Treatment Of Glaucomatous Optic Neuropathy Research Articles

The Chick Embryo and Its Structures as a Model System for Experimental Ophthalmology

The possibilities of using the chick embryo and its individual structures as a model system in experimental ophthalmology are considered. Cultures of the retina and spinal ganglia from chick embryos are used in the development of new methods for the treatment of glaucomatous optic neuropathy and ischemic optic neuropathy. The chorioallantoic membrane is used for modelling vascular pathologies of the eye, screening of anti-VEGF drugs, and assessing biocompatibility of implants. Co-culturing of chick embryo nervous tissue and human corneal cells makes it possible to study the processes of corneal reinnervation. The use of chick embryo cells and tissues in the "organ-on-a-chip" system opens up wide opportunities for fundamental and applied ophthalmological studies.

Сравнительный анализ гемодинамических и электрофизиологических показателей на фоне комплексного лечения глаукомной оптической нейропатии эндоназальным электрофорезом в сочетании с электростимуляцией

Цель. Сравнительная оценка комплексного лечения глаукомной оптической нейропатии с введением препарата танакан с помощью эндоназального электрофореза в сочетании с электростимуляцией по данным ЗВП и ультразвукового доплеровского картирования. Материалы и методы. Исследование проводилось в Самаркандской областной глазной больнице и клинике Самаркандского государственного медицинского университета. Под наблюдением находились 80 пациентов (116 глаз) с глаукомной оптической нейропатией (ГОН) в возрасте от 40 до 78 лет, из них 44 (55%) женщины и 36 (45%) мужчин, с установленным диагнозом первичной открытоугольной и закрытоугольной глаукомы II или III стадии в условиях компенсации внутриглазного давления (21,3±3,2). Все пациенты были разделены на три гомогенные группы. В третьей группе помимо нейропротекторного лечения и эндоназального электрофореза использовалась чрескожная электростимуляция зрительного нерва с помощью аппарата ЭСОМ. Результаты. Отмечалось улучшение остроты зрения в 1,32 раза у пациентов со II стадией и в 1,4 раза – у лиц с III стадией болезни во 2-й основной группе уже через месяц после проведенной терапии по сравнению с группой контроля. Суммарные границы периферического поля зрения также были достоверно расширены во 2-й основной группе. Также следует отметить улучшение гемодинамических показателей сосудов зрительного нерва в этой группе со сравнительно сниженным индексом резистентности в большей степени, изменение которого составило от 0,66 до 0,57 к 6-му месяцу наблюдения. Кроме того, увеличение амплитуды зрительных вызванных потенциалов подтверждает достоверный положительный эффект чрескожной электростимуляции (p≤0,05) во 2-й основной группе. Заключение. Использование эндоназального электрофореза с препаратом танакан в сочетании с чрескожной электростимуляцией в комплексном лечении ГОН снижает риск развития атрофии зрительного нерва и наряду с улучшением зрительных функций удлиняет положительный эффект основного лечения. Предложенный в работе метод комплексного лечения позволит повысить эффективность терапии пациентов с компенсированной первичной глаукомой, улучшит прогноз по зрению и качество реабилитационных мероприятий. Purpose. To assess comparative effectiveness of complex treatment of glaucomatous optic neuropathy with drug tanakan using endonasal electrophoresis in combination with electrostimulation based on VEP and ultrasound doppler mapping. Materials and methods. The study was carried out in Samarkand regional eye hospital and Samarkand state medical university. Under observation were 80 (116 eyes) patients with glaucomatous optic neuropathy aged 40 to 78, from them 44 (55%) – female, 36 (45%) – male with fixed diagnosis primary open angel and angle closure glaucoma of the II or III stages in compensated intraocular pressure (21.3±3.2). All patients were divided into three groups. In the third group patients beside neuroprotective treatment and endonasal electrophoresis took transcutaneous electrostimulation of the optic nerve with ESOM apparatus. Results. An improvement of the visual acuity in 1.32 times in the II stage and 1.4 times in the III stage in the II main group was noted compare to control one. Total boundaries of the peripheral visual field also were reliably enlarged in the II main group. It should be noted that hemodynamic index of vessels of the optic nerve with comparatively low index of the resistance were higher also in the given group and made up from 0.66 to 0.57 in the 6-months of observation. On top of that, enlargement of the visual evoke potential amplitude supported reliable positive effect of the transcutaneous electrostimulation (p≤0.05) in the II main group. Conclusion. The usage of endonasal electrophoresis with tanakan following with percutaneous electrostimulation in complex treatment of glaucomatous optic neuropathy protect from the development of the atrophy of optic nerve and along with improvements of visual functions prolong positive effect of the main treatment. Proposed complex treatment enables to increase effectiveness of treatment patents with compensate primary glaucoma, improves visual prognosis and quality of the rehabilitation measurements.

