Cause Of Acute Visual Loss Research Articles

Optic Neuritis in the New Millennium

Abstract Optic neuritis (ON) is a common cause of acute visual loss due to optic neuropathy in adults. Although typical demyelinating ON usually recovers, some forms of autoimmune inflammatory ON may result in permanent disability. The relatively recent discovery of novel autoantibodies and their roles in the pathogenesis of ON, including aquaporin 4 (AQP4) in neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein (MOG) antibody in MOG-associated disease (MOGAD) has led to paradigm shifts in both the acute and chronic management of ON. We performed a comprehensive literature review to assess current and upcoming perspectives on ON by searching for contemporary articles (from 2015 to 2024) for articles that reported updates in diagnostic tools and methods, such as antibody testing. This monograph reviews these recent advances in the evaluation and management of ON.

Statin Treatment on Cardiovascular Risk After Retinal Artery Occlusion: A Historical Cohort Study

IntroductionRetinal artery occlusion (RAO) is a major cause of acute visual loss and patients with RAO have an increased risk for subsequent cardiovascular events. However, there is little evidence of whether the use of statins is associated with the prevention of cardiovascular events in patients with RAO. We investigated whether statin treatment in patients with RAO is associated with a lower risk of cardiovascular events.MethodsThis study was a historical cohort study with nested case–control analysis. Using the nationwide health insurance claims database in Korea, we retrospectively established a cohort of newly diagnosed RAO patients without prior cardiovascular events between January 2008 and March 2020. We defined the case group as those who had cardiovascular events (stroke or myocardial infarction) and the control group as RAO patients without primary outcome matched by sex, age, comorbidities, and duration of follow-up (1:2 incidence density sampling). Conditional logistic regression was performed.ResultsAmong 13,843 patients newly diagnosed with RAO, 1030 patients had cardiovascular events (mean follow-up period of 6.4 ± 3.7 years). A total of 957 cases were matched to 1914 controls. Throughout the study period, the proportion of patients taking statin was less than half. Statin treatment after RAO was associated with a low risk of cardiovascular events (adjusted OR, 0.637; 95% CI 0.520–0.780; P < 0.001). A longer duration of statin exposure was associated with a lower cardiovascular risk.ConclusionsIn patients with newly diagnosed RAO, treatment with statins, particularly long-term use, was associated with a low risk of future cardiovascular events.

Case report: A surprising cause of acute vision loss

Methanol poisoning is a common problem because of accidental ingestion of methanol or drinking adulterated liquor containing methanol. Exposure apart from ingestion is rare. Here we present a case in which acute vision loss occurred after inhalation.

Retrobulbar neuritis associated with empty sella syndrome: A diagnostic challenge

A 35-year-old female presented with sudden diminution of vision to finger counting at half meters in right eye (RE) since 15 days. RE showed grade III RAPD. Rest of the ocular examination was normal. She had no significant past medical history. Neuroimaging showed empty sella. We suspected retrobulbar neuritis (RBN) as a cause of loss of vision since there was no evidence of acute change in morphology of sella turcica like hemorrhage, trauma or ischemia, furthermore there were no pathological findings in RE and visual cortex to explain acute visual loss. Therefore, we prescribed intravenous steroids followed by oral steroids. Vision in RE improved to 6/12 after 15 days. We found that RBN can be a cause of sudden vision loss in cases with empty sella syndrome (ESS) and can pose diagnostic challenge that whether the vision loss is due to ESS or RBN. RBN can be a cause of acute vision loss in patients with ESS and can create diagnostic confusion.

Patent foramen ovale as a cause of acute vision loss.

Patent foramen ovale as a cause of acute vision loss.

Protective Effects of Oroxylin A on Retinal Ganglion Cells in Experimental Model of Anterior Ischemic Optic Neuropathy.

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute vision loss in older people, and there is no effective therapy. The effect of the systemic or local application of steroids for NAION patients remains controversial. Oroxylin A (OA) (5,7-dihydroxy-6-methoxyflavone) is a bioactive flavonoid extracted from Scutellariae baicalensis Georgi. with various beneficial effects, including anti-inflammatory and neuroprotective effects. A previous study showed that OA promotes retinal ganglion cell (RGC) survival after optic nerve (ON) crush injury. The purpose of this research was to further explore the potential actions of OA in ischemic injury in an experimental anterior ischemic optic neuropathy (rAION) rat model induced by photothrombosis. Our results show that OA efficiently attenuated ischemic injury in rats by reducing optic disc edema, the apoptotic death of retinal ganglion cells, and the infiltration of inflammatory cells. Moreover, OA significantly ameliorated the pathologic changes of demyelination, modulated microglial polarization, and preserved visual function after rAION induction. OA activated nuclear factor E2 related factor (Nrf2) signaling and its downstream antioxidant enzymes NAD(P)H:quinone oxidoreductase (NQO-1) and heme oxygenase 1 (HO-1) in the retina. We demonstrated that OA activates Nrf2 signaling, protecting retinal ganglion cells from ischemic injury, in the rAION model and could potentially be used as a therapeutic approach in ischemic optic neuropathy.

