Aims: The main aim of this work was to find out if there is a correlation between vessel density (VD) and results of measured perfusion values in ophthalmic artery and in central retinal artery of the same eye in a group with hypertension glaucoma (HTG). Materials and methods: The file included 20 patients with HTG, thereof 13 women of average age 68.7 years (49–80 years) and 7 men of average age 58.4 years (27–81 years). Criteria for inclusion in the study: visual acuity 1,0 with possible correction less than ±3 diopters, approximately the same changes in visual fields in every patient, intraocular pressure (IOP) less than 18 mmHg, no other ocular or neurological diseases. VD was measured by Avanti RTVue XR by Optovue firm, perfusion parameters were measured using Doppler ultrasound with Affinity 70G machine by Philips firm. The peak systolic velocity (PSV) and end diastolic velocity (EDV) and resistance index (RI) were measured both in ophthalmic artery (AO) and in central retinal artery (CRA). Visual field (VF) was examined by quick threshold glaucoma program by Medmont M 700 machine. The sum of sensitivities in apostilbs (abs) was evaluated in the range 0–22 degrees of visual field. The results of sensitivities in visual field were compared to VD and perfusion parameters in CRA and AO of the same eye. Results: Pearson’s correlation coefficient (p = 0,05) was used to assess the dependency between chosen parameters. By comparing VF and VD from measured areas, strong correlation (r = 0.64, resp. 0.65) was revealed. It was then proved that VD (WI-VDs) correlates with RICRA weakly (r = -0.35) and moderately strongly (WI-VDa r = -0.4, PP-VDs r = -0.43 and PP-VDa r = -0.45). This means that with increasing resistance index in CRA the density in VD decreases. The other correlations between VD and perfusion parameters (PSV and EDV) in CRA and AO were not significant. Conclusion: Measured values showed that the vascular component of VD has a huge impact on the changes in visual fields in HTG. Weak to moderate influence exists between VD and RI in CRA. OCTA has proven to be more suitable than Doppler ultrasound for determining the condition of blood circulation in the eye.
The study provides an up-to-date overview of pathogenesis, functional and structural changes in normal tension glaucoma (NTG) and its differences from high tension glaucomas (HTG). The authors point to less known facts which make both diagnostic groups different. First of all, there are electrophysiological findings that verify pathology in the complete visual pathway in HTG in contrast to NTG where the retinal ganglion cell response is relatively normal but the abnormalities are in the visual pathway. This corresponds to the findings of functional magnetic resonance imaging of the brain with a significant decrease in activity in HTG compared to NTG. We found a higher decrease in activity in HTG following application of the colour paradigm compared to NTG where we did not see a similar difference. We also investigated the central corneal thickness (CCT) in both diagnostic groups. We did not find a statistically significant difference. However, we found the effect of CCT on progression of the changes in visual fields in HTG. In relation to suspicion of abnormally low cerebrospinal pressure and a possible cerebrovascular fluid flow disturbance in NTG, we examined the optic nerve thickness (OND) and optic nerve sheath diameter (OSD) at a distance of 4, 8, 16 and 20mm from the posterior pole of the eye. In the comparison with the healthy population, we did not find any abnormalities except for the width of the optic chiasma that was markedly lower in NTG. In relation to a possible impairment of cerebral perfusion we determined the degrees of cerebral atrophy using magnetic resonance imaging by measuring the bicaudate ratio (BCR) and white matter lesions using the Fazekas scale. We did not find a difference between HTG and NTG in BCR. We found statistically significant changes in BCR which correlated with the changes in visual fields. The higher values of the pattern defect were associated with increased brain atrophy (BCR). We did not detect similar relations in the Fazekas scale. We found a significant difference in this parameter among NTG, HTG and a control group. We found the most advanced changes in the patients with HTG. Conclusion: In HTG, impairment of retinal ganglion cells and subsequently also their axons, including visual cortex occurs because of a high intraocular pressure. In NTG, the retinal ganglion cells are relatively normal like the visual cortex, but alteration occurs in their axons. The cause is not a high intraocular pressure but most probably ischemia.
Aim: The aim of the study was to determine whether hypertensive glaucoma (HTG) with different types of treatment leads to significant damage in any of the evaluated parameters. Sample and methodology: The sample, consisting of 36 HTG patients (72 eyes), was divided into three subgroups: In the first group, patients were treated with combination therapy (latanoprost + timolol, latanoprost + dorzolamide + timolol, dorzolamide + timolol). The group consisted of seven women and five men, with an average age of 64 years (49-81). In the second group, patients were treated with beta-blockers (carteolol, betaxolol, timolol). The group consisted of five women and five men, with an average age of 62 years (27-77). In the third group, patients were treated with prostaglandins (latanoprost, bimatoprost). The group consisted of eleven women and three men, with an average age of 61 years (61-78). Criteria for inclusion in the study were visual acuity of 1.0 with a possible correction of less than ±3 dioptres, approximately the same changes in the visual fields of all patients, an intraocular pressure (IOP) of less than 18 mmHg, and no other ocular or neurological disease. The retinal nerve fibre layer (RNFL) on the optic nerve target and vessel density (VD) was measured using an Avanti RTVue XR from Optovue. We determined the values of VD in whole image (WI) and VD of peripapillary (PP). In both cases, we then measured all vessels (VDa) and small vessels (VDs). The visual field was examined by means of a fast threshold glaucoma program with a Medmont M 700 instrument. In addition to the sum of sensitivities in apostilbs (asb) in the range of 0-22 degrees, the overall visual field defect (OD) was also evaluated. The statistical analysis was carried out using a multivariate regression model with adjustment for age and gender. The measured values of the third group were taken as baseline. Results: In the statistical analysis, we have found differences in visual field in the combination treatment group (p = 0.0006) and differences were recorded for RNFL in the beta-blocker group (p = 0.04).
The aim of the study was to compare the treatment of hypertensive glaucoma (HTG) in the early stages with carteolol and latanoprost by assessing the change in vessel density (VD) and retinal nerve fibre layer (RNFL). Methods: The first group with diagnosed HTG consisted of 46 eyes treated with carteolol; the second group consisted of 52 eyes treated with latanoprost. The following examinations were evaluated in all patients: intraocular pressure (IOP), retinal nerve fibre layer (RNFL), vessel density (VD) and visual field examination (glaucoma fast threshold test). The results were compared before treatment and 3 months after treatment. Results: There was no difference in the overall visual field defect (OD) between groups before treatment. After treatment, there was a decrease in IOP in both groups (carteolol-treated group had a mean decrease of 5.8 mmHg and latanoprost-treated eyes had a mean decrease of 7 mmHg). This difference was not statistically significant (p = 0.133). No similar difference was observed for RNFL (p = 0.161). In contrast, the change in the VD parameter was statistically significant between groups (p < 0.05), with a greater difference observed in the carteolol-treated group of eyes. Carteolol had a better effect on the VD.
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