Spaceflight-Associated Neuro-Ocular Syndrome (SANS)
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Disease Entity
Disease
Spaceflight-associated Neuro-Ocular Syndrome (SANS), formerly called visual impairment and intracranial pressure (VIIP) syndrome[1], is a neuro-ophthalmic condition observed predominantly after long-duration space flight(LDSF) . It is a constellation of findings characterised by optic disc edema, posterior globe flattening, choroidal/retinal folds, optic nerve sheath distension, and a hyperopic refractive shift.[2][3]
Etiology
- The exact etiology of spaceflight-associated neuro-ocular syndrome remains incompletely understood. Current evidence suggests that SANS is not caused by a single mechanism, but rather represents a multifactorial response to long-duration space flight. Proposed mechanism pathway of SANS is shown in Figure 1.[4]
- Given the limitations in sample sizes and the inherent complexity of identifying the signs that define SANS, the analysis results show insufficient evidence to identify a single, well-supported cause. Thus, it is likely that SANS has a multifactorial origin, incorporating key clinical highlights from various proposed theories.[5]
- Only about 12 astronauts travel to space each year, averaging 3 astronauts every three months. This limited sample size poses challenges in characterizing SANS. [4]
Risk Factors
- Although prolonged exposure to microgravity is the central initiating factor in SANS, the development and severity of the syndrome appear to be influenced by several interacting etiological mechanisms and risk modifiers. These can be organised into mission-related, physiological, environmental, biochemical, and individual suspecitibity factors, as summarised in Table 1 and 2.
Table 1. Etiological Mechanism
| Factor | Proposed mechanism | Main SANS relevance |
| Long-duration microgravity | Loss of normal gravitational gradient | Central initiating exposure; risk increases with mission duration |
| Cephalad fluid shift | Redistribution of fluid toward head, neck, orbit, and intracranial compartments | Head/orbital congestion, optic disc edema, optic nerve sheath distension |
| Impaired jugular venous outflow | Cranial and orbital venous congestion | May worsen CSF drainage and optic nerve sheath distension |
| Impaired vortex vein drainage | Reduced choroidal venous outflow increases choroidal volume | Choroidal thickening, folds, posterior globe flattening, hyperopic shift |
| Altered CSF dynamics | Altered CSF pressure, pulsatility, or drainage around optic nerve | Optic nerve sheath distension and optic disc edema |
| Optic nerve sheath compartmentalization | Localized CSF trapping or altered exchange within the optic nerve sheath | Asymmetric disc edema; persistent sheath distension |
| Altered translaminar pressure gradient | Changed relationship between IOP and retrolaminar CSF pressure | Optic nerve head remodeling; RNFL thickening |
| Impaired orbital/optic nerve lymphatic drainage | Reduced clearance of perineural and orbital fluid | Perineural fluid accumulation; persistent optic nerve sheath changes |
Table 2. Risk Modifiers
| Risk modifier | Proposed influence | Clinical relevance |
| Elevated ambient CO2 | May promote cerebral vasodilation and alter venous/ICP regulation | Potential contributor; exact role uncertain |
| Folate/B12 one-carbon pathway variation | May modify endothelial, vascular, or connective tissue susceptibility | Associated with susceptibility to SANS-related findings |
| High salt intake | May increase fluid retention and worsen fluid-shift physiology | Potentially increases cephalad fluid congestion |
| Intensive resistive exercise | May transiently alter venous, intrathoracic, intracranial, and orbital hemodynamics | Possible aggravating factor in susceptible astronauts |
| Space radiation exposure | May contribute to vascular, retinal, lens, or neuroinflammatory effects | More relevant to lunar/Martian missions; possible retinal microvascular risk |
| Individual anatomy/connective tissue differences | Variation in ocular, vascular, orbital, or connective tissue response | May explain heterogeneity, asymmetry, and persistence |
Pathophysiology
- The pathophysiology of spaceflight-associated neuro-ocular syndrome (SANS) is not completely understood. Current evidence indicates that SANS is a multifactorial disorder arising from the interaction of various factors, including microgravity-induced fluid shifts, altered cerebrospinal fluid (CSF) dynamics, venous and lymphatic congestion, changes in the translaminar pressure gradient, choroidal expansion, and individual susceptibility. (Table 3)
- These mechanisms together help explain the major clinical and imaging findings associated with SANS, such as optic disc edema, optic nerve sheath distension, posterior globe flattening, choroidal and retinal folds, cotton-wool spots, and a hyperopic refractive shift.
