Effect of treatment with carteolol and latanoprost in newly diagnosed primary open-angle glaucoma on peripapillary vessel density.

BACKGROUND AND AIM: In a previous follow-up of glaucoma patients taking carteolol or latanoprost, we found a greater progression of visual field changes with the prostaglandin than the betablocker. In the present study we compared the impact of carteolol and latanoprost on peripapillary vessel density in newly diagnosed primary open-angle glaucoma (POAG) patients. METHODS: The study consisted of two groups of POAG patients. There were 46 patient eyes treated with carteolol (Carteol LP 2%) in the first group and 52 eyes treated with latanoprost (Xalatan 0.005%) in the second. Intraocular pressure (IOP), vessel density (VD) and visual field were assessed in all patients. VD was measured peripapillary by optical coherence tomography angiography (OCTA) with the Avanti RTVue XR in eight segments: Inferior Temporal - IT (1); Temporal Inferior -TI (2); Temporal Superior - TS (3); Superior Temporal - ST (4); Superior Nasal - SN (5); Nasal Superior - NS (6); Nasal Inferior - NI (7) and Inferior Nasal - IN (8). The measurements were compared before and after three months of treatment. The visual field was examined with a fast threshold glaucoma program using a Medmont M 700 instrument from Medmont International Pty Ltd. and only when a diagnosis of POAG was done. The overall defect (OD) was assessed. RESULTS: Before treatment, there was no difference between groups in either OD or VD. After treatment, there was a decrease in IOP in both groups. In the carteolol-treated group, the mean decrease was 5.8 mmHg and in the latanoprost-treated eyes, the mean decrease was 7 mmHg. The difference was not statistically significant (P=0.133). After treatment with carteolol, there was a statistically significant increase in VD in segments 4, 5 and 6. After latanoprost treatment, VD was statistically significantly improved only in segment 5. A greater increase in VD values was found in eyes treated with carteolol than in eyes treated with latanoprost. CONCLUSION: Carteolol had a better effect on vessel density than latanoprost.

Visual Neuroprosthesis - Stimulation of Visual Cortical Centers in The Brain. Design of Non-Invasive Transcranial Stimulation of Functional Neurons.

PURPOSE: The purpose of the article is to present the history and current status of visual cortical neuroprostheses, and to present a new method of stimulating intact visual cortex cells. METHODS: This paper contains an overview of the history and current status of visual cortex stimulation in severe visual impairment, but also highlights its shortcomings. These include mainly the stimulation of currently damaged cortical cells over a small area and, from a morphological point of view, possible damage to the stimulated neurons by the electrodes and their encapsulation by gliotic tissue. RESULTS: The paper also presents a proposal for a new technology of image processing and its transformation into a form of non-invasive transcranial stimulation of undamaged parts of the brain, which is protected by a national and international patent. CONCLUSION: The paper presents a comprehensive review of the current options for compensating for lost vision at the level of the cerebral cortex and a proposal for a new non-invasive method of stimulating the functional neurons of the visual cortex.

Peripapillary retinal nerve fiber layer following vessel density correction at different IOP values.

PURPOSE: The aim of this study was to define the thickness of the retinal nerve fiber layer (RNFL) in the peripapillary region of the retina after adjusting for the effect of vessel density (VD) in patients with pathological intraocular pressure (IOP). PATIENTS AND METHODS: 69 patients (122 eyes) with IOP >21 mmHg (range 21-36 mmHg, mean 23.65±2.70 mmHg). 32 were men (average age 55±13 years) and 37 were women (average age 52±14 years). IOP was measured using the Ocular Response Analyser (ORA). VD and RNFL were measured peripapillary by OCT (Avanti RTVue XR) in eight segments: Inferior Temporal - IT (1); Temporal Inferior - TI (2); Temporal Superior -TS (3); Superior Temporal - ST (4); Superior Nasal - SN (5); Nasal Superior - NS (6); Nasal Inferior - NI (7) and Inferior Nasal - IN (8). The VD value was subtracted from the total RNFL value. RESULTS: A corrected value for the RNFLc nerve fiber layer thickness (RNFLc) was introduced to account for VD across the RNFL volume in each segment. Person's correlation coefficient (r) was used to assess the correlation between IOP and RNFLc. The strongest correlations in RNFLc were in segments 5 (r=-0.32, P=0.002) and 8 (r=-0.21, P=0.037). CONCLUSION: The greatest changes in RNFLc (RNFL minus VD) were in eyes with pathological IOP in segments 5 and 8, the location of the retinal ganglion cell magnocellular fibers. That is, when the thickness of the nerve fiber layer was reduced by correcting for vessel density, there was a significant correlation in segments 5 (r =-0.32, p<0.05) and 8 (r =-0.21, P<0.05) with intraocular pressure. The results suggest use of a corrected RNFL from VD value as more appropriate for detecting early changes in glaucoma.

