Optic Nerve Sheath Distention as a Protective Mechanism Against the Visual Impairment and Intracranial Pressure Syndrome in Astronauts

Abstract

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 ...

MRI-based quantification of ophthalmic changes in healthy volunteers during acute 15° head-down tilt as an analogue to microgravity

“…Thus, the ONS distension observed within the bulbar subarachnoid region suggests that CSF pressure was elevated during acute 15°HDT, as expected. The ONS distension observed in most subjects shows that the ONS can expand in response to elevated ICP; however, because of the nonlinear mechanical behaviour of soft tissues, we expect that further increases in ICP would result in reduced or even negligible changes in ONS area [28]. It is possible that subjects who had little to no change in ONS cross-sectional area may have already had stiffened ONS tissues (e.g.…”

Quantitative magnetic resonance image assessment of the optic nerve and surrounding sheath after spaceflight

“…Interestingly, this subject had the largest increase in ONS area immediately post flight (R + 1) and also displayed the largest observed ONS cross-sectional areas both pre-and post flight. It is possible that in-flight ONS distention subsided after landing and before the first postflight scan, or that ICP was elevated before launch and had already saturated the ONS's compensatory threshold 30 . Previously, Kramer et al 6 found a geometrically larger ONS in subjects with globe flattening, another sign of SANS.…”

“…npj Microgravity (2020)30 Published in cooperation with the Biodesign Institute at Arizona State University, with the support of NASA1234567890():,;…”

The escape of retrobulbar cerebrospinal fluid in the astronaut’s eye: mission impossible?

“…Wostyn and De Deyn [20,21] recently hypothesized that astronauts with less compliant ON sheaths may be more likely to develop optic disc swelling, and that the ON sheath response to changing CSF pressure, measured by intrathecal infusion tests, may be a potential predictive biomarker for optic disc edema in astronauts. Hansen and Helmke [22] demonstrated that the human ON sheath expands rapidly in vivo after small CSF pressure changes during intrathecal infusion tests until a saturation point is reached at which no further dilatation occurs.…”

“…Hansen and Helmke [22] demonstrated that the human ON sheath expands rapidly in vivo after small CSF pressure changes during intrathecal infusion tests until a saturation point is reached at which no further dilatation occurs. From this point of view, a greater degree of ON sheath rigidity that prevents further ON sheath expansion may result in increased SAS pressure, given that smaller increases in CSF volume will produce significant increases in CSF pressure in the ON sheath [20,21]. Thus, variations in elasticity within the structure of the ON sheath may produce varying degrees of optic disc swelling between astronauts and even asymmetric disc edema in the same astronaut [20,21].…”