Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study

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Pediatrics and Neonatology (2017) xx, 1e8

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Original Article

Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study ´le ´my Tosello a,b,*, Estelle Pipon c, Candice Fabre a, Barthe Catherine Gire a, Kathia Chaumoitre b,c a

Department of Neonatology, Assistance Publique-Hoˆpitaux de Marseille, Hoˆpital Nord, 13015, Marseille, France b Aix Marseille University, UMR 7268 ADE´S/EFS/CNRS, Marseille, France c Department of Medical Imaging, APHM, Hoˆpital Nord, 13015, Marseille, France Received May 22, 2017; received in revised form Nov 13, 2017; accepted Jan 2, 2018

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Keywords lenticulostriate vasculopathy; magnetic resonance imaging; newborn; outcome

Abstract Background: Lenticulostriate vasculopathy (LSV) is a hyperechogenicity of the lenticulostriate branches of the basal ganglia and/or thalamus’ middle cerebral arteries and is frequently seen in neonatology. Our study primarily describes the perinatal data and long-term follow-up of newborns with lenticulostriate vessel hyperechoic degeneration. Secondly, it describes the cerebral imaging data as a function of perinatal factors and neurodevelopmental follow-up of these newborns. Methods: This retrospective study assesses the outcome of newborns with LSV hyperechogenicity on cerebral ultrasound (two grades). These children were born between January 2008 and September 2015 and were treated in a large level III neonatal intensive care unit. Thirty-four term-equivalent age children underwent MRIs using a standardized protocol of T2, T1 3D, diffusion and spectro-MRI sequences. The MRIs retrospectively measured the white matter and basal ganglia apparent diffusion coefficients (ADC). Results: Fifty-eight neonates, ranging from 25 to 42 weeks gestational age (GA), were diagnosed with LSV. There was a significantly increased high-grade LSV when accompanied by fetal heart rate abnormalities (p Z 0.03) and the neonate’s need for respiratory support at birth (P Z 0.002). The mean ADC score was substantially superior in the high-grade versus the low-grade LSVs (p Z 0.023). There were no noteworthy outcome differences between a high and low grade LSV. The mean ADC for basal ganglions was appreciably higher in children with a severe prognoses (death or developmental disorder) as compared to children with no abnormalities (p < 0.01). Conclusion: From the results of our study, it appears that a low-grade LSV could be considered as a normal variant. There are no unifying diagnostic criteria for LSV on cerebral ultrasound. With a

* Corresponding author. Department of Neonatology, Assistance Publique des Ho ˆpitaux de Marseille (APHM), Ho ˆpital Nord, Chemin des Bourrely, 13015, Marseille. France. E-mail address: [email protected] (B. Tosello). https://doi.org/10.1016/j.pedneo.2018.01.002 1875-9572/Copyright ª 2018, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BYNC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002

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C. Fabre et al cerebral MRI, the use of ADC values of basal ganglia may well underscore the importance of such data in predicting long-term outcomes. Copyright ª 2018, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/ 4.0/).

1. Introduction Lenticulostriate vasculopathy (LSV) is a hyperechogenicity of the lenticulostriate branches of the basal ganglia and/or thalamus’ middle cerebral arteries.1 This frequent neonate echocardiographic abnormality is reported in 0.4e5.8% of newborns having had a brain ultrasound.2 LSV occurs in nearly 2.5% of preterm infants (20% of premature infants),3 and has no existing validated ultrasound criteria. Its most recent classifications describe a low grade LSV as having 1 or 2 fine striations, and a high grade has 3 striations or more.4 Nevertheless, the clinical significance, etiology and longterm consequences seen on a neonatal cerebral ultrasound (CUS) is unclear. By using magnetic resonance imaging (MRI), some authors have described LVS as an “increased T2 signal structure” corresponding to structures previously identified in ultrasounds. Others find no correlation between the ultrasound, scanner or MRI brain scans images. Advanced brain imaging techniques such as diffusion weighted MRI to obtain the diffusion coefficiency would therefore be interesting in describe these abnormalities. Initially, LSV was considered as associated with Cytomegalovirus 5; however, this association was extended to include other congenital infections, and then further encompassed non-infectious etiologies. These etiologies include perinatal asphyxia, twin pregnancies, twin twin transfusion syndrome, congenital malformations, and prematurity.6 LSV etiology investigations are essentially based on retrospective studies of a small number or series of cases with heterogeneous populations, thus biasing the interpretation of the results. A few studies have addressed the medium to long-term development of newborns with the relationships between LSV and perinatal factors being discordant. Our study’s primary objective was to describe the perinatal data and long-term follow-up of neonates with hyperechoic degeneration of lenticulostriate vessels. Secondary objectives described cerebral imaging data as a function of perinatal factors and neurodevelopmental follow-up.

