Investigating the role of intracranial pressure in glaucoma
Even when we can lower intraocular pressure substantially some people still continue to show progressive vision loss from glaucoma. One factor that may play an important role in the development of glaucoma is cerebral spinal fluid pressure. It is of interest that cerebral spinal fluid pressure decreases with age in a manner that mirrors the increase in prevalence of glaucoma. To more fully understand the effect that modifying cerebral spinal fluid pressure has on the health of the optic nerve and thus the risk of glaucoma, we will employ a suite of novel experimental models and state-of-the-art in vivo tools. Our studies involve acute and chronic modification of translaminar pressure. We will undertake studies in young and older animals to assess age-related modification of glaucoma risk. Our multidisciplinary approach will allow us to marry up risk factors with the cellular and molecular changes that predispose to the development of glaucoma. This will study will provide an explanation for many long lingering clinical paradoxes in glaucoma, as well as highlighting novel therapeutic targets for further study.
Intracranial pressure can counteract the effect of intraocular pressure elevation on optic nerve structure and function. A. Intraocular and intracranial pressure are forces that oppose each other across the lamina cribrosa. Using optical coherence tomography we show that there was more backward bowing of the optic nerve surface (arrow lines) and retinal compression (arrowheads) with IOP elevation when ICP was normal (B. ICP 5 mmHg) compared with a high ICP (D. 30 mmHg). Using the electroretinogram we show that high ICP prevents ganglion cell dysfunction caused by elevated IOP. Black traces indicate baseline waveforms and colored traces indicate waveforms when IOP was 70 mmHg. The response is more affected when ICP was normal (C, orange trace), and less affected when ICP was high (E, blue trace). Adapted from Zhao et al (2015).
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