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Original research
Effect of gestational age on cerebral lesions in neonatal encephalopathy
  1. Lauren Binet1,
  2. Thierry Debillon1,2,
  3. Jonathan Beck3,
  4. Antoine Vilotitch4,
  5. Isabelle Guellec5,
  6. Anne Ego2,6,
  7. Marie Chevallier1,2
  8. on behalf of the LYTONEPAL research group
    1. 1 Neonatal Intensive Care Unit, Grenoble Alpes University Hospital, Grenoble, France
    2. 2 Université Grenoble Alpes, CNRS, Public Health Department, Grenoble Alpes, Grenoble Institute of Engineering, TIMC-IMAG, Grenoble, France
    3. 3 Department of Neonatology, Reims University Hospital Alix de Champagne, Reims, France
    4. 4 Univversité Grenoble Alpes, Data Engineering Unit, Public Health Department, Grenoble Alpes University Hospital, Grenoble, France
    5. 5 7 Neonatal Intensive Care Medicine Department, University Hospital Nice Cote d'Azur, Nice, France
    6. 6 Université de Paris, CRESS, Obstetrical Perinatal and Pediatric Epidemiology Research Team, EPOPé, INSERM, INRAE, F-75004, Paris, France
    1. Correspondence to Dr Marie Chevallier; MChevallier3{at}chu-grenoble.fr

    Abstract

    Objective To determine the risk on brain lesions according to gestational age (GA) in neonates with neonatal encephalopathy.

    Design Secondary analysis of the prospective national French population-based cohort, Long-Term Outcome of NeonataL EncePhALopathy.

    Setting French neonatal intensive care units.

    Patients Neonates with moderate or severe neonatal encephalopathy (NE) born at ≥34 weeks’ GA (wGA) between September 2015 and March 2017.

    Main outcome measures The results of MRI performed within the first 12 days were classified in seven injured brain regions: basal ganglia and thalami, white matter (WM), cortex, posterior limb internal capsule, corpus callosum, brainstem and cerebellum. A given infant could have several brain structures affected. Risk of brain lesion according to GA was estimated by crude and adjusted ORs (aOR).

    Results MRI was available for 626 (78.8%) of the 794 included infants with NE. WM lesions predominated in preterm compared with term infants. Compared with 39–40 wGA neonates, those born at 34–35 wGA and 37–38 wGA had greater risk of WM lesions after adjusting for perinatal factors (aOR 4.0, 95% CI (1.5 to 10.7) and ORa 2.0, 95% CI (1.1 to 3.5), respectively).

    Conclusion WM is the main brain structure affected in late-preterm and early-term infants with NE, with fewer WM lesions as GA increases. This finding could help clinicians to estimate prognosis and improve the understanding of the pathophysiology of NE.

    Trial registration number NCT02676063, ClinicalTrials.gov.

    • magnetic resonance imaging
    • neonatology

    Data availability statement

    Data may be obtained from a third party and are not publicly available. De-identified participant data are available on request from tdebillon@chu-grenoble.fr, principal investigator. The latter will make the request to the research laboratory hosting the database. (MESP Laboratory, TIMC Grenoble University Hospital). Reuse conditions may be authorised subject to strict analysis conditions and a specific purpose.

    https://doi.org/10.1136/archdischild-2023-326131

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      Data availability statement

      Data may be obtained from a third party and are not publicly available. De-identified participant data are available on request from tdebillon@chu-grenoble.fr, principal investigator. The latter will make the request to the research laboratory hosting the database. (MESP Laboratory, TIMC Grenoble University Hospital). Reuse conditions may be authorised subject to strict analysis conditions and a specific purpose.

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      Footnotes

      • Collaborators Lytonepal research group: Auvergne Rhône-Alpes: N. Bouchon-Guedj (Chambéry), G. Remerand (Clermont-Ferrand), M. Chevallier (Grenoble), O. Claris (Lyon, HFME), C.M. Loys (Lyon, Croix Rousse), H. Patural (Saint-Etienne); Bourgogne Franche-Comté: T. Dabudyk (Besançon), C. Chantegret (Dijon); Bretagne: J.M. Roué (Brest), M. Gromand (Rennes), A. Busnel (St-Brieuc), A. Sevestre (Vannes); Centre Val-de-Loire: J. Guerreiro (Orléans), G. Favrais (Tours); Grand Est: J. Nakhleh (Mulhouse), N. Bednarek (Reims), D. Astruc, (Strasbourg), B. Kassis-Makhoul (Troyes); Hauts de France: G. Ghostine (Amiens), J. Ghesquiere (Arras), L. Egreteau (Calais), S.M. Dhahbi (Creil), S. Klosowski (Lens), F. Flamein (Lille), J. Balitalike (Valenciennes); Ile-de-France: D. Brau (Argenteuil), V. Zupan-Simunek (Clamart), C. Huon (Colombes), M. Tauzin (Créteil), M. Merhi (Evry), N. Le Sache (Le Kremlin-Bicêtre), B. Heller Roussin (Montreuil), D. Mellah (Meaux), A. Lapillonne, E. Leroy Terquem (Paris, Necker), J. Patkai (Paris, Port Royal), V. Biran (Paris, Robert Debré), I. Guellec (Paris, Trousseau), A. Durandy (Poissy), P. Boize (Pontoise), F. Goudjil (St Denis); Nouvelle Aquitaine: P. Jouvencel (Bayonne), O. Brissaud (Bordeaux), F. Mons (Limoges), K. Norbert (Pau), A. Parizel (Poitiers); Occitanie: G. Cambonie (Montpellier), M. Di Maio (Nîmes), R. Salloum (Perpignan), M.O. Marcoux (Toulouse); Pays de Loire: S. Le Bouedec (Angers), C. Flamant (Nantes), Y. Montcho (Le Mans); Provence Alpes Côte d’Azur: C. Desrobert (Marseille La Conception), V. Brevaut-Malaty (Marseille, Nord), F. Casagrande (Nice), R. Salloum (Perpignan); Martinique: S. Ketterer Martinon (Fort de France); Normandie: A. Cénéric (Caen), J. Mourdie (Le Havre), A. Chadie (Rouen); La Réunion: M. Carbonnier (Saint-Pierre), D. Ramful (Saint-Denis).

      • Contributors TD, AE wrote the grant proposal and supervised data collection for the LyTONEPAL cohort. MC, TD and AE designed this study, and drafted, reviewed and revised the manuscript. LB contributed to the statistical analysis and writing of the manuscript. AV carried out the statistical analysis and reviewed the manuscript. JB assisted in the collection of data for all brain imaging. IG critically reviewed the manuscript for important intellectual content. MC is guarantor.

      • Funding 2013 French Program for Hospital Clinical Research (PHRC-N-13-0327). The funder had no role in the design and conduct of the study.

      • Competing interests None declared.

      • Provenance and peer review Not commissioned; externally peer-reviewed.

      • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.