糖尿病视网膜病变患眼玻璃体视盘牵拉综合征的临床特征、对视功能的影响及玻璃体切割手术的疗效观察
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摘要
目的：观察糖尿病视网膜病变（diabetic retinopathy，DR）患眼中玻璃体视盘牵拉(vitreopapillary traction，VPT)的临床特征、发生机制及对视功能的影响，评估经睫状体扁平部玻璃体切割手术(pars plan vitrectomy，PPV)治疗PDR患眼VPT的效果以指导临床工作者对其诊疗。
方法：38例患者42只眼纳入研究。所有纳入研究的VPT患者分别做以下检查：最佳矫正视力（best-corrected visual acuity，BCVA）、眼压（intraocular pressure，IOP）、裂隙灯前节检查、双目间接检眼镜眼底检查、荧光素眼底血管造影（fundus fluorescein angiography，FFA）、光相干断层扫描（Optical Coherence Tomography，OCT）、视觉诱发电位（Visual evokedpotentials，VEP）及视野检查。分析时，以31例患者的对侧无VPT眼作为对照组，对比分析患眼的图像特征及BCVA、VEP和视野的改变。对符合手术标准的16例VPT患者18只眼行PPV，手术中剥除增殖膜并行全视网膜光凝术（Panretinal photocoagulation，PRP），根据患者情况术后采用气体或者硅油填充，晶状体混浊者同时行超声乳化手术联合PPV。手术后1、3、6个月进行随访，采用手术前相同的仪器设备行相关检查，对比分析手术前后盘沿视网膜厚度、视盘渗漏、BCVA、VEP、视野改变情况。
结果：
1. VPT在间接眼底镜、FFA及OCT下的临床特征：
1.1经散瞳眼底镜检查视盘可表现为：1）.视盘无任何改变2）.视盘区域性边缘不清，轻度隆起，多位于视盘鼻侧及视盘上、下方3）.视盘边界不清，充血隆起。
1.2FFA视盘可表现为：1）视盘无异常荧光2）视盘水肿，表面毛细血管扩张渗漏晚期呈高荧光，可分为限局性水肿、弥漫性水肿3）视盘新生血管（neovascularization of the disc, NVD），早期显影随后荧光素渗漏晚期呈强荧光4）视盘增殖膜，呈遮蔽荧光或荧光着染。
1.3OCT显示所有患者视盘隆起最高点有线性高反射信号附着并伸入玻璃体腔，生理凹陷变窄或消失，可同时合并盘周视网膜浆液性脱离、黄斑水肿或黄斑牵拉移位。
2.结合FFA及OCT将VPT分3类：（1）单纯不全玻璃体后脱离型7只眼，占16.67%（2）不全玻璃体后脱离伴NVD型13只眼，占30.95%（3）视盘增殖膜型22只眼，占52.88%。
3. VPT对视功能的影响：
42只VPT患眼BCVA为0.70±0.38明显低于对照组0.36±0.14（P﹤0.01），其中BCVA<0.1者5只眼，占11.90%；BCVA≥0.1，但<0.3者20只眼，占47.62%；BCVA≥0.3者17只眼，占40.48%。VEP异常率为61.90%，其中5只眼接受F-VEP均显示各波潜伏期均中度延长,37只眼接受P-VEP显示P100潜伏期为(121.90±10.43)ms、振幅为(4.50±2.04)μv，对照组P100潜伏期为(104.00±5.06)ms、振幅为(7.29±3.06)μv，两者相比差异有显著统计学意义（P﹤0.01），VPT患眼P100潜伏期明显延长、振幅明显降低。视野检查显示有生理盲点扩大或视野向心性缩小者26只眼，占61.90%。OCT测量VPT患眼盘沿视网膜厚度为(544.70±183.71)μm与对照组同一位置盘沿视网膜厚度(260.35±43.87)μm明显增厚（P﹤0.01）。
4. PPV的临床疗效：
BCVA由手术前的0.89±0.30提高为手术后6个月时的0.50±0.34，其中BCVA提高者16只眼，占88.89%，BCVA稳定者2只眼，占11.11%。手术前后差异有显著统计学意义（P﹤0.01）。18只患眼中16只眼接受P-VEP，2只眼接受F-VEP。 P-VEP检查P100潜伏期由手术前的（131.90±10.43）ms缩短为手术后6个月（103.53±5.61）ms，振幅由手术前的(3.60±0.94))μv提高到手术后6个月（6.32±2.24）μv，手术前后两者差异均具有显著统计学意义（P﹤0.01）；2只眼F-VEP结果显示各波潜伏期均轻度延长。OCT测量盘沿视网膜厚度手术前为（577±159.67）μm，手术后6个月时为（312.67±65.19）μm，手术后盘沿视网膜厚度明显下降（P﹤0.01）。手术后1、3、6个月BCVA、VEPP100潜伏期、振幅、盘沿视网膜厚度的变化组间进行比较，除3个月与6个月变化无统计意义（P﹥0.05），余差异均有统计学意义（P﹤0.05）；
视野检查手术后生理盲点扩大改善者3只眼，余多数患眼出现视野向心性缩小或视野周边暗点。
手术后所有患者OCT显示手术后视盘牵拉解除，视神经纤维贴附，视盘生理凹陷形态逐渐恢复。FFA显示视盘边界清晰，视盘渗漏消失且未见视盘低荧光。
结论：
1. VPT在PDR中并不少见，FFA和OCT联合应用可确诊VPT的存在，并对其手术疗效进行评估。
2. VPT导致视神经纤维及视盘滋养血管睫状后动脉的正常解剖结构和功能改变而损害视功能。
3. PPV手术能彻底解除视盘的牵拉，使视神经形态恢复及视功能改善，避免长期的VPT导致不可逆的视神经萎缩。
4.虽然VPT存在的时间和强度与视功能损害程度之间的关系仍需进一步的研究，但是主张早期行PPV手术。
Purpose: To observe the clinical characteristics, pathogenesis and effectson visual function of vitreopapillary traction (VPT) in diabetic retinopathy(DR).To evaluate the therapeutic effects of pars plana vitrectomy for VPT inDR.