Distal Nasal Part of the Visual Field and RNFL in Primary Open-Angle Glaucoma.

Purpose: The aim of this study was to compare changes in the conventionally undiagnosed distal nasal visual field with RNFL in patients with early primary open-angle glaucoma (POAG). Material and Methods: 59 eyes of 32 patients (18 women, 14 men) with early stage POAG were included. All eyes were found to have a normal visual field (fast threshold program of 50 degrees nasally and 22 degrees temporally) with the Medmont M700. Visual acuity was 1.0 (with a possible correction ±3 D), and they had no other ocular pathology except glaucoma. The visual field was subsequently examined with the same instrument by moving the fixation point 40 degrees temporally (spatially adaptive program) and simultaneously turning the head 10 degrees nasally. A total of 89 examination points were included using flicker stimuli in a range of 0-120 degrees nasally. Nerve fiber layer (RNFL) and vessel density (VD) was measured using the in-built software of the Avanti RTVue XR instrument. Using Pearson's correlation coefficient, the results of visual field examination with RNFL without and after correction (by subtracting VD from total RNFL value) in the superior-nasal (SN-5) and inferior-nasal (IN-8) segments were compared. Results: In all eyes, changes were found in the distal periphery of the nasal part of the visual field. No correlation was noted by comparison with RNFL. After adjusting RNFL for VD, we observed no correlation in the SN segment (5) (r=-0.03) and a very weak correlation in the IN segment (8) (r=-0.16). Conclusion: With a normal visual field tested by the rapid threshold glaucoma program, changes in the distal part of the nasal periphery of the visual field were found in the entire cohort and did not correlate with the RNFL and RNFL results after correction from VD.

Axons of retinal ganglion cells on the optic nerve disc following vessel density correction at different IOP values.

The present study aimed to determine how the vascular density (VD) in each segment peripapillary influences the retinal nerve fiber layer (RNFL) and to eliminate its contribution to RNFL in pathological intraocular pressure (IOP). In a cohort of 69 subjects (mean age, 45±6 years old) with untreated ocular hypertension (122 eyes in total) enrolled in this study, Ocular Response Analyser IOP was measured during routine outpatient care. Its value was >21 (range, 21-36) mmHg in all eyes. Furthermore, peripapillary VD and RNFL were measured using optical coherence tomography in the following eight segments: Inferior temporal (segment 1); temporal inferior (segment 2); temporal superior (segment 3); superior temporal (segment 4); superior nasal (segment 5); nasal superior (segment 6); nasal inferior (segment 7); and inferior nasal (segment 8). The visual field examination was performed with the fast threshold glaucoma program using the Medmont M 700. The overall defect was evaluated. Person's correlation coefficient was used to assess the correlation between VD and IOP. The largest changes were observed in peripapillary segments 1, 4, 5, 6, 7 and 8. The second part of the work was to eliminate the contribution of VD to RNFL. The partial correlation coefficient r was used to adjust RNFL from VD to assess the dependence between the selected parameters. The largest changes in RNFL were in segments 5 and 8 after they had been 'cleaned' of peripapillary VD. In conclusion, the present study revealed that the largest changes in RNFL after VD adjustment were observed for the incipient hypertensive glaucoma in segments 5 and 8.

OCTA and Doppler Ultrasound in Primary Open-Angle Glaucoma and Normal-Tension Glaucoma.

