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choroida · 7 months

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Fundus Photography: Capturing the Window to Eye Health

Fundus photography, also known as retinal photography, is a crucial diagnostic tool used in ophthalmology to capture images of the back of the eye. These images, known as fundus photos, provide valuable insights into the health of the retina, optic nerve, and blood vessels, aiding in the detection and management of various eye conditions.

Importance of Fundus Photography in Ophthalmology

In ophthalmology, where accurate diagnosis is key to effective treatment, fundus photography plays a vital role. It allows ophthalmologists to visualize and document pathological changes in the eye, facilitating early detection of conditions such as diabetic retinopathy, glaucoma, and age-related macular degeneration.

Fundus Photo Equipment and Techniques

Types of Fundus Cameras

There are several types of fundus cameras available, ranging from traditional tabletop models to handheld devices and even smartphone attachments. Each type has its advantages and is suited to different clinical settings.

Preparation for Fundus Photography

Before capturing fundus images, proper patient preparation is essential. This includes dilating the pupils using eye drops to allow better visualization of the retina and ensuring optimal lighting conditions in the examination room.

Fundus Photo Procedure

Patient Preparation

Patients undergoing fundus photography are usually instructed to avoid caffeine and other stimulants that could affect pupil dilation. They are also informed about the procedure and reassured about its non-invasive nature.

Capturing the Image

During the procedure, the patient positions their chin on a rest while the photographer adjusts the camera settings and focuses the lens on the eye. Multiple images may be taken from different angles to capture a comprehensive view of the fundus.

Image Interpretation

Once the images are captured, they are reviewed by the ophthalmologist for signs of abnormalities such as hemorrhages, exudates, or changes in vessel caliber. These findings help guide further diagnosis and treatment decisions.

Common Uses of Fundus Photography

Diabetic Retinopathy Screening

Fundus photography is widely used in diabetic retinopathy screening programs to detect early signs of retinal damage caused by diabetes. Regular screening is essential for preventing vision loss in diabetic patients.

Glaucoma Detection

In glaucoma management, fundus photography aids in assessing the optic nerve head and monitoring changes over time. It helps identify signs of optic nerve damage, such as cupping, which are indicative of glaucomatous damage.

Macular Degeneration Monitoring

Age-related macular degeneration (AMD) is a leading cause of vision loss in older adults. Fundus photography enables clinicians to track the progression of AMD and evaluate the effectiveness of treatments such as anti-VEGF therapy.

Advantages of Fundus Photography

Fundus photography offers several advantages over traditional methods of retinal examination, including non-invasiveness, high-resolution imaging, and the ability to document changes over time. It also allows for easy sharing of images for consultation and education purposes.

Challenges and Limitations

Despite its benefits, fundus photography has some limitations. Patient cooperation, particularly in maintaining steady fixation, can affect image quality. Technical challenges such as glare and artifacts may also impact interpretation.

Future Trends in Fundus Photography

Advancements in technology, including artificial intelligence and telemedicine, are likely to shape the future of fundus photography. Automated image analysis algorithms and remote screening platforms hold promise for improving accessibility and efficiency in eye care.

Conclusion

Fundus photography is a valuable tool in the armamentarium of ophthalmologists, enabling detailed visualization of the retina and aiding in the diagnosis and management of various eye conditions. With ongoing innovations, its role in eye care is expected to expand further in the future.

FAQs

How often should fundus photography be performed?

The frequency of fundus photography depends on individual risk factors and the presence of underlying eye conditions. Your eye care provider can recommend the appropriate screening intervals.

Is fundus photography covered by insurance?

In many cases, fundus photography is covered by insurance, especially when performed for medical reasons such as diabetic retinopathy screening. However, coverage may vary depending on your insurance plan.

Are there any risks associated with fundus photography?

Fundus photography is considered safe and non-invasive. However, temporary side effects such as blurred vision from pupil dilation may occur but typically resolve within a few hours.

Can fundus photography detect all eye conditions?

While fundus photography is effective in detecting many eye conditions, it may not capture certain pathologies that are located deeper within the eye or require specialized imaging techniques.

Is fundus photography painful?

No, fundus photography is a painless procedure. Patients may experience mild discomfort from pupil dilation drops, but the actual imaging process is quick and discomfort-free.

#choroid #choroida #eyes #health #medical care #eyecare #fundus examination #eye health #medical devices #medical equipment

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vaidyaeyehospital · 10 months

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What are the tests Performed to Diagnose Glaucoma?

Several tests are performed to diagnose glaucoma, a group of eye conditions that can lead to optic nerve damage and vision loss. The specific tests may vary based on the suspected type of glaucoma and the individual's eye health. Here are common tests performed to diagnose glaucoma:

1-Tonometry:

Measures intraocular pressure (IOP), which is a key risk factor for glaucoma. Elevated IOP can indicate a higher risk of glaucoma, although normal IOP does not rule out the condition.

2-Ophthalmoscopy:

Allows the eye care professional to examine the optic nerve for signs of damage. Changes in the appearance of the optic nerve head, such as cupping, may suggest glaucoma.

3-Visual Field Test (Perimetry):

Assesses the full horizontal and vertical range of what a person can see in their field of vision. Glaucoma often leads to peripheral vision loss, which can be detected through this test.

4-Gonioscopy:

Examines the drainage angle of the eye to determine if it is open or closed. This helps in classifying the type of glaucoma, such as open-angle or angle-closure glaucoma.

5-Pachymetry:

Measures the thickness of the cornea. Corneal thickness can influence intraocular pressure readings, and thin corneas may be associated with a higher risk of glaucoma.

6-Optical Coherence Tomography (OCT):

Uses light waves to create detailed cross-sectional images of the optic nerve and retina. It helps in assessing the thickness of the retinal nerve fiber layer, which can be indicative of glaucomatous damage.

7-Retinal Imaging:

Captures high-resolution images of the retina, helping to detect any structural changes or damage related to glaucoma.

8-Visual Acuity Test:

Measures how well an individual can see at various distances using an eye chart. While not specific to glaucoma, changes in visual acuity may be observed in advanced stages of the condition.

9-Corneal Hysteresis Measurement:

Evaluates the cornea's ability to absorb and return energy during deformation. This measurement can provide additional information about the biomechanical properties of the cornea and the risk of glaucoma progression.

It's important to note that glaucoma diagnosis is often a combination of these tests, and regular eye examinations are crucial, especially for individuals at higher risk, such as those with a family history of glaucoma or individuals over the age of 40. If you have concerns about your eye health, consult with an eye care professional for a comprehensive examination and appropriate testing.

For more information, Consult Dr. Vaidya Eye Centre as they provide best Glaucoma Treatment in Mumbai or you can contact us on 9004496621.

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amitshahneuro · 11 months

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Why are VEPs performed?