- Cephalad Fluid Shift
- The most widely accepted initiating mechanism of SANS is the cephalad redistribution of body fluids during extended exposure to microgravity. On Earth, gravity maintains a hydrostatic gradient that causes fluid to pool in the lower body. In the absence of gravity, this gradient is disrupted, leading to a headward shift of venous, interstitial, lymphatic, and CSF-related fluids. This results in congestion in the head, neck, orbit, and intracranial compartments, which may alter venous drainage, CSF outflow, and orbital tissue pressure.[6]
- This cephalad fluid shift helps explain several findings associated with SANS. Increased pressure in the orbital and intracranial compartments can contribute to optic nerve sheath distension and optic disc edema. Concurrent choroidal vascular congestion may increase choroidal volume, leading to choroidal folds, posterior globe flattening, and axial shortening, which clinically manifests as a hyperopic shift.
- Intracranial Pressure and the “IIH-like” Hypothesis
- SANS was previously referred to as visual impairment and intracranial pressure syndrome due to its similarities with certain findings seen in terrestrial idiopathic intracranial hypertension (IIH).
- Elevated intracranial pressure could theoretically be transmitted along the optic nerve sheath, leading to optic nerve sheath distension, optic disc edema, and posterior globe flattening. [7]
- However, SANS is not simply IIH occurring in space. Astronauts experiencing SANS often lack the classic symptoms associated with IIH, such as severe headaches, pulsatile tinnitus, diplopia, transient visual obscurations, nausea, and vomiting.
- Lumbar puncture measurements conducted after returning to Earth have shown normal to only borderline elevated CSF opening pressures in some cases. Therefore, sustained global intracranial hypertension alone is unlikely to account for the entire SANS phenotype.
- Altered CSF Dynamics and Optic Nerve Sheath Compartmentalization
- In microgravity, the flow, pulsatility, and drainage of CSF may be affected by the absence of normal gravitational forces and by venous congestion.
- Rather than producing uniformly elevated intracranial pressure, these changes could lead to localized CSF accumulation or altered CSF exchange within the optic nerve sheath.[8]
- The optic nerve sheath may act as a partially separate compartment. CSF compartmentalization within the optic nerve sheath has been proposed as a mechanism for optic nerve sheath distension and optic disc edema, even in the absence of markedly elevated global CSF pressure.
- This theory may also explain the asymmetric nature of SANS findings, as the anatomy, compliance, and CSF communication within the optic nerve sheath can vary between individuals and between eyes.
- Venous Congestion and Choroidal Expansion
- Venous congestion is another significant contributor to SANS.
- During spaceflight, impaired jugular venous drainage and venous stasis have been observed, suggesting altered cranial venous outflow in microgravity.
- Increased venous pressure may hinder CSF absorption and impair orbital venous drainage, further contributing to optic nerve sheath distension and disc edema.[9]
- The choroid is particularly relevant due to its high vascularity. Impaired drainage of the vortex veins can lead to choroidal engorgement and thickening.
- This choroidal expansion can mechanically alter the contour of the posterior globe, resulting in choroidal folds, retinal folds, and posterior globe flattening.
- Such flattening may shorten the axial length of the eye, leading to the hyperopic refractive shift commonly reported in astronauts following long-duration spaceflight.
- Translaminar Pressure Gradient
- The translaminar pressure gradient refers to the pressure difference across the lamina cribrosa, which is influenced by intraocular pressure anteriorly and CSF pressure posteriorly.
- Changes in this gradient may contribute to optic nerve head deformation and optic disc edema.
- In SANS, the translaminar pressure gradient can be altered not only by changes in intracranial or CSF pressure but also by local orbital pressure, optic nerve sheath pressure, venous congestion, and variations in intraocular pressure regulation during exposure to microgravity. [10]
- Lymphatic and Glymphatic Dysfunction
- Impaired lymphatic or glymphatic drainage may contribute to SANS.
- The optic nerve and meninges possess lymphatic-like drainage pathways that are involved in the clearance of fluid from the subarachnoid space around the optic nerve.
- In microgravity, reduced gravitational assistance and increased venous congestion may hinder the clearance of perineural fluid.
- This can lead to persistent distension of the optic nerve sheath and optic disc edema.
