LAUSR

To the Editor: I wish to thank Drs. Wostyn, Gibson, and Mader for the very interesting letter1 concerning my article, Choroidal blood flow: Review and potential explanation for the choroidal venous anatomy including the vortex vein system,2 especially in regard to spaceflight-associated neuroocular syndrome. In this letter, the authors start by reviewing some of the physiologic changes that occur with spaceflight, such as redistribution of blood volume to the head and as a consequence, to the choroid. Macias et al3 reported rapid increases in peripapillary choroidal thickness during spaceflight with a much longer period of normalization after return to earth. In other reported eyes, the choroidal thickness has not returned to normal. Drs. Wostyn, Gibson, and Mader suggest there may be choroidal vascular remodeling secondary to chronic venous congestion. I think this idea has merit. As an extension, and possible clarifying idea, we recently published wide-angle indocyanine green angiography data from eyes of patients with central serous chorioretinopathy and peripapillary pachychoroid syndrome as compared with controls.4 In this study, we found that eyes with either disorder have large anastomotic connections between vortex vein systems, whereas controls, in keeping with Hayreh’s primary observations,5 did not. These anastomotic connections seemed to be the result of vascular remodeling in the venous outflow of the choroid. We proposed that these anastomotic connections would alter the hemodynamics of venous outflow and could contribute to increased local fluid loading within the proximal vessels of the choroid to include the choriocapillaris. This may cause the observed choroidal vascular hyperpermeability, which is a unifying finding in central serous chorioretinopathy.6 It is entirely possible that venous overloading of the choroid during spaceflight could cause remodeling of venous drainage in the choroid, potentially including intervortex anastomoses. One would expect that if these anastomotic connections were established, the choroidal hemodynamics may be permanently altered, which may explain the phlegmatic normalization of choroidal thickness even after return to normal gravity on earth. I would be very interested in collaborating on imaging studies of astronauts. Drs. Wostyn, Gibson, and Mader propose that there is increased resistance to venous drainage during spaceflight, and this may cause increased transudation. Note, as is mentioned in the choroidal blood flow article, resistance is the opposition to blood flow. In the article, it was proposed that the control of venous outflow from the choroid could involve a Starling resistor effect. This mechanism seems to ensure that the venous pressure in the choroid is higher than the intraocular pressure. In space, the intraocular pressure increases, which may indirectly affect venous outflow resistance through the Starling resistor. In spaceflight, the redistribution and the increase in venous pressure may be a more important determinant of blood flow than local resistance changes in the choroid. This is an area in need of more research. Nedergaard and colleagues proposed the glymphatic system in the brain7 and more recently extended this idea to the eye.8 The glymphatic system is a perivascular system that is associated with fluid flow through tissue parenchyma of the brain or retina and can cause clearance of molecules such as b-amyloid. The perivascular pathways for movement of solutes and macromolecules seem to be an important method of transport in neural tissues. The choroid is not neuronal tissue, of course, and its interaction with the glymphatic system is not well defined, but Drs. Wostyn, Gibson, and Mader raise fascinating issues.