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Lucia Carichino, Giovanna Guidoboni, Annahita Amireskandari, Brent Siesky, Alon Harris; Effect of Cerebrospinal Fluid Pressure on Central Retinal Artery Hemodynamics: a Mathematical Model. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4459.
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To investigate the influence of cerebrospinal fluid pressure (CSF-p) on central retinal artery (CRA) hemodynamics. This investigation is motivated by several studies that suggested low CSF-p as a possible risk factor for glaucoma. In particular, there is evidence of lower CSF-p in normal-tension glaucoma subjects.
A mathematical model is developed to simulate the effect of CSF-p on CRA hemodynamics. The model incorporates a description of the lamina cribrosa (LC) deformation and the blood flow in the CRA. The LC is modeled as a homogeneous linearly elastic circular plate of constant finite thickness, which deforms under the combined action of intraocular pressure (IOP), CSF-p and scleral tension. The CRA is modeled as a fluid-structure interaction system. The walls of the CRA deform under the action of an external pressure that varies along the vessel length to include CSF-p, IOP and the compression induced by LC deformation. Numerical simulations are performed at constant IOP=15mmHg and constant mean arterial pressure 62mmHg, while the CSF-p is varied in the range between 1 and 30mmHg.
As CSF-p increases, the CRA blood velocity (v) and flow rate (Q) predicted by the mathematical model show a complex behavior, see Figure 1 and 2. The CRA hemodynamic response can be divided in three phases. In phase A and C the system is dominated by the trans-LC pressure gradient. More precisely, in phase A the trans-LC pressure gradient decreases with CSF-p elevation, leading to an increase in v and Q, while in phase C the gradient increases with CSF-p elevation, leading to a decrease in v and Q. In phase B the trans-LC pressure gradient is small enough to be overcome by the scleral tension. This leads to a less steep decrease in v and Q when compared with phase C, which results from the direct action of elevated CSF-p on the pre-laminar CRA segment.
Low CSF-p has been associated with primary open angle glaucoma (POAG). The exact mechanisms responsible for this association remain unclear. Our model suggests that the contribution of CSF-p alterations to POAG pathophysiology might be mediated by secondary retinal blood flow changes.
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