R. Werth et M. Moehrenschlager, The development of visual functions in cerebrally blind children during a systematic visual field training, REST NEUROL, 15(2-3), 1999, pp. 229-241
Sixteen children aged 1 to 15 years who were blind due to an ischemic postg
eniculate 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 wh
o were blind due to a postgeniculate lesion following perinatal asphyxia an
d 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 v
isual field and the functional luminance difference threshold were assessed
with a specially designed are perimeter. In all children blindness had alr
eady persisted for at least one year. Visual functions developed within a t
raining period of three months in 15 of 22 children who received visual fie
ld training whereas there was no spontaneous recovery in the control group.
The functional luminance difference threshold was still elevated above nor
mal in the case of 5 children who recovered from blindness. In 2 children t
he latency of saccades elicited by light targets in the formerly blind visu
al area was significantly longer than the latency of saccades elicited by t
argets 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 a
n effect of scattering light. The findings support the assumption that syst
ematic stimulation of cerebrally blind areas may facilitate the development
of visual functions in brain damaged children. The cerebral lesions associ
ated 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 b
asis of the shrinkage of the blind areas.