Yoko Ito , Yuki Takatsudo , Peter L. Gehlbach , Keisuke Mori
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GIF-formatted pseudo-animation was generated with OCT images acquired initially in a static eye state, followed by scans immediately after ocular excursions.</p></div><div><h3>Results</h3><p>Initial stages of PVD included peripheral PVD with (stage 1a) or without (stage 1b) interposed material between the posterior vitreous cortex and the retina, and perifoveal PVD expanding to the periphery (stage 2). All stage 1 PVDs presented anterior to the papillomacular vitreous liquefaction. All eyes demonstrated mobility of the vitreous gel at the anterior face of the vitreous liquefaction; however, the adherent cortical vitreous layer comprising the posterior wall of the lacuna showed no mobility. Mobility of the posterior vitreous cortex was not present in eyes with stage 1a PVD and increased with the progression of the stage of PVD (<em>p</em> = 3.60×10<sup>−6</sup>).</p></div><div><h3>Conclusion</h3><p>During nonpathological PVD, macula is protected from tractional insults conveyed by mobile vitreous due to overlying vitreous liquefaction. However, the vitreoretinal interface anterior to the lacunae experiences tractional forces until vitreoretinal separation occurs. These observations reinforce the hypothesis that vitreous liquefaction, vitreous mobility, and vitreoschisis formation contribute to PVD initiation and support that premacular lacunae protect the macula during PVD initiation and early progression.</p></div>","PeriodicalId":100071,"journal":{"name":"AJO International","volume":"1 2","pages":"Article 100021"},"PeriodicalIF":0.0000,"publicationDate":"2024-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950253524000212/pdfft?md5=8cd23e5d8e2639844b99c1fda0f6bd0c&pid=1-s2.0-S2950253524000212-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Vitreous mobility during the posterior vitreous detachment initiation demonstrated by pseudo-motion optical coherence tomography\",\"authors\":\"Yoko Ito , Yuki Takatsudo , Peter L. 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All stage 1 PVDs presented anterior to the papillomacular vitreous liquefaction. All eyes demonstrated mobility of the vitreous gel at the anterior face of the vitreous liquefaction; however, the adherent cortical vitreous layer comprising the posterior wall of the lacuna showed no mobility. Mobility of the posterior vitreous cortex was not present in eyes with stage 1a PVD and increased with the progression of the stage of PVD (<em>p</em> = 3.60×10<sup>−6</sup>).</p></div><div><h3>Conclusion</h3><p>During nonpathological PVD, macula is protected from tractional insults conveyed by mobile vitreous due to overlying vitreous liquefaction. However, the vitreoretinal interface anterior to the lacunae experiences tractional forces until vitreoretinal separation occurs. 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引用次数: 0
摘要
目的记录早期玻璃体后脱离(PVD)过程中玻璃体视网膜界面发生的解剖学变化。方法在与年龄相关的 PVD 早期阶段,对 27 只正常眼睛进行广角和假动光学相干断层扫描(OCT)检查。静态阶段的广角检查由蒙太奇传统 OCT 图像组成。结果PVD的初期阶段包括后玻璃体皮质和视网膜之间有(1a期)或无(1b期)中间物质的周边PVD,以及向周边扩展的眼周PVD(2期)。所有1期PVD都出现在乳头状玻璃体液化的前方。所有眼球的玻璃体液化前方的玻璃体凝胶都有流动性;但是,构成裂孔后壁的粘附皮质玻璃体层没有流动性。结论在非病理性 PVD 期间,由于上覆玻璃体液化,黄斑可免受移动玻璃体带来的牵引性损伤。然而,裂孔前方的玻璃体视网膜界面会受到牵引力的影响,直至玻璃体视网膜分离。这些观察结果加强了玻璃体液化、玻璃体移动和玻璃体裂孔形成有助于PVD发生的假设,并支持黄斑前腔隙在PVD发生和早期发展过程中保护黄斑的观点。
Vitreous mobility during the posterior vitreous detachment initiation demonstrated by pseudo-motion optical coherence tomography
Purpose
To document the anatomical changes occurring at the vitreoretinal interface during early posterior vitreous detachment (PVD).
Methods
Wide-angle and pseudo-motion optical coherence tomography (OCT) were obtained on 27 normal eyes during the early stages of age-related PVD. The wide-angle examination in a static phase consisted of montaged conventional OCT images. GIF-formatted pseudo-animation was generated with OCT images acquired initially in a static eye state, followed by scans immediately after ocular excursions.
Results
Initial stages of PVD included peripheral PVD with (stage 1a) or without (stage 1b) interposed material between the posterior vitreous cortex and the retina, and perifoveal PVD expanding to the periphery (stage 2). All stage 1 PVDs presented anterior to the papillomacular vitreous liquefaction. All eyes demonstrated mobility of the vitreous gel at the anterior face of the vitreous liquefaction; however, the adherent cortical vitreous layer comprising the posterior wall of the lacuna showed no mobility. Mobility of the posterior vitreous cortex was not present in eyes with stage 1a PVD and increased with the progression of the stage of PVD (p = 3.60×10−6).
Conclusion
During nonpathological PVD, macula is protected from tractional insults conveyed by mobile vitreous due to overlying vitreous liquefaction. However, the vitreoretinal interface anterior to the lacunae experiences tractional forces until vitreoretinal separation occurs. These observations reinforce the hypothesis that vitreous liquefaction, vitreous mobility, and vitreoschisis formation contribute to PVD initiation and support that premacular lacunae protect the macula during PVD initiation and early progression.