- While the exact role of orbital lymphatic and glymphatic dysfunction is not yet fully understood, this mechanism may help explain the lasting structural changes observed after astronauts return to Earth, such as optic nerve sheath distension and choroidal folds.[11]
- Environmental and Biochemical Modifiers
- The ambient levels of carbon dioxide on the International Space Station are higher than those on Earth.
- This condition, known as hypercapnia, may lead to cerebral vasodilation and could affect venous pressure or the regulation of intracranial pressure, although its exact contribution to SANS remains uncertain.
- Radiation exposure becomes increasingly pertinent during exploration-class missions that extend beyond low Earth orbit. [12]
- Space radiation can affect the lens, retina, retinal microvasculature, and the central nervous system, potentially contributing to cotton-wool spots or other microvascular changes. [13]
- However, radiation is currently regarded as a potential modifying factor rather than the primary cause of SANS.
- Individual biochemical susceptibility may also play a role.
- Variations in folate- and vitamin B12-dependent one-carbon metabolism have been linked to ophthalmic findings associated with SANS.
- These metabolic pathways may influence endothelial function, vascular regulation, connective tissue properties, or tissue remodeling. This could explain why only some astronauts develop clinically significant SANS despite similar mission experiences.
- Integrated Mechanistic Model
- Microgravity causes a cephalad fluid shift, leading to congestion in the head, neck, orbital regions, venous systems, and intracranial spaces.
- This congestion alters venous drainage, cerebrospinal fluid (CSF) dynamics, optic nerve sheath pressure, choroidal volume, and the translaminar pressure gradient.
- Collectively, these changes produce the characteristic SANS phenotype, which includes optic disc edema, optic nerve sheath distension, posterior globe flattening, choroidal and retinal folds, cotton-wool spots, and a hyperopic refractive shift.
- The variability of SANS can likely be attributed to differences in mission duration, spacecraft environment, venous and cerebrospinal fluid anatomy, ocular structure, nutritional status, one-carbon metabolism, and tissue susceptibility.
- This variability explains why findings can be asymmetric, vary in severity, and sometimes persist in astronauts after they return to Earth.
Table 3. Pathophysiological Mechanisms Linked to SANS Findings
| Mechanism | Proposed effect | Clinical / imaging correlate |
|---|---|---|
| Cephalad fluid shift | Headward redistribution of venous, interstitial, lymphatic, and CSF-related fluid | Head/orbital congestion, optic disc edema, optic nerve sheath distension |
| Altered CSF dynamics | Abnormal CSF flow, pulsatility, or drainage around the optic nerve | Optic nerve sheath distension, disc edema |
| Optic nerve sheath compartmentalization | Localized CSF trapping or impaired exchange within the optic nerve sheath | Asymmetric optic disc edema, persistent sheath distension |
| Venous congestion | Impaired jugular and orbital venous drainage | Increased orbital pressure, impaired CSF absorption, optic nerve sheath changes |
| Choroidal expansion | Increased choroidal volume from impaired vortex vein drainage | Choroidal folds, posterior globe flattening, hyperopic shift |
| Altered translaminar pressure gradient | Change in pressure relationship across the lamina cribrosa | Optic nerve head remodeling, RNFL thickening, disc edema |
| Lymphatic/glymphatic dysfunction | Impaired clearance of perineural and orbital fluid | Persistent optic nerve sheath distension and disc swelling |
| Elevated ambient CO₂ | Possible cerebral vasodilation and altered venous/ICP regulation | Potential aggravation of cephalad congestion |
| One-carbon metabolism variation | Possible biochemical susceptibility affecting vascular/connective tissue response | Variable astronaut susceptibility |
| Radiation exposure | Possible retinal microvascular and neuroinflammatory effects | Potential contributor to cotton-wool spots or future deep-space ocular risk |
Diagnosis
Symptoms
- Symptoms include decreased near-visual acuity (hyperopic refractive shift), visual scotomas, headaches [2] and deterioration of distance.[14]
- The most frequent symptomatic complaint among astronauts experiencing SANS is decreased near vision caused by a hyperopic shift in vision of up to 1.5 diopters which can appear as early as after 3 weeks of microgravity exposure.[2]
- Self-reported SANS-related symptoms correlated with spaceflight time in a dose-dependent manner with 23% claiming disturbances in near-sightedness after short-duration space flight (SDSF) and up to 47% claiming similar symptoms after LDSF onboard the ISS.[2]
- Despite bearing superficial similarities to terrestrial idiopathic intracranial hypertension, astronauts do not experience diplopia, pulsatile tinnitus or transient visual obscurations,[2] the common symptoms of IIH.[15]
- Less frequently observed symptoms also include visual scotomas[2] and headaches. No changes in best corrected visual acuity, color vision or other complaints have been noted to date.