The aim of this study was to determine whether the values of vessel density (VD) and perfusion parameters in the ophthalmic artery (OA) and central retinal artery (CRA) of the same eye differ in patients with hypertensive glaucoma (HTG) from patients with normotensive glaucoma (NTG). The first group consisted of 20 HTG patients (40 eyes). Patients with HTG were verified to have primary open-angle glaucoma (POAG). The second group consisted of 20 HTG patients (40 eyes). VD was used to determine the Avanti RTVue XR from Optovue (USA). Peak systolic velocity (PSV), end-diastolic velocity (EDV) and resistance index (RI) were measured in both the central retinal artery (CRA) and ophthalmic artery (OA) using Doppler sonography on the Affinity 70G from Philips (USA). The visual field (VF) was examined by a fast threshold glaucoma program using a Medmont M700 (Australia). We showed no differences in VF, VD, PSV-OA and EDV-CRA between the two groups. Statistically significant differences between the two groups were observed in PSV in CRA (p = 0.04), EDV in OA (p = 0.009) and in RI in both CRA and OA. Other values were without significant differences in both groups. In both HTG and NTG, we observed in PSV-CRA, EDV-OA, RI-CRA and RI-OA.

Optic neuropathy associated with acute pancreatitis: A case report.

The present article describes a case of a 24-year-old patient who suffered from acute pancreatitis. The patient simultaneously developed visual acuity loss and changes in the visual field. When examined, the finding was physiological, including the fundoscopy. Neither fluorescein angiography or optical coherence tomography demonstrated any retinal abnormalities; electroretinography was physiological as well. The visual evoked potentials (VEP) showed abnormalities in amplitudes. Patient's visual field was reduced to 40˚. The follow-up examination 13 months after the first symptoms proved a progression of changes in the visual field and prolonged latency of P100 peak in VEP. The retinal nerve fibre layer stayed unchanged, but the vessel density on the optic nerve head decreased. Magnetic resonance brain imaging showed non-specific subcortical and paraventricular focuses in the white matter of both hemispheres. There were no other abnormalities detected by magnetic resonance imaging. Neurological examination was normal. In conclusion, the present study verified this decrease of visual functions as a lesion in the visual pathway using VEP, which was also confirmed by magnetic resonance brain imaging.

Ethambutol-induced optic neuropathy.

PURPOSE: A case report of a 40-year-old patient with tuberculosis treated with ethambutol is described. Within six months of starting treatment, there was a painless sudden decline in visual function. Despite the known complications of ethambutol treatment, it was discontinued after another three months. METHODS: In the case report, we highlight the damage to the dominantly peripheral visual pathways. Using electrophysiological examinations, we showed a significant alteration in the optic nerves. Optical Coherence Tomography (OCT) showed progressive loss of vessel density and nerve fibre layer of retinal ganglion cells. Perimetric examination showed both a central decrease in sensitivity and mainly scotomas in the temporal parts of the visual fields. Although there was improvement in visual fields over time, OCT findings indicated progression of ethambutol-induced optic neuropathy (EON). Magnetic Resonance Imaging confirmed the alteration in the peripheral part of the visual pathway (intraorbital, intracranial parts of optic nerves, chiasma, and optic tracts). CONCLUSION: Even though EON is not an unknown complication, new cases still occur and, unfortunately, with an irreversible course. Therefore, it is important to draw attention constantly to this complication and to consider it not only in ophthalmologists' surgeries.

Bilateral optic neuropathy as a complication of allogeneic hematopoietic stem cell transplantation.

