Optic Nerve Head Edema Research Articles

Comparative characteristics of ophthalmological symptoms of orbitocranial and orbital cavernous venous malformation

BACKGROUND: Cavernous venous malformation of the orbit, formerly known as cavernous hemangioma of the orbit, refers to vascular malformations with slow blood flow, and is a frequent lesion of the orbit in adults. The spread of cavernous venous malformation of the orbit into the cranial cavity is extremely rare.
 AIM: The aim of this study is a comparative analysis of ophthalmological manifestations of orbitocranial and orbital cavernous venous malformation.
 MATERIALS AND METHODS: The analysis was performed on 50 patients operated in N.N. Burdenko National Scientific and Practical Center for Neurosurgery from 2004 till 2023. Two groups of patients with сavernous venous malformation of the orbit were identified: group 1 — with malformation spreading into the cranial cavity, group 2 —with malformation localized in the orbit only.
 RESULTS: In 29 patients, cavernous venous malformation of the orbit spread into the cranial cavity through superior orbital fissure, inferior orbital fissure, optic canal and/or through combinations thereof; in 21 patients, the malformation was located in the orbit only. Females prevailed in both groups; the average age was 44 years. The first group included patients with the following features: visual impairments were more frequent and more prominent, oculomotor disorders caused mainly by the involvement of oculomotor and abducens nerves; optic nerve atrophy, slight proptosis. The second group was identified by more prominent proptosis, more mild visual impairments, oculomotor disorders caused by the presence of the malformation in the orbit, at the eye fundus, optic nerve head edema prevailed.
 CONCLUSIONS: Ophthalmic symptoms due to topographic and anatomical variants of a cavernous malformation.

Features of Peripapillary Hyperreflective Ovoid Mass-Like Structures in Nonarteritic Anterior Ischemic Optic Neuropathy Patients and Normal Controls.

To determine the characteristics of peripapillary hyperreflective ovoid mass-like structures (PHOMS) in patients with nonarteritic anterior ischemic optic neuropathy (NAION) and in normal adults. A total of 406 included eyes were divided into four groups: acute NAION group, chronic NAION group, unaffected group, and normal eyes group. PHOMS were detected on optical coherence tomography slices from optical coherence tomography angiography scans centered on the optic nerve head (ONH). The differences in age, sex, and ONH parameters were investigated between eyes with PHOMS and eyes without PHOMS among groups. The prevalence of PHOMS in acute eyes (43.48%) and fellow eyes (28.20%) was significantly higher than that in normal eyes (11.76%) (acute vs. normal, P < 0.001; fellow vs. normal, P = 0.014). In the acute group, the PHOMS score of size was negatively correlated with age in acute eyes (r = -0.486, P = 0.03). The size of PHOMS was negatively correlated with age and cup/disc ratio and positively correlated with retinal nerve fiber layer thickness in the nasal and inferior sectors in the normal groups. No differences in age, sex, ONH parameters, or visual field defects were found between eyes with PHOMS and eyes without PHOMS. The prevalence of PHOMS increased significantly in acute nonoptic disc drusen (NODD)-NAION eyes and fellow eyes. PHOMS could also be found among normal adults. PHOMS may be a nonspecific sign secondary to ONH edema and axoplasmic stasis. The high prevalence of PHOMS in acute NODD-NAION eyes may indicate axoplasmic stasis secondary to tissue edema.

Combined Salvage Treatments in a Case of Neurosyphilis

Purpose: Visual loss and optic nerve head (ONH) edema are hallmarks in diagnosing optic neuritis, perineuritis, neuroretinitis and papillitis, but clinicians often disregard the role that intracranial hypertension could play in neurosyphilis. Methods: A case of syphilitic optic neuropathy with visual loss and bilateral ONH edema was presented, where the detailed diagnosis procedure of chronic intracranial hypertension and its treatment were described.

Idiopathic Intracranial Hypertension: A Case Report

Background: Optic nerve head edema is a serious finding for which multiple etiologies need to be considered. When optic nerve head edema is observed bilaterally, among the top differentials is idiopathic intracranial hypertension (IIH), also known as primary pseudotumor cerebri. An emergent magnetic resonance image with and without contrast as well as venography and lumbar puncture with opening pressure measurement must be performed to diagnose and determine management. Case Report: This case specifically features a 30-year-old Caucasian female with bilateral optic disc edema secondary to IIH. In addition to discussing the details regarding this patient’s case, this report highlights pertinent imaging, visual testing, and co-management. Conclusion: Important caveats to treatment and management of the condition, and other underlying complications of IIH are discussed. Close monitoring of papilledema, visual acuity, and visual field, along with co-management with neurology and neuro-ophthalmology will provide optimum care.