Visual Evoked Potentials (VEPs) are performed for several reasons, primarily related to their diagnostic and clinical applications in assessing the visual system and specific neurological conditions. Here are some key reasons why VEPs are performed:

1. Diagnosis of Optic Nerve Disorders:VEPs are valuable in diagnosing and evaluating conditions that affect the optic nerve, such as optic neuritis, which is often associated with multiple sclerosis. Abnormal VEP responses can help confirm the presence of optic nerve damage.

2. Monitoring Multiple Sclerosis: VEPs are frequently used to monitor the progression of multiple sclerosis (MS). Changes in VEP responses over time can indicate the development or progression of demyelination in the visual pathway, which is a common feature of MS.

3. Assessing Visual Pathway Function: VEPs provide a quantitative assessment of the function of the visual pathway, from the eye to the visual cortex. This information is essential in evaluating the integrity of the visual system.

4. Glaucoma Evaluation: VEPs can be used in the assessment of glaucoma, a condition characterized by elevated intraocular pressure and optic nerve damage. They can help detect early signs of glaucomatous damage to the optic nerve before visual field loss occurs.

5. Visual Disorders Diagnosis: VEPs can assist in diagnosing various visual disorders, including congenital and acquired visual impairments, where the source of the problem may be related to the visual pathway or the brain's processing of visual information.

6. Differentiating Between Organic and Functional Visual Loss: In cases of unexplained vision loss, VEPs can be used to help distinguish between organic (physiological or neurological) and functional (psychological) causes. Organic causes often result in abnormal VEP responses.

7. Evaluating Visual Rehabilitation: VEPs can be used to assess the effectiveness of visual rehabilitation strategies, such as interventions for amblyopia (lazy eye) or visual prosthetic devices.

8. Research and Scientific Studies: VEPs are also employed in scientific research to gain insights into the functioning of the visual system and the processing of visual information in the brain.

It's important to note that VEPs are a valuable tool in the diagnostic process, but they are typically used in conjunction with other clinical assessments, medical history, and imaging studies to provide a comprehensive understanding of a patient's condition. The specific reason for performing a VEP may vary depending on the patient's symptoms and medical history.

It's essential to consult with Dr. Amit Shah, a healthcare professional or Neurologist in Malad practicing at Dr. Amit Shah Neurology Clinic for a proper diagnosis and individualized care.

#dr. amit shah #best neurologist in mumbai #neurologist in malad #Dr. Amit Shah Neurology Clinic #Why are VEPs performed #Visual Evoked Potentials

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markbeyerwrites · 2 years

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Seeming to be a bag lady and being a bag lady are not the same. Go look at a bag lady and this becomes axiomatic: there‘s a sour, rancid odor ten feet around her — the stench of a sort that takes weeks to ferment; hair like matted sackcloth; watery eyes, blurred and vaguely unfocused, or else glaucomatous; pants crotch stained by piss, soaked and dried a dozen times (the root source of the reek?). Yet here she is, in disguise.

(via What Beauty on Litsy)

#TokenRealist DareToReadThis booktofilm filmproducer hollywoodoption

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pathologyucgconference · 2 years

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Deep learning in ophthalmology and artificial intelligence

Deep learning-based artificial intelligence (AI) has attracted a lot of attention internationally recently. However, DL is only now starting to have an impact on healthcare. DL has been widely embraced in image recognition, speech recognition, and natural language processing. To detect diabetic retinopathy, retinopathy of prematurity, the glaucoma-like disc, macular oedema, and age-related macular degeneration, DL has been used to fundus images, optical coherence tomography, and visual fields in ophthalmology.

Screening, diagnosing and monitoring severe eye illnesses in individuals in primary care and community settings may be achieved using telemedicine and L in ocular imaging. However, there are also possible drawbacks to the use of DL in ophthalmology, such as technical and clinical difficulties, the inexplicability of algorithm outputs, medicolegal concerns, and physician and patient resistance to the 'black box' AI algorithms. In the future, DL might completely change how ophthalmology is practised. A description of the cutting-edge DL systems outlined for ophthalmic applications, potential difficulties in clinical deployment, and future directions are provided in this paper.

Diabetic retinopathy

The effective three-pronged approach to preventing blindness from DR consists of community-based screening, prompt referral, and appropriate treatment. However, finding sufficient screening resources is still difficult. The use of AI can provide mass population screening with minimal labour and maximum effectiveness, properly identify the pre-defined referrable disease for quick treatment, and so have far-reaching effects.

The early detection of retinopathy of prematurity is the cornerstone of management. A fully automated DL system was able to precisely diagnose plus illness despite the fact that expert- and telemedicine-based screening are well-established methodologies.

Screening is possible for the possibly blinding condition of glaucoma. On wide-angle OCTs, DL algorithms have been taught to recognise glaucoma-like disc and glaucomatous nerve fibre layer damage.

10th World Digital Pathology & AI Event on April 04-06, 2023 in Berlin, Germany

Current Uses of AI in Ophthalmology

Glaucoma subspecialty is a rapidly developing topic, and new technological developments are frequently published in the literature. The first use of AI in glaucoma focuses on intraocular pressure (IOP), with higher IOP levels causing glaucomatous alterations including a larger cup/disc ratio. To define IOP parameters more accurately for tracking the evolution of glaucoma, a continuous monitoring contact lens has been created.

Age-related macular degeneration, diabetic retinopathy, and retinopathy of prematurity are the three main themes of AI in the retina subspecialty (AMD). AI has been trained to recognise clinically significant macular oedema in diabetic retinopathy, enabling early diagnosis and treatment of DR. AI developments have also had an impact on retinopathy of prematurity, or aberrant blood vessel growth in the retina as a result of preterm delivery. ROP emergence and advancement have been quantified using computerized algorithms and machine learning techniques. Finally, AMD is a significant contributor to visual loss in the field of the retina and can be detected with OCT and fundus photography. Artificial intelligence's top priorities are both detection methods. In fact, research has shown that AMD diagnosis

Current Imaging Modalities in Neuro-Ophthalmology

Prior to exploring AI applications in neuro-ophthalmology, it is crucial to review the current imaging techniques now in use. Computed tomography (CT) and magnetic resonance imaging (MRI) are the two main imaging modalities used in neuro-ophthalmology, and each has certain benefits and drawbacks depending on the condition that an ophthalmologist is trying to diagnose. Additionally, it's critical to identify vascular anomalies that could be causing ocular disease with CT angiography (CTA) and MR angiography (MRA). Additionally, visual field testing with Humphrey Visual Field (HVF) perimetry is a crucial diagnostic technique.