Methods: A total of38DR patients (44eyes) with VPT were enrolled.All the patients had undergone best-corrected visual acuity (BCVA),slit lampmicroscope,stereoscopic fundus photography,intraocular pressure(IOP),fundus fluorescein angiography (FFA), optical coherence tomography(OCT), visual evoked potentials (VEP) and visual field examination. Thecontralateral eyes without VPT of31patients were selected as the control toanalyze the clinical characteristics of VPT and the effects on visual function.Furthermore, of which16patients (18eyes) who meet the operationrequirements were performed to pars plana vitrectomy （PPV） in thisprospective and self-reflection study. Panretinal photocoagulation (PRP) werecompleted during the operation. According to patient’s conditions, combinedsurgery of anterior and posterior segment and silicon oil tamponade wereundergone. Comparatively analyze the changes in OCT retinal thickness at theedge of optic disc, FFA leakage of optic disc, BCVA, latency and amplitude ofVEP, visual field before PPV，1month,3months and9months after PPV.
Results:
1. The clinical characteristics of VPT:
1.1By the Funduscopy examination, appearances of optic discs are as follows:
1) normal optic discs.2) The mild elevated optic discs with regional blurredmargins, most often located in the nasal side of the optic disc or insuperior,inferior areas.3) The congestion and elevation of optic discs with blurred margins.
1.2According to FFA, findings of optic discs are as follows:1) normalfluorescent.2) Papilloedema with telangiectasia and fluorescein leakage wasdivided into localized edema and diffuse edema, the optic discs showedirregular hyperfluorescence at the late phase.3) Neovascularization of the discfilled early and rapidly,and with local strong fluorescence due to fluorescenceleakage at middle and late stage.4) Proliferative membrance on optic discshowed blocked fluorescence or fluorescence staining.
1.3OCT showed that optic disc swelling and physiological depression narrowor nearly disappearance, and traction of the optic disc by a linear mid-highreflected signal, associated with peripapillary serous retinal detachment,macula oedema or displacement.
2. VPT can be classified into3types based on FFA and OCT images:incomplete posterior vitreous detachment was found in7eyes(16.67%),incomplete posterior vitreous detachment with neovascularization of the disc(DNV) was found in13eyes (30.95%), proliferative membrance on opticdisc was found in22eye (52.88%).
3. The effects on visual function of VPT:
BCVA of42eyes with VTP was (0.70±0.38) lower than that of controlgroup significantly，which was (0.36±0.14)(P﹤0.01). There were5eyes(11.90%) with BCVA<0.1,20eyes (47.62%) with BCVA≥0.1，but<0.3,17eyes(40.48%) with BCVA≥0.3. The abnormal rate of VEP was26/42(61.90%).Among them,5eyes had undergone Flash-VEP which showedpotential time moderate delay and amplitude declination;37eyes hadundergone pattern-VEP which showed that P100latency and amplitudewas(104.00±5.06)ms and (4.50±2.04)μv respectively, and in control groupwas(104.00±5.06)ms and (7.29±3.06)μv respectively, there was significantdifference between the two groups(P﹤0.01). Automated perimetry disclosedenlarged blind spot and/or concentric constriction of the visual field was foundin26eyes (61.90%). OCT showed that retinal thickness at the edge of opticdisc in42eyes with VTP was (544.70±183.71)μm thicker than that of control group significantly，which was (260.35±43.87)μm (P﹤0.01).
