Optic Disc Edema In Astronauts Research Articles

Optic Disc Edema in Astronauts from a Choroidal Point of View.

INTRODUCTION: Optic disc edema has been well documented in astronauts both during and after long-duration spaceflight and is hypothesized to largely result from increased pressure within the orbital subarachnoid space brought about by a generalized rise in intracranial pressure or from sequestration of cerebrospinal fluid within the orbital subarachnoid space with locally elevated optic nerve sheath pressure. In addition, a recent prospective study documented substantial spaceflight-associated peripapillary choroidal thickening, which may be a contributing factor in spaceflight-associated neuro-ocular syndrome. In the present article, based on the above, we offer a new perspective on the pathogenesis of microgravity-induced optic disc edema from a choroidal point of view. We propose that prolonged microgravity exposure may result in the transudation of fluid from the choroidal vasculature, which, in turn, may reach the optic nerve head, and ultimately may lead to fluid stasis within the prelaminar region secondary to impaired ocular glymphatic outflow. If confirmed, this viewpoint would shed new light on the development of optic disc edema in astronauts.Wostyn P, Gibson CR, Mader TH. Optic disc edema in astronauts from a choroidal point of view. Aerosp Med Hum Perform. 2022; 93(4):396-398.

The odyssey of the ocular and cerebrospinal fluids during a mission to Mars: the "ocular glymphatic system" under pressure.

A significant proportion of the astronauts who spend extended periods in microgravity develop ophthalmic abnormalities including optic disc edema, globe flattening, chorioretinal folds, and hyperopic refractive error shifts. A constellation of these neuro-ophthalmic findings has been termed "spaceflight-associated neuro-ocular syndrome". Understanding this syndrome is currently a top priority for NASA, especially in view of future long-duration missions (e.g., Mars missions). The recent discovery of an "ocular glymphatic system" can potentially help to unlock mechanisms underlying microgravity-induced optic disc edema. Indeed, a major paradigm shift is currently occurring in our understanding of transport of fluids and solutes through the optic nerve following the recent discovery of an optic nerve glymphatic pathway for influx of cerebrospinal fluid. In addition, the recent identification of an entirely new glymphatic pathway for efflux of ocular fluid may have profound implications for fluid dynamics in the eye. Observations pertaining to this ocular glymphatic pathway provide critical new insights into how intracranial pressure can alter basic fluid transport in the eye. We believe that these novel findings have the potential to be game changers in our understanding of the pathogenesis of optic disc edema in astronauts. In the present review, we integrate these new insights with findings on the intracranial and neuro-ophthalmologic effects of microgravity in one coherent conceptual framework. Further studies in this area of investigation could not only provide exciting new insights into the mechanisms underlying microgravity-induced optic disc edema but also offer opportunities to develop countermeasure strategies.

Potential Involvement of the Ocular Glymphatic System in Optic Disc Edema in Astronauts.

INTRODUCTION: A significant proportion of the astronauts who spend extended periods in microgravity develop ophthalmic abnormalities, including optic disc edema, optic nerve sheath distention, globe flattening, chorioretinal folds, hyperopic refractive error shifts, and nerve fiber layer infarcts. A constellation of these neuro-ophthalmic findings has been termed spaceflight-associated neuro-ocular syndrome. An increased understanding of factors contributing to this syndrome is one of the top priorities for ESA and NASA because the length of missions is expected to increase substantially in the future. As discussed in the present article, the very recent discovery of an ocular glymphatic clearance system can potentially help to unlock mechanisms underlying microgravity-induced optic disc edema. Observations pertaining to the ocular glymphatic pathway provide supporting evidence for the hypothesis, originally proposed by our group, suggesting that the glymphatic outflow from the eye into the optic nerve may be impeded under prolonged microgravity conditions, leading to optic disc edema.Wostyn P, De Winne F, Stern C, Mader TH, Gibson CR, De Deyn PP. Potential involvement of the ocular glymphatic system in optic disc edema in astronauts. Aerosp Med Hum Perform. 2020; 91(12):975977.