Physical Examination
- Visual acuity- Increased hyperopic sphere.[2]
- Cycloplegic and manifest refraction= normal to near normal vision.
- Fundoscopic exam -Disc edema, cotton wool spots, glutting of the superior and inferior nerve fibers[14], and choroidal folds.[2][16]. Asymptomatic cases of bilateral, asymmetrical optic disc edema can occur in SANS.[14](Figure 2)
- Optical coherence tomography-OCT is a key modality for detecting and monitoring optic disc edema, retinal nerve fiber layer thickening, peripapillary wrinkles, choroidal folds, and structural changes in the posterior segment of the eye.
(Tonometry assessments for IOP are not reliable indicators for development of SANS, as dictated by NASA Lifetime Surveillance of Astronaut Health.[14])
Signs
- Astronauts with SANS may have disc edema, choroidal folds, cotton wool spots, nerve fiber layer thickening on OCT, globe flattening and hyperopic shift.[2]
- While these signs may originate during spaceflight, no cases thus far have engendered a life-threatening or mission-endangering potential.[14]
- When compared to IIH optic nerve edema, the optic nerve in SANS has linear areas of fold (vs concentric “Patons lines”) and the posterior fundus shows choroidal folds that may appear before retinal folds.[4]
- Reduction of optic nerve edema with directed alleviation of ICP etiologies in IIH is associated with residual optic nerve atrophy; this finding is not demonstrated in SANS.
Diagnostic procedures
- Diagnostic procedures in astronauts experiencing SANS to date have included pre and post post MRI, pre-, intra-, and post flight OCT, orbital ultrasound, and occasional postflight lumbar punctures.[2]
- As per NASA protocol, currently on ISS to address SANS includes visual acuity testing software, ocular ultrasound, ophthalmic imaging, and optical coherence tomography, including OCT MulitColor Imaging.
- Pre and Post flight MRI are indicated. MRI imaging may show increases to optic nerves sheath diameter and optic nerve diameter with “kinks” to the optic nerve visible as T2 hyper intensities (96%).[17][14]Posterior globe flattening and pituitary dome concavity with posterior stalk deviation were also seen within the microgravity exposure cohorts.[17]Cephalad brain shift has also been demonstrated on post flight MRI.Diffusion Tensor Imaging (DTI), an advanced MRI-based neuroimaging technique utilizing vector-dependent analysis of tissue water molecule movements to determine cerebral axonal organization. In addition, time-wise analysis of MRI neuroimaging of astronauts may provide utility in determining time-dependent progression and recovery in SANS.[4] (Figure 3)
- Although the clinical picture of SANS is unique to the microgravity environment, similar OCT changes have been observed in head down tilt (HDT) bed rest studies on earth.[18] A 70-day trial of HDT bed rest found optic disc swelling and increased peripapillary retinal thickening, signs also seen in SANS. [18] These HDT bed rest studies, as well as HDT bed rest in the setting of hypercapnia, have become an increased interest in a potential terrestrial analog for studying SANS and its countermeasures.
- Orbital ultrasound is used on the ISS and has detected qualitative globe flattening.[4]
- OCT and funduscopic examination are performed with remote data transmission to terrestrial Subject Matter Experts (e.g. Ophthalmologists)during missions and has demonstrated optic disc edema, chorioretinal folds, and cotton wool spots.[2][14]
- OCT Angiography (OCTA) has recently been introduced to the ISS and will provide more comprehensive, quantitative data on the changes in choroidal blood flow, which may increase the understanding of SANS and its cephalad fluid shift theory. Retinal and choroidal vessel microalterations as depicted in OCT- Angiography (OCTA) imaging demonstrate favorable insight into terrestrial retinal and choroidal disease processes.[4] Due to the non-invasive nature, industrial-grade resolution of posterior orbit structures, patient-consistency, and operator receptivity, the OCT2 imaging modality is the current diagnostic imaging test of choice for initial unmasking and observation of SANS. [19](Figure 4)
- Lumbar puncture along with MRI have also been used to assess SANS but are limited to terrestrial use. Lumbar punctures performed in the context of SANS demonstrate normal to borderline increased opening CSF pressures which have been documented as high as 28.5 cmH20 at 2 months after landing.[2]
- ICP condition surveillance utilizing population-based data is not currently possible as solely astronauts observing optic disk edema were retrieval of post-flight ICP measurements acquired from.[4]
Figure 4:Optical Coherence Tomography of Pre-flight (top) and 30 days prior to return (R-30, bottom), comparison on optical coherence tomography with R-30 showcasing peripapillary wrinkles, choroidal folds, and optic disc edema. Courtesy of NASA. Image available to open public at https://bjo.bmj.com/content/107/7/895.long.
