Second-order spatial summation in amblyopia

Abstract

Amblyopes show bilateral loss of sensitivity for second-order (contrast defined) stimuli that can be further suppressed by flanking second-order stimuli (whereas flanks facilitate sensitivity in normal observers). The suppressive flank effect in amblyopes might be explained by abnormal pooling of second-order contrast across visual space. In this study, we investigate whether amblyopes show abnormal second-order spatial summation by measuring contrast detection thresholds for 1c/deg modulations of random noise (stimuli 1-12 cycles) in amblyopic observers, strabismic observers with no visual acuity loss, and normal (control) observers. Non-control observers showed substantial bilateral loss of sensitivity relative to the control observers, as expected. However, all observers showed essentially equal second-order spatial summation: contrast detection threshold decreased with approximately the square root of the number of cycles, and then became independent of size at 6-8 cycles (similar asymptotes). We conclude that the pooling of second-order contrast across visual space is unaffected by amblyopia.

The amblyopic deficit for 2nd order processing: Generality and laterality

“…If this was so then it would suggest anomalous spatial summation for second-order stimuli by the amblyopic eye at low modulation frequencies (<1 c/d). Spatial summation for second-order stimuli has been found to be normal at 1 c/d (Wong & Levi, 2005) but it is yet to be investigated below 1 c/d.…”

“…The psychophysical deficit in amblyopia is extensive involving not only contrast sensitivity (Hess & Howell, 1977;Levi & Harwerth, 1977) but also the encoding of spatial position (Bedell & Flom, 1981;Hess, Campbell, & Greenhalgh, 1978;Lagreze & Sireteanu, 1991), global motion (Aaen-Stockdale & Hess, 2008;Ho et al, 2005;Simmers et al, 2003), global form (Husk & Hess, 2013;Simmers, Ledgeway, & Hess, 2005;Simmers et al, 2011), contrast-defined form (Hong, Levi, & McGraw, 2001) and motiondefined form (Husk, Farivar, & Hess, 2012;Giaschi et al, 1992). The site of the amblyopic deficit is thought to be primarily in the striate cortex (Kiorpes & McKee, 1999) but the extent to which the extra-striate cortex is separately affected is not clear (Kiorpes et al, 1998).…”

Temporal Synchrony Deficits in Amblyopia

“…A mblyopia traditionally is thought of in terms of a purely spatial deficit as reflected by reduced acuity, 1 reduced contrast sensitivity, 2,3 spatial distortions/inaccuracy, [4][5][6] and reduced sensitivity for global spatial tasks. [7][8][9][10] However, more recently evidence has emerged for a deficit in amblyopia for global motion 11 including optic flow 12 and for the maximum spatial displacement supporting motion perception for random dot kinematograms (Dmax). [13][14][15] The fact that low level motion performance is thought to be normal in amblyopia 16 raises the question of whether these global motion deficits could be a consequence of the spatial loss in amblyopia.…”

New Perspectives in Amblyopia Therapy on Adults: A Critical Role for the Excitatory/Inhibitory Balance

“…Interestingly, the balance between excitation and inhibition has been suggested to be impaired during development also in amblyopic human subjects and cortical over-inhibition could underlie the degradation of spatial vision abilities (Polat, 1999; Levi et al, 2002; Wong et al, 2005). In agreement with this hypothesis, repetitive transcranial magnetic stimulation (rTMS), which increases cortical excitability, transiently improves contrast sensitivity in adult amblyopes, likely acting on the excitation/inhibition balance (Thompson et al, 2008).…”