10th World Digital Pathology & AI Conference on April 04-06, 2023 in Berlin, Germany

Applications of AI in Neuro-Ophthalmology

Papilledema, anterior ischemic optic neuropathy (AION), non-arteritic anterior ischemic optic neuropathy (NAION), and differentiating AION and NAION from glaucomatous optic neuropathy are three conditions of particular importance to neuro-ophthalmology, despite the fact that glaucoma, retina, and neuro-ophthalmology share many similarities (GON).

The laterality of a diseased process is crucial in neuro-ophthalmology for reducing the list of possible diagnosis. For instance, distinct disease conditions often lead to unilateral and bilateral optic disc edoema. In order to start the process of making a diagnosis, it is crucial for AI to be able to discriminate between the laterality of the right and left eye. In this regard, Liu et alDLS .'s rivalled Jang et almuch .'s bigger data set, achieving 98.78% accuracy. This leads to the intriguing finding that DLS can be reliable even with little amounts of data.

Conclusions

Ophthalmic AI systems are useful because they reduce the amount of time needed to analyse image data, give ophthalmologists a better knowledge of how diseases proceed, and help with prognosis, staging, and early diagnosis.

10th World Digital Pathology & AI Summit on April 04-06, 2023 in Berlin, Germany

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storesandmarket · 6 years

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Now is National #Glaucoma Week 2018 June 4-10 Get your #eyes tested and avoid #blindness! #GlaucomaScreening #GlaucomaAwareness #nationalglaucomaweek #Glaucomatous #glaucomasucks #tonometry #tonometer #blindness #glaucomatest #glaucomaweek #EyeHealth #ophthalmology #optometry #oftalmologo #oftalmologos #optometristas #Oftalmología #glaucomasurgery #Ophthalmic #glaucomacure #ojos #eye

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lupinepublishers · 4 years

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Lupine Publishers | A Review of Metabolic Sensors in Glaucoma

Trends in Ophthalmology Open Access Journal (TOOAJ)

Abstract

Glaucoma is the second leading cause of irreversible blindness worldwide. It is a multifactorial, progressive, chronic optic neuropathy that is characterized by loss of retinal ganglion cells (RGC) and optic nerve head (ONH) cupping including extra cellular matrix (ECM) remodelling and fibrosis at the lamina cribrosa (LC). Clinically this results in chronic, progressive peripheral visual field loss. The pathogenesis of glaucoma is not yet fully understood. Therefore, there is an urgent need to identify and target the underlying mechanisms governing ECM remodelling of the LC, in order to stop the progressive, chronic damage to the LC/ONH and irreversible visual field loss. This review identifies and examines some of the key metabolic processes and cellular sensors involved in the pathogenesis of ECM fibrosis in general but herein specifically in glaucoma, including mitochondrial dysfunction and adenosine monophosphate activated protein kinase (AMPK) upregulation. Furthermore, the development of novel therapeutics such as nicotinamide (NAM) and metformin are discussed as promising potential future therapeutic options for glaucoma.

Keywords: Glaucoma; Fibrosis; Extracellular Matrix (Ecm) Mitochondrial Dysfunction; Adenosine Monophosphate Activated Protein Kinase (Ampk); Nicotinamide (Nam); Metformin

Introduction

Glaucoma is the second leading cause of irreversible blindness worldwide. More than 67 million people are affected by glaucoma, which has a global prevalence of 3.5% in persons over the age of forty years [1]. Glaucoma is heterogenous group of progressive optic neuropathy disorders resulting in loss of peripheral field vision. The primary risk factor associated with the development of glaucoma is elevated intraocular pressure (IOP). Currently, lowering IOP is the only pharmacological treatment available for managing glaucoma [2]. However, there is a subset of glaucoma patients with normal IOP. Studies have shown that normal tension glaucoma (NTG) accounts for approximately 30% of all patients diagnosed with glaucoma [1]. This poses a significant treatment obstacle, as the efficacy of IOP lowering drops is highly variable among this cohort of NTG patients [3]. The major clinical presentations of glaucoma include cupping and pallor of the ONH. Glaucoma is characterized by loss of retinal ganglion cells (RGC) and optic nerve head (ONH) cupping [3]. This dysfunction occurs in the cells of the lamina cribrosa (LC) region, which is a three-dimensional (3D), fenestrated, mesh like structure located in the ONH. Under normal circumstances, the LC functions as a structural support to unmyelinated RGC axons as they pass through posteriorly, before exiting the eye to the brain, becoming the optic nerve [4,5]. The LC is a biomechanically weaker structure when compared to the rest of the sclera and is thereby the putative site of RGC damage in glaucoma. Laminar cupping is connective tissue-based, with the LC progressively moving posteriorly and excavating beneath the anterior sclera canal leading to remodelling of extracellular matrix (ECM), stiffness and consequently fibrosis of the LC connective tissue in the ONH [3], which is driven by profibrotic growth factors such as transforming growth factor- beta (TGFβ) [6] and backward bowing. This results in optic nerve axon compression, axonal loss and, ultimately, chronic, progressive peripheral visual field defects [7].

The cellular mechanisms involved in glaucoma are not fully understood. Understanding these processes will lead to new methods of preventing chronic glaucomatous vision loss when conventional IOP-lowering treatments either fail to prevent progression (up to 20% of glaucoma patients continue to progress to blindness) [5], or adequate target pressures cannot be achieved due to ineffectiveness of or poor tolerance to medication. Thus, there is an urgent need to identify and target the underlying mechanisms of metabolism governing remodelling of the LC, in order to stop the progressive, chronic damage to the LC/ONH and irreversible visual field loss. This review aims to identify and examine some of the key metabolic processes and cellular sensors involved in the pathogenesis of fibrosis in glaucoma and investigate potential therapeutic options.

Fibrosis

Whilst the pathogenesis of glaucoma has yet to be fully elucidated, it is known that connective tissue fibrosis is one of the major pathological drivers of the disease. The term fibrosis is defined as the process of unchecked wound healing [8]. Fibrosis is involved in the pathogenesis of many systemic diseases involving multiple tissue and organ systems such as the heart, liver, lungs and kidneys. Fibrosis results in chronic, progressive, pathological destruction of tissue and organ function [9,10]. The normal wound healing response of tissues to damage is a highly complex process, involving activation of the coagulation cascade, inflammation, angiogenesis, cellular proliferation and tissue remodelling [10]. Activated fibroblasts, known as collagen producing myofibroblasts that are highly contractile, drive the wound healing response to an acute injury by remodelling extracellular matrix (ECM) resulting in the restoration of tissue integrity and previously damaged parenchymal cells [11-12]. This normal wound healing process becomes dysregulated and uncontrolled in states of chronic inflammation, recurrent or repetitive injury or chronic hypoxia, resulting in tissue fibrosis. The ECM is composed primarily of fibrous proteins (primarily collagens, glycoproteins such as fibronectins and vitronectins, and laminins) and proteoglycans [11]. ECM provides structural and biochemical support to cells and tissues in multicellular organisms, in addition to functioning biochemically as a substrate for cell adhesion, growth and differentiation. Thus, ECM is essential for normal connective tissue structure, architecture, differentiation, and homeostasis [14].

