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Such visuovestibular cortical interaction could underlie the perceptual mechanisms that attempt to resolve visual motion from self-motion percepts while simultaneously optimizing visual form perception under natural conditions of vestibular activation such as during locomotion.
The occipito-temporal cortical activations were in the lateral occipital complex, a part of the ventral visual pathway active during visual form perception. Thus, macrospatial form perception preferentially recruits this region of extrastriate visual cortex, compared to microspatial form perception.
Visual risk factors include low-level visual difficulties such as reduced contrast perception [41] [44] and higher-level visual form perception deficits [45] [48].
One role for a vestibular modulation of visual motion signals at cortical level would be optimizing visual form perception.
A role for vestibular signals in optimizing visual form perception does not obviate a vestibular role in resolving the self- versus object-motion conflict.
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Since visual motion usually occurs when an object with a particular form is moving, we speculate that motion processing is tightly linked to form processing (Kourtzi et al., 2008) even for non-form motion, and therefore, the right ventral visual dominance for form perception might serve as the basis of the motion perception laterality effect we have observed in this study.
Low visual acuity people declared either severe difficulties in long or short distance vision to question 1 and 2 and form perception or visual impairment to question 3. The worst severity in terms of visual impairment (blind >LV >NVP) was always retained.
This 'linking' of information is a critical intermediate stage in the perception of visual form [3] and has lead to the notion of an 'association field' [4], [5] that integrates information from neighbouring filters tuned to similar orientations (see Field and Hayes [6] and Hess and Field [7] for reviews).
Alternatively, if ventral visual cortex is only engaged when motion contributes to form perception, then a ventral visual lesion should only impair motion perception when form representations are evoked (e.g. by structure-from-motion stimuli), but not when only basic motion perception is tapped (e.g. motion coherence or motion detection).
Thus our findings shed light on the initial stage of form perception in the visual cortex.
The lesion site in the patients was either to the left or to the right ventral visual pathway, and all patients exhibited form perception deficits (Table 1), either object agnosia and/or pure alexia.
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