Study on the deformations of the lamina cribrosa during glaucoma.
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 18.6μm under the intraocular pressure of 40mmHg, 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.



The 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.
State Key Laboratory of Nonlinear Mechanics (LNM), Institute of Mechanics, Chinese Academy of Sciences, Beijing 100190, China.
Hanjing
H
Tian
State Key Laboratory of Nonlinear Mechanics (LNM), Institute of Mechanics, Chinese Academy of Sciences, Beijing 100190, China.
Long
L
Li
State Key Laboratory of Nonlinear Mechanics (LNM), Institute of Mechanics, Chinese Academy of Sciences, Beijing 100190, China; School of Engineering Science, University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: songf@lnm.imech.ac.cn.
Fan
F
Song
D005901:Glaucoma / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007429:Intraocular Pressure; D008954:Models, Biological; D009900:Optic Nerve / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D020221:Optic Nerve Injuries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
Deformation; Glaucoma; Lamina cribrosa; Optic nerve injury; Reissner’s thin plate theory