Abnormalities in higher cortical visual processing

Abstract

Sixty percent of the human brain is formed by visual pathways and high visual centers. Thirty visual centers work normally in concordance with systematic and constant communication with each other. Visual cortical areas include primary and secondary areas. Normal visual processing includes the signalization and neuronal processing initiated from the retina through the lateral geniculate body to the striate cortex.1,2 Visual cortical areas include Broadman-17 (primary visual cortex, area striata, visual area V1) area related to shape and size of the objects in striate cortex at lobus occipitalis; Broadman-18 (area parastriata, prestriate cortex, visual area V2) area related to the analysis of object motion in parastriate cortex at lobus occipitalis; Broadman-19 associated with visual area V3 in posterior parietal lobe related to visual integration and cortical color vision; V4 and V5 areas in superior temporal sulcus, related to motion perception (M cells) input, direction and depth perception; visual area V6 in parietal cortex associated with extra-personal perception.2,3 Lesions in visual areas 18 and 19 are associated with visual agnosia. The injury in left may be associated with pure alexia. Defects in the posterior parietal cortex cause optic ataxia while the damage to the medial supero-temporal cortex and medial temporal visual cortex results in loss of visual motion perception (akinetopsia) in different directions. The damage to the inferotemporal cortex causes visual agnosia. Damage to V4 results in loss of color vision, achromatopsia, while damage to V6 causes an inability to distinguish two-dimensional patterns.4–6