Abstract
Previous psychophysical studies have shown impairments in motion processing, a dorsal visual stream function, in children with autism (e.g., Spencer et al., 2000). Since the dorsal stream receives input mainly from the magnocellular (M), and little from the parvocellular (P), pathway, these findings may reflect abnormal processing in the M pathway in autism. To test this abnormal M pathway hypothesis, and to determine whether such abnormalities are present early in life, we compared M and P pathway function in infants with an older sibling with autism (i.e., “at-risk” infants, who have a ∼10% chance of ultimately being diagnosed with autism, and added risk for sub-clinical social and communication deficits) with typical infants. M and P pathway function was assessed by obtaining luminance (L) and red/green chromatic (C) contrast sensitivities, respectively (see Dobkins et al., 1999). L and C sensitivities were determined in 88 typical and 11 at-risk 6-month-olds, using forced-choice preferential looking. The results of a 2-factor ANOVA (factor 1=subject group: at-risk vs. typical, factor 2=stimulus type: L vs. C) yielded a significant interaction ((F(1,97) = 5.4, p < 0.05). These results suggest abnormalities in the relative integrity of M vs. P pathways in at-risk infants. Specifically, differences were observed for L sensitivity (at-risk: mean log = 1.53, se = 0.07; typical: mean log = 1.38, se = 0.04), but not C sensitivity (at-risk: mean log = 1.51, se = 0.08; typical: mean log = 1.54, se = 0.03). Although L sensitivity in at-risk infants was actually enhanced, this nonetheless suggests abnormalities in M pathway processing, which could potentially serve as a phenotypic marker for autism, and may explain some of the cognitive/behavioral problems of individuals with autism. Preliminary data will be presented investigating correlations between these visual data at 6-months and social-communicative behaviors at 10-months, and diagnostic outcomes at 24-months.
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