Pulsatile ocular blood flow in primary open-angle glaucoma and ocular hypertension

PURPOSE: To compare pulsatile ocular blood flow measurements in untreated ocular hypertensive (OHT) subjects and primary open-angle glaucoma (POAG) patients. DESIGN: A prospective observational study in an institutional setting. METHODS: A total of 97 subjects were recruited to the study (50 ocular hypertensives, 24 glaucoma patients, and 23 normal subjects). "High-risk" OHT had intraocular pressure (IOP) > 25 mm Hg; "low-risk" OHT had IOP 相似文献   

Electro-oculogram changes in patients with ocular hypertension and primary open-angle glaucoma

Recent evidence suggests that retinal hypoxia and ischemia affect the standing potential of the eye and the activity of the photoreceptors. To test whether chronically elevated intraocular pressure would produce similar effects, we measured electro-oculograms in two groups of patients: ocular hypertensive patients and patients with primary open-angle glaucoma. There were significant differences among the average electro-oculogram ratios of these groups compared to age-similar controls. The control observers had an average light-peak/dark-trough ratio of 2.86, the ocular hypertensive patients had an average ratio of 2.44, and the patients with primary open-angle glaucoma had an average ratio of 2.07. This indicates that long-term elevations in intraocular pressure can decrease the light peak of the electrooculogram, even in patients with no other evidence of glaucomatous damage. This deficit may have its origins in the sensitivity of the outer retina to choroidal ischemia.     

Condition of ocular blood supply in patients with primary open-angle glaucoma with normal pressure

The condition of discharge of intraocular fluid (IOF), the value of systemic arterial pressure (AP), the condition of mean dynamic arterial pressure in the ocular artery (Pm.ophth.) an the perfusion ocular pressure (Pperf.) were examined in patients with normal pressure glaucoma (NPG). A decrease in the IOF discharge from 0.16 +/- 0.02 cu mm per 1 mm Hg at the NPG initial stage to 0.11 +/- 0.01 cu mm per 1 mm Hg at the NPG deteriorated stage was established. The value of decrease of the systemic AP within an interval of 100 to 116 mm Hg is observed in patients with NPG by 6.9 times more often as compared to the controls (in 42.2% and 6.1% of cases, respectively). A reliable reduction of Pm.ophth. by 4.0 mm Hg and of Pperf.--by 4.9 mm Hg was found in patients with NPG as compared with Pm.ophth. and Pperf. in the controls with the same systemic AP values; the deficit of the ocular volumetric blood flow reached 10.9%. The treatment of NPG patients must be related with improving the IOF discharge, with reducing the genuine intraocular pressure (Po) to a tolerable level, and with increasing the systemic AP, Pm.ophth. and Pperf. to the mean statistically normal level.     

Short-term variability of systemic blood pressure and submacular choroidal blood flow in eyes of patients with primary open-angle glaucoma

Purpose  

To analyse short-term variability of systemic blood pressure and choroidal blood flow in glaucoma patients, and compare them with ocular hypertensive patients and controls.     

原发性开角型青光眼眼部血流动力学以及高血压对其的影响

目的　探讨原发性开角型青光眼眼部血流动力学以及高血压对其的影响。方法　研究对象为我院确诊的原发性开角型青光眼患者 4 9例 4 9眼 ,其中 19例有全身高血压病史。根据是否合并高血压分为 2组 ,应用彩色多普勒成像技术检测眼动脉 (OA)、视网膜中央动脉 (CRA)和后短睫状动脉 (SPCA)的血流动力学指标 ,取年龄相匹配的正常人 18例作为对照组。结果　青光眼患者的CRA及SPCA的收缩期峰值流速 (PSV) ,分别为 (7.6 4cm·s-1± 2 .6 0cm·s-1,9 2 1cm·s-1± 1.16cm·s-1)、舒张期血流速度 (EDV )(2 .0 4cm·s-1± 0 .95cm·s-1,2 .98cm·s-1± 0 .88cm·s-1)及平均流速 (MV) (3.87cm·s-1± 1 34cm·s-1,4 92cm·s-1±1 12cm·s-1)均低于正常对照组 ,阻力指数 (RI) (均为 0 70±0 0 6 )明显高于正常对照组。合并高血压的青光眼患者CRA及SPCA的PSV(9 4 5cm·s-1± 2 38cm·s-1,10 2 3cm·s-1±1 2 5cm·s-1)、EDV(3 0 8cm·s-1± 1 12cm·s-1,3 5 2cm·s-1± 1 10cm·s-1)和MV (4 92cm·s-1± 1 5 2cm·s-1,5 5 4cm·s-1± 1 2 6cm·s-1)明显高于非高血压的青光眼患者。结论　青光眼患者的球后血管的血流速度明显下降 ;无高血压的青光眼患者的血流速度低于合并全身高血压的青光眼患者。     

