RESUMO
Optic neuritis (ON) is a debilitating condition that through various mechanisms, including inflammation or demyelination of the optic nerve, can result in partial or total permanent vision loss if left untreated. Accurate diagnosis and promptly initiated treatment are imperative related to the potential of permanent loss of vision if left untreated, which can lead to a significant reduction in the quality of life in affected patients. ON is subtyped as "typical" or "atypical" based on underlying causative etiology. The etiology of ON can be differentiated when appropriate diagnostic testing is performed. Using history taking, neuroimaging, and visual testing to localize the underlying pathology of ON in a time-sensitive manner is critical in mitigating these unsatisfactory outcomes. Herein, we examine the differences in presentation, pathophysiology, and treatments of typical ON causes, like multiple sclerosis (MS), and atypical causes such as neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG) ON. The present investigation places focus on both neuroimaging and visual imaging in the differentiation of ON. Additionally, this review presents physicians with a better understanding of different presentations, treatments, and prognoses of ON.
RESUMO
Decreased melatonin levels have been linked to both Alzheimer's disease (AD) and Parkinson's disease (PD), which are the two most prevalent neurodegenerative disorders. The development of sleep disorders is widespread in patients diagnosed with AD or PD. In this regard, calcification of the pineal gland, typically seen in the third decade, has been associated with a reduction in melatonin production. Recent studies have suggested that exogenous melatonin application can be utilized to treat sleep disorders in patients with neurodegenerative diseases. Furthermore, research has shown that deficiencies in melatonin levels in patients with AD or PD begin before a diagnosis of either disease is made. These findings could encourage further research on melatonin as a potential biomarker for the diagnosis or a possible area for the early treatment of these diseases. Many clinical studies have also produced data denoting melatonin treatment as a method to reduce the detrimental neurocognitive effects of these diseases. Further research on the role of melatonin in neurodegenerative diseases could expand symptomatic and prophylactic treatment options for diseases such as AD and PD. This review investigates melatonin's physiological properties, its role in AD and PD, and current findings on its potential therapeutic benefits in AD and PD patients.
