Placental pathology associated with lenticulostriate vasculopathy (LSV) in preterm infants.

OBJECTIVE: Our aim was to examine the frequency and type of placental abnormalities in neonates with LSV. STUDY DESIGN: We prospectively reviewed cranial ultrasounds (cUS) from neonates born at ≤32 weeks of gestation at Parkland Hospital between 2012 and 2014. Our cohort included neonates with LSV and gestational age and sex matched controls with normal cUS. We retrieved placental pathology reports retrospectively and compared placental abnormalities in both groups. RESULTS: We reviewed 1351 cUS from a total of 407 neonates. Placental pathology evaluations were complete for 64/65 (98%) neonates with LSV and 68/70 (97%) matched controls. There were no significant differences for any type of placental abnormities between LSV and control groups. However, infants with highest stage LSV were more likely to have large for gestational age (LGA) placentas (p = 0.01). CONCLUSION: The association between LSV and LGA placenta may indicate a shared vascular response to an adverse prenatal environment.

Intrauterine Transmission of SARS-COV-2 Infection in a Preterm Infant.

We present a preterm infant who developed a fever and mild respiratory disease on the second day of life. Infant severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nasopharyngeal testing was positive at 24 and 48 hours of life. Placenta histopathology revealed SARS-CoV-2 infection by electron microscopy and immunohistochemistry. Further understanding of the risk factors that lead to in utero transmission of SARS-CoV-2 infection is needed.

Lenticulostriate vasculopathy in preterm infants: a new classification, clinical associations and neurodevelopmental outcome.

OBJECTIVE: To examine the inter-rater reliability for the diagnosis of LSV on cranial ultrasound (cUS), determine the risk factors associated with LSV and its progression, and examine neurodevelopmental outcome. STUDY DESIGN: Prospective case-control study of neonates ≤32wks of gestation assessed for LSV by serial cUS (n = 1351) between 2012 and 2014 and their neurodevelopment at 18-36mon-corrected age compared to controls. RESULTS: Agreement for LSV on cUS improved from Κappa 0.4-0.7 after establishing definitive criteria and guidelines. BPD was the only variable associated with the occurrence and the progression of LSV. Cytomegalovirus (CMV) infection occurred in one neonate (1.5%). Neurodevelopmental outcome of neonates with LSV did not differ from controls. CONCLUSIONS: Establishment of well-defined stages of LSV improves the reliability of the diagnosis and allows identification of neonates with progression of LSV. Although LSV was associated with BPD, it was not associated with congenital CMV infection.

Lenticulostriate vasculopathy in neonates: Is it a marker of cerebral insult? Critical review of the literature.

Although lenticulostriate vasculopathy (LSV) was recognized nearly 30 years ago, neonatologists and radiologists still question its clinical significance. The diagnosis of LSV may be highly subjective, resulting in many false negatives when the radiologist is not familiar with the lesion or false positive if over-read by those with special interest in this finding. There has been an increase in incidence of LSV since its recognition in 1985 which might reflect nothing more than a growing awareness of this finding on neonatal cranial ultrasound. On the other hand, improved ultrasound imaging technology may have enhanced identification of LSV. Prospective studies evaluating the presence, significance and diagnosis of LSV are limited and have produced conflicting results. Therefore, the associated risk factors and clinical relevance of LSV on cranial ultrasound remain unclear. This review will examine the existing literature.

Lenticulostriate vasculopathy in neonates: Perspective of the radiologist.

Lenticulostriate vasculopathy (LSV) is a diagnosis dependent on neonatal cranial ultrasound (US). The diagnosis of LSV requires the presence of linear or branching echogenicities in the area of the basal ganglia and/or thalamus on gray scale cranial US. Although the diagnosis of LSV is dependent on cranial US, there are no convincing correlates observed on either computerized tomography or magnetic resonance imaging. Moreover, the radiographic criteria for LSV on cranial US remain vague, and intra-observer correlations are generally reported to be poor. The purpose of this review is to examine the issues associated with the use of cranial US and the diagnosis of LSV, including alternative imaging, clinical abnormalities and the significance of LSV on cranial US.