Fibrosis in Glaucoma

Fibrosis is characterized by a pathological deposition and accumulation of ECM by myofibroblasts. It is already known that there is an excessive accumulation of ECM in glaucomatous LC tissue, trabecular meshwork (TM) cells and Schlemm’s Canal [11], which results in ONH remodelling and damage. In response to elevated IOP, the ECM genes of glaucomatous LC cells become structurally stiffer and less compliant than normal LC cells, thereby acting as a pro-fibrotic driver of disease [12-15]. ECM stiffness is also a hallmark of tissue ageing. It is known that aged tissues display decreased levels of proteins cadherin and catenin, thin basement membranes and apoptotic resistant, senescent fibroblasts which release fibronectin, matrix metalloproteinases (MMPs) and pro-fibrotic cytokines [13]. Furthermore, aged tissues display a defective upregulation of cross-linked collagen fibres which drives tissue stiffness and rigidity [12], and older age is a significant risk factor for glaucoma. Several other pro-fibrotic mediators are overexpressed in glaucoma, including cytokine transforming growth factor ß (TGFß) and thrombospondin-1 (TSP-1) [3]. TGFß, which is present in the aqueous humour, is a pro-fibrotic cytokine that induces the differentiation of fibroblasts to their collagen secreting form, myofibroblasts. TGFß controls ECM synthesis and activates ECM through the signal transducer family Smad proteins [16,17]. When activated, Smad proteins translocate to the nucleus where they function to regulate gene transcription [13,15]. Our group has shown that LC cells from glaucoma donors [9] have many characteristics of myofibroblasts including the expression of α-SMA, and a marked expression of pro-fibrotic ECM genes and proteins (e.g. collagen 1A1, periostin, fibronectin) upon stimulation with TGFβ [10], cyclic stretch11, and oxidative stress [12]. In another study, we found an increase of F-actin stress fibres (indicating enhanced cellular reorganisation) and increased substrate stiffness elicits a myofibroblastic phenotype in human LC cells [13,14].

Mitochondrial Dysfunction in Glaucoma

Mitochondria, commonly known as the ‘powerhouse’ of the eukaryotic cell, are cellular organelles responsible for the energy production of the cell, and the regulation of cellular metabolism [18]. Mitochondria produce adenosine triphosphate (ATP) primarily through oxidative phosphorylation (OXPHOS), in addition to glycolysis and the Krebs cycle (citric acid cycle). Energy disruption, particularly mitochondrial dysfunction, which results in the toxic accumulation of reactive oxygen species (ROS) within cells has been studied in several disease models over the past decade including cancer, diabetes, and neurodegenerative diseases including Alzheimer’s Disease, muscular dystrophy [19]. A number of studies have examined the role of mitochondrial dysfunction in both human and animal models of glaucoma.

Mitochondrial Dysfunction Studied in Glaucomatous TM Cells

TM cells in glaucomatous human POAG patient eyes were shown to have dysfunctional and defective mitochondria, which resulted in uncontrolled, elevated IOP. These TM cells were more also more vulnerable to Ca2+stress when compared to healthy aged, matched controls, and authors postulated that this vulnerability contributes to sustained, chronic rise in IOP [20]. A recent study of a cohort of ocular hypertensive patients with a longstanding history of raised IOP (‘susceptible’), but whom had never developed glaucoma was performed. Lascaratos etl al found that the ‘susceptible’ patient cohort with ocular hypertension demonstrated both higher levels of mitochondria and ADP phosphorylation, and were better able to withstand and manage cellular stresses such as oxidative stress and excess calcium, versus patients with glaucoma and aged matched controls [21]. They concluded that enhanced mitochondrial activity in a systemic capacity confers protection to the development of RGC damage, ON damage and ultimately the development of glaucoma in addition to identifying mitochondria as a disease biomarker [21]. It has been shown via electron microscope analysis that mitochondria found in the ON in glaucomatous eyes are notably smaller and fewer when compared to normal age matched eyes [22,23] Furthermore, studies have demonstrated a reduced number of cristae within mitochondria, which means cells contain less tools to perform effective OXPHOS. Consequently, cells possess lower and deficient energy capacity [19,23]. This has a direct downstream effect on axonal survival in circumstances such as glucose depletion. Axons require functional mitochondria in order to survive on lactate, which normally bypasses the process of glycolysis on conversion to pyruvate. However, it has been demonstrated in glaucomatous optic nerves that mitochondria are not capable of effective regeneration, thereby leading to downstream axonal death [22].

Mitochondrial Dysfunction Studied in Glaucomatous Retinae

In glaucoma, defective mitochondrial function is associated with both disease susceptibility and disease resistance [19]. In fact, in vivo studies of mice have demonstrated mitochondrial dysfunction to be one of the primary detectable features of stressed RGC’s in response to elevated IOP [24]. Inman et al. demonstrated that defective mitochondrial DNA and metabolic dysregulation occur prior to evidence of neurodegeneration [19]. It is established that RGC’s require a large quantity of ATP due to the dense axonal volume of mitochondria surrounding the OHN. Mitochondrial dysfunction in RGCs, which results in defective cellular repair process thereby enhances their susceptibility to apoptosis and subsequent glaucomatous pathogenesis [25]. Harun et al. studied DBA/2J mice models and showed that monocarboylate transporters (MCT), which function as lactate and ketone transportation molecules, are under expressed in glaucomatous retinae, and result in decreased ATP production [26] Mice received an injection of MCT2 (AAV2:MCT2) in order to restore MCT2 to normal cellular levels, and it was shown that RGCs were preserved in this group of mice. Importantly, following the induction of MCT2 overexpression in DBA/2 J retinae via AAV2:MCT2 injection, mitochondrial function in the retinae of these mice improved. Additionally, an increase in RGC density and an enhancement of energy homeostasis were also noted in DBA/2J mice versus the untreated cohort. This study demonstrates both the neuroprotective effect of MCT2 on glaucomatous RGCs, in addition to highlighting the potential therapeutic benefit enhanced cellular energy input may have in glaucoma treatment in the future [26].

