Diagnosis and Therapy of Impairment of Higher Visual Function

Abstract

Visual information is processed in the brain from the primary visual cortex to the posterior association cortex, the latter being responsible for higher level processing. Visual-form and spatial information are separately processed through the ventral and dorsal pathways, respectively, in the posterior association cortex. Visual hemispatial agnosia is a symptom that is observed after injury to the right temporal-parietal cortex. Bilateral parietal lobe damage causes Bálint syndrome, which is characterized by simultanagnosia, psychic paralysis of gaze, and optic ataxia. On the other hand, damage to the ventral pathway results in visual agnosia, which is divided into three types depending on the processing level of visual information. Prosopagnosia is a special type of visual agnosia and appears after bilateral damage to the ventral mesial temporal lobe. Topographical disorientation can be of two types depending on the location of the lesion (on mesial parietal lobe or mesial occipito-temporal lobe). Various strategies including utilization of brain compensatory mechanism, reinforced learning of lost functions, and electrical/magnetic brain stimulation are now available for the treatment of these higher visual dysfunctions.