4. The therapeutic effects of PPV for VPT:
Among18eyes, BCVA was (0.89±0.30) before surgery and (0.50±0.34)6months after surgery, the difference was statistically significant (P<0.01).BCVA of16eyes (88.89%) increased,2eyes (11.11%) didn’t change. Amongthem,16eyes were performed to pattern-VEP and2eyes were performed toFlash-VEP. Pattern-VEP showed that P100latency and amplitude were(131.90±10.43)ms,(3.60±0.94)μv and (103.53±5.61)ms,(6.32±2.24)μvrespectively before surgery and6months after surgery. The latency andamplitude were improved significantly at6months follow-up compared withthe preoperational result (P<0.01). The retinal thickness at the edge of opticdisc was (577±159.67)μm,(312.67±65.19)μm respectively before surgery and6months after surgery, the retinal thickness was reduced significantlycompared with the preoperational result (P<0.01).The result of BCVA, latencyand amplitude of VEP, retinal thickness at the edge of optic disc hadsignificant change at each time-point before and1,3,6months after surgery,except for between3months and6months.
Visual field examination disclosed the improvement of enlarged blindspot was3eyes after surgery, but most of eyes were occurred concentricconstriction of the visual field and peripheral field scotomas.
OCT showed that traction to optic disc was released in all eyes afteroperation, with recovering of optic nerve fiber and physiological cup ofpapilla. FFA showed that the leakage optic disc with clear margin completelydisappeared and no hypofluorescence at the late phase were observed.
Conclusions:
1. VPT is not rare in proliferative diabetic retinopathy. The combinedapplication of FFA and OCT not only effectively diagnose VPT, but alsoevaluate the therapeutic effects of PPV.
2. VPT can impair visual function by the anatomical and functional changes ofoptic nerve fibres and posterior ciliary arteries.
3. Surgical release of this VPT may improve the anatomical and functional outcome significantly to avoid irreversible optic nerve atrophy.
4. It still remains unclear how duration and intensity of vitreopapillary tractioncontributes to the amount of optic nerve damage. Nevertheless, we advocatethat early vitrectomy should be considered as soon as visual function isreduced.
方法：38例患者42只眼纳入研究。所有纳入研究的VPT患者分别做以下检查：最佳矫正视力（best-corrected visual acuity，BCVA）、眼压（intraocular pressure，IOP）、裂隙灯前节检查、双目间接检眼镜眼底检查、荧光素眼底血管造影（fundus fluorescein angiography，FFA）、光相干断层扫描（Optical Coherence Tomography，OCT）、视觉诱发电位（Visual evokedpotentials，VEP）及视野检查。分析时，以31例患者的对侧无VPT眼作为对照组，对比分析患眼的图像特征及BCVA、VEP和视野的改变。对符合手术标准的16例VPT患者18只眼行PPV，手术中剥除增殖膜并行全视网膜光凝术（Panretinal photocoagulation，PRP），根据患者情况术后采用气体或者硅油填充，晶状体混浊者同时行超声乳化手术联合PPV。手术后1、3、6个月进行随访，采用手术前相同的仪器设备行相关检查，对比分析手术前后盘沿视网膜厚度、视盘渗漏、BCVA、VEP、视野改变情况。
结果：
1. VPT在间接眼底镜、FFA及OCT下的临床特征：
1.1经散瞳眼底镜检查视盘可表现为：1）.视盘无任何改变2）.视盘区域性边缘不清，轻度隆起，多位于视盘鼻侧及视盘上、下方3）.视盘边界不清，充血隆起。
1.2FFA视盘可表现为：1）视盘无异常荧光2）视盘水肿，表面毛细血管扩张渗漏晚期呈高荧光，可分为限局性水肿、弥漫性水肿3）视盘新生血管（neovascularization of the disc, NVD），早期显影随后荧光素渗漏晚期呈强荧光4）视盘增殖膜，呈遮蔽荧光或荧光着染。
1.3OCT显示所有患者视盘隆起最高点有线性高反射信号附着并伸入玻璃体腔，生理凹陷变窄或消失，可同时合并盘周视网膜浆液性脱离、黄斑水肿或黄斑牵拉移位。
2.结合FFA及OCT将VPT分3类：（1）单纯不全玻璃体后脱离型7只眼，占16.67%（2）不全玻璃体后脱离伴NVD型13只眼，占30.95%（3）视盘增殖膜型22只眼，占52.88%。
3. VPT对视功能的影响：
42只VPT患眼BCVA为0.70±0.38明显低于对照组0.36±0.14（P﹤0.01），其中BCVA<0.1者5只眼，占11.90%；BCVA≥0.1，但<0.3者20只眼，占47.62%；BCVA≥0.3者17只眼，占40.48%。VEP异常率为61.90%，其中5只眼接受F-VEP均显示各波潜伏期均中度延长,37只眼接受P-VEP显示P100潜伏期为(121.90±10.43)ms、振幅为(4.50±2.04)μv，对照组P100潜伏期为(104.00±5.06)ms、振幅为(7.29±3.06)μv，两者相比差异有显著统计学意义（P﹤0.01），VPT患眼P100潜伏期明显延长、振幅明显降低。视野检查显示有生理盲点扩大或视野向心性缩小者26只眼，占61.90%。OCT测量VPT患眼盘沿视网膜厚度为(544.70±183.71)μm与对照组同一位置盘沿视网膜厚度(260.35±43.87)μm明显增厚（P﹤0.01）。