Munson's Sign: An Obvious Finding to Explain Acute Vision Loss.

Keratoconus is a progressive disorder affecting the cornea, which causes the cornea to become weakened and conical in appearance. The resultant decrease in structural integrity of the cornea predisposes affected individuals to acute corneal hydrops, a break in Descemet’s membrane, the deepest layer of the cornea, resulting in pain and acute vision loss. We present here a case of this little-known cause of acute vision loss, and an example of Munson’s sign, which is a v-shaped protrusion of the lower eyelid on downward gaze that is characteristic of advanced keratoconus. We hope to highlight Munson’s sign as a simple identifier of keratoconus in an otherwise undiagnosed individual suspected of having acute corneal hydrops.

Saturday Night Retinopathy After Intranasal Heroin

Purpose: To describe the clinical features of a case of Saturday night retinopathy (SNR) following intranasal heroin use. Methods: Ophthalmological examination, including optical coherence tomography and fluorescein angiogram, was performed. Serial images were obtained at follow-up visits at 1 week and 1 month. Results: The visual acuity was no light perception vision and there was an afferent pupillary defect in the affected eye. There was also evidence of complete ophthalmoplegia, globe proptosis, conjunctival chemosis, and corneal epitheliopathy and funduscopic evidence of ophthalmic artery occlusion. Follow-up imaging showed choroidal and retinal nonperfusion. Magnetic resonance imaging demonstrated edematous extraocular muscles and a bilateral hippocampal ischemia. Conclusions: This is the first case of SNR following intranasal heroin use and opioid-associated hippocampal ischemia. As physicians witness the impacts of the country’s opioid epidemic, it is important to recognize SNR as a cause of acute visual loss.

Vascular hypoperfusion in acute optic neuritis is a potentially new neurovascular model for demyelinating diseases.

PurposeOptic neuritis is highly correlated with multiple sclerosis and is a major cause of acute visual loss and long-term neuronal degeneration. Primary cerebral hypoperfusion has been reported in brain demyelinating diseases. This study investigated whether peripapillary perfusion is changed in patients with acute optic neuritis (AON).MethodsThis three-year cohort study was conducted from September 1 2012, to August 31, 2015. Two hundred and forty-one patients with non-glaucomatous acute optic neuropathy were screened, and 42 non-highly myopic patients who had suffered their first episode of unilaterally idiopathic AON were studied. All cases received spectral-domain optical coherence tomography (OCT) examination, general survey, and standard corticosteroid therapy. OCT images were analyzed using a customized MATLAB program for measuring peripapillary choroidal thickness (PCT). Multivariate regression models were constructed to identify factors that are significantly related to peripapillary perfusion.ResultsDecreased PCT was found in eyes experiencing AON combined with disc swelling (the ratio of lesion eye PCT/fellow eye PCT was 0.87 ± 0.08; range, from 0.75 to 1.00). In comparison to the healthy fellow eyes, approximately every 26% increase in the thickness of the retinal nerve fiber layer due to axonal swelling was associated with a 10% decreased thickness of PCT. Thinner PCT is also correlated with poorer trough vision, which may lead to poorer final vision. These findings were obvious in patients with optic papillitis but not in patients with retrobulbar neuritis.ConclusionsPeripapillary vascular hypoperfusion was found in patients experiencing AON combined with disc swelling. These findings are unlike those for other ocular inflammatory diseases but are consistent with cerebral hypoperfusion, which is found in brain demyelinating diseases; thus, these findings may represent a new neurovascular model in this field.

The enigma of nonarteritic anterior ischemic optic neuropathy: an update for the comprehensive ophthalmologist.