Mitochondrial Dysfunction in Blood Analyses of Glaucoma Patients

Mitochondrial dysfunction in lymphocytes of a cohort of primary open angle glaucoma (POAG) patients has been examined [27]. Lee et al. analysed ATP production and cellular respiration in POAG patients and found that POAG lymphoblasts displayed decreased levels of complex 1-driven ATP synthesis and complex-1 driven maximal respiration when compared to controls. Complex 1 (NADH: ubiquinone oxidoreductase), whose role is electron transport, is the biggest enzymatic complex of the mitochondrial respiratory chain [28]. There was no difference in complex-2 linked respiration between the two groups, nor was there any difference in ATP production when cells were grown on galactose media (thereby reliant on mitochondria OXPHOS [27]). Similarly, another recent study conducted a comparative analysis of mitochondrial OXPHOS complex-1 dysfunction in patients with Leber Hereditary Optic Neuropathy (LHON) when compared to POAG patients. LHON is a mitochondrially inherited disorder involving complex-1 mutations, and is characterized by the quick, aggressive and irreversible loss of RGCs [29]. POAG, LHON and normal lymphoblasts were cultured on galactose media, and the growth rates of the groups were examined. POAG lymphoblasts and LHON lymphoblasts grew 1.47 and 2.35 times slower than control lymphoblasts. Furthermore, when compared to controls, POAG lymphoblasts demonstrated an 18% reduction in complex-1 activity, versus a 29% decreased in LHON lymphoblasts. Finally, when complex-1 ATP synthesis between the groups was compared to control samples, a 19% reduction was noted among the POAG group whereas a 17% decrease was observed in LHON patients [29]. This study demonstrates OXPHOS impairment in both POAG and LHON patients and proposes that the milder dysfunction of the POAG group versus LHON patients might reflect a less aggressive nature and progression of glaucoma. Finally, this study highlights the potential role of restoring mitochondrial function as a promising therapeutic target for diseases characterized by mitochondrial dysfunction, including glaucoma. A study using Gene-Set Analyses was conducted on a cohort of POAG and NTG patients to assess mitochondrial gene associations [30]. Khawaja et al. identified a strong association between POAG and lipid metabolism pathways (P<0.002) and butanoate metabolism, which is a carbohydrate metabolism pathway (P<0.004). This study demonstrates an important role of lipid and carbohydrate metabolism in the disease pathogenesis of POAG.

Mitochondrial Dysfunction in Glaucomatous LC Cells

Our group has demonstrated that glaucoma LC cells proliferate at a higher rate than normal LC cells [15] and show mitochondrial dysfunction [16]. Kamel et al. conducted a detailed mitochondrial bioenergetic assessment on normal and glaucoma human LC cells [31] which revealed significantly abnormal mitochondrial respiratory bioenergetic function in human glaucoma LC cells when compared to controls. Decreased ATP production at basal levels, reduced OXPHOS and increased glycolysis were observed. Furthermore, MCT1 (OXPHOS marker), MCT4 (glycolysis marker), MTHFD2 (folate-mediated one-carbon metabolism marker), and GLS2 (glutaminolysis marker) were overexpressed in the glaucoma patient cohort. Thus, the findings of this study indicate that glaucoma cells undergo a process of ‘metabolic reprogramming’, and essentially switch from OXPHOS to aerobic glycolysis. This phenomenon is known as ‘the Warburg effect’, and it is a well-known, longstanding feature of neoplastic cells and cancer associated fibroblasts (CAF) [32,33].

The Role of Nicotinamide (NAM) in Glaucoma

NAD+ is activated by caloric restriction, fasting, exercise and AMPK. NAD+ is metabolised to nicotinamide (NAM) by NAD+ consuming enzymes such as CD38, Sirtuins and poly adenosine diphosphate ribose polymerase (PARPs). NAM is a water-soluble form of niacin (Vitamin B3). NAM can be converted to nicotinamide mononucleotide (NMN) by nicotinamide phosphoribosyl transferase (NAMPT) and then to NAD+ by nicotinamide mononucleotide adeneylytransferase 1 and 3 (NMNAT 1-3), via the salvage and pathway. Nicotinamide N-Methyl Transferase (NNMT) catalyses the methylation of NAM to N-methyl-nicotinamide (metNAM), which is subsequently metabolised further to N1-methyl-2-pyridine-5-carboxamide (2py) or N1-methyl-4-ppyridone-3-carboxamide (4py) utilizing the methyl donor S-adenosyl methionine (SAM) from the methionine cycle. 2py and 4py are the primary metabolites of NAM. NAM in reversing or halting disease pathogenesis. For example, NAM supplementation studied in obesity models in mice resulted in reduced oxidative stress and inflammation as well as repleted glycogen storage capacity [34]. NAM supplementation however, had no direct effect on lifespan, rather it enhanced healthspan [34].

The potential role of bioavailable NAM as a drug therapeutic target has been studies in animal models of glaucoma [24]. Williams, et al. studied DBA/2J mice models and showed that nicotinamide has a neuroprotective role in glaucoma. In glaucoma, reduced levels of NAD+, mitochondrial damage and glutathione depletion result in fragile, vulnerable RGCs. A single molecule of low dose NAM (NAMLo), high dose NAM (NAMHi) and finally NMNAT gene therapy was administered [24]. NAMLo mice demonstrated neuronal protection against glaucoma development, with no mitchondrial dysfunction, and decreased levels of DNA damage observed. NAMLo had no impact on IOP levels. 93% of NAMHi mice displayed no cellular signs optic nerve damage. Furthermore, NAMHi had a protective effect on IOP levels. This study implies that NAMHi confers not only a protective effect against glaucoma development but a protective effect on cellular types other than RGCs [24]. Another recent study led by Hiu, et al. demonstrated an improvement of inner retinal function in glaucoma patients following the administration of NAM supplementation [35]. They conducted a randomised control trial of fifty-seven patients with known, well controlled glaucoma. Patients were commenced on a regimen of NAM over three months. (1.5g/day for 6/52 followed by 3.0g/day for 6/52). Photopic negative response (PhNR) which is an electroretinogram (ERG) parameter was used as the measurement of inner retinal function (Saturated PhNR amplitude = Vmax). The study found that Vmax improved by 14.8%(p=0.02) in patients receiving NAM versus 5.2% (p=0.27) in the placebo group. When comparing visual field (VF) mean deviation (MD) 27% of patients on NAM improved by ≥1dB, and additionally fewer patients on NAM demonstrated any worsening of VF (4%), versus the control group (p=0.02). This study further highlights a promising potential for NAM supplementation in the treatment of glaucoma, although it is clear that further studies must be performed on a larger scale in order to fully elucidate the effectiveness and determine the long term safety of NAM in glaucoma therapy.