4. PPV的临床疗效：
BCVA由手术前的0.89±0.30提高为手术后6个月时的0.50±0.34，其中BCVA提高者16只眼，占88.89%，BCVA稳定者2只眼，占11.11%。手术前后差异有显著统计学意义（P﹤0.01）。18只患眼中16只眼接受P-VEP，2只眼接受F-VEP。 P-VEP检查P100潜伏期由手术前的（131.90±10.43）ms缩短为手术后6个月（103.53±5.61）ms，振幅由手术前的(3.60±0.94))μv提高到手术后6个月（6.32±2.24）μv，手术前后两者差异均具有显著统计学意义（P﹤0.01）；2只眼F-VEP结果显示各波潜伏期均轻度延长。OCT测量盘沿视网膜厚度手术前为（577±159.67）μm，手术后6个月时为（312.67±65.19）μm，手术后盘沿视网膜厚度明显下降（P﹤0.01）。手术后1、3、6个月BCVA、VEPP100潜伏期、振幅、盘沿视网膜厚度的变化组间进行比较，除3个月与6个月变化无统计意义（P﹥0.05），余差异均有统计学意义（P﹤0.05）；
视野检查手术后生理盲点扩大改善者3只眼，余多数患眼出现视野向心性缩小或视野周边暗点。
手术后所有患者OCT显示手术后视盘牵拉解除，视神经纤维贴附，视盘生理凹陷形态逐渐恢复。FFA显示视盘边界清晰，视盘渗漏消失且未见视盘低荧光。
结论：
1. VPT在PDR中并不少见，FFA和OCT联合应用可确诊VPT的存在，并对其手术疗效进行评估。
2. VPT导致视神经纤维及视盘滋养血管睫状后动脉的正常解剖结构和功能改变而损害视功能。
3. PPV手术能彻底解除视盘的牵拉，使视神经形态恢复及视功能改善，避免长期的VPT导致不可逆的视神经萎缩。
4.虽然VPT存在的时间和强度与视功能损害程度之间的关系仍需进一步的研究，但是主张早期行PPV手术。
Purpose: To observe the clinical characteristics, pathogenesis and effectson visual function of vitreopapillary traction (VPT) in diabetic retinopathy(DR).To evaluate the therapeutic effects of pars plana vitrectomy for VPT inDR.
Methods: A total of38DR patients (44eyes) with VPT were enrolled.All the patients had undergone best-corrected visual acuity (BCVA),slit lampmicroscope,stereoscopic fundus photography,intraocular pressure(IOP),fundus fluorescein angiography (FFA), optical coherence tomography(OCT), visual evoked potentials (VEP) and visual field examination. Thecontralateral eyes without VPT of31patients were selected as the control toanalyze the clinical characteristics of VPT and the effects on visual function.Furthermore, of which16patients (18eyes) who meet the operationrequirements were performed to pars plana vitrectomy （PPV） in thisprospective and self-reflection study. Panretinal photocoagulation (PRP) werecompleted during the operation. According to patient’s conditions, combinedsurgery of anterior and posterior segment and silicon oil tamponade wereundergone. Comparatively analyze the changes in OCT retinal thickness at theedge of optic disc, FFA leakage of optic disc, BCVA, latency and amplitude ofVEP, visual field before PPV，1month,3months and9months after PPV.
Results:
1. The clinical characteristics of VPT:
1.1By the Funduscopy examination, appearances of optic discs are as follows:
1) normal optic discs.2) The mild elevated optic discs with regional blurredmargins, most often located in the nasal side of the optic disc or insuperior,inferior areas.3) The congestion and elevation of optic discs with blurred margins.
1.2According to FFA, findings of optic discs are as follows:1) normalfluorescent.2) Papilloedema with telangiectasia and fluorescein leakage wasdivided into localized edema and diffuse edema, the optic discs showedirregular hyperfluorescence at the late phase.3) Neovascularization of the discfilled early and rapidly,and with local strong fluorescence due to fluorescenceleakage at middle and late stage.4) Proliferative membrance on optic discshowed blocked fluorescence or fluorescence staining.
1.3OCT showed that optic disc swelling and physiological depression narrowor nearly disappearance, and traction of the optic disc by a linear mid-highreflected signal, associated with peripapillary serous retinal detachment,macula oedema or displacement.
2. VPT can be classified into3types based on FFA and OCT images:incomplete posterior vitreous detachment was found in7eyes(16.67%),incomplete posterior vitreous detachment with neovascularization of the disc(DNV) was found in13eyes (30.95%), proliferative membrance on opticdisc was found in22eye (52.88%).