More recently, artificial intelligence application on a lightweight convolutional neural network (CNN) with an EfficientNet encoder that studies OCT images inflight and may detect SANS changes.[20]
Laboratory test
- Laboratory testing for enzymatic deficiencies in cyanocobalamin- and folate-dependent 1-carbon pathways may shed light on predisposition for SANS development in astronauts.[21]
Management
General treatment
- SANS-directed therapeutics follow a multi-faceted countermeasure approach.
- These include aiding potential enzymatic defects in folate- & cyanocobalamin-dependent 1-carbon pathways, securing a relative decrease in TLPD via utility of swim goggles[4] and selective use of acetazolamide for reduction in ICP.[14]
- Additional treatment modalities includes ensuring proper nutritional supplementation during spaceflight<[21], targeted exercise regimes with selective preference for non-intensive resistive exercises[4], and simulation of earth-like gravitational environments during spaceflight.[4][14]
- Several pairs of “Space Anticipation Glasses” of varying powers are routinely deployed with ISS crewmembers in order to mitigate any hyperopic shifts experienced during the LDSF.[2] Considering the cephalad fluid shift seen in microgravity, some efforts have focused on simulating gravity by creating relative lower body negative pressure to mimic gravity.[22]
Medical therapy
- Acetazolamide (Diamox Sequel) 500mg and 250mg for 6 and 2 weeks, respectively, may afford utility via decreases in cerebral pressures, as evidenced by post-LDSF lumbar puncture opening pressures in this case study.[14]
- Clinical support for administration of acetazolamide during spaceflight remains debatable.[14] TLPD assessments may provide the required clinical context for relief of optic disk edema via subsequent modifications in IOP and ICP.[14]
- Among the non-medical therapy tried in the past[23] was an intake of traditional Chinese herbs as a countermeasure effect against weightlessness(-6° HDT used to simulate weightlessness).
- During bed rest, the near vision and IOP showed a wavelike decreases when herbs were taken. The effect of these herbs are not been tested in people with flight
Medical follow up
- Follow up with visual field (VF) perimetry testing within 72-hours upon return from spaceflight can ascertain the contribution of optic disc edema, if present, to formation of blind spots.[14]
- In addition, assessment of OCT Retinal nerve fiber layer (RNFL) thickness at regular intervals post-spaceflight can aid in understanding the impact of chronic optic disc edema on RNFL pruning.[14]
- Signs of SANS may persist even after a return to normal earth gravity including the presence of mildly elevated CSF opening pressures[2] choroidal folds, and disc edema.[16][24].
Complications
- Certitude in permanence of SANS-associated visual acuity discrepancies remains uncertain; however, clear lack of consistency exists in time to reinstatement of normal visual function following presentation of SANS.[14][2]
- No permanent visual loss has yet occurred in any ISS crew members due to SANS.
Prevention
- Because SANS results in structural and sometimes residual changes in vision, and because it increases as spaceflight duration increases, NASA has continued attention and investigation in this matter, however, it has been somewhat limited due to small sample size of humans on spaceflight. Therefore HDTBR studies on Earth continue to be important[25]
- NASA has determined risk of SANS for each type of Design Reference Mission (DRM) Category, including
- Low Earth Orbit
- Lunar Orbital
- Lunar Orbital+ Surface
- Mars
(As updated 5/2025, only MARS travel (730-1224 days) requires mitigation actions for SANS)[26]
- Prevention protocol of SANS remains undetermined, however heightened efforts by NASA via an intensified occupational monitoring program for all active-duty astronauts, including specified attempts to characterize ICP-related signs: protrusion of the optic nerve head (ONH) ( shown to occur within the first 24 hours of increased ICP. Additionally, low salt diets, less intensive resistive exercise, and good nutrition may delay the development of SANS as explained above. [14]
- There have been some attempts to lower ICP without affecting cerebral perfusion such as negative pressure suits(specially inferior half of body up to 20mmHg) and thigh cuffs[27].