BACKGROUND: The authors present a case study which describes the development of bilateral optic neuropathy as a complication of allogeneic hematopoietic stem cell transplantation (HSCT) in a patient who underwent a transplant for B-cell acute lymphoblastic leukemia (B-ALL). The patient, who was in remission with regard to the underlying hematological disease, developed edema of both optic discs and maculas three months after transplantation. The morphological finding regressed after treatment with corticoids and comprehensive systemic anti-infective therapy. However, the loss of function was not entirely restored. CASE REPORT: One year after the healing, the atrophy of the optic discs persisted, with corresponding findings in vessel density (VD), retinal nerve fibre layer (RNFL) and visual field changes. Electrophysiological examination by pattern electroretinogram (PERG) showed an alteration in retinal ganglion cells in the left eye, but with significant damage to nerve fibres on both sides. Visual evoked potential (VEP) verified bilateral non-inflammatory neurogenic lesions. This finding was also confirmed by functional magnetic resonance imaging (fMRI). Examination by structural magnetic resonance imaging (MRI) showed inflammatory changes in the optic nerve sheaths over time and a consequent marked narrowing of them. CONCLUSION: The authors believe that edema of the optic discs and maculas was caused by a combination of several factors. Firstly, MRI showed inflammatory changes in the optic nerve sheaths, which led to a blockade of axoplasmic transport. Another factor that may have played a part in the outcome was endothelial damage to blood vessels with impaired microcirculation supplying the optic nerve fibres, which contributed to the occurrence of macular edema.

The Relationship Between the Thickness of cpRNFL in Segments and Intraocular Pressure.

Purpose: The aim of this study was to investigate whether the retinal nerve fibre layer (RNFL) in some segments of the optic nerve disc in pathological intraocular pressure is more damaged in eyes without antiglaucoma treatment. Patients and Methods: The cohort consisted of 69 subjects (122 eyes), 32 males (6x one, 26x both eyes) aged 21 to 76 years and 37 females (4x one and 30x both eyes) aged 22 to 75 years, who were measured to have IOP greater than 21 mmHg (21-36) in routine ambulatory care. Measurements were performed using the Ocular Response Analyser, taking into account corneal hysteresis. RNFL thickness was measured using the Avanti RTVue XR and was assessed in 8 segments (1-IT, 2-TI, 3-TS, 4-ST, 5-SN, 6-NS, 7-NI, 8-IN). The visual field was examined with a fast threshold glaucoma program using the Medmont M700. The overall defect (OD) was evaluated. Pearson's correlation coefficient r was used to assess the dependence between the selected parameters. Results: The largest peripapillary changes in RNFL were observed in segments 1, 4, 5 and 8. It should be emphasized that segments 1 and 4 have been temporarily shifted. Segments 5 and 8 then corresponded to the upper (at no. 12) and lower (at no. 6) sectors. Conclusion: The most important result of this study is the finding that the greatest changes in the RNFL layer were observed in pathological IOP at segment 5 (r=-0.3) and 8 (r=-0.28), at the point where the fibres of the magnocellular retinal ganglion cells enter the retina.

Comparison of the Effect on Vessel Density and RNFL between Carteolol and Latanoprost.

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.

Visual neuroprosthesis: present and future perspectives.

The purpose of this study is to provide an overview of the replacements used in lost vision in the form of the bionic eye, to show their deficiencies and outline other possibilities for non-invasive stimulation of functional areas of the visual cortex. The review highlights the damage not only to the primary altered cellular structures, but also to all other horizontally and vertically localised structures. Based on the results of a large number of functional magnetic resonance imaging and electrophysiological methods, the authors focus on the pathology of the entire visual pathway in pigmentary retinopathy (PR) and age-related macular degeneration (AMD). This study provides a recent overview of the possible systems used to replace lost vision. These range from stimulation with intraocular implants, through stimulation of the optic nerve and lateral geniculate nucleus to the visual cortex. The second part deals with the design of image processing technology and its transformation into the form of transcranial stimulation of undamaged parts of the brain, which is protected by a patent. This is comprehensive overview of the current possibilities of replacement of lost vision and a proposal for a new non-invasive methods of stimulation of functional neurons of the visual cortex.

OCT angiography, RNFL and the visual field at different values of intraocular pressure.