3. The effects on visual function of VPT:
BCVA of42eyes with VTP was (0.70±0.38) lower than that of controlgroup significantly，which was (0.36±0.14)(P﹤0.01). There were5eyes(11.90%) with BCVA<0.1,20eyes (47.62%) with BCVA≥0.1，but<0.3,17eyes(40.48%) with BCVA≥0.3. The abnormal rate of VEP was26/42(61.90%).Among them,5eyes had undergone Flash-VEP which showedpotential time moderate delay and amplitude declination;37eyes hadundergone pattern-VEP which showed that P100latency and amplitudewas(104.00±5.06)ms and (4.50±2.04)μv respectively, and in control groupwas(104.00±5.06)ms and (7.29±3.06)μv respectively, there was significantdifference between the two groups(P﹤0.01). Automated perimetry disclosedenlarged blind spot and/or concentric constriction of the visual field was foundin26eyes (61.90%). OCT showed that retinal thickness at the edge of opticdisc in42eyes with VTP was (544.70±183.71)μm thicker than that of control group significantly，which was (260.35±43.87)μm (P﹤0.01).
4. The therapeutic effects of PPV for VPT:
Among18eyes, BCVA was (0.89±0.30) before surgery and (0.50±0.34)6months after surgery, the difference was statistically significant (P<0.01).BCVA of16eyes (88.89%) increased,2eyes (11.11%) didn’t change. Amongthem,16eyes were performed to pattern-VEP and2eyes were performed toFlash-VEP. Pattern-VEP showed that P100latency and amplitude were(131.90±10.43)ms,(3.60±0.94)μv and (103.53±5.61)ms,(6.32±2.24)μvrespectively before surgery and6months after surgery. The latency andamplitude were improved significantly at6months follow-up compared withthe preoperational result (P<0.01). The retinal thickness at the edge of opticdisc was (577±159.67)μm,(312.67±65.19)μm respectively before surgery and6months after surgery, the retinal thickness was reduced significantlycompared with the preoperational result (P<0.01).The result of BCVA, latencyand amplitude of VEP, retinal thickness at the edge of optic disc hadsignificant change at each time-point before and1,3,6months after surgery,except for between3months and6months.
Visual field examination disclosed the improvement of enlarged blindspot was3eyes after surgery, but most of eyes were occurred concentricconstriction of the visual field and peripheral field scotomas.
OCT showed that traction to optic disc was released in all eyes afteroperation, with recovering of optic nerve fiber and physiological cup ofpapilla. FFA showed that the leakage optic disc with clear margin completelydisappeared and no hypofluorescence at the late phase were observed.
Conclusions:
1. VPT is not rare in proliferative diabetic retinopathy. The combinedapplication of FFA and OCT not only effectively diagnose VPT, but alsoevaluate the therapeutic effects of PPV.
2. VPT can impair visual function by the anatomical and functional changes ofoptic nerve fibres and posterior ciliary arteries.
3. Surgical release of this VPT may improve the anatomical and functional outcome significantly to avoid irreversible optic nerve atrophy.
4. It still remains unclear how duration and intensity of vitreopapillary tractioncontributes to the amount of optic nerve damage. Nevertheless, we advocatethat early vitrectomy should be considered as soon as visual function isreduced.
引文
1Kroll P, Wiegand W, Schmidt JC. Traction vitreoretinal opticopathy inproliferative diabetic vitreoretinopathy. Ophthalmologe,1995,92:687-691
2Rumelt S, Karatas M, Pikkel J, et al.Vitreopapillary traction syndromeassociated with central retinal vein occlusion.. Arch Ophthalmol,2003,121:1093-1097
3Carsten H,Meyer,Stefan Mennel, et al. Functional and anatomical resultsof vitreopapillary traction after vitrectomy. Acta OphthalmologicaScandinavica,2007，221-222
4Shannon Cabrera,Allen Katz.Vitreopapillary traction:cost-effectivediagnosis by optical coherence tomography. Can J Ophthalmol,2006,41:763-765
5Burton J. Wisotsky BJ, Carmelina B. Vitreopapillary traction as a causeof elevated optic nerve head. Am J Ophthalmol,1998,126:137-138
6Swanson EA, Izatt JA, Hee MR, et al. Optical coherence tomography.Opt Lett,1993,18:1864-1866
