Comparison of the SITA Faster-a new visual field strategy with SITA Fast strategy.

AIM: To compare visual field defects using the Swedish Interactive Thresholding Algorithm (SITA) Fast strategy with SITA Faster strategy, a newly developed time-saving threshold visual field strategy. METHODS: Ninety-three participants (60 glaucoma patients and 33 normal controls) were enrolled. One eye from each participant was selected randomly for the study. SITA Fast and SITA Faster were performed using the 24-2 default mode for each test. The differences of visual field defects between the two strategies were compared using the test duration, false-positive response errors, mean deviation (MD), visual field index (VFI) and the numbers of depressed test points at the significant levels of P<5%, <2%, <1%, and <0.5% in probability plots. The correlation between strategies was analyzed. The agreement between strategies was acquired by Bland-Altman analysis. RESULTS: Mean test durations were 246.0±60.9s for SITA Fast, and 156.3±46.3s for SITA Faster (P<0.001). The test duration of SITA Faster was 36.5% shorter than SITA Fast. The MD, VFI and numbers of depressed points at P<5%, <2%, <1%, and <0.5% in probability plots showed no statistically significant difference between two strategies (P>0.05). Correlation analysis showed a high correlation for MD (r=0.986, P<0.001) and VFI (r=0.986, P<0.001) between the two strategies. Bland-Altman analysis showed great agreement between the two strategies. CONCLUSION: SITA Faster, which saves considerable test time, has a great test quality comparing to SITA Fast, but may be not directly interchangeable.

Viscocanalostomy combined with trabeculotomy and mitomycin C in the treatment of primary congenital glaucoma.

AIM: To evaluate the long-term outcome of viscocanalostomy combined with trabeculotomy and mitomycin C in the treatment of primary congenital glaucoma. METHODS: This is a retrospective study. Forty-two eyes of 26 patients with primary congenital glaucoma were enrolled. Intraocular pressure (IOP), corneal diameter (mm) and cup/disc (C/D) were measured before and after the surgery respectively. Follow-up period was 30mo. RESULTS: The mean preoperative IOP was 30.6±7.35 mm Hg. Of the 42 eyes, 2 eyes were required conversion to trabeculectomy for the absence of Schlemm's canal. Of remained 40 eyes, 38 eyes (95%) achieved successful IOP control. The average postoperative IOP was 11.69±4.18 mm Hg at 12mo. The mean reduction was 18.91 mm Hg (P<0.0001). Eighteen (75%) eyes presented a reduction in corneal diameter, and 25 (62.5%) eyes presented a C/D ratio reversal after the surgery. There was no serious complication in any patients over the follow-up period. CONCLUSION: Viscocanalostomy combined with trabeculotomy and mitomycin C is useful in the management of primary congenital glaucoma.

[The effect of AQP4 knock out on retinal electrophysiology in laser-induced ocular hypertension mice].

OBJECTIVE: To investigate the effect of aquaporin 4 (AQP4) knock out (KO) on the dysfunction of retinal ganglion cells (RGC) in laser-induced ocular hypertension (OHT) mice. METHODS: Experimental study. AQP4 KO mice (n = 18, 36 eyes) and wide type (WT) mice (n = 18, 36 eyes) were used. Unilateral OHT was induced by laser photocoagulation in KO and WT mice after anesthesia. A simultaneous recording of PERG was performed by homemade electrodes. Intraocular pressure (IOP) was measured with an IcareLAB rebound tonometer every day at noon before and after surgery. The data was analysed by ANOVA and t test. RESULTS: In AQP4 KO mice, the mean P50 and P95 amplitudes were significantly (P < 0.01) reduced compared with WT mice [P50: KO: (5.53 ± 1.31) vs WT: (8.14 ± 1.24) µv t = 5.70 and P95: KO: (7.71 ± 1.89) vs WT: (11.30 ± 2.61) µv, t = 3.83, respectively]. The latencies of AQP4 KO mice in both P50 and N95 were shorter than those of WT (t = 5.70 and t = 3.83 respectively, P < 0.01). The mean IOP was significantly (P < 0.05) increased after photocoagulation in AQP4 KO and WT mice compared with pre-photocoagulation [KO post: (14.78 ± 1.80) mm Hg(1 mm Hg = 0.133 kPa) vs KO pre-photocoagulation: (6.61 ± 0.90) mm Hg and WT post: (16.44 ± 1.46) mm Hg vs WT pre-photocoagulation: (7.31 ± 0.98) mm Hg, respectively] with animals under general anesthesia. IOP was lowered mildly but significantly in KO mice when compare with WT mice (t = 3.09, P < 0.05) lasting seven days. IOP was gradually decreased to baseline values at day eight in both of KO and WT mice. CONCLUSIONS: Our results indicate that AQP4 null may damage retinal function that can be detected by the measurement of PEGR, a sensitive parameter to reflect the function of RGC.

[The effect of AQP4 gene on the activation of retinal glial cells in chronic high intraocular pressure mice].

OBJECTIVES: To investigate whether aquaporin 4 (AQP4) gene can affect the activation of glial cells and cause the injury of retina of chronic high intraocular pressure mice models, and to discuss its possible mechanism. METHODS: Experimental study. The chronic high intraocular pressure models were established by burning the scleral venous of the right eye, which as the experiment group, and the left eye without any treatment as the control group. The intraocular pressure (IOP) was measured by rebound tonometer. Selected each of the successful model of chronic high intraocular pressure male AQP4 knockout mice (AQP-/-) and their wild-type (WT) male mice 40, divided the two type of mice into five groups after scleral venous burn according to the time of establishing models (24 h, 3 d, 1 w, 2 w, 4 w after scleral venous burn), 8 mouse in each group. And then producing the paraffin sections of mouse eye. Immunohistochemical staining methods was used to observe the expression of the glial fibrillary acid protein (GFAP) in retina glial cells, and observe the expression of the AQP4 in the retina of the WT mouse. Image was acquired under the fluorescence microscopy. The intraocular pressure was analyzed by t-test. RESULTS: After scleral venous burn (24 h, 3 d, 1 w, 2 w, 4 w), there were significant difference (t = 6.66 - 18.08, all P value < 0.05) in the IOP of the AQP4-/- mice (11.30 ± 1.59, 11.20 ± 1.15, 10.60 ± 1.53, 10.75 ± 1.45, 10.45 ± 1.39) and WT mice (11.50 ± 2.56, 11.25 ± 1.65, 10.75 ± 1.33, 10.60 ± 1.33, 10.40 ± 1.19) between the experimental groups and control groups (6.60 ± 0.94, 6.35 ± 0.99, 6.55 ± 0.94, 6.45 ± 0.99, 6.50 ± 0.94 and 6.60 ± 1.05, 6.50 ± 0.89, 6.40 ± 1.09, 6.30 ± 1.13, 6.50 ± 1.05). Since 24 hours after the scleral venous burn, the expression of GAFP of the two type mice began to increase and reached to peak at 1 week after burning. This peak of WT mice was more obvious than that of AQP4-/- mice. The concentration of GAFP began to decrease at 2 weeks after burning and reached to bottom at 4 weeks later. To the WT mice, the expression of AQP4 was remarkable higher in experimental group than that in control group at 1 week after the scleral venous burn. The expression of AQP4 was related to the expression of GAFP in high intraocular pressure of WT mice at 1 w, 2 w, and 4 w after the scleral venous burn. CONCLUSIONS: The chronic high intraocular pressure models can be established successfully by burning the scleral venous. AQP4 gene can affect the activation of the glial cells in chronic high intraocular pressure mice and lead to the injury of retina.