Nicotinamide adenine dinucleotide (NAD+) is found in the cytoplasm, mitochondria and nuclei of eukaryotic cells [36]. NAD+ plays a central role in the regulation of several biological processes including metabolism, cell signalling, DNA repair and cellular longevity [37]. Reduction in NAD+ levels have been associated with several age-related diseases, including carcinoma, cardiovascular disease (CAD), neurodegenerative and metabolic disorders [38]. NMNAT2, an enzyme producing NAD is essential for RGCs, healthy axons and in the prevention of axonal degeneration [39]. NMNAT2 is a survival factor necessary for axon survival. NMNAT2 null mice demonstrate truncated RGC axons and have no optic tract. Furthermore, siRNA knockdown of NMNAT2 results in the degeneration of neurons despite the absence of injury [39]. Mice were injected with AAV2.2 which contained the Nmnat1 gene. >70% of mice treated with this vector were found to have no clinical or pathological signs of optic nerve damage. Finally, mice were treated with both Nmat1 gene in addition to NAMLo. 84% of mice receiving this combination therapy were free of any glaucomatous damage, therefore it is postulated that a combination therapy confers additional protection and reduces vulnerability of the RGC cells of the LC to glaucomatous changes [24]. A number of studies have examined the potential therapeutic role of NAM in Parkinsons Disease (PD) patients. One mouse model study conducted by Harrison et al. showed that NAM administration improved locomotor responses and lessened dopamine depletion, thereby demonstrating a neuroprotective role for NAM [40]. Conversely, however, other studies have shown that NAM is associated with PD and exacerbates neurodegeneration [41]. Interestingly, levels of NNMT and metNAM were found to be raised in PD brains [42]. These conflicting reports warrant further analyses and studies in order to accurately elucidate the role of NAM in PD and neurodegenerative diseases.

Nicotinamide N-Methyl Transferase (NNMT)

Nicotinamide N-Methyl Transferase (NNMT) is a cytosolic enzyme that is expressed at the highest level in the liver [40]. NNMT catalyses the methylation of NAM to N-methyl-nicotinamide (metNAM), which is subsequently metabolised further to N1-methyl-2-pyridine-5-carboxamide (2py) or N1-methyl-4-ppyridone-3-carboxamide (4py) utilizing the methyl donor S-adenosyl methionine (SAM) [37,40] [Figure 1]. NNMT eliminates NAM from the NAD+ synthesis pathway, resulting in depleted levels of NAD+. NNMT is expressed in several tissues such as the heart, brain, kidney and muscle, and its upregulation and overexpression has been linked with various disease pathogenesis such as cancer, metabolic, neurodegenerative and inflammatory disorders [37,43]. Furthermore, there have been several associations between high levels of SAM, which is a homocysteine precursor, and insulin resistance and cardiovascular disease (CAD) [44,45]. Importantly, high levels of serum NNMT and NAM are associated with increased severity of CAD [46]. In mice models, techniques such as genetic knockdown and drug inhibition of NNMT was found to be protective against obesity and type two diabetes [47]. Authors treated mice with a molecular analogue of NAD (JBSNF000088), which inhibited NNMT activity. Mice treated with the analogue displayed lowered body weight, an improvement to normal glucose tolerance and an improvement in insulin sensitivity [47].

Future Directions and Conclusion

The cellular mechanisms involved in glaucoma are yet to be fully elucidated. Understanding these processes will lead to new methods of preventing chronic glaucomatous vision loss when conventional IOP-lowering treatments either fail to prevent progression (up to 20% of glaucoma patients continue to progress to blindness) or adequate target pressures cannot be achieved due to ineffectiveness or poor tolerance to medication. Thus, there is a clear unmet need to target the underlying mechanisms governing the progressive fibrotic remodelling of the LC, to halt the progressive and ongoing fibrotic damage to the LC/ONH and visual field loss. It is clear that there are multiple systemic cellular processes at play simultaneously, and when combined, result in the development of glaucoma. Glaucoma may be described as a multifactorial disease entity, and it is likely that in the future, there will be no ‘one size fits all’ therapeutic option. It is evident, however, that mitochondrial dysfunction plays an integral role in the aetiology of glaucoma, and that the dysregulation of this organelle directly results in RGC susceptibility and vulnerability. Several studies have highlighted promising therapeutic targets in halting or even reversing this progression, including nicotinamide, insulin and metformin. AMPK is a highly conserved master regulator of metabolism, both at the cellular and organismal levels, whose function is extremely relevant not only for normal physiology, but also for the understanding of many metabolic diseases [54]. The examination of novel mechanisms of AMPK as the key metabolic sensor in LC cells in glaucoma will be vital to understand the driving force underlying fibrotic changes occurring in the LC. These activated LC myofibroblasts drive the fibrotic processes occurring in the LC. The glaucoma LC cells adapt to their pro-fibrotic role by increasing their proliferation, reducing apoptosis, and augmenting their metabolism. These activated LC myofibroblasts essentially undergo ‘metabolic reprogramming’ to utilise alternative high-energy sources to enhance cellular growth and development. Halting the pro-fibrotic activity and metabolism of glaucoma LC cells by restoring AMPK expression and activity to normal levels, could lead to a new therapeutic approach to reduce fibrosis in glaucoma. In conclusion, glaucoma is a multifactorial, progressive, chronic optic neuropathy. The second leading cause of irreversible blindness worldwide, the development of novel therapeutics to combat this disease is of paramount importance. This review has identified several key metabolic sensors whose dysregulation and dysfunction directly drive and promote disease development and progression. Whilst there have been several potential treatment options investigated for this disease in the last decade, it is clear that further research and clinical trials to fully determine the suitability and effectiveness of therapeutic targets are necessary.

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Borrowed Time and Borrowed World

read it on the AO3 at https://ift.tt/2UgtBsf

by Hyperion327

Take in this sight. Take in the vast expanse of greyness, unrelenting and abandoned by the Gods. Taste the ash on your tongue, smell it on the scant wind. Listen to the roar of what was once the main artery of a continent, now clogged and rotten like the heart of some gout-ridden nobleman gasping his last. There was once a city here, now ash. There were once lives here, now dust. Giant burned out torches tower where trees once stood, the force and the flame burning away their leaves and limbs and leaving behind only blackened stakes that point to the glaucomatous sky like the site of a great witch burning.

After the end, an alpha, his mate, and their pup make their way eastward, in the hopes of finding something, anything.

Words: 6581, Chapters: 1/1, Language: English

Series: Part 6 of A Rock to Cling to While We Catch Our Breath

Fandoms: Teen Wolf (TV)

Rating: Explicit

Warnings: Graphic Depictions Of Violence, Major Character Death, Rape/Non-Con

Categories: M/M

Characters: Derek Hale, Stiles Stilinski, Original Child Character(s), Scott McCall, Isaac Lahey, Melissa McCall, Sheriff Stilinski

Relationships: Derek Hale/Stiles Stilinski, Isaac Lahey/Scott McCall

Additional Tags: Alternate Universe - Post-Apocalypse, Gore, Body Horror, Implied/Referenced Rape/Non-con, Implied/Referenced Cannibalism, Time Skips, Post-apocalyptic road trips, Dark Derek Hale, Dark Stiles Stilinski, Werewolf Stiles Stilinski, Religious Discussion, Stand alone work, This is the third time I've used that road trip tag, Are you guys sensing a theme yet? Cause I sure am

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ao3-sterek · 5 years

Text

Borrowed Time and Borrowed World

read it on the AO3 at https://ift.tt/2UgtBsf

by Hyperion327

After the end, an alpha, his mate, and their pup make their way eastward, in the hopes of finding something, anything.