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute optic nerve injury, and frequently presents to comprehensive ophthalmologists. We review the typical and atypical clinical features and current literature on various treatment modalities for NAION. The epidemiology and clinical presentation of this disease can be variable, making a definitive diagnosis difficult in many cases. In addition, the differential diagnoses for this disorder, although comprising much less prevalent entities, are quite broad and can have substantial systemic implications if these alternatives go unrecognized. NAION has many systemic associations and comorbidities that deserve inquiry when the diagnosis is made. There are currently no widely accepted, evidence-based treatments for NAION. All recommendations made to patients to reduce their risk of sequential eye involvement, including avoidance of potential nocturnal hypotension, erectile dysfunction medication, and treatment of obstructive sleep apnea, have theoretical bases. NAION is a common cause of acute vision loss in adult and older patients, and thus, comprehensive ophthalmologists need to be able to diagnose and appropriately manage this disorder. We anticipate fruitful results from current and future trials aimed at neuroprotection in the affected eye and prevention of sequential eye involvement.

Should plasma exchange be offered to patients with multiple sclerosis-associated optic neuritis?

Should plasma exchange be offered to patients with multiple sclerosis-associated optic neuritis?

Genetic causes of acute visual loss

AbstractGenetic causes of acute visual loss are relatively rare, but these still need to be considered in the differential diagnosis, especially in the relevant clinical context. In this presentation, classical genetic disorders affecting the optic nerve will be discussed with a particular focus on Leber hereditary optic neuropathy (LHON). LHON is a primary mitochondrial DNA (mtDNA) disorder and three point mutations within the mitochondrial genome account for the vast majority of cases, namely: m.3460G&gt;A, m.11778G&gt;A and m.14484T&gt;C. It typically affects young adult males who present with bilateral severe visual loss in the second or third decade of life. In addition to the canonical LHON mutations, other pathogenic mtDNA mutations have been reported that can result in both syndromic and non‐syndromic optic neuropathies. Acute visual loss in genetic disorders can also be secondary to pathology involving the retrochiasmal visual pathways, for example, in MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke‐like episodes). The cardinal clinical manifestations in this group of patients are homonymous hemianopic visual field defects or cortical blindness.

Inflammatory and infectious causes of acute visual loss

AbstractIn this course comprehensive review of inflammatory and infectious causes of acute visual loss will be presented. This will include pre‐and retrochiasmal‐chiasmal visual pathway lesions. The lecture will focus on clinical presentation with localizing symptomatology and signs, recommended diagnostic tests, differential diagnosis and treatment possibilities. Also, known pathophysiology of various disorders will be discussed. At the conclusion of presentation the audience will be familiar with the wide range of neuro‐ophthalmological disease states that can result in acute visual loss.

Vascular causes of acute visual loss

AbstractAcute optic neuropathy due to a vascular cause is essentially a syndrome of ischemic optic neuropathy. The mechanism of ischemic optic neuropathy involves a fall in perfusion pressure to the optic nerve which, in susceptible individuals, leads to infarction of the prelaminar or retrolaminar portion of the optic nerve. Ischemic optic neuropathy can be subdivided into anterior ischemic optic neuropathy and posterior ischemic optic neuropathy . A special category is post‐operative ischemic optic neuropathy. This lecture will discuss the clinical features that distinguish these forms of ischemic optic neuropathy , the risk factors associated with them and the approach to their management.

Neoplastic causes of acute visual loss

AbstractVisual loss in relation with cancer has greatly increased in adult as in child. Not only because improvement of diagnostic techniques, but because survival rate has dramatically improved. Acute visual loss may be associated to direct or metastatic involvement of the eye or may be a consequence of cancer therapy including chemotherapy, radiation as newer modality like intra‐arterial injections. Considering the possible immunodysfunction in these patients infection as autoimmune disorders should be considered in the differential diagnosis of acute uni or bilateral visual loss. Clinical features and therapeutic options will be discussed through clinical cases.

Bilateral acute visual loss from Rathke's cleft cyst apoplexy in a patient with dengue fever.

Hemorrhagic complications of optic pathway diseases are extremely rare causes of acute visual loss associated with dengue fever. In this paper we report a patient presenting with dengue fever and bilateral acute visual loss caused by chiasmal compression due to Rathke's cleft cyst apoplexy. Considering the importance of early diagnosis and treatment to visual recovery, apoplexy of sellar and suprasellar tumors should be considered in the differential diagnosis of patients with acute visual loss and dengue fever.

