Biomechanics of optic nerve head (ONH) has attracted increasing attention in recent years due to its association with ganglion cell damage and tissue remodeling resulted vision impairments [1, 2]. The ONH is exposed to both intraocular pressure (IOP) and intracranial pressure (ICP), separated by the lamina cribrosa (LC) which is regarded as the primary site of axonal injury in glaucoma[3]. The elevated IOP was widely acknowledged as a major risk factor for glaucoma. However, a large number of glaucoma patients never have an increase in IOP [4]. In studies that have looked at lumbar puncture (LP) data, patients with open-angle glaucoma were found to have lower ICPs than non-glaucomatous controls[5]. It suggests that higher translaminar pressure difference across the LC rather than IOP alone may have an important role in the pathogenesis of ONH damage. There were few computational models had been established to investigate the ICP’s role on ONH, such as Ethier et al. found elevated ICP could induce decreased strain within LC using finite element model[6]. However, less experimental data are available for delineating the role of ICP on the behaviors of LC. In this work, we present one dataset from LP patients and reconstruct its two-dimensional computational model of the ONH based on the patient’s images to delineate the role of ICP on ONH mechanics. The changes of LC depth, BMO width and papillary height were compared between the simulation and clinical dataset. The maximum principal strain of LC was calculated to reinforce its link with mechanosensitive cells in ONH.

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