The aim of the present study was to investigate the relationship between intraocular pressure (IOP), vessel density (VD), retinal nerve fiber layer (RNFL) parameters and overall defect (OD) of the visual field in eyes where antiglaucoma treatment had not yet been initiated. A total of 61 subjects (122 eyes) who had an IOP of >20 mmHg on several occasions, in at least one eye, in routine outpatient care were included. These were subjects who had never been treated for hypertension glaucoma. The cohort was divided into four subgroups. In the first group, there were 18 eyes with an IOP value of <20 mmHg. In the second group, there were 39 eyes with IOP values of 20-22 mmHg. The third group consisted of 32 eyes with IOP values of 22-24 mmHg and the final group consisted of 33 eyes with IOP values of >24 mmHg. The IOP results were compared with VD, RNFL and OD using Pearson's correlation coefficient to assess the relationship between the selected parameters. RNFL and OD were moderately correlated only in the group of eyes with an IOP value >24 (r=0.48); in the other groups the correlation was very weak. However, changes in visual field were already observed in eyes with IOP 20-22 mmHg (r=-0.27). There was a moderate correlation in eyes with an IOP value >24 mmHg (r=-0.53). The most significant result observed was the relationship between VD and RNFL. In eyes with an IOP value ≤20, a moderate to strong correlation between these parameters was observed. This relationship increased with increasing IOP values up to a very strong correlation in the group with an IOP value >24 mmHg. A moderate to strong dependence between VD and RNFL in eyes with an IOP value ≤20 mmHg was observed, and this dependence was very strongly correlated in the eyes with an IOP value >24 mmHg.

Changes of intraocular lens position induced by Nd:YAG capsulotomy.

AIMS: The aim of this study was to evaluate the changes in IOL position (axial shift, tilt and decentration) in the capsular bag after Nd:YAG laser capsulotomy and to create a user-friendly software that is optimized for the output of available imaging technology, then verify the relationship between the biometric parameters of the eye and the extent of changes in the IOL position. PATIENTS AND METHODS: The study included 35 artephakic eyes that underwent laser capsulotomy. Before and at least one hour after capsulotomy, all patients underwent the following assessments: optical biometry (Lenstar LS900), OCT with anterior segment module (Optovue Avanti) and IOL photography in infrared mode using reference unit (Verion). The original software solution was designed for the graphical evaluation of the differences between centering, axial displacement and tilt of IOL. Changes in IOL position were evaluated as simple differences before and after the laser procedure and as differences in absolute values (abs). RESULTS: The following results show the average differences in IOL position: ACD=0.02±0.23 mm (abs=0.11±0.20 mm), IOL decentration in x-axis = -0.001±0.091 mm (abs=0.065±0.063 mm), IOL decentration in y-axis =0.012±0.119 mm (abs=0.048±0.53 mm), tilt in horizontal plane TILT-H=0.11±0.83° (abs=0.51±0.66°) and tilt in vertical plane TILT-V = -0.14±0.49° (abs=0.26±0.44°). All changes were insignificant (P>>0.05). In total, 74.29% of IOLs showed a hypermetropic shift. A moderate positive correlation was found between the absolute differences in horizontal tilt and keratometry (r=0.45). Relationship with other changes and parameters were weak. CONCLUSION: In conclusion, the use of the original software solution developed by the authors showed that changes in IOL centering, axial displacement and tilt occur after Nd:YAG capsulotomy, but average differences were insignificant. In almost 3/4 cases, there was a hypermetropic axial displacement of the IOL.

Temporal Visual Field Border.

PURPOSE: The aim of the study was to determine the physiological temporal visual field border, based on theoretical calculations and by perimetric examination itself. MATERIALS AND METHODS: A perimetry test was performed on 15 healthy subjects - seven women (27-30 years old) and eight men (28-46 years old), all of whom had healthy eyes with a visual acuity value of 1.0. The visual field was evaluated using a Medmont M700 with nasal displacement of the fixation point of 40 degrees. In total, 179 examined points of visual field were included. The model of the entry of temporal rays into the eye was created on the basis of the measured biometric values of the eye and with the help of the AD systems AutoCad and SolidWorks. RayViz for SolidWorks was able to simulate the passage of light rays through the model. RESULTS: The temporal part of the subjective visual field border was up to 110 degrees in all eyes. Modelling of the input rays based on geometric optics in one of the participants in the testing revealed a theoretical temporal boundary of the visual field of 102 degrees. CONCLUSION: Theoretical calculations of geometric optics have shown that the temporal boundary of the visual field reaches up to 102 degrees in a healthy individual. By perimetric examination, this limit reached 110 degrees.

