Interocular suppression in strabismic amblyopia results in an attenuated and delayed hemodynamic response function in early visual cortex

  • Farivar R
  • Thompson B
  • Mansouri B
 et al. 
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Factors such as strabismus or anisometropia during infancy can disrupt normal visual development and result in amblyopia, characterized by reduced visual function in an otherwise healthy eye and often associated with persistent suppression of inputs from the amblyopic eye by those from the dominant eye. It has become evident from fMRI studies that the cortical response to stimulation of the amblyopic eye is also affected. We were interested to compare the hemodynamic response function (HRF) of early visual cortex to amblyopic vs. dominant eye stimulation. In the first experiment, we found that stimulation of the amblyopic eye resulted in a signal that was both attenuated and delayed in its time to peak. We postulated that this delay may be due to suppressive effects of the dominant eye and, in our second experiment, measured the cortical response of amblyopic eye stimulation under two conditions--where the dominant eye was open and seeing a static pattern (high suppression) or where the dominant eye was patched and closed (low suppression). We found that the HRF in response to amblyopic eye stimulation depended on whether the dominant eye was open. This effect was manifested as both a delayed HRF under the suppressed condition and an amplitude reduction.

Author-supplied keywords

  • 1
  • 10
  • 11
  • 1167
  • 12
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  • 16
  • 2011
  • amblyopia
  • and delayed hemodynamic response
  • b
  • citation
  • content
  • cortex
  • doi
  • f
  • farivar
  • function in early visual
  • functional imaging
  • hemodynamic modulation
  • hemodynamic response
  • hess
  • http
  • interocular suppression in strabismic
  • journal of vision
  • journalofvision
  • mansouri
  • org
  • r
  • results in an attenuated
  • thompson
  • visual cortex
  • visual development
  • www

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  • R. Farivar

  • B. Thompson

  • B. Mansouri

  • R. F. Hess

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