7Puliafito CA, Hee MR, Schuman JS, et al. Diseases of the optic nerve. In:Optical Coherence Tomography of Ocular Diseases. Slack Inc. NewJersey,1996,pp:357-368
8Yoshihiro Saito,Nami Ueki.Transient optic disc edema by vitreous in aquiescent eye with proliferative diabetic retinopathy mimicking diabeticpapillopathy.Br J Ophthalmol,2005,25:83-85
9Katz B, Hoyt WF. Intrapapillary and peripapillary hemorrhage in youngpatients with incomplete posterior vitreous detachment. Signs ofvitreopapillary traction. Ophthalmology,1995,102:349-354
10Sebag J,Buckingham B,Charles MA.Biochemical abnormalities invitreous of humans with proliferative diabetic retinopathy. ArchOphthalmol,1992,110:1472-1479
11Kakehashi A, Schepens CL, de Sousa-Neto A, et al. Biomicroscopicfindings of posterior vitreoschisis. Ophthalmic Surg,1993,24:846-850
12Schwartz SD,Alexander R,Hiscott P,et al. Recognition of vitreoschisis inproliferative diabetic retinopathy. Ophthalmology,1996,103:323-328
13Appen RE, Chandra SR, Klein R, et al. Diabetic papilopathy. Am JOphthalmol,1980,90:203-209
14Kroll P, Wiegand W, Schmidt J. Vitreopapillary traction in proliferativediabetic retinopathy. Br J Ophthalmol,1999,83:261-264
15Regillo CD, Brown GC, Savino PJ, et al. Diabetic papilopathy-patientcharacteristics and fundus findings.Arch Ophthalmol1995;113:889-895
16Antcliff RJ, Marshall J. The pathogenesis of edema in diabeticmaculopathy. Semin Ophthalmol,1999,14:223-232
17Funatsu H, Yamashita H, Ikeda T, et al. Angiotensin II and vascularendothelial growth factor in the vitreous fluid of patients with diabeticmacular edema and other retinal disorders. Am J Ophthalmol,2002,133:537-543
18Funatsu H,Yamashita H, Mona H,et al. Increased levels of vascularendothelial growth factor and interleukin-6in aqueous humor of diabeticwith macular edema. Am J Ophthalmol,2002,133:70-77
19Karatas M, Ramirez JA, Ophir A. Diabetic vitreopapillary traction andmacular edema.Eye,2005,19,676-682
20Pendergast SD, Martin DF,Proia AD,et al. Removal of optic disc stalksduring diabetic vitrectomy. Retina,1995,15:25-28
21Early Treatment Diabetic Retinopathy Study Research Group. Earlyphotocoagulation. For diabetic Retinopathy ETDRS report number9Ophthalmology,1991,98(suppl):766-85
22Shimura M, Yasuda K, Nakazawa T, et al. Quantifying alterations ofmacular thickness before and after panretinal photocoagulation inpatients with severe diabetic retinopathy and good vision.Ophthalmology,2003,110:2386-94
1Bishop PN. Structural macromolecules and supramolecular organizationof the vitreous gel. Prog Retin Eye Res,2000,19:323-344
2Scott JE. The chemical morphology of the vitreous. Eye6:553-555
3Sebag J. Anatomy and pathology of the vitreo-retinal interface. Eye,1992,6:541-552
4Russell SR, Shepherd JD, Hageman GS. Distribution of glycoconjugatesin the human internal limiting membrane. Invest Ophthalmol.VisSci,1991,32:1986-1995
5Sebag J. Anatomy and pathology of the vitreo-retinal interface.Eye,1992,6:541-552
6Scott JE. The chemical morphology of the vitreous. Eye,1992,6:553-555
7Scott JE, Chen Y, Brass A.Secondary and tertiary structures involvingchondroitin and chondroitin sulphate in solution,investigated by rotaryshadowing electron microscopy and computer simulation. Eur JBiochem,1992,209:675-680
8Sebag J. Abnormalities of human vitreous structure in diabetes. GraefesArch Clin Exp Ophthalmol,1993,231:257-260
9Sebag J, Ansari RR, Dunker S, Suh KI. Dynamic light scattering ofdiabetic vitreopathy. Diabetes Technol Ther,1999,1:169-76
10Tomι CC, De Rojas Silva MV, Rodrνguez-Garcνa J. Levels ofpentosidine in vitreous of eyes with proliferative diabetic retinopathy,proliferative vitreoretinopathy and retinal detachment. Graefes ArchClin Exp Ophthalmol,2005,243:1272-6
11Kakehashi A, Kado M, Akiba J. Variations of Posterior vitreousdetachment. Br J Ophthalmol,1997,81(7):527-32
12Kang SW, Hyung SM, Choimy, et al. Induction of vitreolysis andvitreous detachment w ith hyaluronidase and perfluo rop ropane gas.Korean J Ophthalmol,1995,9:69-78
13Tolentino FI et al. Vitreoretinal disorders. Diagnosis and Management.Philadecphia: WB. Saunders,1976,130
14Takahashi M et al. Arch Ophthalmol,1980,98:665