High diagnostic accuracy of T2FLAIR at 3 T in the detection of optic nerve head edema in acute optic neuritis.

Optic nerve head edema (ONHE) detected by fundoscopy is observed in one-third of patients presenting optic neuritis (ON). While ONHE is an important semiological feature, the correlation between ONHE and optic nerve head MRI abnormalities (ONHMA), sometimes called "optic nerve head swelling," remains unknown. Our study aimed to assess the diagnostic accuracy of T2 fluid-attenuated inversion recovery (FLAIR) MRI sequence in detecting ONHE in patients with acute ON. In the present single-center study, data were extracted from two prospective cohort studies that consecutively included adults with a first episode of acute ON treated between 2015 and 2020. Two experienced readers blinded to study data independently analyzed imaging. A senior neuroradiologist resolved any discrepancies. The primary judgment criterion of ONHMA was assessed as optic nerve head high signal intensity on gadolinium-enhanced T2FLAIR MRI sequence. Its diagnostic accuracy was evaluated with both the gold standard of ONHE on fundus photography (FP) and peripapillary retinal nerve fiber layer thickening on optic coherence tomography (OCT). A total of 102 patients were included, providing 110 affected and 94 unaffected optic nerves. Agreement was high between the different modalities: 92% between MRI and FP (k= 0.77, 95% CI: 0.67-0.88) and 93% between MRI and OCT (k= 0.77, 95% CI: 0.67-0.87). MRI sensitivity was 0.84 (95% CI: 0.70-0.93) and specificity was 0.94 (95% CI: 0.89-0.97) when compared with the FP. Optic nerve head high T2FLAIR signal intensity corresponds indeed to the optic nerve head edema diagnosed by the ophthalmologists. MRI is a sensitive tool for detecting ONHE in patients presenting acute ON. In patients with optic neuritis the high T2FLAIR (fluid-attenuated inversion recovery) signal intensity of the optic nerve head corresponds indeed to optic nerve head edema, which is a useful feature in optic neuritis etiological evaluation and treatment. Optic nerve head edema is a prominent clinical feature of acute optic neuritis and is usually diagnosed during dilated or non-dilated eye fundus examination. Agreement was high between magnetic resonance imaging, fundus photography, and optical coherence tomography. Optic nerve head high T2 fluid attenuation inversion recovery signal intensity is a promising detection tool for optic nerve head edema in patients presenting acute optic neuritis.

The efficacy of local glucocorticosteroid therapy in nonarteritic anterior ischemic optic neuropathy

BACKGROUND: Non-arteritic anterior ischemic optic neuropathy is the second most common optic neuropathy after glaucoma. The effectiveness of the glucocorticosteroid therapy use for the non-arteritic anterior ischemic optic neuropathy treatment remains a subject of debate. Currently, the search for markers of the diseases therapeutic window is under way.&#x0D; AIM: The aim of this study is to evaluate the use of local glucocorticosteroid therapy as an emergency care for non-arteritic anterior ischemic optic neuropathy.&#x0D; MATERIALS AND METHODS: 41 patients with non-arteritic anterior ischemic optic neuropathy were enrolled in the study. To evaluate optic nerve head and macula morphometric characteristics, optical coherence tomography was performed, additionally, diameters of arteries and veins were assessed at 4 vascular arcades. Patients were divided into 2 groups according to the presence of intraretinal fluid. The first (main) group consisted of 23 patients with intraretinal fluid, in the second (control) group 18 patients without intraretinal fluid were included. The first group was further divided into two subgroups according to the medical aid recourse periods up to 5 days, and from 6 to 21 days (subgroup 1 9 patients, subgroup 2 14 patients).&#x0D; RESULTS: Correlations between the dynamics of optic nerve head edema changes and the caliber of arteries (negative correlation) and that of veins (positive correlation) were revealed. Sub-tenon injection of long-acting glucocorticosteroid did not lead to morpho-functional improvement in first group patients. Local short-acting glucocorticosteroid therapy accomplished in the acute period of the disease made it possible to achieve an improvement in best corrected visual acuity during the first month in group 1 patients without any further worsening of it.&#x0D; CONCLUSIONS: When providing emergency care to patients with non-arteritic anterior ischemic optic neuropathy during the first 5 days from the disease onset, the local use of glucocorticosteroid therapy is advisable.

