Original ArticleAbnormal Magnocellular Pathway Visual Processing in Infants at Risk for Autism
Section snippets
Subjects
The data from 13 6-month-old high-risk infants contributed to this study (5 female infants, 8 male infants). These infants were recruited through advertisements in the San Diego area, as well as referrals from other laboratories studying autism at the University of California, San Diego (UCSD). The older siblings of the high-risk infants were diagnosed with ASD (autistic disorder; Asperger syndrome; or pervasive developmental disorder-not otherwise specified [PDD-NOS]) by a licensed clinical
Results
Shown in Figure 3A are group mean log luminance and chromatic contrast sensitivities for 13 high-risk infants (white bars) and 26 low-risk matched control infants (grey bars). The results of a two-factor analysis of variance (ANOVA) (1 = subject group, 2 = stimulus type [luminance vs. chromatic]) yielded no significant main effects. However, the interaction between subject group and stimulus type was significant [F(1,37) = 10.45, p = .0026]. As can be seen in Figure 3A, this interaction was
Discussion
The data from our study of high-risk infants provide preliminary evidence that familial risk for ASD is associated with abnormal processing of luminance contrast in early infancy. Because luminance sensitivity is mediated by the M visual pathway, these results suggest that abnormal M pathway function may be an endophenotypic marker for ASD. It is important to point out that although the current study observed enhanced luminance sensitivity in high-risk infants, this should still be considered
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