Physiological and Morphoragical Studies on Senescence of Higher Visual Center

用图形翻转视觉诱发皮层电位(VECP)对人和动物衰老过程中的视功能进行定量评价。结果显示，老年人的对比度阈值升高，即对较高空间频率的敏感度降低，而亮度阈值升高。时间频率曲线也有整体抑制，上半视野敏感度降低，蓝黄色缺陷和调节幅度降低。对植入人工晶状体的人工晶状体眼的研究证实，晶状体透明度降低、黄化和老年性斜视并不能完全解释老年人视觉功能低下的原因。青少年帕金森病患者停用L-多巴后，VECP的P100峰潜伏期延长，提示患者存在多巴胺缺乏，可作为临床衰老模型。老年组小鼠的视神经纤维计数明显减少。人们认为，除了眼睛本身，还有神经元的衰老。这一结果可以通过以下日常生活经验来说明。晚上，如果一只猫爬在墙上，在视野中快速奔跑，老年人就很难识别这只猫是一只印花猫。然而，令人惊讶的是，在视觉功能中发现的衰老没有在其他感官中发现的那么严重。随着研究的深入，还需进一步研究大脑对视网膜的反馈机制和代偿机制。

Visual functions in senescence were assessed quantitatively by the pattern reversal visually evoked cortical potentials (VECP) in human subjects and animals. The results obtained in the elderly showed an elevation of contrast threshold, ie, lowered sensitivity, for higher spatial frequency, and a rise in the luminance thresholds. There was also an overall suppression in the temporal frequency curves, a sensitivity decrease for the upper half of the visual field, a blue-yellow defect and a decrease in the amplitude of accommodation. Studies of the pseudophakic eye with an intraocular lens verified that the lower transparency and yellowish changes of the crystalline lens and senile miosis do not entirely account for the depressed visual function in the elderly. The delay of P100 peak latency of the VECP in patients with juvenile Parkinson's disease after cessation of L-dopa indicated the deficiency of dopamine in these patients, which in turn was considered as a clinical model of senescence. Optic nerve fiber counts in mice showed a significant decrease in the aged group. It was considered that there is neuronal senescence other than in the eye itself.The results can be illustrated by the following daily life experience. In the evening, an elderly person would have difficulty in identifying a cat as a calico cat if the cat were atop a wall and running quickly through the visual field. It was surprising, however, that the senescence found in the visual function was not as great as that found in the other sensory organs. As further studies, investigation of the feedback mechanism from the brain to the retina and the compensatory mechanism should be made.