Effects of retinal ganglion cell loss on magno-, parvo-, koniocellular pathways in the lateral geniculate nucleus and visual cortex in glaucoma

Effects of retinal ganglion cell loss on magno-, parvo-, koniocellular pathways in the lateral geniculate nucleus and visual cortex in glaucoma
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DOI:
10.1016/s1350-9462(03)00026-0
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发表时间:
2003-07-01
影响因子:
17.8
通讯作者:
Gupta, N
Gupta, N
中科院分区:
医学1区
文献类型:
--
作者:
Yücel, YH;Zhang, QA;Gupta, N

文献摘要

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青光眼是世界性失明的主要原因,视网膜神经节细胞死亡是其病理标志。越来越多的证据表明,青光眼损伤从视网膜神经节细胞延伸到大脑的视觉中心。在单侧青光眼的实验性灵长类动物模型中,在外侧膝状核的大细胞、小细胞和角细胞通路中观察到退行性变化;这些变化与眼压和视神经损伤的严重程度有关。神经病理学发现也存在于由未受影响的对侧眼睛驱动的外侧膝状体核层中。最后,有关于视觉皮层变化与不同程度的视网膜神经节细胞损失相关的信息。讨论了这些发现对于完善有关进展病理学以及青光眼检测和治疗概念的影响。 (C) 2003 Elsevier Science Ltd. 保留所有权利。
Glaucoma is a leading cause of world blindness, and retinal ganglion cell death is its pathological hallmark. There is accumulating evidence that glaucomatous damage extends from retinal ganglion cells to vision centers in the brain. In an experimental primate model of unilateral glaucoma, degenerative changes are observed in magnocellular, parvocellular, and koniocellular pathways in the lateral geniculate nucleus; and these changes are presented in relation to intraocular pressure and the severity of optic nerve damage. Neuropathological findings are also present in lateral geniculate nucleus layers driven by the unaffected fellow eye. Finally, there is information on changes in the visual cortex in relation to varying degrees of retinal ganglion cell loss. The implications of these findings for refining concepts regarding the pathobiology of progression, and the detection and treatment of glaucoma, are discussed. (C) 2003 Elsevier Science Ltd. All rights reserved.