Known Physiological and Anatomical Changes That Result from Optical and Motor Deficits

Abstract

Mammals compensate for optical deficits occurring at a young age by anatomical and physiological changes in the visual cortex. Not much compensation is found at the level of the retina or the lateral geniculate nucleus. In the case of binocular function, orientation selectivity, and direction selectivity, this is what one would expect, because these are all properties of the visual cortex rather than of the retina or the lateral geniculate. The mechanisms that produce acuity and contrast sensitivity changes are also often found at the cortical level, even though acuity and contrast sensitivity are properties of the retina and lateral geniculate as well. The compensation is specific for the deficit. Monocular deprivation affects ocular dominance rather than orientation selectivity, and orientation deprivation affects orientation selectivity rather than ocular dominance. There is a rearrangement of the connections within the cortex, and the columns specific for the deprived features contract, while the columns specific for the non-deprived features expand. The physiological properties of the cells change correspondingly. There is a limit to how far compensation can occur through anatomical and physiological changes. This is not important for monocular, orientation, and direction deprivation, because columns for left and right eyes are near each other and so are columns for vertical and horizontal orientations and cells for rightward and leftward movement. It is, however, important for strabismus, when the angle of strabismus is large. In this case, compensation occurs through some form of physiological suppression rather than through anatomical rearrangements.