American journal of ophthalmology case reports · 2024
Paracentral acute middle maculopathy in a patient with Myelin Oligodendrocyte glycoprotein antibody associated optic neuritis.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Heroor Aniruddh, Tyagi Mudit, Kekunnaya Ramesh, Chattannavar Goura
Аннотация
PURPOSE: There is insufficient literature reporting the concurrent occurrence of retinal ischemic lesions with optic neuritis. In this case report, we present a distinctive instance of Optic Neuritis with a positive Myelin Oligodendrocyte glycoprotein (MOG) antibody, accompanied by retinal ischemia manifesting as paracentral acute middle maculopathy (PAMM) lesions.
OBSERVATIONS: Our patient is a 25-year-old female who tested positive for MOG antibodies and exhibited retinal PAMM lesions without any apparent underlying ischemic cause. She received intravenous pulse steroid therapy, and her symptoms and signs completely resolved one month later.
CONCLUSION: PAMM can serve as an initial manifestation of Myelin Oligodendrocyte glycoprotein Antibody Associated Disease (MOGAD). This case has the potential to contribute to the existing literature, facilitating a deeper exploration of the pathophysiology of retinal ischemia in MOG associated optic neuritis.
OBSERVATIONS: Our patient is a 25-year-old female who tested positive for MOG antibodies and exhibited retinal PAMM lesions without any apparent underlying ischemic cause. She received intravenous pulse steroid therapy, and her symptoms and signs completely resolved one month later.
CONCLUSION: PAMM can serve as an initial manifestation of Myelin Oligodendrocyte glycoprotein Antibody Associated Disease (MOGAD). This case has the potential to contribute to the existing literature, facilitating a deeper exploration of the pathophysiology of retinal ischemia in MOG associated optic neuritis.