Impaired ocular blood flow regulation in patients with open-angle glaucoma and diabetes

Background: To elucidate the potential impact of diabetes mellitus on primary open‐angle glaucoma pathology through vascular deficiency. Design: Cross‐section analysis from a longitudinal, prospective study. Participants: Eighty‐four open‐angle glaucoma patients (20 diabetic open‐angle glaucoma patients and 64 non‐diabetic open‐angle glaucoma patients) Methods: Patients were analyzed for ocular structure, ocular perfusion pressure (OPP), retrobulbar blood flow and retinal capillary perfusion. Statistical analysis was performed by SPSS version 18.0. Comparisons between groups were made as well as multivariate linear regression analysis. Main Outcome Measure: Retrobulbar blood flow and the retinal microcirculation. Results: Central retinal artery peak systolic velocity was 13.5% lower in diabetic patients (P = 0.007). In diabetic open‐angle glaucoma patients, ocular perfusion pressure positively correlated with central retinal artery and temporal posterior ciliary artery peak systolic velocity (R = 0.476, P = 0.039 and R = 0.529, P = 0.02, respectively), and with central retinal artery and nasal posterior ciliary artery resistance index (R = 0.537, P = 0.018 and R = 0.566, P = 0.012 respectively). Average retinal nerve fibre layer positively correlated with central retinal artery peak systolic velocity and temporal posterior ciliary artery end diastolic velocity (R = 0.501, P = 0.029 and R = 0.553, P = 0.019, respectively), and negatively correlated with superior and inferior retinal avascular space in the diabetic group (R = ?0.498, P = 0.030 and R = ?0.700, P = 0.001, respectively); no correlations were found in the non‐diabetic group. Negative correlations between retrobulbar and retinal circulations were only found in the diabetic open‐angle glaucoma patients, whereas positive correlations between retinal flow and non‐flow were only found in non‐diabetic open‐angle glaucoma patients. Conclusion: Diabetes may interfere with normal vascular regulation and contribute to glaucoma progression.     

Electrophysiological and psychophysical flicker sensitivity in patients with primary open-angle glaucoma and ocular hypertension

Temporal sensitivity was assessed in patients with primary open-angle glaucoma (POAG) and ocular hypertension (OHT). Three measures of flicker sensitivity were obtained: psychophysical modulation thresholds, visual-evoked potentials (VEPs), and focal electroretinograms (FERGs). We found elevated psychophysical thresholds at higher temporal frequencies (30-50 Hz) in patients with POAG, relative to thresholds for age-matched controls. The OHT patients had elevated psychophysical thresholds only at 50 Hz. On the other hand, VEP amplitudes in POAG patients were reduced at all temporal frequencies, with the magnitude of the loss increasing with temporal frequency. The OHT patients, however, showed no reductions in VEP amplitude at any temporal frequency. Finally, POAG patients' FERG amplitudes were reduced at 30-50 Hz; whereas FERG amplitudes in the OHT patients were normal at all temporal frequencies. These results indicate that OHT patients can exhibit psychophysical threshold losses at high temporal frequencies which are not observed in the suprathreshold electrophysiological amplitude measures. On the other hand, patients with POAG show both psychophysical and VEP losses across a range of temporal frequencies. In addition, the decreases in FERG amplitudes in POAG patients suggest changes in the functioning of the outer retina in this disease.     

