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Reply to “Peripapillary Hyper‐Reflective Ovoid Masslike Structures in Astronauts”

Dear Editor, We read with great interest the paper recently published in Annals of Neurology by Petzold and colleagues and would appreciate the opportunity to make a comment. In their longitudinal, prospective study, the authors investigated the occurrence and development of peripapillary hyperreflective ovoid mass-like structures (PHOMS) in patients with multiple sclerosis (MS), healthy controls, and non-MS disease controls. PHOMS are a new finding in spectral domain optical coherence tomography, which are seen in a variety of conditions with optic disc swelling, such as idiopathic intracranial hypertension (IIH). Petzold and colleagues found that the proportion of PHOMS was significantly higher in patients with MS (16%) when compared with healthy control subjects (0%). In non-MS disease controls, the condition associated most frequently with PHOMS was IIH (62%). According to the authors, the presence of PHOMS in MS might be attributable to axoplasmic stasis, impaired “glymphatic” outflow from the eye to the brain, or a change of the translaminar pressure gradient at the optic disc. It would be interesting to investigate whether PHOMS can also be found in astronauts returning from long-duration missions to the International Space Station. We believe that PHOMS in astronauts could originate through the same mechanisms as proposed by Petzold and colleagues. In microgravity conditions, elevation of optic nerve sheath pressure, attributable to a rise in intracranial pressure and/or sequestration of cerebrospinal fluid within the orbital subarachnoid space, might lead to a reduction or reversal of the normal posteriorly directed trans-lamina cribrosa pressure difference (TLCPD), defined as intraocular pressure minus optic nerve subarachnoid space pressure. We have previously proposed that this might block the glymphatic efflux of ocular fluid into the optic nerve, ultimately leading to optic disc edema in astronauts. This glymphatic theory of microgravity-induced optic disc edema is supported by very recent observations pertaining to the discovery of an entirely new ocular glymphatic pathway for removal of fluid and metabolites from the intraocular space via the proximal optic nerve in rodents. Indeed, it was found that the TLCPD is a major driver of the ocular glymphatic outflow and that increased intracranial pressure inhibits the ocular glymphatic efflux. Obviously, further research is required to provide evidence for the presence of PHOMS in astronauts. If confirmed, given that a similar mechanism has been proposed by Petzold and colleagues to account for the development of PHOMS in MS, anterograde ocular glymphatic transport blockage might also be considered as a possible underlying mechanism for the occurrence of PHOMS in astronauts.