Werth R, Moehrenschlager M
Institute for Social Pediatrics and Adolescent Medicine, University of Munich, München, Germany.
Restor Neurol Neurosci. 1999;15(2-3):229-41.
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.
16名年龄在1至15岁之间、因围产期窒息后丘脑后缺血性脑损伤而失明的儿童,以及6名年龄在1至13岁之间、因丘脑后创伤性脑损伤而失明的儿童参加了系统的视野训练。31名因围产期窒息后丘脑后病变而失明的儿童和12名因丘脑后创伤性病变而失明的儿童作为对照组。这些儿童未接受视野训练或接受无效的视野训练。使用专门设计的弧形视野计评估功能性视野的扩展和功能性亮度差异阈值。所有儿童失明已持续至少一年。在接受视野训练的22名儿童中,有15名在三个月的训练期内视觉功能得到了发展,而对照组没有自发恢复。5名从失明中恢复的儿童的功能性亮度差异阈值仍高于正常水平。在2名儿童中,以前失明视野区域中由光目标引发的扫视潜伏期明显长于视野正常区域中目标引发的扫视潜伏期。控制了光散射,以排除我们将训练期间视野扩大解释为视觉功能发展迹象的情况是散射光的影响。这些发现支持这样一种假设,即对脑性失明区域进行系统刺激可能有助于脑损伤儿童视觉功能的发展。治疗期间视觉功能得到改善的与受损视觉功能相关的脑损伤与以下假设一致,即纹状和纹状外视觉皮层以及下层白质中的保留组织是盲区缩小的解剖学基础。