拉坦前列腺素与噻吗心安治疗原发性开角型青光眼和高眼压症对照研究

目的　以噻吗心安为对照,评估新型异丙酯前列腺素Ｆ２α的苯基替代衍生物拉坦前列腺素（ＰｈＸＡ４１）对于眼压升高病人的降眼压疗效和副作用。方法　３４ 例（６６ 只眼） 原发性开角型青光眼或高眼压症患者入选,随机分组,１７ 例（３２ 只眼）滴用０．０５ｇ·Ｌ－１ 拉坦前列腺素每天１ 次,１７ 例（３４ 只眼）滴用５ｇ·Ｌ－１ 噻吗心安每天２ 次,共治疗１２ｗｋ。结果　１２ｗｋ治疗期间,两种药物均能有效降低眼压（Ｐ＜ ０－０１） ,且效应持续。各次随访均显示,拉坦前腺素的降眼压效果显著优于噻吗心安（Ｐ＜ ０－０５）。１２ｍｏ 时,拉坦前列腺素组的眼压降低了９－５±３－１ｍ ｍＨｇ（３６－８ ％）（１ｍ ｍＨｇ＝ ０．１３３ｋＰａ） ,噻吗心安组降低了７－４±２－６ｍ ｍＨｇ（２９－６％ ）（ Ｐ＜ ０－０１）。拉坦前列腺素治疗后,少数病例发现角膜上皮点状脱落。噻吗心安组的平均心率减少４ 次·ｍｉｎ－１（Ｐ＜ ０－０５） 。结论　０ ．０５ｇ·Ｌ－１ 拉坦前列腺素每天１ 次与５ｇ·Ｌ－１ 噻吗心安每天２ 次相比,具有更强的降眼压作用,而且耐受性良好。因此,拉坦前列腺素将成为青光眼药物治疗的有效选择。     

Finger blood flow in patients with low tension glaucoma and primary open-angle glaucoma.

Finger blood flow was studied by means of laser Doppler flowmetry in 12 patients with low tension glaucoma (LTG), 12 patients with primary open-angle glaucoma (POAG) and 12 normal subjects. Baseline flow, flow after immersion of the hand in warm water (+40 degrees C), and flow after exposure of the hand in cold water (+4 degrees C) were measured. Statistically significant differences were not found in each flow between the three groups of the patients (p greater than 0.05). Vasospastic response to warm and cold water was observed in 25% of LTG patients, 17% of POAG patients, and 25% of normal subjects. There was no significant difference between LTG, POAG, and normal subjects in finger blood flow.     

高眼压症及原发性开角型青光眼患者的24 h眼压波动规律

目的 通过24 h眼压测量来深入分析对比高眼压症与原发性开角型青光眼(POAG)患者的眼压曲线特征。方法 收集2016年1月~2019年3月在我科门诊诊断为高眼压症的患者52例(104眼)及POAG尚未接受降眼压治疗的患者38例(76眼)。入院后行24 h眼压检查,用非接触性眼压计从早9时起每隔2 h测量眼压1次,至次日7时结束。分析2组患者的平均眼压,峰值眼压及时间点,谷值眼压及时间点,昼夜眼压波动及双眼眼压压差值及其分布情况,比较2组眼压波动的异同点。结果 104眼高眼压症患者的平均眼压为(18.73±1.71)mmHg(1 mmHg=0.133 kPa),平均峰值眼压为(22.36±2.40) mmHg,平均谷值眼压为(15.63±2.09) mmHg,平均昼夜眼压波动为(6.72±2.24) mmHg。76眼POAG患者的平均眼压为(20.65±2.53) mmHg,平均峰值眼压为(25.78±2.81) mmHg,平均谷值眼压为(17.45±2.54) mmHg,平均昼夜眼压波动为(8.34±2.37) mmHg。2组的峰值及谷值眼压值分布最多的时间点均为凌晨3时及夜晚21时,大部分患者的峰值眼压时间点在门诊时间之外。高眼压症组中昼夜眼压波动位于5~8 mmHg的占比最大,为54.81%(57/104),POAG组中昼夜眼压波动>8 mmHg的占比最大,为53.95%(41/76)。高眼压症组中,16例患者经24 h眼压检查后监测到眼压波动异常,占比为30.77%(16/52);POAG组中经24 h眼压检查后有29例患者可以监测到眼压波动异常,占比为76.32%(29/38)。结论 24 h眼压监测中,POAG患者较高眼压症患者的平均眼压、峰值眼压、谷值眼压、昼夜眼压波动及双眼压差均有增加。对于24 h眼压发现眼压波动较大的高眼压症患者应在后续加强密切随访,而对于POAG患者24 h眼压监测可在治疗前提供眼压的基线水平,为后续治疗提供参考及评估依据,因此建议将24 h眼压作为高眼压症及POAG的常规检查手段。     

