Contrast enhancement of the retinal image and image distortion associated with macular degeneration.

F S Sjöstrand
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Abstract

An analysis of image distortion in connection with macular degeneration revealed that seeing objects requires brightness contrast enhancement. Thus macular degeneration changes neural interaction controlling bipolar cell responses to light stimulating photoreceptors to reverse spatial brightness contrast enhancement with the consequence that objects cannot be seen. This shows that the contrast of the retinal images is too low for vision without enhancement. However images consisting of randomly arranged small spots of different brightness are seen because of cones enhancing bipolar cell responses to rod input and rods enhancing bipolar cell responses to cone input. This residual vision and the observation that image distortion disappears at low light intensities reveal that macular degeneration is a functional disorder with intact photoreceptor function. The affection may therefore be caused by a reduction of blood flow through the choriocapillaries associated with ageing. The analysis of image distortion associated with the affection led to a simple way to determine the size of the affected retinal area, making it possible to follow the progression of the affection in a direct and simple way. Basic aspects are described of synaptic interaction within the information processing unit that determines the responses of the bipolar cells to photoreceptor input. This unit is the first information processing unit that has been revealed thanks to the extension of the analysis of the nervous system to the nanometer level at which information is processed. The minute size of the information processing unit, the special conditions for synaptic transmission combined with the short distances separating the synapses create special conditions for neural interaction at the nanometer level, establishing conditions for high speed neural communication.

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视网膜图像的对比度增强和与黄斑变性相关的图像失真。
对与黄斑变性有关的图像失真的分析表明,要看到物体需要亮度对比度增强。因此,黄斑变性改变了控制双极细胞对光刺激光感受器反应的神经相互作用,从而逆转了空间亮度对比增强,结果是看不到物体。这表明,视网膜图像的对比度太低,视觉没有增强。然而,由于视锥细胞增强双极细胞对视杆输入的响应,视杆细胞增强双极细胞对视锥输入的响应,因此可以看到由随机排列的不同亮度的小点组成的图像。这种残余视觉和在低光强度下图像失真消失的观察表明,黄斑变性是一种具有完整光感受器功能的功能障碍。因此,这种影响可能是由与衰老有关的绒毛膜毛细血管的血液流动减少引起的。对与情感相关的图像失真的分析导致了一种简单的方法来确定受影响的视网膜区域的大小,使得以直接和简单的方式跟踪情感的进展成为可能。描述了信息处理单元内突触相互作用的基本方面,这种相互作用决定了双极细胞对光感受器输入的反应。这是由于神经系统的分析扩展到处理信息的纳米级,首次揭示的信息处理单元。信息处理单元的微小尺寸,突触传递的特殊条件,再加上突触之间的距离短,为神经在纳米级的相互作用创造了特殊条件,为神经的高速通信奠定了条件。
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