Words: 6581, Chapters: 1/1, Language: English

Series: Part 6 of A Rock to Cling to While We Catch Our Breath

Fandoms: Teen Wolf (TV)

Rating: Explicit

Warnings: Graphic Depictions Of Violence, Major Character Death, Rape/Non-Con

Categories: M/M

Characters: Derek Hale, Stiles Stilinski, Original Child Character(s), Scott McCall, Isaac Lahey, Melissa McCall, Sheriff Stilinski

Relationships: Derek Hale/Stiles Stilinski, Isaac Lahey/Scott McCall

read it on the AO3 at https://ift.tt/2UgtBsf

#ao3feed #sterek fics #sterek #fics

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ao3feed-scisaac · 5 years

Text

Borrowed Time and Borrowed World

read it on the AO3 at https://ift.tt/2UgtBsf

by Hyperion327

After the end, an alpha, his mate, and their pup make their way eastward, in the hopes of finding something, anything.

Words: 6581, Chapters: 1/1, Language: English

Series: Part 6 of A Rock to Cling to While We Catch Our Breath

Fandoms: Teen Wolf (TV)

Rating: Explicit

Warnings: Graphic Depictions Of Violence, Major Character Death, Rape/Non-Con

Categories: M/M

Characters: Derek Hale, Stiles Stilinski, Original Child Character(s), Scott McCall, Isaac Lahey, Melissa McCall, Sheriff Stilinski

Relationships: Derek Hale/Stiles Stilinski, Isaac Lahey/Scott McCall

read it on the AO3 at https://ift.tt/2UgtBsf

#scisaac #ao3feed #fanfic

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lupine-publishers-oajbeb-blog · 5 years

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Lupine Publishers | Lupine Publishers | The Possibility of Complex Treatment of Optic Nerve Atrophy based on Etiopathogenetic Approach using the New Classification of this Ophthalmopathology

Open Access Journal of Biomedical Engineering and Biosciences

Lupine Publishers | Open Access Journal of Biomedical Engineering and Biosciences

Abstract

Application of treatment, differentiated based on the degree of functional changes and stages of atrophy, type of atrophy and nature of the lesion, significantly alters the effectiveness of treatment when compared to the isolated electropharmocological stimulation and even more so compared to the traditional medication method of treatment.

Keywords: New clinical classification and treatment of optic nerve atrophy

Abbrevations: ONA: Optic Nerve Atrophy; PONA: Partial Optic Nerve Atrophy

Introduction

Optic nerve atrophy (ONA) is the end result of disease, intoxication, genetically determined abnormality or injury of retinal ganglion cells and/or their axons situated between the retina and the lateral geniculate bodies of the brain. The prevalence percentage of various optic nerve diseases in the eye disease hospital is approximately 1-1.5%, 19 to 26% of those cases resulting in complete atrophy of the optic nerve and incurable blindness. Causes of ONA are: diseases of retina and optic nerve (inflammation, dystrophy, including glaucomatic and involutional, poor circulation due to hypertension, atherosclerosis, diabetes, etc., swelling, profuse bleeding, compression and damage of the optic nerve), diseases and injuries of the orbit, Central nervous system diseases (optic-chiasm leptomeningitis, abscesses and brain tumors with increased intracranial pressure, neurosyphilis, demyelinating disease, traumatic brain injury), intoxication with methyl alcohol, antibiotics (streptomycin, gentamicin), anti- malarial drugs (quinine, hingamin). ONA may be a component or sole manifestation of a number of hereditary diseases (congenital amaurosis, hereditary optic nerve atrophy, etc.) [1,2].

Table 1:Clinical Classification of the Partial Optic Nerve Atrophy.

Treatment of optic nerve atrophy is a very complex and difficult problem because of the extremely limited regenerative ability of the neural tissue. All depends on how widespread the degenerative process in the nerve fibers is and whether their viability is preserved. Some progress in the treatment of optic nerve atrophy has been achieved with the help of pathogenetically directed influences aimed to improve the viability of nervous tissue. The development of new methods of treatment of partial optic nerve atrophy (PONA) has greatly enhanced the possibility of rehabilitation of patients with this pathology. However, the abundance of methods in the absence of clear indications complicates the choice of a treatment plan in each individual case. [1,3,4,5,6,7] The analysis of literature on diagnosis and treatment of PONA showed lack of clear classification and the existence of various approaches to the assessment of the severity of the disease[2,8,9,10]. The following classification presented in Table 1 was used to determine the treatment plan [7,9]. The purpose of work. To create a method of optic nerve atrophy treatment differentiated depending on severity and other individual characteristics of the patient and to analyze the effect of the application of this technique.

Material and Methods

To treat the patients with partial atrophy of the optic nerve, we use the following methods. Infita-a low-frequency pulse physiotherapy device designed to expose the central nervous system (CNS) to low-frequency pulse electromagnetic field (without direct contact with the patient), which results in an improved central blood flow, saturation of blood with oxygen, and increased redox processes in the nervous tissue. It has as the following characteristics: no output signal - a triangular voltage pulse with negative polarity, pulse frequency 20 - 80 Hz (most frequently used 40 - 60 Hz), pulse duration of 3 ± 2 V, recommended number of procedures 12 - 15, starting with 5 minutes, increasing to 10 and then 12 minutes beginning with the fifth procedure and so on up to 12 treatments. Treatment method, hereinafter called the direct electropharmacological stimulation (EPS), includes installation of a soft PVC catheter into the retrobulbar space and a repeated inoculation of various medications through it into the retrobulbar space selected based on the etiopathogenesis of the atrophy. All patients were infused with a 10% solution of piracetam and exposed to electrical stimulation through a needle electrode inserted into the retrobulbar space through the catheter with the device "AMPLIPULS" 40 minutes later [11,12].

