Ischemic optic neuropathy

Athappilly, Geetha; Pelak, Victoria S.; Mandava, Naresh; Bennett, Jeffrey L.

doi:10.1179/174313208x319107

Cited by 18 publications

(7 citation statements)

References 58 publications

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“…Apoptotic and necrotic cell death types constitute the damaged region in many retinal neuropathologies for which the role of IR was proposed (Athappilly et al, 2008; Bresnick et al, 1975; Hayreh, 2013; Osborne et al, 1999). Thus, understanding the apoptotic and necrotic pathways involved in IR-induced neuronal injury can provide us with clinically effective treatments for many retinal diseases.…”

Section: Discussionmentioning

confidence: 99%

Retinal ganglion cell (RGC) programmed necrosis contributes to ischemia–reperfusion-induced retinal damage

Dvoriantchikova

Degterev

Ivanov

2014

Experimental Eye Research

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Retinal ischemia–reperfusion (IR) injury remains a common cause of blindness and has a final pathway of retinal ganglion cell (RGC) death by apoptosis and necrosis. RGC apoptosis was intensively studied in IR injury, while RGC necrosis did not receive nearly enough consideration since it was viewed as an accidental and unregulated cellular event. However, there is evidence that necrosis, like apoptosis, can be implemented by a programmed mechanism. In this study, we tested the role of RGC programmed necrosis (necroptosis) in IR-induced retinal injury. We employed the mouse model of retinal IR injury for in vivo experiments. The oxygen and glucose deprivation (OGD) model was used as an IR model in vitro. Primary RGCs were isolated by an immunopanning technique. Necrostatin 1 (Nec1) was used to inhibit necroptosis in in vitro and in vivo experiments. The changes in gene expression were assessed by quantitative RT-PCR. The distribution of proteins in the retina and in RGC cultures was evaluated by immunohistochemistry and immunocytochemistry, respectively. Our data suggest that proteins (Ripk1 and Ripk3), which initiate necroptosis, were present in normal and ischemic RGCs. Treatment with Nec1 significantly reduced retinal damage after IR. Increased RGC survival and reduced RGC necrosis following OGD were observed in Nec1-treated cultures. We found significantly reduced expression of genes coding pro-inflammatory markers Il1b, Ccl5, Cxcl10, Nos2 and Cybb in Nec1-treated ischemic retinas. Thus, our findings suggest that RGC necroptosis contributes to retinal damage after IR through direct loss of cells and induction of associated inflammatory responses.

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Section: Discussionmentioning

confidence: 99%

Retinal ganglion cell (RGC) programmed necrosis contributes to ischemia–reperfusion-induced retinal damage

Dvoriantchikova

Degterev

Ivanov

2014

Experimental Eye Research

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“…When the patient can communicate, they usually report painless vision loss. The diagnosis is primarily clinical, and the eye exam confirms the presence of an afferent pupillary defect and optic disc pallor and edema with sparing of the remaining peripheral retina on fundoscopy [13]. A crucial finding on examination is the presence of a small cup-to-disc ratio (disc at risk), meaning a crowded optic-nerve head with a small physiological cup [12,14,15].…”

Section: Discussionmentioning

confidence: 99%

Waking Up Blind in the ICU: A Case Report of Ischemic Optic Neuropathy in a Burn Patient

Quiroga

Asif

Lagziel

et al. 2019

Cureus

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The objective of this report is to analyze and summarize the current literature of ischemic optic neuropathy (ION), a rare complication in severe burn and trauma victims, while presenting an urban burn center's experience with the condition. This is an unfortunate condition and this report will raise awareness to a potential complication in the burn patient population as well as in critically ill patients in other settings.We present the case of a 27-year-old healthy male patient admitted to our Burn Center with 85% total body surface area (TBSA) full-thickness burns sustained in a house fire. The patient had a complicated hospital course but improved over time and was weaned off of prolonged ventilation and sedation. Subsequently, he complained of bilateral blindness. A fundoscopic examination demonstrated bilateral pale optic nerves with sparing of the remaining peripheral retina consistent with ION. The patient suffered complete bilateral vision loss. He had multiple factors that could have instigated the development of ION, including several episodes of septicemia, hypovolemic shock and severe adult respiratory distress syndrome (ARDS) with refractory hypoxemia requiring a prolong ventilation support and vasopressor therapy. Due to the advancement of the treatment of acute burns, the survival rate of patients that once would have succumbed to their burn injury, is increasing. With these new achievements, we are facing new challenges and complications. ION has a significant impact on the quality of the patient’s life. The early diagnosis will not necessarily translate into a benefit for these patients as no treatment has been proven successful. Extensive retrospective and prospective studies are necessary to identify and treat this patient population.

