Finite element modeling of effects of tissue property variation on human optic nerve tethering during adduction

Abstract

Tractional tethering by the optic nerve (ON) on the eye as it rotates towards the midline in adduction is a significant ocular mechanical load and has been suggested as a cause of ON damage induced by repetitive eye movements. We designed an ocular finite element model (FEM) simulating 6° incremental adduction beyond the initial configuration of 26° adduction that is the observed threshold for ON tethering. This FEM permitted sensitivity analysis of ON tethering using observed material property variations in measured hyperelasticity of the anterior, equatorial, posterior, and peripapillary sclera; and the ON and its sheath. The FEM predicted that adduction beyond the initiation of ON tethering concentrates stress and strain on the temporal side of the optic disc and peripapillary sclera, the ON sheath junction with the sclera, and retrolaminar ON neural tissue. However, some unfavorable combinations of tissue properties within the published ranges imposed higher stresses in these regions. With the least favorable combinations of tissue properties, adduction tethering was predicted to stress the ON junction and peripapillary sclera more than extreme conditions of intraocular and intracranial pressure. These simulations support the concept that ON tethering in adduction could induce mechanical stresses that might contribute to ON damage.

The impact of horizontal eye movements versus intraocular pressure on optic nerve head biomechanics: A tridimensional finite element analysis study

“…The classic physiopathology theory of glaucoma poses that an increase in intraocular pressure (IOP) would lead to compression of the axons at the lamina cribrosa (LC) with consequent ischemia and axoplasmic flow blockage, and hence the death of RGC [ 2 ]. However, although high IOP is recognized as the most important risk factor for glaucoma [ 3 ], this is not the only mechanical load experienced by the optic nerve, as it is also influenced by cerebrospinal fluid pressure [ 4 , 5 ], IOP fluctuations [ 6 ], vascular pulsatility [ 7 ], and eye movements [ [8] , [9] , [10] , [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] ], among other factors.…”

“…A recent FE study performed by Jafari et al [ 10 ], in which a 6° ocular rotation was generated, has also confirmed these findings. Thus, as a result, it has been hypothesized that eye movements could also contribute to the development of glaucomatous optic neuropathy [ 8 , 9 , 11 , 12 ].…”

“…On the other hand, eye anatomy has typically been reconstructed variably in FE studies. As a result, different eye regions and tissues have been included and excluded in posterior ocular models [ [8] , [9] , [10] , [11] , [12] , [31] , [32] , [33] , [34] , [35] , [36] , [37] ]. Biologically the eye is comprised of three tunics, namely: fibrous (cornea and sclera), vascular (iris, ciliary body, and choroid), and nervous (retina), and it is located within the orbit and surrounded by fat [ 38 ].…”

“…Nevertheless, some ocular models have not included the choroid [ [8] , [9] , [10] , 12 , 31 , 32 , 34 , 36 , 37 ], and some others neither the nervous tunic [ 9 , 10 , 12 , 33 ]. Besides that, the retina has usually been regarded as an extension of the prelaminar tissue [ 40 ] and adipose tissue has not been commonly incorporated.…”

“…Furthermore, the optic nerve's SAS has been commonly modeled as empty, with the cerebrospinal fluid pressure (CSFP) applied inside it [ 8 , 9 , 11 , 12 , [31] , [32] , [33] , [34] , 37 ]. However, the SAS is not an empty space; rather, it is a complex structure that includes very dense layers of trabeculae, collagen-based structures that act as supportive pillars between the arachnoid and the pia mater [ 39 , [42] , [43] , [44] ], and allow the flow of cerebrospinal fluid among its spaces.…”