Pituitary apoplexy without chiasm compression: A case report.

The present report presents a rare case in which a patient with pituitary apoplexy (PA) without compression of the optic chiasm experienced diagnosable visual impairment in the ensuing months. Endocrinologically, the condition was a prolactinoma followed by bleeding into the pituitary gland. Due to the unexplained functional changes in the patient, an electrophysiological examination (pattern electroretinogram and pattern visual evoked potentials) was performed, which verified a bilateral non-inflammatory neurogenic lesion. This finding was confirmed by functional magnetic resonance imaging (fMRI) examination. Structural MRI did not reveal chiasm compression in the time sequence or alteration of the optic nerves (the diameter of the optic nerve at different distances from the eye and the diameter of the optic nerve sheath at different distances from the eye). Similarly, neither the retinal nerve fiber layer (RNFL) nor the vessel density was altered. The present report suggests that changes in visual fields may be due to ischemia in the area of the chiasm and optic nerves, similar to PA.

The influence of central corneal thickness on progression of normotensive glaucoma.

OBJECTIVES: To verify whether there is a relation between central corneal thickness (CCT) and progression of normotensive glaucoma (NTG), to assess the impact of early changes in the visual field on their progression in time. METHODS AND PATIENTS: The sample consisted of two groups of patients with NTG. In the first group there were 50 eyes of 25 persons (15 females and 10 males) average age 63 years who had been treated with prostaglandins. The second group consisted of 50 eyes of 25 persons (16 females and 9 males) average age of 62 years who had had no local therapy. All patients were cardiologically compensated and had no other internal or neurological disease. Visual acuity was 1.0 with a possible correction (less than ±3 dioptres) in all patients. The IOP ranged between 10-15 mmHg in all patients. If hypotensive ophthalmological therapy was initiated, it had been stable for the last five years. In all patients, we monitored CCT, excavation in the papilla (c/d), pattern defect (PD) and overall defect (OD) of the visual field. In 2013, changes in the visual fields were approximately the same in all patients. We compared the results of the visual fields after five years, i.e. the results were obtained in 2018. CCT was measured, using the ultrasound pachymeter Tomey SP-100. PD and OD of the visual field using the glaucoma fast threshold program with the MEDMONT M 700 device. For statistical comparison, we used the paired t test and correlation analysis. RESULTS: In both groups, we found progression of PD in time (P=0.0000, P=0.0001, respectively). In the patients treated with prostaglandins, OD had not statistically significantly changed (P=0.49) in contrast to the untreated patients (P=0.001). There was no statistically significant relation between CCT and PD in any of the groups. It was similar between the CCT and OD. In the treated NTG patients, we found a weak correlation between the changes in PD in time (r=0.2846, P=0.0438) and moderately strong relation for OD (r=-0.63). The finding was similar in untreated patients PD (r=-0.2, P=0.162) and OD (r=-0.443, P=0.001). CONCLUSION: We found no relationship between progression of changes in the visual fields in CCT. Progression of changes in the visual fields was higher in patients who had more advanced changes at the beginning of observation. The untreated patients had progression of changes in the visual fields both in PD and OD in contrast to those who were taking prostaglandins and presented changes only in PD.

Effect of prostaglandins and beta blockers on progression of hypertensive and normotensive glaucomas.

