The Effect of Gravity on the Eyes

Of course we take gravity for granted – it’s reliable and has not changed in the billions of years that life has evolved. As a result of this consistent experience, we have evolved systems to get the blood back up to the heart. We have valves in our veins, muscle pumps and the negative thoracic pressure of respiration to pull the blood uphill. But the venous blood in our heads can just fall back down to the heart, so our jugular veins are generally valveless and when we are upright they are empty with zero pressure. These aspects of human anatomy and physiology have interesting implications for our eyes, for glaucoma, or for intracranial hypertension. Patients often ask, “Is it OK for me to do downward-facing dog?”

Firstly, arterial pressure is regulated carefully to maintain constant blood flow to the brain and to the eye. Usually, we measure the blood pressure at the brachial artery, roughly at the level of the heart. There is some variation in how the blood pressure changes when lying down and in healthy volunteers there may be a small decrease because the heart doesn’t have to push so hard to get the blood up to the head. By these measures, there are small decreases in the estimated ocular perfusion pressure when lying down, but these estimates are based on calculations rather than direct measurements¹. If we measure the blood pressure at the level of the head, by elevating the arm with the cuff beside the ear, we see a bit more of a gravity effect, at least in the brachial artery.

In our experiments with tipping volunteers at different angles on a table, we found the arterial pressure in the brachial artery at the level of the eye went up with inversion, even more than the intraocular pressure (IOP). This meant that ocular perfusion pressure increased a little in most people and we saw some compensatory vasoconstriction in the retinal vasculature. Generally, the arterial pressure and blood flow in the eye is not greatly affected by gravity or posture.

Up to your neck with pressure

It is fascinating to think about how giraffes cope with their gravity-induced blood flow challenges. Indeed, giraffes have been described as living on the extreme end of physiology. When standing tall they need very high blood pressure to push blood all the way up to their brains, yet they avoid hypertensive diseases, perhaps because they have different gene expression in their cardiovascular muscles to keep them supple. When bending down to drink they need to divert blood away from their brains to prevent a catastrophic stroke, so there is a complicated vascular structure at the base of the giraffe skull (called the rete mirabile, or ‘wonderful net’) which is essentially a pressure-sensitive arteriovenous shunt. Their oesophageal swallowing action also assists with venous return to the heart. It is interesting to think about the physical limits to these evolutionary modifications, but they are also inspirations for therapeutic targets for hypertension. Could we make our heart muscle, our arteries, or indeed our sclera or Tenon capsule, as elastic and limber as a giraffe’s?

While arterial regulation keeps cranial blood pressure and blood flow fairly constant, the veins have much more dynamic changes with gravity and posture. At atmospheric pressure and with our head raised, in a sitting or standing position, the veins of the head are generally collapsed. An important exception to this is the episcleral veins of the eye, which maintain a pressure 6–10 mmHg above atmospheric pressure. Little is known about how the episcleral pressure is regulated in humans, but arteriovenous connections have been suggested from animal work, which would be our own version of the pressure-sensitive rete mirabile in the eye². This would also be an important therapeutic target, as interventions to reduce the episcleral venous pressure would be useful in glaucoma, including after glaucoma surgery (unlike existing glaucoma eye drops).

When we lie down, especially if the head is lower than the heart, the veins of the head fill up like a simple fluid column. In a head-down position we have a raised venous pressure in our heads and this drives the intraocular pressure (IOP) and intracranial pressure (ICP) upwards in a predictable way. This becomes most relevant when we think about conditions such as glaucoma or papilloedema as being due to a tension between the IOP and ICP pushing forward or backward on the optic disc (the so-called translaminar pressure difference, TPD).

The most interesting part of our project on tipping people upside down was that while everyone’s IOP increased substantially, in most people the TPD did not appear to change. That is to say the ICP increased by a similar amount to the IOP, as both are driven by the venous pressure. Patients often ask about hobbies and activities, such as bungee jumping or yoga headstands, and I now tend to be more reassuring about whether the raised IOP in a head-down position affects glaucoma. The interesting minority of healthy normal volunteers who had a greater increase in IOP than ICP with head-down, or a greater increase in ICP than IOP with head-down, represent an important new dynamic factor in glaucoma risk. Perhaps some people should sleep with a slight head-up or head-down tilt, depending on their eye conditions and the relative change of each pressure.

