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从脉络膜角度看宇航员的视盘水肿。

Optic Disc Edema in Astronauts from a Choroidal Point of View.

出版信息

Aerosp Med Hum Perform. 2022 Apr 1;93(4):396-398. doi: 10.3357/AMHP.6010.2022.

Abstract

Optic disc edema has been well documented in astronauts both during and after long-duration spaceflight and is hypothesized to largely result from increased pressure within the orbital subarachnoid space brought about by a generalized rise in intracranial pressure or from sequestration of cerebrospinal fluid within the orbital subarachnoid space with locally elevated optic nerve sheath pressure. In addition, a recent prospective study documented substantial spaceflight-associated peripapillary choroidal thickening, which may be a contributing factor in spaceflight-associated neuro-ocular syndrome. In the present article, based on the above, we offer a new perspective on the pathogenesis of microgravity-induced optic disc edema from a choroidal point of view. We propose that prolonged microgravity exposure may result in the transudation of fluid from the choroidal vasculature, which, in turn, may reach the optic nerve head, and ultimately may lead to fluid stasis within the prelaminar region secondary to impaired ocular glymphatic outflow. If confirmed, this viewpoint would shed new light on the development of optic disc edema in astronauts.

摘要

视盘水肿在长期太空飞行期间和之后的宇航员中已有充分记录,据推测主要是由于颅内压普遍升高引起的眼眶蛛网膜下腔压力增加所致,或者是由于脑脊液在眼眶蛛网膜下腔中被隔离,导致视神经鞘内压力局部升高所致。此外,最近的一项前瞻性研究记录了大量与太空飞行相关的视盘周围脉络膜增厚,这可能是与太空飞行相关的神经眼综合征的一个促成因素。在本文中,基于上述内容,我们从脉络膜的角度对微重力引起的视盘水肿的发病机制提出了新的观点。我们提出,长时间的微重力暴露可能导致脉络膜血管中的液体渗出,进而可能到达视神经头部,并最终可能导致由于眼淋巴流出受损而导致前层流区内的液体停滞。如果得到证实,这一观点将为宇航员视盘水肿的发展提供新的视角。

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