- To increase IOP, there has been trials of artificial gravity and googles (that minimally increased IOP and translaminar pressure).
- Although the effect of CO2 has not yet been statistically proven, the NASA has reduced International Space Station ambient CO2. [28]
- In recent studies[29] , by performing lower body negative pressure (LBNP) overnight, there hydrostatic gradients were reintroduced, therefore they were hemodynamically stable and choroid engorgement was attenuated. Therefore, at the first ocular remodeling finding, LBNP may be indicated.
Prognosis
- Although some ocular structural changes from SANS may persist for years after spaceflight, including globe flattening, choroidal folds, and hyperopic shifts, no crew member has yet experienced permanent vision loss after the spaceflight.[4][14]
- Questionnaire analysis of 300 astronauts demonstrated alterations in normal acuity failing exclusivity in astronauts with prior LDSF, with 29% of astronauts participating in SDSF reporting negative adjustments in near-visual acuity.
- Case reports illustrate persistence of post-spaceflight choroidal folds for at least 3 years after spaceflight.[14]
- Optic disc swelling has persisted in some up to 2 years after mission.[24].
- Permanent increases in laxity of the collagenous structures of the eye and orbit including the trabecular fibers of the optic nerve sheath during LDSF may contribute to persistent signs of optic nerve sheath distension and retinal and choroidal folds upon return from spaceflight.[4]
Other Ocular Conditions in Spaceflight
Space-Associated Dry Eye Disease
- While Spaceflight-Associated Neuro-ocular Syndrome (SANS) is widely studied, astronauts also commonly experience dry eye disease due to low humidity, high CO₂ levels, and limited tear evaporation in spacecraft.
- Nearly all long-duration crew members report ocular surface dryness, with studies showing changes in tear film, meibomian glands, and corneal epithelium—collectively termed "space-associated dry eye syndrome."[30][31][32]
Ocular Trauma from Particulate Matter
- Ocular trauma is a concern, as particles from inside spacecraft or sources like lunar and Martian regolith can harm the cornea.
- Simulations show that lunar dust is very abrasive, raising concerns about lasting corneal damage during future missions.[32][33]
Ocular Infections
- Ocular infections have been linked to spaceflight. Space travel weakens immune function, increasing the risk of viral reactivation and susceptibility to bacterial or fungal keratitis.
- Although severe infectious keratitis is rare, it would pose a serious challenge in space due to limited resources.[32][34]
Radiation-Induced Ocular Risks
- Prolonged spaceflight increases ocular risks from cosmic radiation, accelerating posterior sub capsular cataract formation and possibly contributing to retinal microangiopathy.
- Astronauts on missions beyond low Earth orbit face higher cumulative radiation risks, especially on lunar or Martian expeditions.[32][35]
Additional Resources
References
- ↑ Wostyn P, Deyn PP De. Optic Nerve Sheath Distention as a Protective Mechanism Against the Visual Impairment and Intracranial Pressure Syndrome in Astronauts. 2017;(September 2017):2017-2020. doi:10.1167/iovs.17-22600
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 Mader TH, Gibson CR, Pass AF, et al. Optic Disc Edema, Globe Flattening, Choroidal Folds, and Hyperopic Shifts Observed in Astronauts after Long-duration Space Flight. Ophthalmology. 2011;118(10):2058-2069. doi:10.1016/j.ophtha.2011.06.021
- ↑ Yang JW, Song QY, Zhang MX, et al. Spaceflight-associated neuro-ocular syndrome: a review of potential pathogenesis and intervention. Int J Ophthalmol. 2022;15(2):336-341. Published 2022 Feb 18. doi:10.18240/ijo.2022.02.21
- ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 Lee, A.G., Mader, T.H., Gibson, C.R. et al. Spaceflight associated neuro-ocular syndrome (SANS) and the neuro-ophthalmologic effects of microgravity: a review and an update. npj Microgravity 6, 7 (2020). https://doi.org/10.1038/s41526-020-0097-9
- ↑ National Aeronautics and Space Administration – Human Research Program – Human Health Countermeasures Element. Risk of Spaceflight Associated Neuro-ocular Syndrome (SANS). Humanresearchroadmap.nasa.gov. https://humanresearchroadmap.nasa.gov/evidence/reports/SANS.pdf?rnd=0.945882965319735. Accessed October 20, 2020
- ↑ Wostyn P, De Deyn PP. Optic nerve sheath distention as a protective mechanism against the visual impairment and intracranial pressure syndrome in astronauts. Invest Ophthalmol Vis Sci. 2017;58(10):4604-4605. doi:10.1167/iovs.17-22600
- ↑ Mader TH, Gibson CR, Pass AF, Kramer LA, Lee AG, Fogarty J, Tarver WJ, Dervay JP, Hamilton DR, Sargsyan A, Phillips JL, Tran D, Lipsky W, Choi J, Stern C, Kuyumjian R, Polk JD. Optic disc edema, globe flattening, choroidal folds, and hyperopic shifts observed in astronauts after long-duration space flight. Ophthalmology. 2011;118(10):2058-2069. doi:10.1016/j.ophtha.2011.06.021
- ↑ Stenger MB, Tarver WJ, Brunstetter T, Gibson CR, Laurie SS, Lee SMC, Macias BR, Mader TH, Otto C, Sargsyan A, Smith SM, Zwart SR, Ploutz-Snyder R, Bloomberg JJ. Risk of Spaceflight Associated Neuro-ocular Syndrome (SANS). NASA Human Research Program Human Health Countermeasures Element. NASA Johnson Space Center. 2017
- ↑ Mader TH, Gibson CR, Pass AF, Lee AG, Killer HE, Hansen HC, Dervay JP, Barratt MR, Tarver WJ, Sargsyan AE, Kramer LA, Riascos RF, Bedi DG, Pettit DR. Optic disc edema in an astronaut after repeat long-duration space flight. J Neuroophthalmol. 2013;33(3):249-255. doi:10.1097/WNO.0b013e31829b41a6
- ↑ Alperin N, Lee SH, Mazda M, Hushek SG, Roitberg B. Evidence for the importance of extracranial venous flow in patients with idiopathic intracranial hypertension. Acta Neurochir Suppl. 2005;95:129-132. doi:10.1007/3-211-32318-X_28
- ↑ Kramer LA, Sargsyan AE, Hasan KM, Polk JD, Hamilton DR. Orbital and intracranial effects of microgravity: findings at 3-T MR imaging. Radiology. 2012;263(3):819-827. doi:10.1148/radiol.12111986
- ↑ Waisberg E, Ong J, Paladugu P, Kamran SA, Zaman N, Tavakkoli A, Lee AG. Radiation-induced ophthalmic risks of long duration spaceflight: current investigations and interventions. Eur J Ophthalmol. 2024;34(5):1337-1345.
- ↑ Ong J, Tarver W, Brunstetter T, Mader TH, Gibson CR, Mason SS, Smith SM, Zwart SR, Laurie SS, Lee AG. Spaceflight associated neuro-ocular syndrome: proposed pathogenesis, terrestrial analogues, and emerging countermeasures. Br J Ophthalmol. 2023;107(7):895-900. doi:10.1136/bjophthalmol-2021-320434
- ↑ 14.00 14.01 14.02 14.03 14.04 14.05 14.06 14.07 14.08 14.09 14.10 14.11 14.12 14.13 14.14 14.15 14.16 14.17 Stenger M.B., Tarver W.J., Brunstetter T.et al. Risk of Spaceflight Associated Neuro-ocular Syndrome (SANS). NASA Human Research Program Human Health Countermeasures Element https://humanresearchroadmap.nasa.gov/evidence/reports/SANS.pdf NASA Johnson Space Center. 2017; (Available at:) https://humanresearchroadmap.nasa.gov/evidence/reports/SANS.pdf?rnd=0.434276635495143
- ↑ Giuseffi V, Wall M, Siegel PZ, Rojas PB. Symptoms and disease associations in idiopathic intracranial hypertension (pseudotumor cerebri): a case-control study. Neurology. 1991.
- ↑ 16.0 16.1 Mader TH, Gibson CR, Pass AF, et al. Optic disc edema in an astronaut after repeat long-duration space flight. J Neuro-Ophthalmology. 2013;33(3):249-255. doi:10.1097/WNO.0b013e31829b41a6
- ↑ 17.0 17.1 Kramer LA, Sargsyan AE, Hasan KM, Polk JD, Hamilton DR. Orbital and Intracranial Effects of Microgravity: Findings at 3-T MR Imaging. Radiology. 2012;263(3):819-827. doi:10.1148/radiol.12111986
- ↑ 18.0 18.1 Taibbi, G. et al. Ocular outcomes comparison between 14- and 70-day head-down-tilt bed rest. Invest. Ophthalmol. Vis. Sci. 57, 495–501 (2016).
