title: Differences in white matter fiber tract development present from 6 to 24 months in infants with autism.
abstract: OBJECTIVE
  Evidence from prospective studies of high-risk infants suggests that early symptoms of autism usually emerge late in the first or early in the second year of life after a period of relatively typical development. The authors prospectively examined white matter fiber tract organization from 6 to 24 months in high-risk infants who developed autism spectrum disorders (ASDs) by 24 months.
  
  
  METHODS
  The participants were 92 high-risk infant siblings from an ongoing imaging study of autism. All participants had diffusion tensor imaging at 6 months and behavioral assessments at 24 months; a majority contributed additional imaging data at 12 and/or 24 months. At 24 months, 28 infants met criteria for ASDs and 64 infants did not. Microstructural properties of white matter fiber tracts reported to be associated with ASDs or related behaviors were characterized by fractional anisotropy and radial and axial diffusivity.
  
  
  RESULTS
  The fractional anisotropy trajectories for 12 of 15 fiber tracts differed significantly between the infants who developed ASDs and those who did not. Development for most fiber tracts in the infants with ASDs was characterized by higher fractional anisotropy values at 6 months followed by slower change over time relative to infants without ASDs. Thus, by 24 months of age, those with ASDs had lower values.
  
  
  CONCLUSIONS
  These results suggest that aberrant development of white matter pathways may precede the manifestation of autistic symptoms in the first year of life. Longitudinal data are critical to characterizing the dynamic age-related brain and behavior changes underlying this neurodevelopmental disorder.
authors.affiliation: Carolina Institute for Developmental Disabilities and the Department of Psychiatry, University of North Carolina, Chapel Hill, USA. jason.wolff@cidd.unc.edu
authors.forename: Jason J
authors.initials: JJ
authors.lastname: Wolff
authors.forename: Hongbin
authors.initials: H
authors.lastname: Gu
authors.forename: Guido
authors.initials: G
authors.lastname: Gerig
authors.forename: Jed T
authors.initials: JT
authors.lastname: Elison
authors.forename: Martin
authors.initials: M
authors.lastname: Styner
authors.forename: Sylvain
authors.initials: S
authors.lastname: Gouttard
authors.forename: Kelly N
authors.initials: KN
authors.lastname: Botteron
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Dager
authors.forename: Geraldine
authors.initials: G
authors.lastname: Dawson
authors.forename: Annette M
authors.initials: AM
authors.lastname: Estes
authors.forename: Alan C
authors.initials: AC
authors.lastname: Evans
authors.forename: Heather C
authors.initials: HC
authors.lastname: Hazlett
authors.forename: Penelope
authors.initials: P
authors.lastname: Kostopoulos
authors.forename: Robert C
authors.initials: RC
authors.lastname: McKinstry
authors.forename: Sarah J
authors.initials: SJ
authors.lastname: Paterson
authors.forename: Robert T
authors.initials: RT
authors.lastname: Schultz
authors.forename: Lonnie
authors.initials: L
authors.lastname: Zwaigenbaum
authors.forename: Joseph
authors.initials: J
authors.lastname: Piven
mesh_terms: D016880:Anisotropy; D001321:Autistic Disorder / Q000209:etiology / Q000473:pathology*; D001921:Brain / Q000254:growth & development / Q000473:pathology*; D016022:Case-Control Studies; D002659:Child Development Disorders, Pervasive / Q000209:etiology / Q000473:pathology; D002675:Child, Preschool; D056324:Diffusion Tensor Imaging; D005260:Female; D006801:Humans; D007223:Infant; D008279:Magnetic Resonance Imaging; D008297:Male; D009413:Nerve Fibers, Myelinated / Q000473:pathology*; D059906:Neuroimaging