AIM: The aim of the study was to evaluate the progression of changes in the visual fields in patients with hypertensive glaucoma (HTG) and normotensive glaucoma (NTG) following administration of prostaglandins and beta blockers, as well as also in NTG without ophthalmological therapy. Methodos. The HTG group included 12 patients (mean age 66 years) with approximately the same changes in the visual field and central corneal thickness (CCT-568um) treated with prostaglandins, and 12 patients (mean age 60 years, CCT=544um) treated with beta-blockers. The IOP ranged from 12 to 18mmHg for the whole follow-up period. The NTG group consisted of three subgroups. The first subgroup consisted of 14 patients (mean age 58 years) who were treated with prostaglandins. The second subgroup consisted of 10 patients (mean age 57 years) who were treated with beta blockers. The third subgroup consisted of 18 patients (mean age 57 years) who underwent no ophthalmological therapy. IOP was within the range of 8-12 mmHg over the whole follow-up period. In all patients, we monitored the pattern defect (PD) and overall defect (OD) within a period of five years. The treatment was not modified during the treatment period. All patients were compensated for cardiovascular status and had no other internal or neurological disease. Visual acuity was 1.0 with a possible correction (less than 3 dioptres) in all patients. RESULTS: There was no statistically significant difference in HTG during the treatment with prostaglandins in PD (P=0.35) and OD (P=0.09) or beta blockers (P=0.37 and 0.23, respectively). In NTG, the greatest changes occurred in PD (P=0.0001) in untreated patients. OD showed no statistically significant changes (P=0.25). Similarly, the patients on prostaglandins had a statistically significant difference in PD (P=0.04), while OD did not show statistically significant changes (P=0.4). We did not find statistically significant differences in progression in patients with NTG treated with beta blockers PD (P=0.7), OD (P=0.4). CONCLUSION: Treatment of glaucoma with prostaglandins and beta blockers has a significant importance in HTG. However, beta blockers have a higher protective effect on the visual field. This is not true in NTG, where we demonstrated this effect only following the administration of beta blockers.

Optical coherence tomography angiography and the visual field in hypertensive and normotensive glaucoma.

BACKGROUND: Hypertensive glaucoma (HTG) causes damage to the retinal ganglion cells and eventually to the entire visual pathway due to high intraocular pressure (IOP). However, increased IOP will also affect the vessel density (VD) of the posterior pole of the eye and the related retinal ganglion nerve fibres (RNFL). In normotensive glaucoma (NTG), the retinal ganglion cells are relatively intact. The pathology is at the level of ganglion fibres. The unanswered question is what has altered ganglion cell fibres at the level of the retina and optic nerve head in NTG? AIM: The aim of this study was to determine whether there is a correlation between the retinal nerve fibre layer (RNFL) and vessel density (VD) at the same altitudinal half of the retina and the sum of sensitivities of the contralateral half of the visual field of the same eye in hypertensive and normotensive glaucoma (NTG). METHODS: Our group included 20 patients with HTG and 20 patients with NTG. The Pearson's correlation coefficient r was used for evaluation of the relationship of the peripapillary RNFL and VD, visual field (using the fast threshold glaucoma program) as the sum of sensitivities in apostilbs (asb) to the extent of 0-22 degrees. The results of sensitivity were compared with the RNFL and VD of the contralateral altitudinal half of the retina in the same eye. RESULTS: In the HTG group there was a moderate relationship between RNFL and VD (both hemifields), but no relationship between RNFL and VF. VD SH and VF IH showed weak correlation and VD IH and VF SH showed no correlation. In patients with NTG, we found a strong correlation between RNFL and VD (both hemifields), between VD SH and VF IH a moderate correlation, between VD IH and VF SH also a moderate correlation and a weak correlation between RNFL and VF. CONCLUSION: By comparing the RNFL and VD at the same altitudinal halves of the retina, we found a moderate correlation in HTG and a strong correlation in NTG. We found no or a weak correlation between VD and VF in HTG. In NTG the relationship between VD and VF showed a strong correlation. These findings reveal the differences in the diagnostic groups.

Neuroprotection in glaucoma-electrophysiology.

Hypertensive glaucoma is defined as a group of diseases with progressive loss of the neuroretinal margin of the optic disc that causes characteristic degenerative optic neuropathy. The present study provided an updated summary of the physiology and pathology of neurotransmission in the visual path, with the focus on glaucoma. The results of positron emission tomography, functional magnetic resonance imaging and mainly electrophysiological methods demonstrated pathogenesis of nerve cell damage in the visual pathway. Based on these conclusions, neuroprotection in glaucoma was proposed. This consists mainly of the reduction of the intraocular pressure. It is followed by a decrease of glutamate in the synaptic cleft and blockade of its binding to the NMDA receptors. The supply of energy substrates to altered nerve cells is also indispensable. Therapy should be systemic due to impairment of the complete visual path.