- ↑ Ong J, Tarver W, Brunstetter T, et al. Spaceflight associated neuro-ocular syndrome: proposed pathogenesis, terrestrial analogues, and emerging countermeasures. British Journal of Ophthalmology 2023;107:895-900.
- ↑ Kamran, S.A., Hossain, K.F., Ong, J. et al. SANS-CNN: An automated machine learning technique for spaceflight associated neuro-ocular syndrome with astronaut imaging data. npj Microgravity 10, 40 (2024). https://doi.org/10.1038/s41526-024-00364-w
- ↑ 21.0 21.1 National Aeronautics and Space Administration. Human Adaptation to Space Flight: The Role of Nutrition. https://www.nasa.gov/sites/default/files/human-adaptation-to-spaceflight-the-role-of-nutrition.pdf. Accessed October 20, 2020.
- ↑ Arbeille P, Roumy J. Adaptation of the left heart , cerebral and femoral arteries , and jugular and femoral veins during short- and long-term head-down tilt and spaceflights. 2001:157-168. doi:10.1007/s004210100473
- ↑ Xu X, Xu ZM, Liu GY, et al. Effects of head down tilt on intra-ocular pressure, near vision, and visual field and the protection effect of Chinses herbs. Space Medicine & Medical Engineering. 2002(06):419–422.
- ↑ 24.0 24.1 Mader TH, Gibson CR, Otto CA, et al. Persistent Asymmetric Optic Disc Swelling after Long-Duration Space Flight: Implications for Pathogenesis. J Neuro-Ophthalmology. 2017;37(2):133-139. doi:10.1097/WNO.0000000000000467
- ↑ Ong J, Lee AG and Moss HE (2021) Head-Down Tilt Bed Rest Studies as a Terrestrial Analog for Spaceflight Associated Neuro-Ocular Syndrome. Front. Neurol. 12:648958. doi: 10.3389/fneur.2021.648958
- ↑ Laurie S. Risk of Spaceflight Associated Neuro-ocular Syndrome (SANS)Human Health Countermeasures (HHC) May 13, 2025 [current research ongoing]https://humanresearchroadmap.nasa.gov/Risks/risk.aspx?i=105
- ↑ Arbeille P, Herault S, Fomina G, Roumy J, Alferova I, Gharib C. Influences of thigh cuffs on the cardiovascular system during 7-day head-down bed rest. J Appl Physiol (1985) 1999;87(6):2168–2176.
- ↑ Martin Paez Y, Mudie LI, Subramanian PS. Spaceflight Associated Neuro-Ocular Syndrome (SANS): A Systematic Review and Future Directions. Eye Brain. 2020;12:105-117. Published 2020 Oct 19. doi:10.2147/EB.S234076
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- ↑ Ax T, Ganse B, Fries FN, Szentmáry N, de Paiva CS, March de Ribot F, Jensen SO, Seitz B, Millar TJ. Dry eye disease in astronauts: a narrative review. Front Physiol. 2023;14:1281327. -PMC - PubMed
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- ↑ Crucian BE, Choukèr A, Simpson RJ, Mehta S, Marshall G, Smith SM, Zwart SR, Heer M, Ponomarev S, Whitmire A, Frippiat JP, Douglas GL, Lorenzi H, Buchheim JI, Makedonas G, Ginsburg GS, Ott CM, Pierson DL, Krieger SS, Baecker N, Sams C. Immune System Dysregulation During Spaceflight: Potential Countermeasures for Deep Space Exploration Missions. Front Immunol. 2018;9:1437. - PMC - PubMed
- ↑ Waisberg E, Ong J, Paladugu P, Kamran SA, Zaman N, Tavakkoli A, Lee AG. Radiation-induced ophthalmic risks of long duration spaceflight: Current investigations and interventions. Eur J Ophthalmol. 2024;34:1337–1345. - PubMed
- ↑ Redfern AJ, Lee AG. Spaceflight-Associated Neuro-Ocular Syndrome (SANS). Experts InSight American Academy of Ophthalmology. https://www.aao.org/education/audio/spaceflight-associated-neuro-ocular-syndrome-sans Accessed June 18, 2024.
