As nicely reported by Mader et al., 1,2 a significant proportion of the astronauts who spend extended periods in microgravity develop ophthalmic abnormalities, including optic nerve sheath (ONS) distention, optic disc swelling, globe flattening, choroidal folds, and hyperopic shifts, which is also designated as visual impairment and intracranial pressure (VIIP) syndrome. Importantly, astronauts with VIIP can experience decreases in visual acuity that remain unresolved years after flight. 2 Given that the VIIP syndrome is one of the top priorities for the National Aeronautics and Space Administration, especially in view of future long-duration spaceflight missions, including trips to Mars, there is an urgent need to better understand the mechanisms leading to VIIP and to develop countermeasure strategies.Currently, the exact mechanisms causing the VIIP syndrome are unknown. Among the several mechanisms proposed to play a role, a leading hypothesis is that the VIIP syndrome is caused by elevated intracranial pressure (ICP) resulting from microgravity-induced cephalad fluid shifts leading to venous stasis in the head and neck. 3 This stasis could cause impairment of cerebrospinal fluid (CSF) drainage into the venous system and cerebral venous congestion, both of which could lead to a rise in ICP. 3 The increased subarachnoid pressure resulting from intracranial hypertension is thought to be directly transmitted from the intracranial compartment to the intraorbital compartment through the perioptic subarachnoid space (SAS). 2 This elevated CSF pressure at eye level results in ONS distention and anteriorly directed forces that indent the posterior sclera resulting in posterior globe flattening, redundancy and folding of the choroid, and axial shortening. 2 In addition, elevated ICP could result in stasis of axoplasmic flow with optic disc swelling similar to what occurs in patients with terrestrial idiopathic intracranial hypertension. 3 In the present letter, we provide a conceptual framework in which ONS distention may be seen as a compensatory protection mechanism against the other ophthalmic changes of the VIIP syndrome. As noted above, the rise in ICP, resulting from microgravity-induced cephalad fluid shifts, would presumably be propagated from the CSF surrounding the brain down the ONSs to the posterior globe, ultimately resulting in the ophthalmic abnormalities of the VIIP syndrome. 1 However, we believe that the ONS response to the rise in ICP during extended microgravity exposure may play a prominent role in determining whether or not an astronaut is susceptible to developing ophthalmic changes of VIIP. It is important to note that elevated CSF pressure results in dilation of the ONS before papilledema appears. 4 Furthermore, a previous study among patients undergoing intrathecal infusion testing showed that the ONS response measured with ultrasonography was directly correlated with CSF pressure above an individual patient's threshold until a saturation point was reached when no further dilation occurred. 5 ...