The development of visual functions in cerebrally blind children during a systematic visual field training

Sixteen children aged 1 to 15 years who were blind due to an ischemic postgeniculate cerebral lesion after perinatal asphyxia and 6 children aged 1 to 13 years who were blinded after a postgeniculate traumatic cerebral lesion participated in a systematic visual field training. Thirty-one children who were blind due to a postgeniculate lesion following perinatal asphyxia and 12 children who suffered from blindness after a traumatic postgeniculate lesion served as controls. These children received no visual field training or an ineffective visual field training. The extension of the functional visual field and the functional luminance difference threshold were assessed with a specially designed arc perimeter. In all children blindness had already persisted for at least one year. Visual functions developed within a training period of three months in 15 of 22 children who received visual field training whereas there was no spontaneous recovery in the control group. The functional luminance difference threshold was still elevated above normal in the case of 5 children who recovered from blindness. In 2 children the latency of saccades elicited by light targets in the formerly blind visual area was significantly longer than the latency of saccades elicited by targets in the normal area of the visual field. Light scatter was controlled in order to exclude that the widening of the visual field during training which we interpreted as a sign of the development of visual functions was an effect of scattering light. The findings support the assumption that systematic stimulation of cerebrally blind areas may facilitate the development of visual functions in brain damaged children. The cerebral lesions associated with the impaired visual functions which improved during the treatment are in agreement with the assumption that spared tissue in the striate and extrastriate visual cortex and underlying white matter is the anatomical basis of the shrinkage of the blind areas.