The value of lamina cribrosa in the diagnosis and treatment of glaucoma. Remodeling of lamina cribrosa collagen and approaches to its therapeutic treatment

Among the first structures suffering damage with an increase in intraocular pressure (IOP) and in early stage of glaucoma are the lamina cribrosa (LC) and peripapillary sclera (ppScl). Changes in these structures occur at the molecular and cellular level. Extracellular matrix (ECM) is the basis of connective tissue, provides mechanical support for the cells, facilitates intercellular interactions and transport of chemicals, including in LC and ppScl. Mechanical stress causes remodeling and disorganization of the ECM, which leads to changes in the structure of the tissue itself, an increase in its rigidity and a decrease in elasticity. Taking into account the molecular and cellular mechanisms of damage to LC and ppScl, various researchers have developed strategies and tactics for therapeutic intervention on these structures, contributing to a decrease in ECM secretion and, as a consequence, suspension of their remodeling. These approaches may in the future form the basis for the treatment of glaucomatous optic neuropathy.

Comparative Analysis of Hemodynamic and Electrophysiological Parameters against the Background of Complex Treatment of Glaucomatous Optic Neuropathy with Endonasal Electrophoresis in Combination with Electrical Stimulation

This article discusses a comparative analysis of hemodynamic and electrophysiological parameters in the context of complex treatment of glaucomatous optic neuropathy with electrical stimulation with endonasal electrophoresis. All this justifies the need for new approaches in the treatment of glaucoma and the great clinical significance of neuroprotective therapy (Russ Herman, 2010; Shepard Allan R. et al., 2010).

Clinical And Functional Effectiveness Of Endonasal Electrophoresis In Combination With Electrostimulation In Complex Therapy Of Glaucomatous Optic Neuropathy

The aim of the study was the clinical and functional assessment of the complex treatment of glaucomatous optic neuropathy with the administration of the drug tanakan in the form of endonasal electrophoresis in combination with electrical stimulation according to IST and ultrasound Doppler mapping. We examined 43 (74 eyes) patients with GON aged from 58 to 76 years. The results of the study showed that this method effectively delays the development of optic nerve atrophy and, along with the improvement of visual functions, lengthens the positive effect of the main treatment, which was confirmed by a significant improvement in hemodynamic parameters according to the ultrasound Doppler study.

Efficacy of the combination of carteolol hydrochloride + latanoprost in the treatment of glaucoma and ocular hypertension

ABSTRACTIntroduction: The only evidence-based mechanism for prevention and treatment of glaucomatous optic neuropathy is decreasing the intraocular pressure (IOP). Prescribing multiple ocular hypotensive agents, such as the combination of carteolol and latanoprost, may synergistically improve IOP; however, doing so may increase the complexity of a medication regimen, in turn, impairing patient adherence. Fixed-combination glaucoma medications offer convenience and effectiveness. New to this class of glaucoma medication is fixed combination carteolol-latanoprost (FCCL).Area covered: This review intends to give the reader a better understanding of the efficacy of the combination of carteolol and latanoprost separately, and where FCCL fits into the vast medical arsenal of IOP drops. Furthermore, it outlines the particular pharmacologic mechanisms targeted, the pharmacokinetics, effectiveness, the advantages of fixed-combination administration, and tolerability.Expert opinion: The combination of carteolol and latanoprost, separately or in a fixed-combination, is more effective than either drug alone. Given the early stage in development of FCCL, it has yet to be determined how FCCL compares to other fixed-combination medications. However, pending further approval, fixed-combination carteolol-latanoprost may represent a reasonable alternative for a patient whose IOP is inadequately controlled on a prostaglandin analog alone and for whom a simplified combination is preferred.

