Abstract
Abstract
Space flight‐associated neuroocular syndrome (SANS) is a consequence of long‐duration space flight and is detected in two‐thirds of astronauts. In‐flight, this can cause a change in the refraction of the eyes, requiring graded hypermetropic ‘superfocus adjustable’ glasses, optic nerve head oedema and choroidal folds. While the optic disc oedema resolves on returning to gravitational force, the choroidal folds and axial length shortening remain. Controversy remains over the role of intracranial pressure in the development of these changes. A recent case report has re‐energised the debate as to whether nutraceuticals and an individual's genetic expression of the 1‐carbon metabolic pathway are a major component for the development of this condition. The strict 6° head down tilt bed rest platform remains the cornerstone for evaluating analogous pathological changes and trialling potential targeted therapies. The translational application of a glucagon‐like peptide 1 receptor agonist for the treatment of raised intracranial pressure in idiopathic intracranial hypertension may be of significance as a potential countermeasure for SANS. The aim of this narrative review is to explore the controversies in the integration of the presumed pathophysiological factors and to debate suitable countermeasures.