Objective To observe the functional and morphological changes of macular after panretinal photocoagulation（PRP）in the patients with diabetic retinopathy（DR）.Methods A total of 57 eyes of 34 patients with DR undergoing PRP were enrolled in this prospective and self-reflection study. Comparatively analyze the changes of the best visual acuity（BCVA）, optical coherence tomography (OCT) and multi-focal electroretinography (mfERG) before PRP,20 days, 3 months and more than 9 months after PRP. Statistical analyses were performed by wilcoxon, chisquare, Dunnett-t, LSD-t tests and spearman related analyses. The changes of macular function and foveal retinal thickness before and after PRP were comparatively analyzed.Results BCVA of all patients reduced at 9 months after PRP（P=0.022）.The amplitude density of mfERG P1 of ring 2 decreased at 20 days after PRP（P=0.039）,then recovered at 3 months and decreased again at 9 months（P=0.014）.The amplitude density of mfERG P1 of ring 3-5 decreased at 20 days,3 months and more than 9 months after PRP（20 days: ring 3: P=0.000,ring 4: P=0.001, ring 5: P=0.000；3 months: ring 3:P=0.000, ring 4: P=0.006, ring 5: P=0.001; more than 9 months: ring 3: P=0.000,ring 4: P=0.000, ring 5: P=0.000）. The amplitude density of mfERG P1 of ring 1 was significantly lower at 9 months after PRP（P=0.050）. The foveal retinal thickness increased at 20 days after PRP(P=0.007), then recovered at 3 months or later. Cystoid macular degeneration was found in 6 eyes(10.5%) at 20 days after PRP.Conclusions After the treatment of PRP, there were some extend reduction of the macular function, a transient increase on foveal retinal thickness. Combined mfERG and OCT can be a comprehensively and objectively assessment of macular function and morphology.
Diabetic vitreopapillary traction syndrome (DVPT) is an important complication of diabetic eye disease, caused by persistent mechanical traction exerted by the vitreous on the optic disc and its surrounding tissues, It can lead to severe consequences such as visual impairment and visual field defects. The core mechanisms involve diabetic vitreous remodeling (including hyperglycemia-induced vitreous liquefaction, abnormal cross-linking, and anomalous posterior vitreous detachment) and the fibrovascular proliferation-traction vicious cycle, both contributing to the initiation and progression. Regarding diagnosis, optical coherence tomography is the cornerstone for visualizing vitreo-papillary anatomical relationships. B-scan ultrasonography is valuable in cases with opaque media. Visual field testing assesses the extent of retinal nerve fiber layer involvement. Fluorescein fundus angiography reveals disruption of the blood-retinal barrier on the optic disc surface. Optical coherence tomography angiography shows promise as a novel tool for early diagnosis and dynamic monitoring by quantifying microvascular abnormalities in the optic disc region. For treatment, conservative observation is suitable for patients with mild symptoms and stable visual function. For those experiencing progressive visual impairment, significant disc edema, or concurrent complications of diabetic retinopathy requiring intervention, active consideration of pars plana vitrectomy is warranted. Future research can focus on neuroprotection and revasrearization strategies, the quantitative relationship between traction intensity and optic nerve injury, and the optimization of individualized treatment strategies based on mechanisms, thereby further improving the diagnosis and treatment level of DVPT.