Aperçu: G.M.
Des études précédentes avaientsignalé que les nourrissons qui ont développé un
trouble du spectre de l'autisme (TSA) ont eu une augmentation du liquide
céphalo-rachidien (CSF) dans l'espace sous-arachnoïdien (c.-à-d. CSF
extra-axial) de 6 à 24 mois. La présente étude a tenté de confirmer et d'étendre cette constatation dans un plus grand échantillon indépendant.
Les
nourrissons qui ont développé un TSA ont eu un volume de CSF
extra-axial significativement plus important à 6 mois comparativement
aux deux groupes de comparaison sans TSA (18% de plus que les
nourrissons à risque élevé sans TSA , Co = d = 0,54). Le volume de CSF extra-axial est resté élevé pendant 24 mois (d = 0,46). Les
nourrissons qui avaient des symptômes d'autisme plus sévères ont un volume
encore plus important de CSF extra-axial de 6 à 24 mois (24% plus élevé à
6 mois, d = 0,70; 15% plus élevé à 24 mois, d = 0,70). Le volume de CSF extra-axial à 6 mois prévoyait que les nourrissons à
risque élevé seraient diagnostiqués avec TSA à 24 mois avec une
précision globale de 69% et une sensibilité correspondante de 66% et une
spécificité de 68%, validée en totalité dans un échantillon séparé.
Biol Psychiatry. 2017 Mar 6. pii: S0006-3223(17)31217-9. doi: 10.1016/j.biopsych.2017.02.1095.
Increased Extra-axial Cerebrospinal Fluid in High-Risk Infants Who Later Develop Autism
Shen MD1, Kim SH2, McKinstry RC3, Gu H4, Hazlett HC2, Nordahl CW5, Emerson RW2, Shaw D6, Elison JT7, Swanson MR2, Fonov VS8, Gerig G9, Dager SR6, Botteron KN3, Paterson S10, Schultz RT11, Evans AC8, Estes AM12, Zwaigenbaum L13, Styner MA2, Amaral DG5, Piven J2; Infant Brain Imaging Study Network; Infant Brain Imaging Study Network, The Infant Brain Imaging Study (IBIS) Network is a National Institutes of Health–funded Autism Center of Excellence project and consists of a consortium of eight universities in the United States and Canada, Piven J14, Hazlett HC14, Chappell C14, Dager S15, Estes A15, Shaw D15, Botteron K16, McKinstry R16, Constantino J16, Pruett J16, Schultz R17, Zwaigenbaum L18, Elison J19, Evans AC20, Collins DL20, Pike GB20, Fonov V20, Kostopoulos P20, Das S20, Gerig G21, Styner M22, Gu H23.
Author information
- 1
- Carolina Institute for Developmental Disabilities and Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina; MIND Institute and Department of Psychiatry and Behavioral Sciences, University of California, Davis, School of Medicine, Sacramento, California. Electronic address: mark_shen@med.unc.edu
- 2
- Carolina Institute for Developmental Disabilities and Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina.
- 3
- Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, Missourt.
- 4
- Carolina Institute for Developmental Disabilities and Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina; Department of Biostatistics, School of Global Public Health, University of North Carolina at Chapel Hill School of Global Public Health, Chapel Hill, North Carolina.
- 5
- MIND Institute and Department of Psychiatry and Behavioral Sciences, University of California, Davis, School of Medicine, Sacramento, California.
- 6
- Department of Radiology, University of Washington Medical Center, Seattle, Washington.
- 7
- Institute of Child Development, University of Minnesota, Minneapolis, Minnesota.
- 8
- Montreal Neurological Institute, McGill University, Montreal, Quebec.
- 9
- Computer Science & Engineering, New York University Tandon School of Engineering, New York, New York.
- 10
- Department of Psychology, Temple University, Philadelphia, Pennsylvania.
- 11
- Center for Autism Research, Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania.
- 12
- Department of Speech and Hearing Science, University of Washington, Seattle, Washington.
- 13
- Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada.
- 14
- Clinical sites-University of North Carolina.
- 15
- University of Washington.
- 16
- Washington University.
- 17
- Children's Hospital of Philadelphia.
- 18
- University of Alberta.
- 19
- University of Minnesota.
- 20
- Data Coordinating Center-Montreal Neurological Institute.
- 21
- Image Processing Core-New York University.
- 22
- University of North Carolina.
- 23
- Statistical Analysis Core-University of North Carolina.
Abstract
BACKGROUND:
We previously reported that infants who developed autism spectrum disorder (ASD) had increased cerebrospinal fluid (CSF) in the subarachnoid space (i.e., extra-axial CSF) from 6 to 24 months of age. We attempted to confirm and extend this finding in a larger independent sample.METHODS:
A longitudinal magnetic resonance imaging study of infants at risk for ASD was carried out on 343 infants, who underwent neuroimaging at 6, 12, and 24 months. Of these infants, 221 were at high risk for ASD because of an older sibling with ASD, and 122 were at low risk with no family history of ASD. A total of 47 infants were diagnosed with ASD at 24 months and were compared with 174 high-risk and 122 low-risk infants without ASD.RESULTS:
Infants who developed ASD had significantly greater extra-axial CSF volume at 6 months compared with both comparison groups without ASD (18% greater than high-risk infants without ASD; Cohen's d = 0.54). Extra-axial CSF volume remained elevated through 24 months (d = 0.46). Infants with more severe autism symptoms had an even greater volume of extra-axial CSF from 6 to 24 months (24% greater at 6 months, d = 0.70; 15% greater at 24 months, d = 0.70). Extra-axial CSF volume at 6 months predicted which high-risk infants would be diagnosed with ASD at 24 months with an overall accuracy of 69% and corresponding 66% sensitivity and 68% specificity, which was fully cross-validated in a separate sample.CONCLUSIONS:
This study confirms and extends previous findings that increased extra-axial CSF is detectable at 6 months in high-risk infants who develop ASD. Future studies will address whether this anomaly is a contributing factor to the etiology of ASD or an early risk marker for ASD.
Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
- PMID: 28392081
- DOI: 10.1016/j.biopsych.2017.02.1095
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