Study on the deformations of the lamina cribrosa during glaucoma

Study on the deformations of the lamina cribrosa during glaucoma
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青光眼时筛板变形的研究

DOI:
10.1016/j.actbio.2017.03.028
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发表时间:
2017-06-01
期刊:
影响因子:
9.7
通讯作者:
Song, Fan
Song, Fan
中科院分区:
工程技术1区
文献类型:
--
作者:
Tian, Hanjing;Li, Long;Song, Fan

文献摘要

被引文献

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筛板是青光眼视神经损伤的主要部位,眼压升高引起的筛板变形与视神经损伤和视野缺损直接相关。然而,到目前为止,人们对活体中的变形知之甚少。这是因为在青光眼的临床诊断和治疗中,在活体上对变形进行完整的观察和精确的测量几乎是不可能的。在本研究中,一个新的力学模型的筛板,采用Reissner的薄板理论。该模型准确地反映了眼压升高时筛板的应力和变形状态,其中剪切变形在以往模型中没有体现,但在视神经损伤中起着关键作用。此外,变形的结构,包括视神经通道和筛板中的板片,首先详细研究。例如,在40 mmHg的眼内压下,椎板片的错位达到18.6 μ m,这足以损伤视神经轴突。本研究结果证实了一些先前提出的关于青光眼患者眼压升高时筛板孔形变形的临床推测。最后,对青光眼发生过程中存在的一些本质性问题,如正常眼压下开角型青光眼的病理机制等进行了讨论。本研究有助于加深对青光眼视神经损伤的认识。意义说明青光眼眼压升高引起视神经损伤的主要部位是筛板。在高眼内压下,靠近筛板周边的视神经通道(通道A)变形为从直圆柱体变成弯曲椭圆角,而靠近筛板中心的视神经通道(通道B)变形为从直圆柱体变成直角。这些变形导致轴突纤维中的轴浆流动障碍和通过通道的毛细血管中的血流受阻,并触发青光眼期间的视野缺损。(C)2017 Acta Materialia Inc.由爱思唯尔有限公司出版。保留所有权利。
The lamina cribrosa is the primary site of optic nerve injury during glaucoma, and its deformations induced by elevated intraocular pressure are associated directly with the optic nerve injury and visual field defect. However, the deformations in a living body have been poorly understood yet so far. It is because that integral observation and precise measurement of the deformations in vivo are now almost impossible in the clinical diagnosis and treatment of glaucoma. In the present study, a new mechanical model of the lamina cribrosa is presented by using Reissner's thin plate theory. This model accurately displays the stress and deformation states in the lamina cribrosa under elevated intraocular pressure, in which the shear deformation is not presented by the previous models, however, is demonstrated to play a key role in the optic nerve injury. Further, the deformations of the structures, involving the optic nerve channels and the laminar sheets in the lamina cribrosa, are first investigated in detail. For example, the dislocation of the laminar sheets reaches 18.6 mu m under the intraocular pressure of 40 mmHg, which is large enough to damage the optic nerve axons. The results here confirm some previously proposed clinical speculations on the deformations of the pore shape in the lamina cribrosa under elevated intraocular pressure during glaucoma. Finally, some essentially clinical questions existed during glaucoma, such as the pathological mechanism of the open-angle glaucoma with normal intraocular pressure, are discussed. The present study is beneficial to deeply understanding the optic nerve injury during glaucoma.Statement of SignificanceThe lamina cribrosa is the primary site of the optic nerve injury induced by elevated intraocular pressure during glaucoma. Under high intraocular pressure, the optic nerve channel near to the periphery of the lamina cribrosa (Channel A) is deformed to become into a tortuous elliptical horn from a straight cylinder, while the optic nerve channel near to the center of the lamina cribrosa (Channel B) is deformed to become into a straight horn from a straight cylinder. These deformations cause both the axoplasm flow obstacle in the axon fibers and the blocked blood flow in the capillaries which pass through the channels, and trigger the visual field defect during glaucoma. (C) 2017 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.