Patrick A. Sibony,Steven S. Laurie,Connor R. Ferguson,Laura P. Pardon,Millennia Young,F. James Rohlf,Brandon R. Macias
Author Response: The Posterior Displacement of the Bruch's Membrane Opening: A Surprising Finding in Spaceflight-Associated Neuro-Ocular Syndrome
idiopathic intracranial hypertension (IIH),spaceflight-associated neuro-ocular syndrome (SANS),papilledema,optical coherence tomography (OCT),optic nerve
Author Response: The Posterior Displacement of the Bruch's Membrane Opening: A Surprising Finding in Spaceflight-Associated Neuro-Ocular Syndrome

We wish to thank Drs. Wostyn, Gibson, and Mader for their interest in our recent publication: “Ocular Deformations in Spaceflight-Associated Neuro-Ocular Syndrome.” The authors have previously commented on the “enigma” of these seemingly paradoxical posterior displacements of Bruch's membrane opening (BMO) in spaceflight-associated neuro-ocular syndrome (SANS). This feature has been independently observed by others,, and appears to be a reproducible optical coherence tomography (OCT) finding in SANS. We agree that the cause is most likely multifactorial, although the precise mechanism is uncertain. The authors suggest that interstitial optic disc edema (due to prelaminar vascular leakage and impaired clearance) may be a contributive factor in displacing the BMO posteriorly. Based on the headward fluid shifts that occur in space, this explanation is plausible, and even likely, but unproven. It is also possible that the disc edema is instead caused by a mild increase in the average intracranial pressure or sequestered perioptic subarachnoid cerebrospinal fluid, which, in either case, can obstruct axoplasmic flow and distend prelaminar axons. Irrespective of the mechanism of optic disc edema, there is some evidence to suggest that swelling of the optic nerve head may not be the principal cause of these posterior BMO displacements. In most cases of SANS, the optic disc edema is so mild that it can only be detected by OCT. Posterior displacements also occurred in our patients with idiopathic intracranial hypertension but were far less frequent, proportionately smaller, and usually associated with high grade papilledema. A subgroup analysis of the crewmembers in our study (see the Table below) showed that the change (Δ) in total retinal thickness (TRT) (d), Δ retinal nerve fiber layer thickness (RNFLT) (e), Δ shape (f), Δ axial length (g), and the presence of choroidal folds (h) and clinically evident disc edema (i), were slightly greater or more frequent in the eyes with posterior BMO displacements than those with anterior displacements. The differences, however, were not statistically significant. In contrast, Δ choroidal thickness (c) was significantly greater in the posterior displacement subgroup than the anterior subgroup. This finding suggests that choroidal thickening may potentially play an important role in the development of posterior deformations in SANS. This would not exclude additional factors. For example, Feola et al. has shown that choroidal thickening may strain the prelaminar optic nerve head and so choroidal expansion and disc edema may synergistically displace the BMO posteriorly. We also speculated that headward fluid shifts might increase orbital tissue pressure. A recent finite element analysis suggests that swelling of the orbital fat might explain the broad flattening of the posterior globe, loss of tension in the peripapillary choroid, and decreased axial length, producing a larger effect than that generated by an elevation in intracranial pressure. If the combination of choroidal expansion and orbital tissue pressure imposes a peripapillary indentation load that spares the BMO, then the reference points on Bruch's membrane layer (BML) would be displaced anteriorly more than the BMO. This alone could explain the “relative” posterior BMO displacements even though the globe overall is indented anteriorly. Figure 4 in our paper summarizes how these factors might hypothetically interact to explain both the anterior and posterior ocular deformations in SANS. For the moment, however, the relative importance of each individual factor, specifically choroidal thickening, orbital tissue pressure, optic disc edema, the translaminar pressure gradient, structural anatomy, and scleral and laminar compliance or dural stiffness, in explaining the ocular deformations in SANS is unknown. We agree with the authors’ conclusion that more research is needed to better understand the effects of headward fluid redistribution on the globe and orbit in the pathogenesis of SANS.