Abstract
Spaceflight-associated neuro-ocular syndrome (SANS) encompasses a unique constellation of neuro-ocular findings in astronauts, including optic disc edema (ODE), globe flattening, chorioretinal folds, and hyperopic refractive shift. Although there are numerous neuro-ocular findings in SANS, the purpose of this review is to describe the novel, emerging concepts of the pathogenesis for the ODE specifically in SANS. While the initial hypotheses on the pathogenesis of ODE in SANS focused on possible elevated intracranial pressures (i.e., papilledema), the most prominent current hypothesis is microgravity-induced cephalad fluid shift. More recent studies however suggest that the pathogenesis of the ODE in SANS is likely multifactorial including possible underlying metabolic and genetic components. We review the literature on ODE in SANS including recent work integrating the complex physiologic interactions of microgravity-induced disruption in intracerebral and intraocular fluid dynamics, vascular congestion, cellular stress responses, and genetic predisposition. We believe that the development of ODE in SANS is likely multifactorial in origin, and further understanding of the mechanical, cellular, metabolic, and genetic components is of utmost importance to develop future countermeasures in preparation for possible future crewed missions to the moon, the asteroid belt, and Mars.
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