Also the following surgical methods can be used -ligation of the superficial temporal artery, implantation of a collagen sponge into the subtenon space, decompression of the optic nerve. In connection with the specifics of performing of surgical procedures in our clinic the technique of their execution is given below. Ligation of the superficial temporal artery. Local anesthesia - lidocaine 2.0 % subcutaneously. A 3 cm long skin incision is made 1 cm in front of the tragus. The tissue is bluntly separated. The superficial temporal artery is ligated with two stitches and overlaps between them. Albucidum powder is infused into the wound. The soft tissue is sutured with catgut suture. Silk sutures are placed on the skin. The wound is treated with a solution of brilliant green dye, aseptic sticker is placed. Implantation of a collagen sponge into the subtenon space. Local anesthesia - lidocaine 2,0 % subcutaneously and dicain 0,5 epibulbarly. A 5-6 mm long skin incision is made in the upper nasal quadrant 5-6 mm away from the limbus, parallel to the limbus. A tunnel is formed between the sclera and the capsule of tenon to the posterior pole using a spatula. An implant of a collagen sponge 10 - 8 mm long and 5 - 6 mm wide, pre-soaked with the solution of emoxipine (cortexin, retinalamin and other drugs or their combinations) is implanted into the tunnel closer to the optic nerve. The suture is placed on the conjunctiva and under the conjunctiva, followed by antibiotics and dexamethasone. After the implantation, antibiotics and a solution of diclofenac is applied locally for 5 - 7 days [13,14].

Decompression of the optic nerve is performed under general anesthesia. Blepharostat is used. An incision is made on the inner side of the conjunctiva. The internal straight muscle is sutured up in front the tendon and is clipped off. Three incisions of the scleral ring around the optic nerve are made. The solution of albucid is applied, and the muscle is locked in place. The suture is placed on the conjunctiva. Dixon and antibiotics are placed under the conjunctiva. The following scheme of treatment was suggested for the peripheral section of the optic nerve:

i. Degree: Emoksipin + dexamethasone subcutaneously in the region of the mastoid process, mildronat + emoxipin subcutaneously in the temple region, vitamin B1 1,0, alternate vitamin B6 1.0 V/m with piracetam 5.0 V/m, low-frequency electromagnetic stimulation.

ii. Degree: Catheterization of the retrobulbar space, direct EPS + long-term melioration: dexamethasone + emoksipin 2 times, piracetam (or other schemes depending on etiology), implantation of a collagen sponge with emoxipin into the subtenon space (ICS), piracetam 20,0 intravenously with physiological saline 200,0.

iii. Degree: Catheterization of the retrobulbar space, direct EFS + piracetam, dexamethasone, emoksipin 2 times a day. Implantation of a collagen sponge with emoxipin into the subtenon space, ligation of the superficial temporal artery, piracetam 20,0 intravenously with physiological saline 200,0.

iv. Degree: Step 1 - decompression of the optic nerve, step 2 or in case step 1 is not possible (severe somatic pathology) - catheterization + direct EFS, piracetam, dexamethasone, emoksipin 2 times retrobulbarly into the catheter. Ligation of the superficial temporal artery (if not done earlier). Implantation of a collagen sponge with emoxipin into the subtenon space, fenotropil tablets according to the treatment scheme, piracetam 20,0 intravenously with physiological saline 200,0.

Treatment scheme for the lesion of the central part of the visual pathway.

a. Stage I: Glycine 1 tablet 3 times a day sublingually for one month, cavinton according to the treatment scheme, then phenotropil (tablets) according to the treatment scheme. "Infita” - percutaneous low-frequency electrical stimulation.

b. Stage II: Cortexin intramuscularly No. 10. Trental intravenously in a physiological saline No. 5 (or aminophylline). Cerebrolysin intravenously No. 5. Glycine 1 tablet 3 times a day for one month. "Infita” low-frequency electrical stimulation.

c. Stage III: Cortexin intramuscularly No. 10. Glycine sublingually 1 tablet 3 times a day for one month. Trental intravenously in a physiological saline No. 5 (or aminophylline). Cerebrolysin or actovegin intravenously No. 5. Piracetam 5,0 intramuscularly No. 10. Antiplatelet agents (aspirin, clopidogrel) if necessary.”Infita” - percutaneous low-frequency electrical stimulation.

d. Stage IV: Cortexin intramuscularly No. 10.Emoxipin intramuscularly No. 10. Trental intravenously No. 5. Cerebrolysin or actovegin or solkoseril No. 10 Piracetam 5,0 intramuscularly No. 10. Antiplatelet agents (aspirin, clopidogrel) if necessary. Catheterization with direct EPS, dexamethasone, piracetam, emoksipin retrobulbarly into the catheter.

In case of total lesion of the visual pathway the elements of both treatment schemes of the corresponding stages are combined. To compare the effectiveness of different PONA treatment schemes three groups of patients were formed. The first group consisted of 358 patients (508 eyes) with optic atrophy of various etiology and pathogenesis, getting treatment, differentiated based on the stage, localization and duration of existence of atrophy. The second group consisted of patients who, regardless of the stage of atrophy, were subjected to a course of electropharmacological stimulation: 107 patients (152 eyes). The control group consisted of 77 patients (126 eyes) who received only medication treatment. The percentage composition of the main types of dystrophy in all three groups was similar.

The main study group consisted of 136 glaucoma patients (183 eyes), 81 patients (122 eyes) with the atrophy of vascular origin, post-inflammatory atrophy was observed in 51 (76 eyes), cerebral in 25 patients (50 eyes), traumatic 52 patients (52 eyes), toxic in 13 patients (25 eyes). The second group included 36 patients with glaucoma (46 eyes), 14 patients (38 eyes) with the atrophy of vascular origin, post-inflammatory atrophy was observed in 16 (24 eyes), cerebral in 5 patients (10 eyes), traumatic in 18 patients (18 eyes), toxic in 8 patients (16 eyes). The control group consisted of 24 patients with glaucoma (42 eyes), 21 patients (32 eyes) with the atrophy ofvascular origin, post-inflammatory atrophy was observed in 14 people (22 eyes), cerebral in 3 patients (6 eyes), traumatic in 8 patients (10 eyes), and toxic in 7 patients (14 eyes). Patients of this group were treated in a conservative manner: emoxipin with mildronate subcutaneously in the temple region, emoksipin with dexamethasone subcutaneously in the area of the mastoid process, taufon under the conjunctiva, piracetam intramuscularly. The result of the treatment of patients with partial atrophy of the optic nerve depending on the type of treatment can be seen in Tables 2 & 3.

Table 2:Results of treating patients with partial atrophy of the optic nerve.

Table 3:Results of treating patients with partial atrophy of the optic nerve.

Note: p<0.01, compared to the values before treatment.

No cases of deterioration were recorded.

Conclusion

Medication therapy combining medications which have various effects on the nervous tissue is effective only for the initial stages of atrophy of the optic nerve. Also, the use of non-invasive physiotherapeutic methods is effective in early stages. The use of direct electropharmacological stimulation is more reasonable for advanced stages, and surgical methods - for severe cases. The use of treatment, differentiated based on the degree of functional changes, the type of atrophy and the nature of the lesion, significantly increases the effectiveness of treatment compared to the isolated use of EPS and even more so compared to medical treatment.

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