Effects of betaxolol and latanoprost on ocular blood flow and visual fields in patients with primary open-angle glaucoma

PURPOSE: To evaluate the effects of betaxolol and latanoprost on ocular blood flow and visual fields in patients with primary open-angle glaucoma (POAG) by means of an observer-masked, prospective clinical study. METHODS: Thirty-two patients with newly diagnosed POAG were included in the study. The patients were randomized into two groups. The first group was treated with betaxolol 0.50% twice daily and the second group with latanoprost 0.005% once daily. Baseline and posttreatment examinations on the first and third months of treatment included intraocular pressure (IOP) measurement, automated visual field testing, and ocular blood flow assessment. For evaluation of visual fields, mean defect and pattern standard deviation indices were used. Ocular blood flow was assessed by means of color Doppler imaging of the central retinal artery (CRA) and the temporal short posterior ciliary artery (PCA). For each vessel, peak systolic (PSV) and end-diastolic (EDV) blood flow velocities were measured and resistivity index (RI) calculated. RESULTS: After exclusion of one noncompliant patient, the study was completed with 31 eyes of 31 patients. Both drugs significantly reduced IOP (p<0.05). The mean IOP lowering effect of latanoprost was significantly higher than that of betaxolol (p=0.03). Visual field indices exhibited no significant changes in either group (p>0.05). There were no significant changes in PSV or EDV measurements of CRA or PCA in either group (p>0.05). RI decreased in both CRA and PCA with both drugs. The mean changes between baseline and 3 month blood flow measurements were not significantly different between betaxolol and latanoprost (p>0.05). CONCLUSIONS: Over a treatment period of 3 months, both betaxolol and latanoprost tended to improve ocular blood flow without one of them being superior to the other. The results suggest that the direct (non IOP-dependent) influence on ocular circulation is better for betaxolol than for latanoprost. In addition, neither drug caused significant generalized improvements in visual fields during this period.     

Minimum concentration of levobunolol required to control intraocular pressure in patients with primary open-angle glaucoma or ocular hypertension

In a double-masked, randomized, comparison titration study to determine the effective dose of topically applied levobunolol, three concentrations of levobunolol (0.25%, 0.5%, and 1%) and of timolol (0.125%, 0.25%, and 0.5%) were evaluated in patients with mild open-angle glaucoma or ocular hypertension. Following a washout of ocular hypotensive medication, twice-daily treatment in both eyes was initiated with the lowest of the three doses of either drug. The concentration was increased if intraocular pressure remained uncontrolled. Intraocular pressure was controlled in 63% (15 of 24) of the patients tested with the lowest concentration of levobunolol and 69% (18 of 26) with the lowest concentration of timolol. Overall, 75% (18 of 24) of the patients in the levobunolol group and 73% (19 of 26) of the patients in the timolol group had adequately controlled intraocular pressure. At the lowest concentrations tested, mean decreases from baseline in intraocular pressure ranged from 6 to 8 mm Hg in both treatment groups.     

Refractive change after dorzolamide use in patients with primary open-angle glaucoma and ocular hypertension.

The purpose of this study was to evaluate refractive and anterior chamber depth changes after short-term dorzolamide use in patients with primary open-angle glaucoma (POAG) and ocular hypertension (OH). This study was prospective and non-comparative and included 34 patients. Baseline refraction and anterior chamber depth were compared to the refraction and anterior chamber depth 14 days after commencing dorzolamide to determine if refraction or anterior chamber depth had been affected. Before dorzolamide use, the mean refractive error was -0.88 +/- 3.53 D (+/-SD). The mean refractive error was -0.94 +/- 3.65 D (+/-SD) two hours post-dose after 14 days of dorzolamide use, which was not significantly different (P = 0.50). The mean pre-treatment anterior chamber depth was 3.088 +/- 0.385 mm (+/-SD), which did not differ significantly from the post-treatment anterior chamber depth mean of 3.092 +/- 0.389 mm (+/-SD) (P = 0.88). The results of the study show that refraction and anterior chamber depth are not significantly altered by short-term dorzolamide use in patients with POAG and OH with no history of previous dorzolamide use.     

