COMPREHENSIVE OPHTHALMOLOGICAL APPROACHES: A STUDY ON CLINICAL PRACTICES AND INTERVENTIONS IN RETINAL AND CORNEAL DISEASES

Аннотация

Neuromyelitis optica is a demyelinating disease that primarily affects the eyes and spinal cord, but can also involve other structures of the central nervous system (CNS) that contain aquaporin-4. Keywords: Clinical manifestations, Diagnostics, prevention, prognosis and treatment. Introduction: Neuromyelitis optica spectrum disorder causes acute optic neuritis, sometimes bilateral, as well as demyelination of the cervical or thoracic spinal cord. It was previously considered a type of multiple sclerosis (MS), but is now recognized as a separate disease. In neuromyelitis optica spectrum disorder, the immune system attacks aquaporin-4, a protein found in astrocytes in the brain, particularly in the spinal cord and optic nerves, or myelin oligodendrocyte glycoprotein (MOG), a protein found in the myelin of oligodendrocytes, and possibly in other areas of the CNS. Astrocytes and oligodendrocytes are damaged by autoimmune inflammatory responses, as well as demyelination. Severe bilateral optic neuritis involving the optic chiasm, leading to loss of vision above or below the horizontal (height visual field defect) or loss of visual acuity (20/200 or worse). Complete spinal cord injury syndrome, especially with paroxysmal tonic spasms Hiccups or nausea and vomiting caused by area postrema syndrome (the area postrema is a structure that controls vomiting and is located at the bottom of the 4th ventricle) Visual evoked potentials help distinguish neuromyelitis optica from other optic neuropathies. Findings in the neuromyelitis optica spectrum disorder include decreased amplitude or prolonged latency. This test is also useful for detecting clinically undetectable damage that may be present before symptoms appear. Methods and Materials: Tests can be performed to differentiate IgG antibodies specific for neuromyelitis optica spectrum disorder (aquaporin 4 antibodies [also called NMO-IgG]) from 59 Mart, 2025-Yil MS. Anti-MOG (myelin oligodendrocyte glycoprotein) antibodies identify a subgroup of patients with neuromyelitis optica who have different clinical features: they have fewer complications and a better recovery than patients with or without AQP4 antibodies. Some patients with clinical signs of neuromyelitis optica do not have antibodies at all and are classified as double seronegative for neuromyelitis optica. Neuromyelitis optica cannot be cured. However, treatment can prevent, slow down, or reduce the severity of exacerbations and reduce the risk of disability in the short term. Eculizumab, a complement C5 inhibitor, is available for the treatment of aquaporin-4 antibody-positive neuromyelitis visual spectrum disorder. Side effects include respiratory tract infections, headache, and pneumonia and can be significant; thus, patients should be monitored closely (3). Because one patient developed meningococcal sepsis, meningococcal vaccination should be considered before initiating treatment. Satralizumab (a monoclonal antibody against the interleukin-6 receptor) and inebilizumab (a monoclonal antibody against CD19 on B cells) are also available for the treatment of aquaporin- 4-positive neuromyelitis optica spectrum disorder. Patients should be monitored closely for infections such as urinary tract infections and respiratory tract infections. Methylprednisolone and azathioprine are often used together. Plasmapheresis may be performed in patients who are ineffective on glucocorticoid therapy. Rituximab, an anti-B-cell antibody, has been shown to reduce relapse rates in a double- blind, placebo-controlled study ( 4 ). Other types of immunomodulatory and immunosuppressive therapy are sometimes used. Natalizumab and fingolimod have been shown to be ineffective and may cause harm. Symptomatic therapy is similar to treatment for MS. Baclofen or tizanidine are prescribed for muscle spasms. Neuromyelitis optica spectrum disorder is usually the result of demyelination involving antibodies to aquaporin-4 or myelin oligodendrocyte glycoprotein. Typical symptoms include vision loss, muscle spasms, para- or tetraparesis, and incontinence. MRI of the brain and spinal cord, as well as the study of visual evoked potentials, are used to diagnose optic spectrum disorders in neuromyelitis. Treatment includes corticosteroids and immunomodulatory or immunosuppressive therapy (e.g., eculizumab, rituximab). The myelin sheath covers a large number of nerve fibers in the central and peripheral nervous system; With its help, the transmission of nerve impulses along the axon occurs at high 60 Mart, 2025-Yil speed. In diseases accompanied by damage to the myelin sheath, the conduction of excitation along the nerve fiber is impaired; Symptoms may reflect a failure in any part of the nervous system. Myelin produced by oligodendroglia in the central nervous system (CNS) differs in its immunochemical properties from that produced by Schwann cells in the peripheral nervous system. Thus, some demyelinating diseases (e.g., Guillain-Barré syndrome,