2. Methods The study has been submitted to the Ethics Committee of the Aix-Marseille University in May 2016 and approved our study.

2.1. Patients Between January 2008 and September 2015, we conducted an observational study and retrospective analysis of

children born between 25 and 42 weeks gestational age (GA) with LSV hyperechogenicity on CUS. The analysis was unicentric and carried out in a French tertiary reference center. Exclusion criteria were infants with congenital abnormalities of the central nervous system, severe other congenital abnormalities, chromosomal and metabolic disorders or had an abnormal CUS with findings other than isolated LSV. Follow-up was completed (57/58, 98.2%) for all but one patient. The medium age of follow up was established at the time of data collection.

2.2. Methods Retrospective data were retrieved from our center through the newborns’ medical files. The perinatal variables studied were: maternal serologic status (toxoplasmosis, rubella, syphilis, human immunodeficiency virus (HIV), Cytomegalovirus (CMV)), alcohol or drug intake, gestational diabetes, autoimmune disease, eclampsia, administration of corticosteroids, magnesium sulphate or Rovalcyte, type of pregnancy, presence of transfuser-transfused syndrome parental and consanguinity. The neonatal variables studied were the duration of pregnancy, birth weight, Apgar, mode of delivery, serologic the newborns’ serologic status (toxoplasmosis, rubella, syphilis, HIV, CMV, listeria, herpes simplex virus (HSV)) in order to conclude that congenital infection is not related to LSV, existence of congenital malformation, Trisomy 21, AFHR (abnormal fetal heart rate) neonatal hypoglycemia, dysthyroidism, perinatal asphyxia, and the need for ventilator support. For preterm infants, sequential CUS were performed within 24 h of birth, at least weekly from the day of birth or admission until discharge or transfer to another hospital, and on the day of the term equivalent MRI examination. Regarding term infants, CUS were performed systematically in term infants with: dysmorphic features, seizures, perinatal asphyxia, low score Apgar (<7 a ` M5), hypotrophy, suspicion of CMV or toxoplasmosis infection, or case-bycase discussion. For our study, the preterm and term infants were excluded based on our criteria mentioned above in the text. For cerebral imaging, we chose an LSV classification, as seen on the CUS, in two grades (performed by two radiologists) according to the classification proposed by Shin et al.7:  Low grade: presence of one or two fine striations (Fig. 1A)  High grade: presence of at least 3 striations (Fig. 1B) We divided LSV into early-onset (first seen on initial or subsequent CUS performed  7 days of birth) and late-onset

Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002

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Figure 1 (A) Low grade: one or two thin echogenic branches (arrow) are visible on either side in the basal ganglia or thalamus. (B) High grade: three or more branches (arrow) are prominently visible in the basal ganglia or thalamus.

(first seen on CUS performed >7 days of birth), according the results of Leijser et al.3 MRI examinations were performed in preterm infants, preferably around or right after term equivalent age; and in term infants, in the 7 first days after the abnormality was first seen. We studied 34 children with MRI at termequivalent age using a standardized protocol of T2, T1 3D, diffusion and spectro-MRI sequences, and retrospectively measured the white matter (WM) and basal ganglia (BG) apparent diffusion coefficient (ADC) (Fig. 2). The main limitation of ADC relates to the orientation dependence of this coefficient (i.e., dependent on the measurement direction) and the lack of structural information. In order to correct any geometric distortion of the head and accentuation of the intracranial vasculature on echo-planar images, we used shorter TE at higher field strengths. The child’s neurodevelopmental outcome was gathered through clinical examination data and/or data provided by the child’s pediatrician. Moderate-severe neurodevelopmental impairment was defined as  1 for moderate to severe cerebral palsy (CP was defined according to Bax 8; referred to a number of non-progressive conditions involving predominantly motor deficiencies of varied semiology, secondary to cerebral anomalies occurring