Radiation Retinopathy: Pathogenesis, Diagnosis, and Treatment

Radiation retinopathy is chronic retinopathy that usually after radiotherapy with delayed onset (6 months-3 years) and slow progression. The primary vascular event is endothelial cell loss. Clinically affected individuals may be asymptomatic or may describe decreased visual acuity. Combining anamnesis, complete ophthalmologic examination, and multimodal imaging is essential for diagnosis. The ophthalmological examination may reveal signs of retinal vascular disease such as microaneurysms (the first structural change detected ophthalmoscopically), cotton wool spots, retinal hemorrhages, perivascular sheathing, capillary telangiectasia, macular edema, and optic nerve head edema. Optical coherence tomography can detect macular edema, intraretinal hyperreflective spots that may develop secondary to ischemia, disorganization in the inner retinal layers, and deterioration in the outer retina. Fundus fluorescein angiography helps detect capillary perfusion anomalies and other signs of vascular disease. Diabetic retinopathy, retinal vein occlusion, ocular ischemic syndrome, hypertensive retinopathy, Coats' disease, and parafoveal telangiectasia should be considered in the differential diagnosis, and sometimes these diseases may accompany radiation retinopathy. Currently, there is still no standard treatment for radiation retinopathy. Anti-vascular endothelial growth factors (anti-VEGF) and steroid therapy are among the effective treatment options. Retinal laser photocoagulation can be applied for neovascular complications. For macular edema, focal laser photocoagulation was less effective than anti-VEGF and steroid therapy in terms of functional gain.

Tubulointerstitial Nephritis and Uveitis Syndrome in the United Arab Emirates

ABSTRACT Purpose To report the first series of tubulointerstitial nephritis (TINU) syndrome from the Middle East. Methods We retrospectively included patients with elevated urine beta-2 microglobulin, and a diagnosis of TINU based on anterior uveitis with or without posterior involvement. Multimodal imaging, duration of follow-up, local and systemic treatment used were recorded. Results 24 eyes of 12 patients (8 male, mean age 20.3 years) met the criteria for TINU. The most common posterior segment clinical finding was optic nerve head edema (41.7%), while on fluorescein angiography 58.3% and 75% of eyes had peripheral vascular and optic disc leakage, respectively. The mean follow-up was 2.5 years and all patients required immunomodulatory treatment. Conclusions Middle Eastern patients with TINU seem to have a male predominance, a bimodal distribution in terms of age, and present with ocular involvement first. Multimodal imaging is paramount in detecting subclinical inflammation and tailoring immunomodulatory treatment.

The Role of Optical Coherence Tomography Angiography in Optic Nerve Head Edema: A Narrative Review.

Optic nerve head (ONH) edema is a clinical manifestation of many ocular and systemic disorders. Ocular and central nervous system imaging has been used to differentiate the underlying cause of ONH edema and monitor the disease course. ONH vessel abnormalities are among the earliest signs of impaired axonal transportation. Optical coherence tomography angiography (OCTA) is a noninvasive method for imaging ONH and peripapillary vessels and has been used extensively for studying vascular changes in ONH disorders, including ONH edema. In this narrative review, we describe OCTA findings of the most common causes of ONH edema and its differential diagnoses including ONH drusen.

Morphologic and Functional Changes of Macula and Optic Nerve Head in Adult Kidney Transplant Recipient

To assess macular and optic nerve head characteristics in patients after kidney transplantation using noninvasive optical coherence tomography (OCT) imaging. The study had a prospective character and was performed during period from November 2019 to November 2020 at the University Clinical Center Tuzla, Tuzla, Bosnia and Herzegovina, and included 59 patients with renal graft who underwent OCT. The obtained OCT images, pathologic changes on the fundus, including macula and optic nerve, were analyzed by reviewing nonparametric measures such as scanning laser ophthalmoscope, B-scan, 3D display, as well as parametric measurements such as central macular thickness, optic nerve head excavation, and retinal nerve thickness fiber (RNFL). There is a statistically significant difference in RNFL values (P=0.031) and cup to disc (P=0.002) ratio in relation to duration of graft. The highest average values of RNFL was in patients with creatinine clearance <30 mL/min, while average cup to disc ratio was lowest in patients with creatinine clearance >60 mL/min. Optic nerve head edema was bilateral in 9 and unilateral in 5 patients. Fundus examination also revealed changes on posterior segment, including retinal detachment (1 patient), bilateral macular edema (9 patients), unilateral macular edema (3 patients), central serous chorioretinopathy (2 patients), and macular pseudo hole (3 patients). Different retinal pathology is present in high incidence in patients secondary to renal transplant. Immunosuppressive therapy, older age, and comorbidities are the usual causes of these changes.