Functional rescue of experimental ischemic optic neuropathy with αB-crystallin

Anterior ischemic optic neuropathy (AION) is an important cause of acute vision loss in adults, and there is no effective treatment. We studied early changes following experimental AION and tested the benefit of a potential treatment. We induced experimental AION in adult mice and tested the effects of short-term (daily for 3 days) and long-term (every other day for 3 weeks) αB-crystallin (αBC) treatment using histological and serial intracranial flash visual evoked potential recordings. One day after experimental AION, there was swelling at the optic nerve (ON) head and increased expression of αBC, a small heat shock protein important in ischemia and inflammation. This upregulation coincided with microglial and astrocytic activation. Our hypothesis was that αBC may be part of the endogenous protective mechanism against injury, thus we tested the effects of αBC on experimental AION. Daily intraveneous or intravitreal αBC injections did not improve visual evoked potential amplitude or latency at days 1-2. However, αBC treatment decreased swelling and dampened the microglial and astrocytic activation on day 3. Longer treatment with intravenous αBC led to acceleration of visual evoked potential latency over 3 weeks, without improving amplitude. This latency acceleration did not correlate with increased retinal ganglion cell survival but did correlate with complete rescue of the ON oligodendrocytes, which are important for myelination. We identified αBC as an early marker following experimental AION. Treatment with αBC enhanced this endogenous, post-ischemic response by decreasing microglial activation and promoting ON oligodendrocyte survival.

An unusual cause of visual loss after Herpes zoster ophthalmicus: a case report

IntroductionThe vascular complications of herpes zoster are well recognised, however, there are few reports of central retinal artery occlusion. Central retinal artery occlusion following herpes zoster ophthalmicus is poorly recognised. This is likely due to the difficulties in obtaining tissue for histopathology to establish causality. We report a case of central retinal artery occlusion and complete internal carotid artery occlusion following herpes zoster ophthalmicus.Case presentationA 44 year old Caucasian female presented with sudden painless loss of vision in her right eye on a background of chronic lymphocytic leukaemia and right sided herpes zoster ophthalmicus. She was initially treated with steroids and antivirals for an underlying presumed vasculitic cause, but review at 24 hours demonstrated a right central retinal artery occlusion. Embolic screen identified complete occlusion of the right internal carotid artery. She was treated with oral antiviral medication for three weeks but had no visual recovery.ConclusionThis case highlights an uncommon cause of acute visual loss. We propose that the underlying small and large vessel occlusion in this patient was due to herpes zoster related vasculopathy. A review of the literature is presented to trace the historical perspective of herpes zoster related vasculopathy.

Neuritis óptica inflamatoria

Inflammatory Optic Neuritis (ON) is the most frequent cause of acute visual loss in young adults. Although the visual prognosis is excellent in the majority of cases, many patients develop pathology, such as multiple sclerosis, in its subsequent evolution. The natural history of ON has been studied in numerous works in recent years; one of the most important of which is Optic Neuritis Treatment Trial. Magnetic Resonance plays a fundamental role in the etiological diagnosis of ON and in predicting the risk of conversion into multiple sclerosis. New exploratory techniques have recently been incorporated, such as optical coherence tomography, useful for diagnosis and prognosis; serum biomarkers have been identified in the diagnosis of other pathologies with an autoimmune nature that produce ON. A better understanding of the clinical and exploratory data of typical ON will make a more rapid and accurate diagnostic study possible. Treatment of ON with steroids must be individualised bearing in mind that they do not alter the long-term prognosis and an immunomodulating therapy must be proposed for patients with a high risk of conversion into multiple sclerosis. This article reviews the existing data in the literature on its clinical manifestations, its etiological and differential diagnosis, and the treatment of inflammatory ON.

Inflammatory optic neuritis

Inflammatory Optic Neuritis (ON) is the most frequent cause of acute visual loss in young adults. Although the visual prognosis is excellent in the majority of cases, many patients develop pathology, such as multiple sclerosis, in its subsequent evolution. The natural history of ON has been studied in numerous works in recent years; one of the most important of which is Optic Neuritis Treatment Trial. Magnetic Resonance plays a fundamental role in the etiological diagnosis of ON and in predicting the risk of conversion into multiple sclerosis. New exploratory techniques have recently been incorporated, such as optical coherence tomography, useful for diagnosis and prognosis; serum biomarkers have been identified in the diagnosis of other pathologies with an autoimmune nature that produce ON. A better understanding of the clinical and exploratory data of typical ON will make a more rapid and accurate diagnostic study possible. Treatment of ON with steroids must be individualised bearing in mind that they do not alter the long-term prognosis and an immunomodulating therapy must be proposed for patients with a high risk of conversion into multiple sclerosis. This article reviews the existing data in the literature on its clinical manifestations, its etiological and differential diagnosis, and the treatment of inflammatory ON.