Pressure gradients

Complex pressure relationships appear at play in glaucoma and papilloedema

Howard Larkin

Posted: Friday, June 1, 2018

In 1908, Kasmir J Noishevsky hypothesised that depression of the optic nerve may be caused by an excess of intraocular pressure (IOP) over cerebrospinal fluid pressure (CSFP) across the lamina cribrosa – and demonstrated it two years later by boring a hole in the skull of a dog with help from the renowned Ivan Pavlov.

More than a century later, evidence continues to mount that a translaminar pressure gradient is involved in papilloedema and glaucomatous excavation, as well as deformation of the posterior pole of the globe and related retinal folds. However, the relationship between CSFP and IOP is complex and cannot yet be directly measured, making it an attractive subject for further research, presenters told the American Academy of Ophthalmology 2017 Annual Meeting in New Orleans, USA.

Assessing effects of the translaminar pressure difference requires understanding specifically what should be measured, said David Fleischman MD, of the University of North Carolina at Chapel Hill, USA. He noted that where CSFP is measured is critical.

For example, while several studies suggest a correlation between IOP and intracranial pressure (ICP), their conclusions are suspect due to various methodological problems. More rigorous recent studies show no correlation between IOP and ICP, Dr Fleischman noted. Both IOP and CSFP can vary with posture, time of day and other factors, he added.

“The translaminar pressure difference is not a static number.”

Two groups have investigated the relationship of orbital CSFP and the intracranial pressure, and these were both performed in dog models with varying results. Dr Fleischman sees orbital pressure as the appropriate point to determine the translaminar pressure difference. Pressure in the orbital space differs from ICP due to the constriction of the optic canal where the optic nerve passes between the skull and the orbit, and impedes free fluid flow. Indeed, differences in size of the two optic canals may explain unilateral and asymmetric papilloedema, he notes, referencing Sohan Hayreh and two recent studies confirming Hayreh’s hypothesis (Bidot S et al. J Neuro-Ophthalmol 2015; 35: 31-36. Bidot S et al. J Neuro-Ophthalmol 2016; 36: 120-125).

Unfortunately, no effective way of measuring orbital CSFP yet exists, Dr Fleischman said.
“This is going to be a big problem for us in terms of quantitative research into the translaminar pressure difference. However, it also makes it an exciting opportunity for research.”

OCT provides indirect evidence of the effect of the translaminar pressure gradient on ocular anatomy in patients with intracranial hypertension, said Patrick A Sibony MD, of Stony Brook University Hospital, New York, USA. OCT shows retinal nerve fibre layer (RNFL) thickness, disc volume, globe shape deformations, retinal folds and changes due to ocular ductions.

Dr Sibony considers OCT measurement of RNFL thickness the best way to monitor papilloedema progression. However, when the disc is swollen, there are segmentation artifacts that can limit its reliability. A decrease in RNLF thickness may be a sign of improvement or axonal attrition; a distinction that can only made by monitoring the visual field.

OCT can also show changes in the shape and displacement of the peripapillary tissues and the lamina cribrosa in response to the intraocular and CSF pressure. Using shape analysis techniques, Dr Sibony has shown anterior shape deformations and displacements (toward the vitreous) with intracranial hypertension that moves posteriorly (away from the vitreous) after treatment. OCT may provide a potentially useful tool for gauging intracranial pressure and the translaminar pressure gradient.

David Fleischman: