Elsevier

Biological Psychiatry

Volume 62, Issue 9, 1 November 2007, Pages 1007-1014
Biological Psychiatry

Original Article
Abnormal Magnocellular Pathway Visual Processing in Infants at Risk for Autism

https://doi.org/10.1016/j.biopsych.2007.02.009Get rights and content

Background

A wealth of data has documented impairments in face processing in individuals with autism spectrum disorders (ASD). Recently, the suggestion has been made that these impairments may arise from abnormal development of a subcortical system involved in face processing that originates in the magnocellular pathway of the primate visual system.

Methods

To test this developmental hypothesis, we obtained visual perceptual data from 6-month-old infants who were at risk for ASD because they had an older sibling diagnosed with the disorder (“high-risk infants”). To measure sensitivity of the magnocellular (M) pathway and, for comparison, of the parvocellular (P) visual pathway, we employed visual stimuli designed to selectively stimulate the two. Sensitivity data from high-risk infants (n = 13) were compared with data from matched control infants (i.e., “low-risk” infants with no family history of ASD, n = 26).

Results

On the P pathway stimulus, high-risk infants exhibited sensitivities that were identical to those of control infants. By contrast, on the M pathway stimulus, high-risk infants exhibited sensitivities nearly twofold greater than those of control infants.

Conclusions

Given that ASD and its symptoms are known to run in families, these preliminary results suggest that ASD may be associated with abnormal M pathway function early in infancy, which may aid in early diagnosis of the disorder.

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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