Visual evoked potentials after photostress in patients with primary open-angle glaucoma and ocular hypertension.

Visual evoked potentials (VEPs) were assessed in basal condition and after photostress in normal subjects, in subjects with ocular hypertension (OHT), and in subjects with primary open-angle glaucoma (POAG). The VEPs recorded in basal condition showed that in patients with OHT and POAG a latency of the P100 peak was higher than in controls. The amplitudes were reduced in POAG patients but not in OHT patients. In all eyes, the VEPs recorded 20 s after photostress showed an increase in latency and a decrease in amplitude. In the control eyes, the functional recovery was complete after 80 s. In the eyes with OHP and in the eyes with POAG, the parameters of VEP after photostress underwent greater changes than in the control eyes. VEPs were superimposable on the basal condition (recovery time) at 73.2 s in OHT patients and at 113.2 s in POAG patients. The longer VEP recovery time after photostress observed in OHT and POAG patients could be attributed to the reduced functionality of the outer layers or the inner retinal layers of the central retina, or both. This test may be useful in the clinical evaluation for early diagnosis of glaucoma.     

Effect of dorzolamide and timolol on ocular blood flow in patients with primary open angle glaucoma and ocular hypertension

BACKGROUND: There is evidence that perfusion abnormalities of the optic nerve head are involved in the pathogenesis of glaucoma. There is therefore considerable interest in the effects of topical antiglaucoma drugs on ocular blood flow. A study was undertaken to compare the ocular haemodynamic effects of dorzolamide and timolol in patients with primary open angle glaucoma (POAG) or ocular hypertension (OHT). METHODS: One hundred and forty patients with POAG or OHT were included in a controlled, randomised, double blind study in two parallel groups; 70 were randomised to receive timolol and 70 to receive dorzolamide for a period of 6 months. Subjects whose intraocular pressure (IOP) did not respond to either of the two drugs were switched to the alternative treatment after 2 weeks. Scanning laser Doppler flowmetry was used to measure blood flow in the temporal neuroretinal rim and the cup of the optic nerve head. Pulsatile choroidal blood flow was assessed using laser interferometric measurement of fundus pulsation amplitude. RESULTS: Five patients did not respond to timolol and were changed to the dorzolamide group, and 18 patients changed from dorzolamide treatment to timolol. The effects of both drugs on IOP and ocular perfusion pressure were comparable. Dorzolamide, but not timolol, increased blood flow in the temporal neuroretinal rim (8.5 (1.6)%, p<0.001 versus timolol) and the cup of the optic nerve head (13.5 (2.5)%, p<0.001 versus timolol), and fundus pulsation amplitude (8.9 (1.3)%, p<0.001 versus timolol). CONCLUSIONS: This study indicates augmented blood flow in the optic nerve head and choroid after 6 months of treatment with dorzolamide, but not with timolol. It remains to be established whether this effect can help to reduce visual field loss in patients with glaucoma.     

Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension

Several lines of evidence suggest that the large optic nerve fibers, which form the magnocellular retinocortical pathway, are preferentially susceptible to early glaucomatous damage. It is evident from studies of the functional architecture of the visual system that the magnocellular pathway underlies the global perception of motion. Therefore, we have developed a psychophysical technique for assessing motion detection thresholds in patients with ocular hypertension (OHT) and primary open-angle glaucoma (POAG). For this purpose we employed a dynamic random dot display that contained varying degrees of a coherent motion signal embedded within a background of random motion noise. We used this technique to measure motion thresholds in POAG patients (n = 37), OHT patients (n = 14), and age-matched controls (n = 39). Motion thresholds were elevated by 70% for the POAG group and 44% for the OHT group relative to controls. In the same patients, no significant deficit in form discrimination was found as measured by Pelli-Robson charts. Our results demonstrate that significant motion perception deficits are evident in POAG and OHT. These findings support the suggestion that significant and selective damage to the magnocellular pathway occurs in OHT and POAG and indicate that motion threshold testing may reveal preclinical optic nerve disease in early POAG.