The spaceflight-induced visual impairment was a serious problem for astronauts remaining for a long time in microgravity.

In the early periods after discovery of the condition, the obvious symptoms - decrease in near-visual acuity, headaches - were reported by astronauts; sometimes as short as after three weeks in microgravity. Thorough medical examination was performed only after landing, determining the extent of anatomical changes post-factum.

How does that look like currently? Do we have diagnostic methods that can be performed in orbit, to determine onset of the condition before the symptoms become perceptible to the affected? And if so - I'm less interested in what these procedures are, and more in their result - how much earlier before perceptible onset can they detect the initial stages of the condition.

This question is motivated by the still unknown problem: is Mars gravity sufficient to prevent the visual impairment? This could be determined through a mission in a spacecraft with a centrifugally introduced Martian level artificial gravity. This shouldn't be as hard as a simulated full 1g, but I'd like to ballpark the mission duration, assuming a simple proportional relation between time until the onset is detected and time when the condition reaches crippling levels - say, if we can detect it after 15 days but it becomes crippling after 450 days (30x the time), then onset on the experimental craft after a year would give the colonists 30 years.


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First off, I'd caution the jump to conclusion in title: There's a reason we re-named VIIP to Spaceflight Associated Neuro-Ocular Syndrome (SANS) - because while we suspect there's elevations of ICP going on, there's still little direct evidence of it and a suspicion that if there is, the ICP elevation alone is likely not sufficient to explain the syndrome in its entirety. We've never done direct ICP measurements in microgravity, and so the explanation of ocular findings in space based on what we'd associate with those findings were we to see them terrestrially is something to be cautious of. We HAVE done a small number of post-flight direct ICP measurements on long-duration astronauts, and some of those values have been moderately elevated.

I'd also REALLY caution against connecting the reports of headaches on orbit with SANS - we have good correlation between headache reports and ISS atmospheric CO2 levels (which vary throughout a mission based on a variety of factors), and CO2 may or may not be related or contributory to SANS. Certainly there's no suggestion among the current medops community that crew-reported headaches are in any way directly related to elevations of ICP.

See Lee, A. G., Mader, T. H., Gibson, C. R., & Tarver, W. (2017). Space flight–associated neuro-ocular syndrome. JAMA ophthalmology, 135(9), 992-994. for a decent catch-up on where we are now currently in our classification of this syndrome.

In brief, the evolution in our understanding of SANS over the last decade has gone from a primary concern with globe flattening and fundoscopically obvious optic disk edema that appeared present in some astronauts, but completely absent in others, to a current understanding based on improved imaging methods such as in-flight Optical coherence tomography (OCT) that suggests this is a spectrum of adaptive (and maladaptive) changes to microgravity that can be observed in every astronaut, with changes observable very early in the mission (within the first few weeks).

The question of why some astronauts go on to develop clinically significant disk edema while others get relatively mild choroidal thickening, while others develop choroidal folds but lack significant disk pathology, while others develop optic nerve sheath diameter thickening and lack other findings, is still open. We suspect there's some underlying anatomical differences that will eventually allow us to predict who's at risk for the more severe clinical changes, but right now the only astronauts we can predict response for are those who have previously flown (because if you've developed clinically significant findings before, we expect you to again).

To the second half of your question, the easy answer is we're just not sure yet because the answer to "how much gravity is needed to offset SANS development" is going to be driven by whatever the underlying physiological mechanism is, which we still haven't identified. I can say that most physicians working this problem would probably agree that ~0.38 G is likely enough to address the impaired cranial venous drainage that comes with microgravity, and if that is the primary upstream contributor to SANS then I'd expect it to address that as well. When you start speculating about whether lunar gravity would be sufficient, you'll get less consensus.


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