during the development of the brain. This condition includes varying degrees of muscle tone, posture, voluntary movement, and automatic movement disorders); moderate to severe cognitive delay (assessed per behavior disturbance) severe visual impairment, defined as visual acuity, 6/60 (metric scale) in the better eye; or severe hearing impairment, defined as requirement of unilateral/bilateral hearing aids or cochlear implants. Follow-up was systematic. The children underwent cerebral MRIs without sedation and their parents received detailed test results (pathology, etiology and cerebral MRI).

2.3. Statistical analysis Data were analyzed using SPSS for Windows. A p-value of less than 0.05 was considered statistically significant. Categorical variables were described by frequencies and percentages, and continuous variables were described by means of standard deviation or medians and maximum/ minimums. Comparative analysis is done using Chi-2 or Fisher test for qualitative variables, and Student test or analysis of variance tests for quantitative variables. ManneWhitney & KruskalleWallis tests were used when the previous tests were not applicable.

Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002

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C. Fabre et al

Figure 2 High grade lenticulostriate vasculopathy on cerebral ultrasound (A and B) term newborn (37 1/7 weeks GA): three or more branches (arrow) are prominently visible in the basal ganglia or thalamus; (C) relation to cerebral MRI with ADC Basal ganglion (ADC value Z 1.42) (circle).

3. Results Between January 2008 and September 2015, 58 neonates ranging from 25 weeks GA to 42 weeks GA were born in our center’s Neonatal Intensive Care Unit and had an LSV hyperechogenicity on CUS. There were 3919 patients benefiting from a CUS between January 2008 and September 2015. The characteristics of this population (obstetrical and neonatal data) are reported in Table 1. There were no significant differences between the high and low grade LSV for these antenatal pathologies. For perinatal factors, low-grade LSV abnormalities were found in 30 children (41% prematurity), and high-grade LSV abnormalities were found in 28 children (58% prematurity). Low and high grade LSV levels were not significantly different in our preterm infants (p Z 0.989). By contrast (Table 2), a high-grade LSV was significantly higher in fetal heart rate abnormalities (p Z 0.03) and in neonates who needed respiratory support at birth (p Z 0.002). Table 3 reports perinatal and outcome data according to the age at which the LSV was discovered. Early onset LSV (<7 days of life) were found in 67.2% of our cohort. The rate of early or late LSV was not significantly different in the preterm population as compared to the term infant. Nevertheless, in the group of children born before 32 weeks GA, the rate of late LSV was significantly higher than early LSV (p < 0.001). A cerebral MRI was performed on 35 patients (60.1%), with 54.2% being performed on prematurely born children. After being completely informed about the MRI procedure and objectives, parents had the option to decline authorizing the examination (n Z 10). One patient was lost to follow-up and 11 patients were transferred to another neonatal unit. The mean ADC value for BG was significantly higher in the high-grade LSV as compared to the low-grade LSV (p Z 0.023) (Fig. 3). This difference was not found in the WM ADC averages.

Table 1

Perinatal characteristics of the neonates. Population N Z 58

Characteristics Obstetrical Data Negative Toxoplasmosis Serology, n (%) Viral fetal diseases CMV Rubella HIV mother Alcohol consumption Drug use Dysthyroidism, n (%) Pre-eclampsia Gestational diabetes Multiple pregnancies Antenatal corticotherapy, n (%) Magnesium Sulphate n (%) AFHRa, n (%) Cesarean, n (%) Neonatal Data Male Gender, n (%) Mean gestational age (SD) Prematurity < 37 weeks, n (%) Prematurity < 32 weeks, n (%) Mean birth weight, g (SD) Hypotrophy (<10 %ile), n (%) Macrosomia (>90 %ile), n (%) Apgar < 7 a ` M5, n (%) Respiratory support at birth, n (%) Hypoxic-ischemic encephalopathy, n (%) Age of first TFU, days, median (IQR) TFU LSV high grade, n (%) MRI brain scan, n (%) Abnormal brain MRI, n (%) a