MTRR 66 and SHMT1 1420 Variants Are Associated with Optic Disc Edema During 30-d Strict Head-down Tilt Bed Rest and CO2 Exposure (P24-036-19)

ObjectivesSome astronauts returning from missions to the International Space Station (ISS) have developed ophthalmic structural changes, including optic disc edema. Incidence of optic disc edema among astronauts has been linked to one-carbon pathway genetic variants and B-vitamin status. A recent 30-d 6-degree head-down tilt bed rest study in which all subjects were exposed to 0.5% CO2 documented the occurrence of optic disc edema in 5 of 11 subjects. The objective of this study was to determine the effect of one-carbon pathway genetics and B-vitamin status on the incidence of optic disc edema in the bed rest subjects. MethodsThe study was conducted at the: envihab facility at the German Aerospace Center in Cologne, Germany. Subjects (6 M/5F) were healthy volunteers, 33 ± 8 y (mean ± SD), having a mean BMI of 23.4 ± 2.2 kg/m2. After a 14-d ambulatory phase in a standard environment (i.e., not hypercapnic), a blood sample was collected to assess vitamin status and single nucleotide polymorphisms (SNPs) associated with one carbon metabolism. We focused on two SNPs (rs1801394, MTRR 66 and rs1979227, SHMT1 1420) based on our earlier findings in astronauts (Zwart et al., FASEB J, 30:141–8, 2016). The 30-d bed rest began after collection of this sample. Optical coherence tomography images were collected before, during (days 15 and 30), and after (6 and 13 days after reambulation) bed rest, and the change in total retinal thickness (TRT) at various distances from Bruch’s membrane opening (BMO) was evaluated against the number of MTRR A66G G alleles and SHMT1 C1420T C alleles. ResultsThe change in TRT at various distances from the BMO in bed rest subjects exposed to mild hypercapnia and headward fluid shifts was strongly associated with the number of MTRR 66 G and SHMT1 1420 C alleles. ConclusionsThis finding may increase understanding of mechanisms involved in optic disc edema in astronauts and patients on Earth, and hence lead to development of targeted countermeasures. Funding SourcesThis work was funded by the NASA Human Health Countermeasures Element of the NASA Human Research Program.

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

Ophthalmic abnormalities including unilateral and bilateral optic disc edema, optic nerve sheath distention, globe flattening, choroidal folds, and hyperopic shifts have been observed in astronauts during and after long-duration spaceflight. An increased understanding of factors contributing to this syndrome, termed spaceflight-associated neuro-ocular syndrome, is currently a top priority for the ESA and NASA, especially since this medical obstacle could impact the visual health of astronauts as well as the success of future missions, including continued trips to the International Space Station, a return to the moon, or a future human mission to Mars. Currently, the exact mechanisms causing this neuro-ocular syndrome are not fully understood. In the present paper, we propose a hypothetical framework by which optic disc edema in astronauts may result, at least partly, from the forcing of perioptic cerebrospinal fluid into the optic nerve and optic disc along perivascular spaces surrounding the central retinal vessels, related to long-standing microgravity fluid shifts and variations in optic nerve sheath anatomy and compliance. Although this hypothesis remains speculative at the present time, future research in this area of investigation could not only provide exciting new insights into the mechanisms underlying microgravity-induced optic disc swelling but also offer opportunities to develop countermeasure strategies.

Dilated Prelaminar Paravascular Spaces as a Possible Mechanism for Optic Disc Edema in Astronauts.

INTRODUCTION: A number of ophthalmic abnormalities, including optic disc edema, have been reported in several astronauts involved in long-duration spaceflights. An increased understanding of factors contributing to this syndrome, initially designated visual impairment and intracranial pressure syndrome and recently renamed spaceflight-associated neuro-ocular syndrome, has become a high priority for ESA and NASA, especially in view of future long-duration missions, including trips to Mars. The underlying pathophysiological mechanisms of this syndrome are still not well understood. In the present paper, we propose that optic disc edema in astronauts may occur, at least in part, as a result of retention of interstitial fluid in distended paravascular spaces at the prelaminar region of the optic nerve head. Preflight, in-flight, and postflight analysis of the optic nerve head and surrounding structures by optical coherence tomography in long-duration International Space Station crewmembers could provide important structural information in this respect.Wostyn P, De Winne F, Stern C, De Deyn PP. Dilated prelaminar paravascular spaces as a possible mechanism for optic disc edema in astronauts. Aerosp Med Hum Perform. 2018; 89(12):1089-1091.

Intracranial pressure-induced optic nerve sheath response as a predictive biomarker for optic disc edema in astronauts.

A significant proportion of the astronauts who spend extended periods in microgravity develop ophthalmic abnormalities. Understanding this syndrome, called visual impairment and intracranial pressure (VIIP), has become a high priority for National Aeronautics and Space Administration, especially in view of future long-duration missions (e.g., Mars missions). Moreover, to ensure selection of astronaut candidates who will be able to complete long-duration missions with low risk of the VIIP syndrome, it is imperative to identify biomarkers for VIIP risk prediction. Here, we hypothesize that the optic nerve sheath response to alterations in intracranial pressure may be a potential predictive biomarker for optic disc edema in astronauts. If confirmed, this biomarker could be used for preflight identification of astronauts at risk for developing VIIP-associated optic disc edema.