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.
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.
Authors: Bernard Z Karmel; Judith M Gardner; Lauren Swensen Meade; Ira L Cohen; Eric London; Michael J Flory; Elizabeth M Lennon; Inna Miroshnichenko; Simon Rabinowitz; Santosh Parab; Anthony Barone; Anantham Harin Journal: Pediatrics Date: 2010-08-02 Impact factor: 7.124
Authors: D L Mills; L Dai; I Fishman; A Yam; L G Appelbaum; M St George; A Galaburda; U Bellugi; J R Korenberg Journal: Dev Neuropsychol Date: 2013 Impact factor: 2.253