = 0.153, p = 0.005) and persisted for 6 months on average. The infants with and without LSV had similar perinatal characteristics, placental pathologies, cytomegalovirus infection rates, and clinical morbidities. The late-onset LSV group comprised 45 (88.2%) infants who had a significantly higher rate of being small for gestational age (SGA) and used oxygen for longer than the infants without LSV. After adjusting a multivariable regression model for GA and SGA, analysis showed that the duration of oxygen usage was an independent risk factor for late-onset LSV development in VLBW infants (odds ratio: 1.030, p = 0.032). Conclusion: LSV may be a nonspecific marker of perinatal insult to the developing brains of preterm infants. Prolonged postnatal oxygen usage may predispose VLBW preterm infants to late-onset LSV development. The long-term clinical impacts of LSV should be clarified.

Highlights

  • Lenticulostriate vasculopathy (LSV) refers to hyperechogenic vessels detected in neonates’ thalami and basal ganglia, using cranial ultrasound

  • GA, gestational age; GDM, gestational diabetes mellitus; HCAM, histological chorioamnionitis; LGA, large for gestational age; LSV, lenticulostriate vasculopathy; NEC, necrotizing enterocolitis; PDA, patent ductus arteriosus; PPROM, preterm premature rupture of the membranes; RDS, respiratory distress syndrome; SGA, small for gestational age; ROP, retinopathy of prematurity. This 7-year retrospective, observational cohort study enrolled all VLBW preterm infants born at a single institution

  • We found that LSV is not an uncommon finding of preterm VLBW and is persistent

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Summary

Introduction

Lenticulostriate vasculopathy (LSV) refers to hyperechogenic vessels detected in neonates’ thalami and basal ganglia, using cranial ultrasound (cUS). Growing awareness of LSV over the past 10 years has led to demonstrations of its associations with a variety of fetal and neonatal diseases, which can antenatally or postnatally affect the developing brain [1]. Grant et al described LSV as branching echogenic structures on cUS images from a neonate with cytomegalovirus (CMV) infection [1]. The incidence of LSV in preterm neonates varies from 2.2% to 32% [3,4]. Our study aimed to determine the prevalence, presentation, and evolution of LSV, and the perinatal risk factors associated with LSV among very-low-birth-weight (VLBW) preterm infants. Results: Of the VLBW infants, 39.2% had LSV before they were 1 year old. LSV was first detected at 112 ± 83 postnatal days, and its detection timing correlated negatively with gestational age (GA)

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