A neurophysiological model for anomalous correspondence based on mechanisms of sensory fusion.
Normal retinal correspondence is not stable. The arguments for the plasticity of correspondence in normal binocular vision have been given into previous papers (Nelson, 1975, 1977). In this paper, both laboratory research and the clinical strabismus literature are reviewed to show similarities between normal and abnormal binocular vision. In particular, it is argued that sensory fusion (Panum's areas) and anomalous retinal correspondence (AC) obey similar principles, and so a sensory fusional model of AC may be developed. Recent advances in the neurophysiology of binocular vision are reviewed, but current laboratory knowledge cannot account for many phenomena known clinically unless certain postulates are made. Two hypothesized intracortical interactions among binocular disparity detectors, termed disparity domain inhibition and spatial domain facilitation, play key roles in extending the neurophysiology of binocular vision to an account of both normally - and clinically - observed plasticities of correspondence. The fusional model of retinal correspondence developed here from postulated domain interactions contrasts with the older concept of fixed corresponding points, an approach which has failed to provide a unified foundation for the treatment of normal and abnormal binocular vision.
D000818:Animals; D002415:Cats; D003867:Depth Perception / Q000502:physiology*; D004292:Dominance, Cerebral; D004948:Esotropia / Q000503:physiopathology; D005403:Fixation, Ocular; D006801:Humans; D008959:Models, Neurological; D012160:Retina / Q000502:physiology; D013285:Strabismus / Q000503:physiopathology*; D014793:Visual Cortex / Q000502:physiology*