September 2019
Volume 19, Issue 10
Open Access
Vision Sciences Society Annual Meeting Abstract  |   September 2019
Less Efficient Magnocellular Processing: A Common Deficit in Neurodevelopmental Disorders
Author Affiliations & Notes
  • Alyse C Brown
    School of Psychological Science and Public Health, La Trobe University
  • Jessica Peters
    School of Psychological Science and Public Health, La Trobe University
  • Carl Parsons
    Port Philip Specialist School, Port Melbourne
  • David P Crewther
    Centre for Human Psychopharmacology, Swinburne University of Technology
  • Sheila G Crewther
    School of Psychological Science and Public Health, La Trobe University
Journal of Vision September 2019, Vol.19, 48a. doi:https://doi.org/10.1167/19.10.48a
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      Alyse C Brown, Jessica Peters, Carl Parsons, David P Crewther, Sheila G Crewther; Less Efficient Magnocellular Processing: A Common Deficit in Neurodevelopmental Disorders. Journal of Vision 2019;19(10):48a. doi: https://doi.org/10.1167/19.10.48a.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Motion is processed within the visual dorsal stream that receives 80% of its input from the rapid processing magnocellular (M) pathway, a pathway critical for the discrimination of rapidly presented sequential stimuli and tracking rapid motion. Deficits in global motion processing are observed in several neurodevelopmental disorders (NDD) leading to our hypothesis that weak motion processing is due to temporal deficiency in M pathway. Thus, M pathway efficiency was behaviourally measured in a sample of NDDs and neurotypicals (mean age 10, range 7–21 years, n=71) via two 4AFC achromatic flicker fusion threshold (FFT) tasks modulated at low and high contrast. The main NDD diagnoses tested were singular or comorbid combinations of Dyslexia, ASD, ID, as well as ADHD which to date have not been reported to have visual anomalies. Autistic tendencies (AQ) was measured in all participants. Diagnosed NDD without ID were individually matched on both chronological age and nonverbal intelligence with typically developing (TD) while ID was matched solely on chronological age. Results showed that young participants with ASD and Dyslexia (aged 7–15yr) including those with comorbid ADHD demonstrated comparable FFTs that were significantly lower than their matched control. However, FFT in the older ASD participants (16+yrs) was only significantly lower at high contrast. Participants with an ID diagnosis which included ASD+ID had inconsistent FFT profile with a large range of thresholds achieved. Interestingly, participants with ADHD alone had significantly higher FFT at high contrast compared to their TD group, possibly due to ADHD prescribed stimulant medication. Higher AQ score was found to correlate with lower FFT (r= −.269, p< .005 n=71). In conclusion, an ID diagnosis was not predictive of a temporal M deficiency however, there was strong evidence for a less efficient M pathway in the ASD and dyslexia diagnoses that could go towards explaining their weak motion processing profiles.

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