15聂爱光,主编.现代黄斑疾病诊断治疗学.北京:北京医科大学中国协和医科大学联合出版社,1996.334-3411
16Schepens. Clinical aspects of pathologic changes in the vitreous body.Am J Ophthalmol,1954,38(1:2):8-21
17Kroll P, Wiegand W, Schmidt JC. Traction vitreoretinal opticopathy inproliferative diabetic vitreoretinopathy. Ophthalmologe,1995,92:687-691
18Rumelt S, Karatas M, Pikkel J, et al.Vitreopapillary traction syndromeassociated with central retinal vein occlusion.. Arch Ophthalmol,2003,121:1093-1097
19Carsten H,Meyer,Stefan Mennel, et al. Functional and anatomicalresults of vitreopapillary traction after vitrectomy. ActaOphthalmologica Scandinavica2007;221-222
20Kroll P, Wiegand W, Schmidt J. Vitreopapillary traction in proliferativediabetic retinopathy. Br J Ophthalmol,1999,83:261-264
21Kakehashi A et al.Retinal breaks in diabetic retinopathy:vitreoretinalrelationships. Ophthalmic Surg,1994,25(10):695
22Gass J.Stereoscopic atlas of macular diseases diagnosis and treatment. St.Louis Mosby,1997,pp904-51
23KakehashiA, Schepens CL, Akba J, et al. Spontaneous resolution offoveal detachments and macular breadk s. Am J Ophthalmol,1995,120:767-775
24Ebatok K. Spontaneous closure of macular hole after posterior vitreousdetachment. Ophthalmic Surg Lasers,2000,31(3):245
25Johnson MW et al. Perifoveal vitreous detachment is the primarypathogenic event in idiopathic macular hole formation. ArchOphthalmol,2001,119:215
26McDonald WE,Michels RG. Vitrectomy for macular tractionncaused byincompleted vitreous separation. Arch Ophthalmol,1998;106:624-628
27Koerner F, Garweg J. Vitrectomy formacular pucker and vitreomaculartraction syndrome. Doc Ophthalmol,1999;97(32)4:449-457
28Bovino JA. Macular Surgery. Norwalk Appleton,1994;107-119
2Rumelt S, Karatas M, Pikkel J, et al.Vitreopapillary traction syndromeassociated with central retinal vein occlusion.. Arch Ophthalmol,2003,121:1093-1097
3Carsten H,Meyer,Stefan Mennel, et al. Functional and anatomical resultsof vitreopapillary traction after vitrectomy. Acta OphthalmologicaScandinavica,2007，221-222
4Shannon Cabrera,Allen Katz.Vitreopapillary traction:cost-effectivediagnosis by optical coherence tomography. Can J Ophthalmol,2006,41:763-765
5Burton J. Wisotsky BJ, Carmelina B. Vitreopapillary traction as a causeof elevated optic nerve head. Am J Ophthalmol,1998,126:137-138
6Swanson EA, Izatt JA, Hee MR, et al. Optical coherence tomography.Opt Lett,1993,18:1864-1866
7Puliafito CA, Hee MR, Schuman JS, et al. Diseases of the optic nerve. In:Optical Coherence Tomography of Ocular Diseases. Slack Inc. NewJersey,1996,pp:357-368
8Yoshihiro Saito,Nami Ueki.Transient optic disc edema by vitreous in aquiescent eye with proliferative diabetic retinopathy mimicking diabeticpapillopathy.Br J Ophthalmol,2005,25:83-85
9Katz B, Hoyt WF. Intrapapillary and peripapillary hemorrhage in youngpatients with incomplete posterior vitreous detachment. Signs ofvitreopapillary traction. Ophthalmology,1995,102:349-354
10Sebag J,Buckingham B,Charles MA.Biochemical abnormalities invitreous of humans with proliferative diabetic retinopathy. ArchOphthalmol,1992,110:1472-1479
11Kakehashi A, Schepens CL, de Sousa-Neto A, et al. Biomicroscopicfindings of posterior vitreoschisis. Ophthalmic Surg,1993,24:846-850
12Schwartz SD,Alexander R,Hiscott P,et al. Recognition of vitreoschisis inproliferative diabetic retinopathy. Ophthalmology,1996,103:323-328
13Appen RE, Chandra SR, Klein R, et al. Diabetic papilopathy. Am JOphthalmol,1980,90:203-209
14Kroll P, Wiegand W, Schmidt J. Vitreopapillary traction in proliferativediabetic retinopathy. Br J Ophthalmol,1999,83:261-264
15Regillo CD, Brown GC, Savino PJ, et al. Diabetic papilopathy-patientcharacteristics and fundus findings.Arch Ophthalmol1995;113:889-895
16Antcliff RJ, Marshall J. The pathogenesis of edema in diabeticmaculopathy. Semin Ophthalmol,1999,14:223-232
17Funatsu H, Yamashita H, Ikeda T, et al. Angiotensin II and vascularendothelial growth factor in the vitreous fluid of patients with diabeticmacular edema and other retinal disorders. Am J Ophthalmol,2002,133:537-543