Нейротрофические факторы и клеточная терапия в лечении глаукомной оптической нейропатии

Нейротрофические факторы и клеточная терапия в лечении глаукомной оптической нейропатии

Dietary factors and the risk of glaucoma: a review.

Glaucoma is an optic neuropathy characterized by a progressive typical pattern of optic neurodegeneration and visual field loss. A relatively high proportion of glauctomatous individuals admit to interest in dietary modification in an attempt to manage their disease. Heavy caffeine consumption appears to have a transient effect on increasing intraocular pressure (IOP). This effect may be clinically insignificant for nonglaucomatous individuals, but the association warrants clinical consideration in those with the disease. Studies investigating the relationship between self-reported antioxidant intake and risk of glaucomatous disease have reported conflicting results. Preliminary studies investigating the relationship between self-reported glaucoma diagnosis and consumption of the oxidants calcium and iron suggest a possible relationship indicating increased risk of the disease with increased consumption of these dietary factors. Initial reports in the literature suggest a potential role for dietary modification in the treatment of glaucomatous optic neuropathy. Further study, with randomized controlled trials, may be necessary to further characterize these relationships.

Effects of antiglaucoma drugs on blood flow of optic nerve heads and related structures

An association between glaucoma development or progression and compromised ocular blood flow has been postulated as a result of population-based studies and prospective cohort studies. Blood flow in the optic nerve head (ONH) is of primary importance in the pathogenesis of glaucoma. The potential to modify the blood flow in the ONH and its related structures has been reported in various agents, including topical antiglaucoma drugs and systemic drugs such as calcium channel antagonists, which are reviewed in this manuscript. Clinical implications of the improvement in ocular blood flow on the treatment of glaucomatous optic neuropathy require further investigation.

Further data on the association between Helicobacter pylori infection and primary open-angle glaucoma

Further data on the association between Helicobacter pylori infection and primary open-angle glaucoma

Retinal ganglion cells survival in a glaucoma model by GDNF/Vit E PLGA microspheres prepared according to a novel microencapsulation procedure

The present experimental work describes the use of a novel protein encapsulation method to achieve protection of the biological factor during the microencapsulation procedure. With this aim, the protein is included in poly(lactic-co-glycolic acid) (PLGA) microspheres without any preliminary manipulation, in contrast to the traditional S/O/W (solid-in-oil-in-water) method where the bioactive substance is first dissolved and then freeze-dried in the presence of lyoprotectors. Furthermore, the presented technique involves the use of an oily additive, vitamin E (Vit E), useful from a technological point of view, by promoting additional protein protection and also from a pharmacological point of view, because of its antioxidant and antiproliferative properties. Application of this microencapsulation technique has been performed for GDNF (glial cell line-derived neurotrophic factor) designed for the treatment of optic nerve degenerative diseases, such as glaucoma, the second leading cause of blindness in the western world. The protein was released in vitro in its bioactive form for more than three months, demonstrated by the survival of their potential target cells (photoreceptors and retinal ganglion cells (RGC)). Moreover, the intravitreal injection of GDNF/Vit E PLGA microspheres in an experimental animal model of glaucoma significantly increased RGC survival compared with GDNF, Vit E or blank microspheres (p < 0.01). This effect was present for at least eleven weeks, which suggests that the formulation prepared may be clinically useful as a neuroprotective tool in the treatment of glaucomatous optic neuropathy.

Neuroprotection of retinal ganglion cells with GDNF-Loaded biodegradable microspheres in experimental glaucoma.

Glaucoma is the second leading cause of blindness worldwide, and also the most common optic neuropathy. The ultimate cause of vision loss in glaucoma is thought to be retinal ganglion cell (RGC) death. Neuroprotection of RGC is therefore an important goal of glaucoma therapy. Currently, glaucoma treatment relies on pharmacologic or surgical reduction of intraocular pressure (IOP). It is critical to develop treatment approaches that actively prevent the death of RGCs at risk in glaucoma. Neurotrophic factors have the ability to promote the survival and influence the growth of neurons. Neurotrophic factor deprivation has been proposed as one mechanism leading to RGC death in glaucoma. Effective neuroprotection in glaucoma likely requires the consistent availability of the active agent for prolonged periods of time. Biodegradable microspheres are especially attractive as drug delivery vehicles for a number of reasons. Sustained GDNF delivery by biodegradable microspheres offers significant neuroprotection to injured RGC in experimental glaucoma. PLGA microsphere-delivered GDNF represents an important neuroprotective strategy in the treatment of glaucomatous optic neuropathy and provides direction for further investigations of this hypothesis.

