GlaucoT Glaucoma Treatment Glasses in the Treatment of Primary Open-Angle Glaucoma

Background: Glaucoma, a neurodegenerative disease, is characterized by the death of retinal ganglion cells and their axons. This damage affects all visual pathways up to the visual center in the brain. Although increased intraocular pressure is considered the most important modifiable risk factor in glaucoma, many factors play a role in its pathogenesis and progression. Different classifications have been proposed for various types of glaucoma. Accordingly, glaucoma; * Open angle or closed angle depending on the iridocorneal angle, * Primary or secondary, depending on the presence of etiological factors that may cause increased intraocular pressure, * According to the age of onset of glaucoma, it can be classified as congenital, childhood or adult glaucoma. In general, POAG is the most common type of glaucoma, accounting for 60-70% of cases. This is followed by secondary glaucomas (30%), primary angle-closure glaucomas (12%) and congenital glaucomas (3%). POAG, also known as simple chronic glaucoma, is a disease with elevated intraocular pressure, cupping at the optic nerve head, and loss of visual field. POAG is an insidious onset, progressive, bilateral anterior optic neuropathy. One of the features that distinguishes it from other types of glaucoma is the open appearance of the iridocorneal angle. The most common type of glaucoma is POAG, and its incidence is 0.5-6.6% over the age of 40 in western countries. The incidence of POAG increases with age. POAG is a progressive neurodegenerative optic neuropathy characterized by high IOP (≥21 mmHg), glaucomatous optic disc, retinal ganglion cells and retinal nerve fiber layer (RNFL) damage, and open iridocorneal angle. POAG is bilateral and usually has an asymmetrical onset. Until the last period, it usually does not give any symptoms. POAG is the most common type of open-angle glaucoma and is one of the leading causes of preventable blindness. Since POAG is asymptomatic in the early stages, the diagnosis is usually made after irreversible visual damage has occurred. With early diagnosis and appropriate treatment, the disease can be caught before significant loss of vision develops. Open iridocorneal angle, IOP above 21 mm Hg, and vertical enlargement of the optic disc cupping are clinical findings of POAG. As a result of the glaucomatous damage, severe visual field and visual acuity losses develop. Although the biggest risk factor for the progression of the disease is high IOP, it is known that other factors also play a role, and glaucoma can develop even under normal pressure. Therefore, lowering the intraocular pressure alone cannot cease optic nerve damage in some patients. The incidence of POAG is increasing with the aging population. While there were approximately 44 million cases of POAG all over the world in 2013, it was estimated that this number would increase to around 53 million in 2020. Ethnical differences are very common, and they are more common in the black race than in the white race and Asian race. The prevalence in the black race, where it is most common, was found to be 5.2% at the age of 60 and 12.2% at the age of 80 years. Its incidence increases with age. In some studies, it was observed at similar rates in men and women, while in some studies it was observed slightly more in men. Family history is a risk factor for POAG. This result reveals the importance of genetic transmission. Although many risk factors such as high IOP, family history, race, advanced age, and myopia have been identified, the main cause of glaucomatous optic neuropathy is unknown. Humor aqueous (HA), produced by the non-pigmented epithelial cells of the ciliary body, is excreted mostly iridocorneal via the juxtacanalicular trabecular network and Schlemm's canal (conventional), and to a lesser extent by the uveoscleral route and enters the venous circulation. POAG 'Rather, it is known that there is a resistance to conventional outflow at the level of the juxtacanalicular trabecular meshwork and the inner wall of Schlemm's canal. In eyes with glaucoma, histological changes in the collagen structure of the trabecular meshwork, the spaces between the trabecular meshwork, and the juxtacanalicular connective tissue, and changes in endothelial cell functions were detected. In addition to these histological changes, collapse in Schlemm's canal is thought to contribute to the increase in resistance to outflow. Along with these, different theories have been proposed that increase the outflow resistance. These theories can be listed as follows: * Occlusion of the trabecular meshwork by accumulated substances, * Loss of trabecular endothelial cells, * Decreased trabecular mesh pore density in Schlemm canal inner wall endothelium, loss of giant vacuoles, * Loss of normal phagocytic activity, * IOP 'Disturbances in the neurological feedback mechanism that concerns the id. In addition, complex mechanisms such as increased oxidative stress, excitotoxicity, hardening of the lamina cribrosa structure, vascular regulation disorder and ischemia, mitochondrial dysfunction, decrease in neurotrophic factors as a result of mechanical stress-induced axoplasmic flow disruption, autoimmunity, low cerebrospinal fluid (CSF) pressure also play a role in the etiopathogenesis. The aim of the treatment is to preserve the visual functions without impairing the patient's quality of life. When making a treatment plan, the stage of glaucoma, the pressure level at which it progresses, and the expected life expectancy of the patient should be considered. Life expectancy and the stage of the disease are important criteria in the choice of treatment. A young patient with mild glaucomatous injury should be treated more aggressively than an 80-year-old patient with moderate glaucomatous injury. Currently, all treatment modalities are aimed at lowering IOP, as IOP is the only factor that can be intervened. According to the treatment protocol accepted all over the world, IOP is tried to be controlled primarily with medical treatment. In cases where medical treatment is insufficient, laser trabeculoplasty or filter surgery is applied. Today, medical treatment of glaucoma begins with eye drops and usually monotherapy (single molecule therapy). If adequate IOP reduction is not achieved with the drug that is started, it is switched to another drug from the same group. If the target pressure is still not reached, combined therapy is started. In combination therapy, drugs that lower IOP by different mechanisms should be combined. Fixed combinations are preferred for ease of use. PAAG 'Drugs used in the treatment of: * Parasympathomimetic drugs (cholinergic drugs), * Sympathomimetic drugs, * Beta blockers, * Hyperosmotic drugs, * Calcium channel blockers, * Prostaglandin analogues, * Carbonic anhydrase inhibitors, * Rho kinase inhibitors. More than half of patients suffer from progressive visual field loss in long-term medical treatment. However, while the annual rate of visual field loss is 32% in inadequately treated patients, this rate is lower in patients with well-controlled IOP. These methods are commonly aimed at lowering IOP. However, no method currently used in the clinic can fully treat glaucoma and glaucoma-related neurodegeneration. Unfortunately, despite adequate pressure control, many patients continue to experience irreversible vision loss. The current treatment approach focuses on IOP-independent treatments and neuroprotection. In this study, flicker light therapy, the effectiveness of which was investigated in the treatment of glaucoma based on some methods used in different diseases, is described for the first time in glaucoma. In Alzheimer's, another neurodegenerative disease, similar to glaucoma, its pathophysiology is characterized by impaired microcirculation in the brain and retina and pathological chronic activation of microglia, resulting in metabolite accumulation in the extracellular matrix and chronic inflammation, followed by neurodegeneration and axon loss. There are many studies on this subject. Studies investigating the neurodegenerative properties of glaucoma have found similarities in the pathophysiology of Alzheimer's disease and glaucoma. 40 Hz flicker of light Alzheimer 's the positive effects on the knitted cortex have also been shown in studies. 40 Hz flicker light is aimed to reduce glaucoma and retinal ganglion cell loss due to glaucoma, by reducing neurodegeneration by decreasing amyloid and metabolite accumulation by increasing both microglial phagocytic activation effect and retinal blood flow. In this study, it was planned to investigate the effect of reducing the progression of glaucomatous damage by applying 40 Hz flicker light therapy for 1 hour a day to POAG patients. It is planned to use visual field test, measurements of retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC) layer thicknesses in optical coherence tomography to investigate the effectiveness of the treatment.