The etiology of lenticulostriate vasculopathy and the role of congenital infections.

Lenticulostriate vasculopathy (LSV) refers to increased echogenicity of the penetrating vessels that supply the basal ganglia and segments of the internal capsule seen on cranial ultrasound. Initially identified in infants with congenital infection, LSV has now been associated with a variety of infectious and non-infectious conditions. Although robust epidemiologic studies are lacking, the available evidence does not support broad evaluation for multiple congenital infections when LSV is identified. We propose screening infants with LSV for congenital cytomegalovirus infection and ensuring that prenatal screening included appropriate testing for syphilis, human immunodeficiency virus, and rubella-immune status. Large, prospective observational studies are needed to determine the incidence of LSV and the relative contribution of infectious and non-infectious conditions to LSV in the neonate.

Lenticulostriate vasculopathy in extremely low gestational age newborns: Inter-rater variability of cranial ultrasound readings, antecedents and postnatal characteristics.

Although lenticulostriate vasculopathy (LSV) was first detected on a cranial ultrasound nearly 30 years ago, its clinical implications and significance remain unknown. The objective of this study was to evaluate the inter-rater reliability of cranial ultrasound readings of LSV, and to explore relationships with potential antecedents and developmental correlates in extremely low gestational age newborns. Of the 1506 infants enrolled during the years 2002-2004, 1450 had at least one set of ultrasound scans evaluated for LSV and 939 had all three sets. To evaluate the inter-rater agreement for identifying LSV, we compared readings from two independent radiologists on days 1-4, 5-14, and on or after day 15. We then evaluated the relationships between LSV and maternal, antenatal, and postnatal characteristics. Our results showed that kappa values were 0.18, 0.33, and 0.36 on days 1-4, days 5-14, and day 15 or greater. Infants who were identified as LSV positive by two readers had higher Score for Neonatal Acute Physiology-II (an illness severity indicator), higher rates of tracheal infection and bacteremia, lower partial pressure of arterial oxygen and pH levels on 2 of the first 3 postnatal days, and they were more likely to have a lower psycho-motor development index at age 2 years. Positive agreement on the presence of LSV was low, as was the kappa value, an index of inter-rater reliability. Infants with high illness severity scores and their correlates were at increased risk of developing LSV, while those who develop LSV appear to be at increased risk of motor dysfunction.

Amplitude-integrated EEG in preterm infants: maturation of background pattern and amplitude voltage with postmenstrual age and gestational age.

OBJECTIVE: Amplitude-integrated electroencephalogram (aEEG) is a single channel EEG recorded from two parietal electrodes. The objective of this study was to test the hypothesis that aEEG maturation follows postmenstrual age (PMA) irrespective of gestational age (GA). METHODS: We recruited inborn infants with a GA <33 weeks and without evidence of neurologic anomaly. Serial aEEG recordings were assessed for: presence of continuous activity and mature sleep-wake cycling (SWC); low base voltage (V), that is, the lowest amplitude margin; high base V, that is, the most common amplitude margin; upper high V, that is, upper margin during highest activity; and span, that is, the difference between upper high and simultaneous high base V. Statistical analysis included logistic regression and repeated measures analysis of variance. RESULTS: We obtained 119 aEEG recordings in 31 preterm infants (GA 25 to 32 weeks; birth weight 600 to 1704 g, PMA 25 to 35 weeks). The frequency of mature SWC increased with PMA independent of GA, while the frequency of continuity increased with PMA and was higher in extremely preterm infants after correcting for PMA. Low base and high base V increased with PMA, while span and upper high V significantly decreased with PMA. In addition, high base V was higher in extremely preterm infants after correcting for PMA. CONCLUSIONS: In preterm infants aEEG matures predominantly with PMA. Our data suggest that some aspects of aEEG maturation are enhanced, rather than inhibited by extremely preterm birth. These data suggest that aEEG in preterm infants may need to be analyzed by comparing results with standards of similar PMA and GA.