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Editors Selection IGR 18-1

Miscellaneous: Pathophysiology of glaucoma: Lessons from microgravity

Comment by Hanspeter Killer & Achmed Pircher on:

69227 The pressure difference between eye and brain changes with posture, Eklund A; Jóhannesson G; Johansson E et al., Annals of Neurology, 2016; 80: 269-276

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The relationship between the intracranial and the intraocular pressure and the translaminar pressure difference (TLCPD) has gained interest in the study of glaucoma (particularly normal-tension glaucoma (NTG)), idiopathic intracranial hypertension (IIH) and the visual impairment/ intracranial pressure (VIIP) syndrome described in astronauts.

Eklund et al. investigated the effect of posture onto the TLCPD in 11 healthy volunteers (age 46 ± 10 years, three males and eight females) by measuring the intracranial pressure (ICP) on lumbar puncture as well as the intraocular pressure simultaneously in supine, sitting and in head-down tilt (HDT) position. The estimated TLCPD at assessed simultaneously measured IOP and ICP was dependent on hydrostatic effects related to body posture.

The pressure behind the lamina cribrosa is virtually not known

The study is nicely conducted, but the results should be interpreted in the light of their limitations.

Firstly, the cohort is small and the age rather young and therefore more representative for IIH patients than patients with NTG.

Secondly, the term intracranial pressure is somehow misleading as it is the lumbar CSF pressure that was measured. Although the CSF pressure at the lumbar site may equal the CSF pressure in the brain¹ it is questionable whether it equals the pressure in the subarachnoid space (SAS) of the optic nerve (ON). Studies applying cysternography demonstrated that in patients with NTG² and patients with papilledema³ CSF does not communicate freely between the intracranial SAS and that of the ON. The SAS of the ON is extremely narrow and due to the mechano-sensitivity of meningothelial cells⁴ that cover the meninges (arachnoid and pia layer) as well as the septae and trabeculae, the lumen of the SAS surrounding the ON is highly dynamic. CSF enters into the orbit through the bony optic canal - the static component, which was shown to influence the expression of papilledema (Bidot). In cases of asymmetric papilledema the CSF pathway along the ON might at least at the side of the less affected ON not be patent.

Thirdly, it is still not clear if and how a higher TLCPD might contribute to optic disc cupping as seen in patients with glaucoma. In fact, the calculated TLCPD in the study from Berdahl et al.⁵ is higher in ocular hypertension compared with that in NTG. The calculated TLCPD in the study from Eklund et al. concerning lumbar CSF pressure measurement in supine position in 11 healthy is even higher than the calculated and as pathologic suggested TLCPD in NTG patients published in the studies from Berdahl et al.⁵ and Ren et al.⁶ Further, a recent study (Pircher et al.) did not show a correlation between the TLCPD and the mean deviation of visual field defects in 38 patients with NTG.

All these questions need to be addressed for further advancement of the TLCPD concept and cannot be eliminated by measuring IOP and CSF-p simultaneously as the pressure behind the lamina cribrosa is virtually not known.

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