Abnormal Attention in Autism Shown by Steady-State Visual Evoked Potentials


Matthew Belmonte

Autism 4(3):269-285 (September 2000)

Address for correspondence: mkb4@Cornell.edu

ABSTRACT: This study examined brain electrical responses as a physiological measure of speed and specificity of attentional shifting in eight adult males with autism. Subjects were required to shift attention between rapidly flashed targets alternating between left and right visual hemifields. When targets were separated by less than 700ms, steady-state brain electrical response in both hemispheres was augmented and background EEG decreased for rightward shifts as compared to leftward shifts. At longer separations, persons with autism showed no modulation of background EEG, and high variability in steady-state response. These results contrast with those in normal controls, where in each hemisphere separately steady-state response increased and background EEG decreased for shifts directed contralaterally to that hemisphere. Group differences were significant at p<0.04 for the steady state response and p<0.0001 for the background EEG. Lack of hemispherically independent modulation in autism may reflect the operation of a nonspecific mechanism of sensory gating.


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CITED IN PUBLICATIONS BY OTHERS:

  1. Bosa CA. As relações entre autismo, comportado social e função executiva. Psicologia: Reflexão e Crítica 14(2):281-287 (2001).
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CITED IN MY OTHER PUBLICATIONS:

  1. Belmonte MK, Yurgelun-Todd DA. Anatomic dissociation of selective and suppressive processes in visual attention. NeuroImage 19(1):180-189 (May 2003).
  2. Belmonte MK, Yurgelun-Todd DA. Functional anatomy of impaired selective attention and compensatory processing in autism. Cognitive Brain Research 17(3):651-664 (October 2003).
  3. Belmonte MK, Cook EH, Anderson GM, Rubenstein JL, Greenough WT, Beckel-Mitchener A, Courchesne E, Boulanger LM, Powell SB, Levitt PR, Perry EK, Jiang YH, DeLorey TM, Tierney E. Autism as a disorder of neural information processing: directions for research and targets for therapy. Molecular Psychiatry 9(7):646-663 (July 2004). Unabridged edition at http://www.cureautismnow.org/conferences/summitmeetings/
  4. Belmonte MK, Allen G, Beckel-Mitchener A, Boulanger LM, Carper RA, Webb SJ. Autism and abnormal development of brain connectivity. Journal of Neuroscience 24(42):9228-9231 (20 October 2004).
  5. Baron-Cohen S, Belmonte MK. Autism: a window onto the development of the social and the analytic brain. Annual Review of Neuroscience 28:109-126 (2005).
  6. Bonneh YS, Belmonte MK, Pei F, Iversen PE, Kenet T, Akshoomoff NA, Adini Y, Simon HJ, Moore CI, Houde JF, Merzenich MM. Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence. Cognitive Neuropsychology 25(5):635-652 (2008).
  7. Baron-Cohen S, Golan O, Chakrabarti B, Belmonte MK. Social cognition and autism spectrum conditions. In: Social Cognition and Developmental Psychopathology (C Sharp, P Fonagy, I Goodyer, eds.), pp 29-56. Oxford: Oxford University Press (4 September 2008).