Neuroprotection in glaucoma: a model for neuroprotection in optic neuropathies.

Efforts to discover modalities and pathophysiologies that might afford successful neurorescue, neurorestoration, and neuroprotection of cells of the central nervous system have focused on processes that affect the central nervous system proper, that is, the brain. Often overlooked in the search for neural protection is the fact that the mammalian optic nerve behaves in many ways as an integral part of the central nervous system. As such, the eye--the optic nerve and retina--affords an ideal clinical model for neuroprotection and neuroprotective agents. Glaucomatous optic neuropathy is the most prevalent of all adult optic neuropathies, and offers an ideal primate and lower mammalian animal model for investigations of neuroprotection. This is especially compelling because while recent studies in glaucoma have shown reduction of intraocular pressure (IOP) to be an effective modality in the treatment of glaucomatous optic neuropathy, not all patients respond to or can achieve meaningful IOP reductions. Therefore much attention has now been focused on neuroprotection as a strategy in therapies for glaucomatous optic neuropathy as a means of preserving retinal ganglion cells and their axonal projections. This review discusses the latest studies on various mechanisms of neuroprotection in the treatment of glaucomatous optic neuropathy.

Increased Production of Tumor Necrosis Factor-α by Glial Cells Exposed to Simulated Ischemia or Elevated Hydrostatic Pressure Induces Apoptosis in Cocultured Retinal Ganglion Cells

Although glial cells in the optic nerve head undergo a reactivation process in glaucoma, the role of glial cells during glaucomatous neurodegeneration of retinal ganglion cells is unknown. Using a coculture system in which retinal ganglion cells and glial cells are grown on different layers but share the same culture medium, we studied the influences of glial cells on survival of retinal ganglion cells after exposure to different stress conditions typified by simulated ischemia and elevated hydrostatic pressure. After the exposure to these stressors, we observed that glial cells secreted tumor necrosis factor-alpha (TNF-alpha) as well as other noxious agents such as nitric oxide into the coculture media and facilitated the apoptotic death of retinal ganglion cells as assessed by morphology, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and caspase activity. The glial origin of these noxious effects was confirmed by passive transfer experiments. Furthermore, retinal ganglion cell apoptosis was attenuated approximately 66% by a neutralizing antibody against TNF-alpha and 50% by a selective inhibitor of inducible nitric oxide synthase (1400W). Because elevated intraocular pressure and ischemia are two prominent stress factors identified in the eyes of patients with glaucoma, these findings reveal a novel glia-initiated pathogenic mechanism for retinal ganglion cell death in glaucoma. In addition, these findings suggest that the inhibition of TNF-alpha that is released by reactivated glial cells may provide a novel therapeutic target for neuroprotection in the treatment of glaucomatous optic neuropathy.

The use of polyunsaturated fatty acids in ocular hypertension.: A study with blue‐on‐yellow perimetry

SummaryThe authors have evaluated the efficacy of systemic treatment with omega‐3 polyunsaturated fatty acids in improving the blue/yellow perimetric indices in patients suffering from ocular hypertension.A total of 40 such patients with mean IOP 22.4±2.6 mmHg, who showed pathological values of mean defect (MD) and the correct pattern standard deviation (CPSD) with blue/yellow perimetry, were treated. Omega‐3 polyunsaturated fatty acids were administered in high doses to them. After three months of therapy, significant improvements in both MD (from —4.845 ± 2.571 dB to —3.720 ± 2.324 dB (p&lt;0.001) and CPSD (from 3.115 ± 1.647 db to 2.860 ± 1.518 dB (p&lt;0.023) were seen in the treated group.Polyunsaturated fatty acids must be considered an efficacious supportive therapy in the prevention and treatment of glaucomatous optic neuropathy.