20 (34.4) 3 (5.1) 1 (1.7) 1 (1.7) 1 (1.7) 1 (1.7) 1 (1.7) 2 (3.4) 11 (18.9) 7 (12.0) 19 (32.7) 6 (10.3) 12 (20.6) 26 (44) 21 (36.2) 36 (4) 29 (50) 18 (31) 2380 (1180) 3 (5.1) 10 (17.2) 16 (27.5) 36 (62) 6 (10.3) 17 (4) 28 (48.2) 35 (60.3) 22 (37.9)

Abnormal fetal heart rate.

Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002

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Hyperechogenicity of lenticulostriate vessels Table 2

Patient characteristics and grade of sonographic LVS.

Perinatal data Maternal age mean, years (SD) Twins, n (%) TTTSa, n (%) Gestational Diabetes, n (%) Maternal hypertension, n (%) Mg Treatmentb, n (%) Antenatal steroids, n (%) GAc mean, weeks (SD) BWd mean, g (SD) Hypotrophy <10 , n (%) Macrosomia >90 , n (%) Male Gender, n (%) Mode of delivery Vaginal, n (%) Cesarean, n (%) Apgar 5 min < 7, n (%) Mechanical ventilation, n (%) AFHRe, n (%) Perinatal asphyxia, n (%) Imaging MRI ADC_BGf, mean (SD) ADC_WMg, mean (SD) Outcome, n (%) Death Severe or moderate neurodevelopmental impairment Normal a b c d e f g h

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Low grade, n Z 30

High grade, n Z 28

P value

32.3 (5) 2 (6.6) 1 (0.58) 4 (2.32) 1 (3.3) 1 (0.58) 8 (26.6) 35 (4.3) 2694.7 (1149.4) 1 (0.45) 5 (2.25) 13 (43.3)

31.1 (6) 5 (17.8) 3 (1.74) 7 (4.06) 1 (3.5) 5 (2.9) 11 (39.2) 33.5 (6.1) 2171.8 (1175.1) 2 (0.9) 5 (2.25) 8 (28.5)

0.523 0.191 0.268 0.257 0.960 0.070 0.306 0.268 0.389 0.807 0.464 0.242

8 (3.6) 10 (4.5) 6 (2.28) 13 (7.54) 3 (1.74) 2 (1.16)

11 (4.95) 16 (7.2) 10 (3.8) 23 (13.34) 9 (5.22) 4 (2.32)

0.805 0.832 0.002 0.038 0.341

1.608 (0.236) 1.108 (0.111)

1.668 (0.214) 1.114 (0.103)

0.023 0.906

2 (1.14) 1 (0.57) 26 (14.56)

3 (1.71) 5 (2.85) 20 (11.4)

0.163h

Twin twin transfusion syndrome. Magnesium Sulphate Treatment. Mean gestational age. Mean birth weight. Abnormal fetal heart rate. Coefficient of Basal ganglia. Coefficient of white matter. Adjusted for GA.

The follow-up was available for 57 children: five (8.6%) children died, six (10.3%) children had a neurodevelopmental disorder and 46 (79.3%) children did not show any abnormality. The median age at the time of the analysis was 27 months (interquartile range [IQR] Z 17.7 months). Outcomes did not appear to have a significant difference between high and low grade LSV. However, the death rate was twofold higher in LSV when discovered earlier rather than later. Finally, the mean ADC for BG is significantly higher in children with a severe prognosis (death or developmental disorder) as compared to children without abnormalities (p < 0.01).

