Abstract

PurposeTo investigate lamina cribrosa (LC) displacement during the Valsalva maneuver in young healthy eyes using enhanced depth imaging (EDI) spectral-domain optical coherence tomography (SD-OCT).MethodsForty-eight eyes of 48 young healthy volunteers (age range: 20–34 years) underwent intraocular pressure (IOP) measurement by Goldmann applanation tonometry as well as Cirrus HD-OCT scans before and during the Valsalva maneuver. The optic nerve head (ONH) parameters (average retinal nerve fiber layer thickness, rim area, disc area, average C/D ratio, vertical C/D ratio, cup volume), anterior LC depth (LCD), subfoveal and peripapillary choroidal thickness, and neural canal opening diameter were measured on compensated OCT and compared during Valsalva challenge. The subjects were asked to take a five-minute break after each Valsalva maneuver.ResultsDuring the Valsalva maneuver, the IOP significantly increased, from 12.7 ± 3.0 mmHg to 16.0 ± 3.2 mmHg (P < 0.001), while the LCD sharply decreased, from 463.4 ± 118.8 μm to 427.3 ± 106.4 μm (P < 0.001). The subfoveal choroidal thickness (300.7 ± 90.6 vs. 309.6 ± 93.5 μm), peripapilllary choroidal thickness (152.2 ± 55.4 vs. 150.8 ± 49.3 μm), neural canal opening diameter (1651.8 ± 204.2 vs. 1651.0 ± 217.6 μm), and all of the ONH parameters did not change significantly (all P > 0.05).ConclusionsThe Valsalva maneuver induced anterior displacement of the LC, but did not alter the choroidal thickness or ONH morphology. The data describe the positional characteristics of the LC in response to the Valsalva maneuver in young healthy eyes.

Highlights

  • Posterior displacement of the lamina cribrosa (LC) caused by increased intraocular pressure (IOP) plays a prominent role in the pathogenesis of glaucoma.[1,2,3] A posteriorly displaced LC can lead to mechanical and vascular damage to the optic nerve head (ONH), including the ganglion cell axons.[1]

  • The data describe the positional characteristics of the LC in response to the Valsalva maneuver in young healthy eyes

  • IOP and cerebrospinal fluid (CSF) pressure dynamics as they impact on the LC have been considered to be a key factor in glaucoma development.[4,5,6,7]

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Summary

Introduction

Posterior displacement of the lamina cribrosa (LC) caused by increased intraocular pressure (IOP) plays a prominent role in the pathogenesis of glaucoma.[1,2,3] A posteriorly displaced LC can lead to mechanical and vascular damage to the optic nerve head (ONH), including the ganglion cell axons.[1]. CSF pressure in NTG eyes is known to be lower than in high-tension glaucoma eyes or healthy controls.[8, 9] In addition, axonal damage and optic neuropathy can be induced by experimental reduction of CSF pressure in monkey eyes.[10]

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