Spaceflight not an eye‐popping experience for astronauts

An astronaut's puffy face is the first visible biomarker of the fluid shift induced by leaving Earth's gravitational field. This outward sign prompted much speculation about the effects of spaceflight on human physiology. It was assumed that the central and headward movement of fluids must be associated with an increase in central venous pressure (CVP). Direct measurements of central venous pressure during space shuttle launches showed that CVP was consistently less than pre-flight supine values on reaching space. About 10 years later, astronauts living for up to 6 months on the International Space Station (ISS) reported vision changes, and lumbar puncture opening pressure was elevated in four astronauts up to 60 days after return to Earth. NASA named the syndrome ‘visual impairment/increased intracranial pressure’, or VIIP, starting a controversy that was partially settled by renaming as spaceflight associated neuro-ocular syndrome (SANS). Spaceflight, with the absence of the normal head-to-foot gravity vector, unloads the body, resulting in musculoskeletal and cardiovascular deconditioning unless appropriate countermeasures are introduced. Unloading is also critical to interpretation of how fluid pressures are distributed in space. CVP is reduced, even though central blood volume is increased, because of the unweighting of tissues around the central veins. How gravitational unloading, hydrostatic pressure differences, blood and cerebrospinal fluid volume redistribution affect intracranial pressure (ICP) during spaceflight is not known. A key study that allows us to speculate on effects of spaceflight directly measured CVP and ICP during parabolic flight in eight participants who previously had an Ommaya reservoir inserted for chemotherapy medications (Lawley et al. 2017). Both CVP and ICP were less in microgravity than during supine rest. Thus, direct measurements of ICP demonstrated that there can be elevated blood volume in the neck veins during unloading in microgravity without an increase in ICP. However, parabolic flight limits microgravity exposure to ∼20 s, so it is unknown if chronic fluid redistribution and possible accumulation of cerebrospinal fluid might have an impact on ICP with long-duration spaceflights. In this issue of The Journal of Physiology, Dr Iwasaki and colleagues (2021) make an important contribution to understanding the potential aetiology of SANS in their report of pre- and post-spaceflight non-invasive estimation of intracranial pressure (nICP). nICP was actually lower or unchanged after spaceflight in 10 of 11 astronauts, a finding counter to the assumption of elevated ICP that prompted the initial syndrome name, VIIP. Their individual subject data further highlight between-person differences, with only two of 11 astronauts experiencing SANS. Together, these observations point to the need for greater focus on other mechanisms responsible for the multiple signs of SANS. Zwart et al. (2016) provide compelling evidence that genetic variations increase susceptibility to SANS, possibly through localized oedema linked to endothelial dysfunction. There are other physical mechanisms that should be considered. Daily life on Earth introduces diurnal variations in hydrostatic gradients such that elevated ICP and intraocular pressure (IOP) during night-time sleep are countered by reductions during the daytime. IOP is greater than ICP, but a mismatch of their ratio, with a greater change proposed for ICP during spaceflight, has been speculated as a potential contributor to the ophthalmic changes observed, including globe flattening. Long-term alterations in hydrostatic gradients change cerebral perfusion pressure (mean arterial pressure at the brain minus ICP) but relatively constant cerebral blood flow or velocity is achieved by autoregulatory adaptation on changing posture or spaceflight. Iwasaki and colleagues (2021) reported higher post-flight cerebral blood velocity but this finding deserves further investigation. Ocular blood flow is influenced by ocular perfusion pressure (OPP = MAP at the eye minus IOP), but there is evidence that ocular vascular resistance operates over a more limited autoregulatory range to increases in OPP (Schmidl et al. 2011). During head-down bed rest or spaceflight, the increase in OPP could increase ocular blood flow, potentially contributing to optic disc oedema (Mohiar, 2020). During spaceflight, a 50% increase in retinal artery blood velocity has been observed, but the mechanism was attributed to compression of the retinal artery rather than an increase in OPP (Sirek et al. 2014). Elevated environmental arterial during spaceflight might dilate arterial resistance vessels, increasing cerebral and ocular perfusion, and affect autoregulation and CO2 reactivity. To date, OPP has not been considered as a potential contributor to SANS. The International Space Agencies have asked researchers to provide accurate data to assist in thoroughly understanding the complex impacts of long-duration spaceflight on risks to astronaut health. As revealed by Iwasaki and colleagues, this task is complicated, not only by variations in human physiology, but also by individualized post-flight medical care dictated by crew surgeons based on symptoms and personal communications with the astronaut. In this study, astronauts received an average of 2 l intravenous fluid and were made available at various times after landing for the scientific investigations. As space exploration moves toward habitation of the Moon and Mars, and to longer duration missions, the mechanisms responsible for SANS need to be identified. The work started by Iwasaki and colleagues with measurements of post-flight nICP is relevant, but measurement on ISS is needed to confirm that high ICP is not, by itself, a contributor to SANS. Rather, genetics, pressure gradients affecting IOP/ICP and OPP, as well as lack of circadian rhythm and countermeasures seem to be areas of focus for future research pursuing protection of vision health in space explorers. None. Both authors have approved the final version of the manuscript and agree to be accountable for all aspects of the work. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. None.

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