4. Discussion The impact of this abnormality in our center over seven years was 1.48%. While according to the literature,2 nevertheless this incidence was reported as increasing.3 Awareness of this abnormality, improved imaging techniques, and the increased risk factors may account for the current LSV rise.4 The LSV model was originally described as

a “mineralizing vasculopathy” suggesting a deposit of basophils in the arterial wall causing CUS echogenicity.9 Nevertheless, this vasculopathy (implied mineralization with positive staining for iron or calcium) was not found in more recent histological reports in neonates with ultrasound LSV. It could however be associated with hypoxic-ischemic lesions.10 Coley et al. have shown that all patients with LSV have cardiac lesions due to cyanosis, poor cardiac output, or both.10 More recently, visualized ultrasound LSV may prove to be transient in preterm infants.3 The various etiological diagnoses of LSV question the physiopathology of the ultrasound abnormality as well as its clinical importance and potentially long-term impact. In our cohort, we classified LSV in two groups according to the number of striations seen in the CUS.7 Low-grade LSV abnormalities were found in 30 children (41% prematurity) and high-grade LSV in 28 children (58% prematurity). Our analyses reported that high grade LSV levels were significantly higher for fetal heart rate abnormalities and when the need for respiratory support in the neonate at birth was necessary. There was, however, no significant difference between LSV of high and

Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002

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C. Fabre et al Table 3

Patient characteristics and age at ultrasound diagnosis.

Perinatal data Maternal age mean, years (SD) Twins, n (%) TTTSa, n (%) Gestational Diabetes, n (%) Maternal hypertension, n (%) Mg Treatmentb, n (%) Antenatal steroids, n (%) GAc mean, weeks (SD) BWd mean, g (SD) Hypotrophy <10 , n (%) Macrosomia >90 , n (%) Male Gender, n (%) Mode of delivery Vaginal, n (%) Cesarean, n (%) Apgar 5 min < 7, n (%) Mechanical ventilation, n (%) AFHRe, n (%) Perinatal asphyxia, n (%) Imaging data Cranial ultrasound: High grade, n (%) ADC_BGf, mean (SD) ADC_WMg, mean (SD) Outcome, n (%) Death Severe or moderate neurodevelopmental impairment Normal a b c d e f g h

LSV early (
LSV late (>7 d), n Z 19

P value

32.5 (6) 2 (5.1) 2 (5.1) 8 (20.5) 2 (5.1) 2 (5.1) 9 (23.0) 36.3 (4.4) 2814.3 (1066.8) 3 (7.6) 8 (20.5) 13 (33.3)

31.9 (5.5) 5 (2.6) 2 (10.5) 3 (15.7) 0 (0) 4 (21.0) 10 (52.6) 30.1 (4.9) 1593.3 (968.0) 0 (0) 2 (10.5) 8 (42 0.1)

0 0.525 0.020 0.446 0.667 0.315 0.062 0.024 <0.001 <0.001 0.182 0.244 0.514

12 (33.3) 17 (43.5) 10 (25.6) 21 (53.8) 1 (2.5) 6 (15.3)

7 (36.8) 9 (47.3) 6 (31.5) 15 (78.9) 3 (15.7) 0 (0)

0.878 0.715 0.064 0.012 0.045

17 (43.5) 1.643 (0.221) 1.109 (0.099)

11 (57.8) 1.650 (0.230) 1.117 (0.119)

0.306 0.889 0.693

4 (10.2) 1 (2.5) 34 (87.1)

1 (5.2) 5 (26.3) 13 (68.4)

0.015h

Twin twin transfusion syndrome. Magnesium Sulphate Treatment. Mean gestational age. Mean birth weight. Abnormal fetal heart rate. Coefficient of Basal ganglia. Coefficient of white matter. Adjusted for GA.

low grades for antenatal pathologies classically described as LSV providers. These results are consistent with the latest studies, notably Cantey et al. in 2015.6 In this review of the literature, no significant association between congenital infections and the onset of LSV were found. On the other hand, the lenticulostriate vessels, perforating branches of the middle cerebral artery supplying the central grey nuclei, are very sensitive to variations in oxygen supply. Indeed, basal and thalamus ganglia having high metabolic demand,11,12 and perforating arteries lacking a rich capillary network,13 are in fact very vulnerable to hypoxicischemic wounds. Our outcome analysis was available for 57 children with a median age of 27-months when data were collected. We did not find any significant differences between high and low grade LSV (adjusted for GA). Very few studies are available on the long-term outcome of newborns with LSV which correspond to a small number of children with discordant results. Most of them showed that LSV, when isolated, had no impact on the neurological outcome of