All of this becomes relevant again with the development of space travel and humans spending longer periods of time without normal gravity. It was recognised after six-month missions on the International Space Station that astronauts would complain of presbyopia symptoms and were found to have hypermetropic shift. However, more concerning observations in astronauts included chorioretinal folds and mild optic disc oedema and it was recognised that there is some overlap between spaceflight-associated neuro-ocular syndrome (SANS) and raised ICP. However, astronauts do not complain of headaches or pulsatile tinnitus, do not experience sixth-nerve palsies and the disc oedema is mild. Lumbar punctures performed soon after returning to Earth have been normal or mildly above normal³. There is, therefore, a gradual shift of fluid towards the head for astronauts, without gravity to pull the fluid down. The usual joke is that astronauts often get puffy faces and wrinkly retinas, but they have beautiful ankles.

Astronauts with SANS have not had serious visual-field loss and the ocular findings improve slowly when they return to Earth. The New Zealand Space Agency seems as unconcerned as I am about this issue, with a top-secret government plan to get some hobby glasses from The $2 Shop. But SANS has been labelled a ‘red light’ issue for space health that could prevent safe Mars missions, partly because Mars has only 0.38 of Earth’s gravity, so the condition would not resolve rapidly after getting there. While around 40% of astronauts get SANS on their first trip, there is a 100% recurrence rate in those astronauts who make a second trip to space⁴. It may be that the variations in healthy volunteers we observed with inversion could be a risk factor for SANS: those people whose ICP increases more than IOP during inversion may be at lower risk of glaucoma but should probably not go to space.

A new way to understand the partial, incomplete features of raised ICP in astronauts is the idea of trapping of fluid in the optic nerve sheath. Detailed microanatomical study of the optic canal was conducted in Dunedin, revealing discontinuities in the subarachnoid space between the orbital optic nerve sheath and the cranium, with collagen fibres arranged in a valve-like pattern that can trap fluid in the orbit⁵. That is, when we stand up, ICP can drop to zero, or even negative pressures and there are advantages to collapsing the subarachnoid space and trapping some fluid in the orbital optic nerve to reduce a sucking strain^6,7. For astronauts this would mean that fluid will tend to accumulate in the optic nerve sheath slowly, without low/negative ICP by day to draw fluid backwards. This exanded optic nerve sheath leads to the hypermetropic shift, choroidal folds, mild disc oedema and other associated radiological findings, such as globe flattening.

Author:  Dr Jesse Gale is a Wellington glaucoma specialist and neuro-ophthalmologist, with roles in private and public hospitals and at the University of Otago Wellington. He is the new chair of the New Zealand branch of RANZCO.

Article published in NZ Optics – July 2026

References

1. Yang JM, Park SW, Ji YS, et al. Postural effects on intraocular pressure and ocular perfusion pressure in patients with non-arteritic anterior ischemic optic neuropathy. BMC Ophthalmol 2017;17(1):47.

2. Zamora DO, Kiel JW. Episcleral venous pressure responses to topical nitroprusside and N-Nitro-L-arginine methyl ester. Invest Ophthalmol Vis Sci 2010;51(3):1614-20.

3. Lee AG, Mader TH, Gibson CR, et al. Spaceflight associated neuro-ocular syndrome (SANS) and the neuro-ophthalmologic effects of microgravity: a review and an update. NPJ Microgravity 2020;6:7.

4. Brunstetter TJ, Mason SS, Osborne S, et al. Predicting Spaceflight-Associated Neuro-Ocular Syndrome in International Space Station Astronauts. JAMA Ophthalmol 2025;143(11):933-7.

5. Liugan M, Xu Z, Zhang M. Reduced Free Communication of the Subarachnoid Space Within the Optic Canal in the Human. Am J Ophthalmol 2017;179:25-31.

6. Morgan WH, Yu DY, Alder VA, et al. The correlation between cerebrospinal fluid pressure and retrolaminar tissue pressure. Invest Ophthalmol Vis Sci 1998;39(8):1419-28.

7. Holmlund P, Stoverud KH, Wahlin A, et al. Posture-Dependent Collapse of the Optic Nerve Subarachnoid Space: A Combined MRI and Modeling Study. Invest Ophthalmol Vis Sci 2021;62(4):26.