Two theories have been defended in the pages of the Archives to explain the difference between the macula-sparing and the macula-splitting hemianopias found in man after interruption of the optic radiation. One theory, championed by Penfield, Evans and MacMillan,1 holds that certain macular fibers in each optic radiation pass, or send collateral branches which pass, through the splenium of the corpus callosum to the contralateral occipital cortex. According to this view, a lesion interrupting the optic radiation before these decussating fibers leave it results in macula-splitting hemianopia, whereas a lesion posterior to that point results in macula-sparing hemianopia.
The other theory, held by Fox and German,2 interprets the clinical findings according to the postulate that the macula is diffusely represented throughout in the striate cortex. Thus, a lesion in the temporal lobe may result in macula-splitting hemianopia because all macular fibers in the optic radiation on one side