18Funatsu H,Yamashita H, Mona H,et al. Increased levels of vascularendothelial growth factor and interleukin-6in aqueous humor of diabeticwith macular edema. Am J Ophthalmol,2002,133:70-77
19Karatas M, Ramirez JA, Ophir A. Diabetic vitreopapillary traction andmacular edema.Eye,2005,19,676-682
20Pendergast SD, Martin DF,Proia AD,et al. Removal of optic disc stalksduring diabetic vitrectomy. Retina,1995,15:25-28
21Early Treatment Diabetic Retinopathy Study Research Group. Earlyphotocoagulation. For diabetic Retinopathy ETDRS report number9Ophthalmology,1991,98(suppl):766-85
22Shimura M, Yasuda K, Nakazawa T, et al. Quantifying alterations ofmacular thickness before and after panretinal photocoagulation inpatients with severe diabetic retinopathy and good vision.Ophthalmology,2003,110:2386-94
1Bishop PN. Structural macromolecules and supramolecular organizationof the vitreous gel. Prog Retin Eye Res,2000,19:323-344
2Scott JE. The chemical morphology of the vitreous. Eye6:553-555
3Sebag J. Anatomy and pathology of the vitreo-retinal interface. Eye,1992,6:541-552
4Russell SR, Shepherd JD, Hageman GS. Distribution of glycoconjugatesin the human internal limiting membrane. Invest Ophthalmol.VisSci,1991,32:1986-1995
5Sebag J. Anatomy and pathology of the vitreo-retinal interface.Eye,1992,6:541-552
6Scott JE. The chemical morphology of the vitreous. Eye,1992,6:553-555
7Scott JE, Chen Y, Brass A.Secondary and tertiary structures involvingchondroitin and chondroitin sulphate in solution,investigated by rotaryshadowing electron microscopy and computer simulation. Eur JBiochem,1992,209:675-680
8Sebag J. Abnormalities of human vitreous structure in diabetes. GraefesArch Clin Exp Ophthalmol,1993,231:257-260
9Sebag J, Ansari RR, Dunker S, Suh KI. Dynamic light scattering ofdiabetic vitreopathy. Diabetes Technol Ther,1999,1:169-76
10Tomι CC, De Rojas Silva MV, Rodrνguez-Garcνa J. Levels ofpentosidine in vitreous of eyes with proliferative diabetic retinopathy,proliferative vitreoretinopathy and retinal detachment. Graefes ArchClin Exp Ophthalmol,2005,243:1272-6
11Kakehashi A, Kado M, Akiba J. Variations of Posterior vitreousdetachment. Br J Ophthalmol,1997,81(7):527-32
12Kang SW, Hyung SM, Choimy, et al. Induction of vitreolysis andvitreous detachment w ith hyaluronidase and perfluo rop ropane gas.Korean J Ophthalmol,1995,9:69-78
13Tolentino FI et al. Vitreoretinal disorders. Diagnosis and Management.Philadecphia: WB. Saunders,1976,130
14Takahashi M et al. Arch Ophthalmol,1980,98:665
15聂爱光,主编.现代黄斑疾病诊断治疗学.北京:北京医科大学中国协和医科大学联合出版社,1996.334-3411
16Schepens. Clinical aspects of pathologic changes in the vitreous body.Am J Ophthalmol,1954,38(1:2):8-21
17Kroll P, Wiegand W, Schmidt JC. Traction vitreoretinal opticopathy inproliferative diabetic vitreoretinopathy. Ophthalmologe,1995,92:687-691
18Rumelt S, Karatas M, Pikkel J, et al.Vitreopapillary traction syndromeassociated with central retinal vein occlusion.. Arch Ophthalmol,2003,121:1093-1097
19Carsten H,Meyer,Stefan Mennel, et al. Functional and anatomicalresults of vitreopapillary traction after vitrectomy. ActaOphthalmologica Scandinavica2007;221-222
20Kroll P, Wiegand W, Schmidt J. Vitreopapillary traction in proliferativediabetic retinopathy. Br J Ophthalmol,1999,83:261-264
21Kakehashi A et al.Retinal breaks in diabetic retinopathy:vitreoretinalrelationships. Ophthalmic Surg,1994,25(10):695
22Gass J.Stereoscopic atlas of macular diseases diagnosis and treatment. St.Louis Mosby,1997,pp904-51
23KakehashiA, Schepens CL, Akba J, et al. Spontaneous resolution offoveal detachments and macular breadk s. Am J Ophthalmol,1995,120:767-775
24Ebatok K. Spontaneous closure of macular hole after posterior vitreousdetachment. Ophthalmic Surg Lasers,2000,31(3):245
25Johnson MW et al. Perifoveal vitreous detachment is the primarypathogenic event in idiopathic macular hole formation. ArchOphthalmol,2001,119:215
26McDonald WE,Michels RG. Vitrectomy for macular tractionncaused byincompleted vitreous separation. Arch Ophthalmol,1998;106:624-628
27Koerner F, Garweg J. Vitrectomy formacular pucker and vitreomaculartraction syndrome. Doc Ophthalmol,1999;97(32)4:449-457
28Bovino JA. Macular Surgery. Norwalk Appleton,1994;107-119