Abstract：
The aim of this experimental study was to investigate the pathogenesis of Terson syndrome (TS), which currently is controversial.
The central retinal artery (in 39 orbits), posterior ciliary arteries (in 8 orbits), and central retinal vein (CRV in 21 orbits) were occluded in rhesus monkeys by exposing them to lateral orbitotomy. Fundus examination and fluorescein fundus angiography were performed before and immediately after cutting the vessels and serially thereafter during the follow-up period. The rationale of the experimental study design is discussed.
In eyes with central retinal artery occlusion, retinal hemorrhages were seen soon after the procedure in 7 eyes, and on follow-up in a total of 15 eyes. In posterior ciliary artery occlusion, retinal hemorrhages were seen soon after the procedure in one eye, and on follow-up in a total of three eyes. In eyes with CRV, all eyes had extensive scattered retinal hemorrhages.
The findings of this experimental study, and my basic, experimental, and comprehensive clinical studies on CRVO, suggest the following concept of the pathogenesis of TS: Compression of the CRV plays a crucial role in the development of TS. The CRV is compressed, as it lies in the subarachnoid space of the optic nerve sheath, by raised cerebrospinal fluid pressure and/or accumulated blood.
venous stasis and raised venous pressure in the retinal veins, leading to venous engorgement, rupture of the retinal capillaries.
retinal hemorrhages. The clinical importance of compression of the CRV and not occlusion of CRV in TS is that optic nerve sheath decompression by opening it and releasing the blood and raised cerebrospinal fluid (CSF) pressure, would result in immediate decompressing of the CRV in the subarachnoid space and restoration of normal circulation and prevent visual loss.
The central retinal artery (in 39 orbits), posterior ciliary arteries (in 8 orbits), and central retinal vein (CRV in 21 orbits) were occluded in rhesus monkeys by exposing them to lateral orbitotomy. Fundus examination and fluorescein fundus angiography were performed before and immediately after cutting the vessels and serially thereafter during the follow-up period. The rationale of the experimental study design is discussed.
In eyes with central retinal artery occlusion, retinal hemorrhages were seen soon after the procedure in 7 eyes, and on follow-up in a total of 15 eyes. In posterior ciliary artery occlusion, retinal hemorrhages were seen soon after the procedure in one eye, and on follow-up in a total of three eyes. In eyes with CRV, all eyes had extensive scattered retinal hemorrhages.
The findings of this experimental study, and my basic, experimental, and comprehensive clinical studies on CRVO, suggest the following concept of the pathogenesis of TS: Compression of the CRV plays a crucial role in the development of TS. The CRV is compressed, as it lies in the subarachnoid space of the optic nerve sheath, by raised cerebrospinal fluid pressure and/or accumulated blood.
venous stasis and raised venous pressure in the retinal veins, leading to venous engorgement, rupture of the retinal capillaries.
retinal hemorrhages. The clinical importance of compression of the CRV and not occlusion of CRV in TS is that optic nerve sheath decompression by opening it and releasing the blood and raised cerebrospinal fluid (CSF) pressure, would result in immediate decompressing of the CRV in the subarachnoid space and restoration of normal circulation and prevent visual loss.
摘要：
本实验研究的目的是探讨Terson综合征(TS)的发病机制,目前是有争议的。
视网膜中央动脉（39个眼眶），睫状后动脉（在8个轨道中），恒河猴的视网膜中央静脉（21个眼眶的CRV）通过暴露于外侧眼眶切开术而闭塞。在切开血管之前和之后立即进行眼底检查和荧光素眼底血管造影，然后在随访期间连续进行。讨论了实验研究设计的基本原理。
在视网膜中央动脉阻塞的眼中，手术后不久，7只眼出现视网膜出血，并在总共15只眼睛的随访中。在睫状后动脉闭塞中，手术后不久，一只眼睛出现视网膜出血，在总共三只眼睛的随访中。在CRV的眼中，所有的眼睛都有广泛的散在视网膜出血。
这项实验研究的结果，和我的基本，实验性的,以及对CRVO的全面临床研究，提示TS发病机理的以下概念：CRV的压缩在TS的发展中起着至关重要的作用。CRV被压缩，因为它位于视神经鞘的蛛网膜下腔，脑脊液压力升高和/或血液积聚。
视网膜静脉的静脉淤滞和静脉压升高，导致静脉充血,视网膜毛细血管破裂.
视网膜出血。在TS中压缩CRV而不是闭塞CRV的临床重要性是通过打开视神经鞘并释放血液和升高脑脊液（CSF）压力来减压，将导致蛛网膜下腔CRV立即减压，恢复正常循环并防止视力丧失。
视网膜中央动脉（39个眼眶），
在视网膜中央动脉阻塞的眼中，
这项实验研究的结果，
视网膜静脉的静脉淤滞和静脉压升高，
视网膜出血。