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“…По дан-ным литературы, 19-20 % слабовидящих пациентов в нашей стране составляют лица, потерявшие зрение вследствие данной патологии [3]. АЗН имеет различные этиологические причины, которые требуют специфиче-ского лечения [1][2][3][4][5][6][7]. Несмотря на успехи современной медицины, совершенствование методов лечения АЗН продолжает оставаться исключительно актуальным [8].…”

Section: Ophthalmology In Russia 2018;15(2):219-224 актуальностьunclassified

Еstimation of Therapeutic Effect of Endonasal Electrophorosis with Methylethylpyridinol in Partial Optic Nerve Atrophy

Разумовская¹,

Разумовский²,

Коровянский³

et al. 2018

Ophthalmology in Russia

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РЕЗЮМЕЦелью исследования было оценить лечебный эффект препарата эмоксипин при введении его методом эндоназального электрофореза больным с частичной атрофией зрительного нерва (ЧАЗН). Пациенты и методы. Лечение было проведено 43 пациентам со средним возрастом 53 ± 2 года, страдающих частичной атрофией зрительного нерва различной этиологии. При этом основную группу составили 22 пациента, которым вводили эмоксипин путем эндоназального электрофореза, группа сравнения -21 человек, которым эмоксипин вводили с помощью парабульбарных инъекций. Каждому пациенту было про-ведено офтальмологическое исследование, которое включало: визометрию, периметрию, рефрактометрию, биомкроскопию, офтальмоскопию, исследование зрительной работоспособности, оценку состояния бульбарной микроциркуляции (общего конъ-юнктивального индекса -ОКИ). Кроме того, проводили электрофизиологические исследования органа зрения: критической частоты слияния мельканий (КЧСМ) и электрической чувствительности глаза (ЭЧ). Результаты. Результаты исследования по-казали эффективность применения препарата эмоксипин для лечения ЧАЗН путем эндоназального электрофореза и выявили улучшение зрительных функций: расширение границ поля зрения на белый, красный и зеленый цвета, снижение зрительной утомляемости, улучшение электрофизиологических показателей и бульбарной микроциркуляции. Заключение. Оценка эффек-тивности применения эмоксипина путем эндоназального электрофореза при частичной атрофии зрительного нерва различной этиологии показала статистически достоверный положительный лечебный эффект (79 %) в виде восстановления зрительных функций. При парабульбарном введении этого препарата, так же как при эндоназальном электрофорезе, в 81 % наблюдалось расширение границ поля зрения от 5 до 25° в различных меридианах, уменьшение количества относительных скотом в поле зрения, в обеих группах наблюдалось улучшение зрительной работоспособности. Среди пациентов, которым проводили эндона-зальный электрофорез, побочных эффектов не наблюдалось. Ключевые слова: частичная атрофия зрительного нерва, эмоксипин, эндоназальный электрофорез, парабульбарные инъ-екции Для цитирования: Разумовская А.М., Разумовский М.И., Коровянский Ю.А., Разумовский Е.С. Оценка лечебного эф-фекта эндоназального электрофореза с метилэтилпиридинолом при частичной атрофии зрительного нерва. Офтальмология. 2018;15(2):219-224. https://doi

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Ischemic optic neuropathy

Cited by 18 publications

References 58 publications

Retinal ganglion cell (RGC) programmed necrosis contributes to ischemia–reperfusion-induced retinal damage

Retinal ganglion cell (RGC) programmed necrosis contributes to ischemia–reperfusion-induced retinal damage

Waking Up Blind in the ICU: A Case Report of Ischemic Optic Neuropathy in a Burn Patient

Еstimation of Therapeutic Effect of Endonasal Electrophorosis with Methylethylpyridinol in Partial Optic Nerve Atrophy

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