Ruowu Hou1, Zheng Zhang2, Diya Yang3, Huaizhou Wang3, Weiwei Chen4, Zhen Li5, Jinghong Sang2, Sumeng Liu2, Yiwen Cao2, Xiaobin Xie6, Ruojin Ren7, Yazhuo Zhang8, Bernhard A Sabel9, Ningli Wang10. 1. Department of Neurosurgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China. 2. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China. 3. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China; Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing, China. 4. Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing, China. 5. Department of Ophthalmology, Xuanwu Hospital, Capital Medical University, Beijing, China. 6. Department of Ophthalmology, Eye Hospital of China Academy of Chinese Medical Sciences, Beijing, China. 7. Eye center, New York Eye and Ear Infirmary, NY, USA. 8. Department of Endoscopic and Microinvasive Neurosugery, Beijing Neurosurgery Institute, Beijing Tiantian Hospital, Capital Medical University, Beijing, China. Electronic address: zyz2004520@163.com. 9. Institute of Medical Psychology, Medical Faculty, Otto-v.-Guericke University of Magdeburg, Magdeburg, Germany. 10. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing, China; Beijing Institute of Ophthalmology, Beijing Tongren Hospital, Capital Medical University, Beijing, China. Electronic address: wningli@vip.163.com.
Abstract
PURPOSE: Because a lowered intracranial pressure (ICP) is a possible mechanism of optic neuropathy, we wished to study the CSF dynamics in the optic nerve chamber by recording possible changes in the optic nerve subarachnoid space pressure (ONSP) and the impact on it when acutely lowering ICP. METHODS: In eight normal dogs pressure probes were implanted in the left brain ventricle, lumbar cistern, optic nerve subarachnoid space and in the anterior eye chamber. Following CSF shunting from the brain ventricle we monitored changes of ICP, lumbar cistern pressure (LCP), ONSP and intraocular pressure (IOP). RESULTS: At baseline, the pressures were different with ICP>LCP>ONSP but correlated with each other (P<0.001). The "trans-lamina cribrosa pressure gradient" (TLPG) was highest for IOP-ONSP, lower for IOP-LCP, and lowest for IOP-ICP (P<0.001). During CSF shunting the ICP gradually decreased in a linear fashion together with the ONSP ("ICP-depended zone"). But when the ICP fell below a critical breakpoint, ICP and ONSP became uncoupled and ONSP remained constant despite further ICP decline ("ICP-independent zone"). CONCLUSIONS: Because the parallel decline of ICP and ONSP breaks down when ICP decreases below a critical breakpoint, we interpret this as a sign of CSF communication arrest between the intracranial and optic nerve SAS. This may be caused by obstructions of either CSF inflow through the optic canal or outflow into the intra-orbital cavity. This CSF exchange arrest may be a contributing factor to optic nerve damage and the optic nerve chamber syndrome which may influence the loss of vision or its restoration.
PURPOSE: Because a lowered intracranial pressure (ICP) is a possible mechanism of optic neuropathy, we wished to study the CSF dynamics in the optic nerve chamber by recording possible changes in the optic nerve subarachnoid space pressure (ONSP) and the impact on it when acutely lowering ICP. METHODS: In eight normal dogs pressure probes were implanted in the left brain ventricle, lumbar cistern, optic nerve subarachnoid space and in the anterior eye chamber. Following CSF shunting from the brain ventricle we monitored changes of ICP, lumbar cistern pressure (LCP), ONSP and intraocular pressure (IOP). RESULTS: At baseline, the pressures were different with ICP>LCP>ONSP but correlated with each other (P<0.001). The "trans-lamina cribrosa pressure gradient" (TLPG) was highest for IOP-ONSP, lower for IOP-LCP, and lowest for IOP-ICP (P<0.001). During CSF shunting the ICP gradually decreased in a linear fashion together with the ONSP ("ICP-depended zone"). But when the ICP fell below a critical breakpoint, ICP and ONSP became uncoupled and ONSP remained constant despite further ICP decline ("ICP-independent zone"). CONCLUSIONS: Because the parallel decline of ICP and ONSP breaks down when ICP decreases below a critical breakpoint, we interpret this as a sign of CSF communication arrest between the intracranial and optic nerve SAS. This may be caused by obstructions of either CSF inflow through the optic canal or outflow into the intra-orbital cavity. This CSF exchange arrest may be a contributing factor to optic nerve damage and the optic nerve chamber syndrome which may influence the loss of vision or its restoration.
Authors: Susanne R Kerscher; Daniel Schöni; Felix Neunhoeffer; Markus Wolff; Karin Haas-Lude; Andrea Bevot; Martin U Schuhmann Journal: Childs Nerv Syst Date: 2019-08-08 Impact factor: 1.475
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