these children.14,15 In a recent retrospective study, the rate of neurodevelopmental abnormalities was 6.3% (7/110), especially in the case of underlying pathology such as congenital heart disease. The association between LSV and neurodevelopmental disorders disappeared in multivariate analysis (LSV of low grade, Odds ratio 3.29 (0.39e27.78) p Z 0.28 and LSV of high grade, 6.90 (0.90e2.94) p Z 0.06).7 Our study’s secondary objectives were to describe cerebral imaging data in terms of perinatal factors and neurodevelopmental follow-up. More than half of the children had a cerebral MRI with diffusion sequence and a metabolic study. The mean BG ADC (higher ADC) was significantly associated with high-grade LSV. There was also a significant difference in the mean BG ADC (higher ADC) between children with normal follow-up, and children with a severe prognosis (death or developmental disorder). In the BG, apparent diffusion coefficient values decrease with maturation (gradual decrease due to fast neuronal densification with ongoing myelination16) and precipitously within the first 2 years, and then decline gradually.17

Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002

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Hyperechogenicity of lenticulostriate vessels

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Figure 3 Relationship between lenticulostriate vasculopathy (LVS) grades and apparent diffusion coefficient (ADC of basal ganglion (BG)); R2 Z 0.471, p Z 0.023.

We also observed a decrease with gestational age at birth (impacting cerebral maturation) (Fig. 3). Added to that, the underlying pathogenesis of LSV is unclear and several potential pathways have been suggested. A delay in maturation linked to the pathogenesis of LSV could be an argument for the increase in the ADC in the high grade context. Few studies have focused on brain exploration using MRI for LSV.18 For Leijser et al.,3 no abnormalities in the BG region were reported in the MRI of 99 preterm at term-equivalent age. Moreover, and in agreement with our results, Leijser et al. demonstrated that newborns with a late LSV onset had significantly lower birth weight than those with an early LSV onset. On the other hand, the first detection of LSV with a CUS was identical between the two groups. The gestational age of birth is an important indicator in the development of LSV with the lenticulostriate vessels being the most vulnerable around this term age. This hypothesis is supported by the fact that term infants have LSV close to their birth, whereas in premature infants, the anomaly appears more often several weeks after their birth (from 31 to 32 weeks of post menstrual age). The main limitations of our study were the retrospective methodology, small cohort and having no control group of normal neonates who underwent a brain ultrasound. However, we assumed that our cohort was at cerebral risk, given their clinical evolution. Neurodevelopmental outcome of preterm infants showed that the distribution of developmental scores was typical for this population. Furthermore, comparison with healthy control term neonates was not available. Second, there was selection bias in the included patient population (in tertiary center, CUS is not a routine). Large, multicenter, prospective cohort studies are needed to determine the incidence of LSV. Our study shows the

necessity to specify the ultrasound criteria and to grade the impairment as well as the interest of a cerebral metabolic study using magnetic resonance spectroscopy techniques.

5. Conclusion Consistent with recent literature, LSV does not appear to be associated with congenital infections but rather with hypoxic-ischemic conditions. From the results of our study, it would seem that low-grade LSV should be considered as a normal variant. As a result, not all newborns having a low-grade LSV as the only CUS abnormality should gain an advantage from having a cerebral MRI at a later date. On the other hand, all children with high-grade LSV require an MRI, and those with increased ADC on the MRI should have close neurological follow-up.

Conflicts of interests The authors declare that they have no conflicts of interest with respect to the authorship or publication of this article.

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Appendix A. Supplementary data Supplementary data related to this article can be found at https://doi.org/10.1016/j.pedneo.2018.01.002.

Please cite this article in press as: Fabre C, et al., Hyperechogenicity of lenticulostriate vessels: A poor prognosis or a normal variant? A seven year retrospective study, Pediatrics and Neonatology (2017), https://doi.org/10.1016/j.pedneo.2018.01.002