In this work, the biomechanical responses of the optic nerve head (ONH) to acute elevations in intracranial pressure (ICP) were systematically investigated through numerical modeling. An orthogonal experimental design was developed to quantify the influence of ten input factors that govern the anatomy and material properties of the ONH on the peak maximum principal strain (MPS) in the lamina cribrosa (LC) and postlaminar neural tissue (PLNT). Results showed that the sensitivity of ONH responses to various input factors was region-specific. In the LC, the peak MPS was most strongly dependent on the sclera thickness, LC modulus, and scleral canal size, whereas in the PLNT, the peak MPS was more sensitive to the scleral canal size, neural tissue modulus, and pia mater modulus. The enforcement of clinically relevant ICP in the retro-orbital subarachnoid space influenced the sensitivity analysis. It also induced much larger strains in the PLNT than in the LC. Moreover, acute elevation of ICP leads to dramatic strain distribution changes in the PLNT, but had minimal impact on the LC. This work could help to better understand patient-specific responses, to provide guidance on biomechanical factors resulting in optic nerve diseases, such as glaucoma, papilledema, and ischemic optic neuropathy, and to illuminate the possibilities for exploiting their potential to treat and prevent ONH diseases.

Current knowledge of traumatic ocular injury is still limited as most studies have focused on the ocular injuries that happened at the anterior part of the eye, whereas the damage to the optic nerve known as traumatic optic neuropathy (TON) is poorly understood. The goal of this study is to understand the mechanism of the TON following the primary blast through a fluid–structure interaction model. An axisymmetric three-dimensional (3D) eye model with detailed orbital components was developed to capture the dynamics of the eye under the blast wave. Our numerical results demonstrated a transient pressure elevation in both vitreous and cerebrospinal fluid (CSF). A high strain rate over 100 s−1 was observed throughout the optic nerve during the blast with the most vulnerable part located at the intracanalicular region. The optic nerve deforming at such a high strain rate may account for the axonal damage and vision loss in patients subjected to the primary blast. The results from this work would enhance the understanding of indirect TON and provide guidance in the design of protective eyewear against such injury.

Purpose: Orbital veins such as the retinal veins and episcleral veins drain into the cavernous sinus, an intracranial venous structure. We studied the effects of acute intracranial pressure (ICP) elevation on episcleral venous pressure, intraocular pressure and retinal vein diameter in an established non-survival pig model. Methods: In six adult female domestic pigs, we increased ICP in 5 mm Hg increments using saline infusion through a lumbar drain. We measured ICP (using parenchymal pressure monitor), intraocular pressure (using pneumatonometer), episcleral venous pressure (using venomanometer), retinal vein diameter (using OCT images) and arterial blood pressure at each stable ICP increment. The average baseline ICP was 5.4 mm Hg (range 1.5-9 mm Hg) and the maximum stable ICP ranged from 18 to 40 mm Hg. Linear mixed models with random intercepts were used to evaluate the effect of acute ICP increase on outcome variables. Results: With acute ICP elevation, we found loss of retinal venous pulsation and increased episcleral venous pressure, intraocular pressure and retinal vein pressure in all animals. Specifically, acute ICP increase was significantly associated with episcleral venous pressure (β = 0.31; 95% CI 0.14-0.48, p < .001), intraocular pressure (β = 0.37, 95%CI 0.24-0.50; p < .001) and retinal vein diameter (β = 11.29, 95%CI 1.57-21.00; p = .03) after controlling for the effects of arterial blood pressure. Conclusion:We believe that the ophthalmic effects of acute ICP elevation are mediated by increased intracranial venous pressure producing upstream pressure changes within the orbital and retinal veins. These results offer exciting possibilities for the development of non-invasive ophthalmic biomarkers to estimate acute ICP elevations following significant neuro-trauma.

Purpose. To characterize the relative contributions of intraocular pressure (IOP) and intracranial pressure (ICP) on lamina cribrosa (LC) behavior, specifically LC depth (LCD) and LC peak strain. Methods. An axially symmetric finite element model of the posterior eye was constructed with an elongated optic nerve and retro-orbital subarachnoid space ensheathed by pia and dura mater. The mechanical environment in LC was evaluated with ICP ranging from 5 to 15 mmHg and IOP from 10 to 45 mmHg. LCD and LC peak strains at various ICP and IOP levels were estimated using full factorial experiments. Multiple linear regression analyses were then applied to estimate LCD and LC peak strain using ICP and IOP as independent variables. Results. Both increased ICP and decreased IOP led to a smaller LCD and LC peak strain. The regression correlation coefficient for LCD was −1.047 for ICP and 1.049 for IOP, and the ratio of the two regression coefficients was −1.0. The regression correlation coefficient for LC peak strain was −0.025 for ICP and 0.106 for IOP, and the ratio of the two regression coefficients was −0.24. A stiffer sclera increased LCD but decreased LC peak strain; besides, it increased the relative contribution of ICP on the LCD but decreased that on the LC peak strain. Conclusions. ICP and IOP have opposing effects on LCD and LC peak strain. While their effects on LCD are equivalent, the effect of IOP on LC peak strain is 3 times larger than that of ICP. The influences of these pressure are dependent on sclera material properties, which might explain the pathogenesis of ocular hypertension and normal-tension glaucoma.

Summary IntroductionThe long-held belief that a ureteral re-implant tunnel should be five times the diameter of the ureter, as proposed by Paquin in 1959, ignores the effect of the orifice on the occurrence of reflux. In 1969, Lyon proposed that the shape of the ureteral orifice (UO) is more important than the intravesical tunnel. However, both theories missed quantitative evidence from principles of physics. The goal of the current study was to test Lyon's theory through numerical models (i.e. to quantify the sensitivity of ureterovesical junction (UVJ) competence to intravesical tunnel length and to the UO).