Assessing retinal function with the multifocal technique

Assessing retinal function with the multifocal technique
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DOI:
10.1016/s1350-9462(00)00013-6
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发表时间:
2000-09-01
影响因子:
17.8
通讯作者:
Hood, DC
Hood, DC
中科院分区:
医学1区
文献类型:
--
作者:
Hood, DC

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由Erich Sutter及其同事开发的多焦点技术可以在几分钟内获得数十个焦点视网膜电图(ERG)反应。虽然这项技术相对较新,但它已经为视网膜疾病的机制提供了见解。然而,由于它是新的,它的工作原理和测量内容仍然存在问题。本章考虑了其中的一些见解和一些问题。第一部分(第2节)描述了如何记录多焦点ERG (mERG),并考虑了它与全视野ERG的关系。mERG反应显示来自视网膜的相对局部区域,并由与全视野ERG相同的成分组成。与完整的ERG相比,mERG的诊断优势也得到了说明。在第3节。损伤对视网膜不同细胞层的影响显示出对mERG的不同影响。这些变化是在一个概念框架内总结出来的。例如,有人认为,当受体外段的疾病,如视网膜色素变性,导致小的,抑制的mERG反应,那么损害是。和预期的一样,在外层。然而,当这些疾病导致mERG反应相当大但非常延迟时,则损害超出了外节段,可能在外丛状层。mERG的隐式时间,而不是振幅,是对受体退行性疾病损伤的更敏感的测量。另一方面,像青光眼这样的疾病,作用于神经节轴突,除非也涉及视网膜内部损伤,否则不会导致mERG容易识别的变化。视网膜内损伤改变了mERG的波形,降低了通常观察到的鼻颞变化。最后,像糖尿病这样的疾病,如果作用于不止一层视网膜,就会产生一系列的影响。在第3节中,回顾了猴子mERG的最新工作,重点是与人类疾病的相关性。为例。阻断由神经节细胞和无突细胞产生的钠基动作电位消除了猴子mERG的鼻颞变化,这些改变的mERG反应类似于一些糖尿病或青光眼患者的反应。最后,在第5节中描述二阶核。二阶核的存在对于理解mERG响应的形状(一阶核)具有重要意义。对mERG模式的全面模拟表明,一阶核由不同波形的响应组成。此外,还认为产生二阶核的非线性自适应机制参与了响应的时间过程的形成。有较大但异常延迟的mERG反应(一阶核)的患者没有可检测到的二阶核。推测二阶核明显减小是外丛状层损伤的诊断,而不是通常认为的内丛状层损伤。(C) 2000 Elsevier Science Ltd.版权所有。
With the multifocal technique, as developed by Erich Sutter and colleagues, scores of focal electroretinogram (ERG) responses can he obtained in a matter of minutes. Although this technique is relatively new, it has already provided insights into the mechanisms of retinal disease. However, because it is new, there also remain questions about how it works and what it measures. This chapter considers some of these insights and some of these questions. The first part (Section 2) describes how the multifocal ERG (mERG) is recorded and considers its relationship to the full-field ERG. The mERG responses are shown to be from relatively local regions of the retina and are comprised of the same components as the full-field ERG. The diagnostic advantage of the mERG as compared to the full-held ERG is also illustrated. In Section 3. the effects of damage to different cell layers of the retina are shown to affect the mERG differently. and these changes are summarized within a conceptual framework. It is argued, for example, that when diseases of the receptor outer segment, like retinitis pigmentosa, result in small, depressed mERG responses, then the damage is. as expected, at the outer segment. However, when these diseases result in mERG responses that are reasonably large but very delayed, then the damage is beyond the outer segment, probably in the outer plexiform layer. The implicit time of the mERG, not amplitude, is the more sensitive measure of damage in degenerative diseases of the receptors. On the other hand, diseases, like glaucoma, which act on the ganglion axon, do not result in easily identified changes to the mERG unless inner retinal damage is involved as well. Inner retinal damage changes the waveform of the mERG and decreases the naso-temporal variation normally observed. Finally, diseases, like diabetes, that act on more than one layer of the retina can have a range of effects. In Section 3, recent work with the monkey mERG is reviewed, with emphasis on the relevance to human diseases. For example. blocking the sodium-based action potentials produced by ganglion and amacrine cells eliminates the naso-temporal variation in the monkey mERG and these altered mERG responses resemble those from some patients with diabetes or glaucoma. Finally, in Section 5 the second-order kernel is described. The presence of a second-order kernel has important implications for understanding the shape of the mERG response (first-order kernel). Full-held simulations of the mERG paradigm illustrate that the first-order kernel is comprised of responses with different waveforms. Further, it is argued that the nonlinear, adaptive mechanisms that produce the secund-order kernel are involved in shaping the time course of the response. Patients with large, but abnormally delayed mERG responses (first-order kernel), do not have a detectable second-order kernel. It is speculated that a markedly diminished second-order kernel is diagnostic of outer plexiform layer damage, not inner plexiform layer damage as is commonly assumed. (C) 2000 Elsevier Science Ltd. All rights reserved.