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The term ‘intraocular pressure’ has traditionally been referred to the ‘pressure in the eye’, although in a strictly physically meaning, the ophthalmologic term ‘intraocular pressure’ only describes the transcorneal pressure difference between the intraocular space and the extraocular surrounding air. An eye with an ‘intraocular pressure’ of 20 mmHg thus has a physically correctly defined pressure of 780 mmHg as sum of the atmospheric pressure (760 mmHg) plus 20 mmHg. For more than 150 years, the intraocular pressure (IOP) defined as transcorneal pressure difference has been considered to be the main risk factor in the pathogenesis of glaucoma. It is, however, the trans-optic nerve head pressure difference that directly affects the optic nerve head (Fig. 1).1,2 It is defined pressure in the intraocular compartment minus pressure in the retrobulbar cerebrospinal fluid space (orbital cerebrospinal fluid pressure [CSF-P]). Taking into the orbital CSF-P as counter-pressure against the IOP, hypotheses may be formed on the pathogenesis of optic nerve head diseases such as glaucoma, retinal vein occlusions and arterial hypertensive retinopathy.

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Figure 1. Transected ocular globe showing the optic nerve head (two black asterisks) and the central retinal vessels in the retrobulbar part of the optic nerve. The white arrow symbolizes the intraocular pressure and the black arrow head points at the optic nerve meninges with the cerebrospinal fluid space and the orbital cerebrospinal fluid pressure. The trans-optic nerve head (trans-lamina cribrosa) pressure difference is intraocular pressure minus orbital cerebrospinal fluid pressure.

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The first hypothesis is that a low orbital CSF-P is associated with the pathogenesis of glaucomatous optic neuropathy. If IOP is normal and orbital CSF-P is abnormally low, the trans-lamina cribrosa pressure difference is increased. It leads to a similar situation as if the IOP is elevated and orbital CSF-P is normal. The situation described first would be normal-(intraocular-)pressure glaucoma. The situation described last is high-(intraocular-)pressure glaucoma. Accordingly, experimental studies and clinical studies suggested that the CSF-P is abnormally low in patients with normal-(intraocular-)pressure glaucoma.3–5

The CSF-P is physiologically correlated with IOP and arterial blood pressure, which is correlated with IOP, so that the pressures in all three fluid-filled compartments (arterial blood system, brain and intraocular space) are correlated with each other. Previous studies showed an association between normal-(intraocular-)pressure glaucoma, low systemic arterial blood pressure and low body mass index. The hypothesis is that in normal-(intraocular-)pressure glaucoma, a low arterial blood pressure is associated with a more marked reduction in CSF-P than reduction in IOP. It results in an increased trans-lamina cribrosa pressure difference, similar as if the IOP is elevated as in high-(intraocular-)pressure glaucoma. It may explain why the optic nerve head appearance is similar in normal-(intraocular-)pressure glaucoma and in high-(intraocular-)pressure glaucoma, despite marked differences in IOP.

Studies have shown an age-related increase in the prevalence of normal-(intraocular-)pressure glaucoma, and a higher prevalence of normal-(intraocular-)pressure glaucoma in Japanese. A recent study by Ren et al. suggested that the CSF-P was correlated with higher body mass index and younger age (own data).5 It may explain the increased prevalence of normal-pressure glaucoma in elderly Japanese with the lower body mass index.

Arterial hypertension is associated with ocular hypertension, however, not with an increased prevalence of glaucoma. The anti-glaucomatous effect of arterial hypertension may be explained by its association with an elevated CSF-P. As a corollary, the increased prevalence of nocturnal arterial blood pressure dipping in patients with normal-(intraocular-)pressure glaucoma may be explained by an associated nocturnal dipping in CSF-P.

The second hypothesis is that an elevated CSF-P may be associated with retinal vein occlusions in arterial hypertensive patients, as the central retinal vein passes through the retrobulbar CSF-P space (Fig. 1). An elevated orbital CSF-P should therefore be a risk factor for the development of retinal vein occlusions. Accordingly, arterial hypertension is a risk factor for the development of retinal vein occlusions. It can be explained by the association between elevated arterial blood pressure and elevated CSF-P. Accordingly, patients with retinal vein occlusions have less marked macular oedema in the evening than in the morning after awakening out of a supine position. In the supine position, the CSF-P is higher than in upright position because of hydrostatic reasons.

The third hypothesis is that papilledema dilated retinal veins in stage IV of hypertensive retinopathy are caused by elevated CSF-P due to the increased blood pressure. Hypertensive retinopathy may thus be the opposite of normal-(intraocular-)pressure glaucoma: in hypertensive retinopathy, a rise in arterial blood pressure is associated with a more marked elevation in CSF-P than elevation in IOP. It may lead to a decreased trans-lamina cribrosa pressure difference and secondary papilledema.

Potential implications of the hypotheses are: carboanhydrase inhibitors may not be given to patients to patients with glaucoma, in particular not to patients with normal-(intraocular-)pressure glaucoma, as these drugs lower the IOP and the CSF-P. Patients with retinal vein outflow disorders may sleep in a slightly elevated head position to reduce the orbital CSF-P overnight. In patients with hypertensive retinopathy, an abnormally high CSF-P may be considered.

In conclusion, the CSF-P as the natural trans-lamina cribrosa counter-pressure against the IOP may play a role in the pathogenesis of nerve head disorders. Glaucoma may be described as a dysregulation of, or an imbalance between, blood pressure, CSF-P and IOP.

References

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  2. References
  • 1
    Morgan WH, Yu DY, Cooper RL, Alder VA, Cringle SJ, Constable IJ. The influence of cerebrospinal fluid pressure on the lamina cribrosa tissue pressure gradient. Invest Ophthalmol Vis Sci 1995; 36: 116372.
  • 2
    Jonas JB, Berenshtein E, Holbach L. Lamina cribrosa thickness and spatial relationships between intraocular space and cerebrospinal fluid space in highly myopic eyes. Invest Ophthalmol Vis Sci 2004; 45: 26605.
  • 3
    Yablonsky M, Ritch R, Pokorny KS. Effect of decreased intracranial pressure on optic disc. Invest Ophthalmol Vis Sci 1979; 18 (Suppl.): 165.
  • 4
    Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology 2008; 115: 7638.
  • 5
    Ren R, Jonas JB, Tian G et al. Cerebrospinal fluid pressure in glaucoma. A prospective study. Ophthalmology 2010; 117: 25966.