Bilateral Optic Neuritis as an Atypical Presentation of Primary Sjögren’s Syndrome (pSS)

Introduction: Primary Sjögren’s syndrome (pSS) is a chronic progressive autoimmune disease that primarily affects exocrine glands with varying symptoms. Here we discuss atypical optic neuritis as an initial presentation of pSS without any sicca symptoms. Case presentation: A 22-year-old woman came to the outpatient clinic with the chief complaint of rapid deteriorating visual acuity that had started one week before—no complaint of the eye or other mucosal dryness. At the initial visit, best corrected visual acuity (BCVA) was hand movement on the right eye and 6/7.5 on the left eye with decreasing color perception. Fundus examination showed bilateral optic nerve head edema. Schirmer test and tear-film break up time were within normal limits. After the initial one gram intravenous methylprednisolone treatment, no significant changes were observed for three consecutive days. Serological investigations revealed raised levels of SS-A native. Improvement happened after being given azathioprine. Conclusion: Optic neuritis may be the initial presentation of Sjögren’s syndrome without sicca symptoms. The presence of a specific antibody, including anti-SSA, is supportive for the diagnosis of such a case.

Optic Disc Edema in Syphilis.

Syphilis is an uncommon cause of optic nerve head edema; however, differentiating syphilis from other etiologies of optic nerve head swelling may be challenging. We describe 4 cases of ocular syphilis presenting with swollen optic nerve head(s) without overt signs of intraocular inflammation to better define the phenotypic presentation of this condition to allow its early recognition and treatment and discuss potential pathophysiological mechanisms of syphilitic optic neuropathy. Retrospective case series of patients presenting to a tertiary neuro-ophthalmology practice with a swollen optic nerve head(s) but no overt signs of intraocular inflammation, which was eventually determined to be secondary to syphilis. Four patients were included in the study. The mean age was 43 years, 2 were women and 2 had bilateral involvement. Two patients had a recent history of skin rash, and one patient was investigated for abdominal pain and elevated liver enzymes. Two patients presented with photopsias and preserved visual function, whereas 2 presented with vision loss. Although chorioretinitis was present in all cases, it was very subtle in all and was only appreciated on fundus autofluorescence (FA) in 3 of 4 cases. Three patients demonstrated evidence of optic perineuritis on neuro-imaging. All patients were treated with a course of intravenous penicillin with a variable degree of visual recovery. Systemic symptoms are common in patients with syphilic optic neuropathy. Optic disc edema as a manifestation of syphilis is usually accompanied by subtle chorioretinitis, which is best appreciated on FA. Optic perineuritis is common in patients with syphilitic optic neuropathy, with its pathophysiology likely similar to meningitis seen in neurosyphilis.

Uveitis and optic nerve edema: when is neuroimaging necessary?

We sought to determine the frequency and clinical characteristics of optic nerve head edema (ONHE) and uveitis in children, in order to better understand when an urgent neurological workup is needed.

Approaches to Potentiated Neuroprotective Treatment in the Rodent Model of Ischemic Optic Neuropathy.

Nonarteritic anterior ischemic optic neuropathy (NAION) commonly causes sudden optic nerve (ON)-related vision loss. The rodent NAION model (rAION) closely resembles NAION in presentation and physiological responses. We identified early rAION-associated optic nerve head (ONH) inflammatory gene expression responses and the anti-inflammatory prostaglandin PGJ2’s effects on those responses. We hypothesized that blocking pro-inflammatory prostaglandin (PGE2) production by inhibiting monoacylglycerol lipase or cyclooxygenase activity and co-administering PGJ2 would potentiate RGC survival following ischemic neuropathy. Deep sequencing was performed on vehicle- and PGJ2-treated ONHs 3d post-rAION induction. Results were compared against responses from a retinal ischemia model. Animals were treated with PGJ2 and MAGL inhibitor KML29, or PGJ2 + COX inhibitor meloxicam. RGC survival was quantified by stereology. Tissue PG levels were quantified by ELISA. Gene expression was confirmed by qPCR. PGJ2 treatment nonselectively reduced inflammatory gene expression post-rAION. KML29 did not reduce PGE2 1d post-induction and KML29 alone increased RGC loss after rAION. Combined treatments did not improve ONH edema and RGC survival better than reported with PGJ2 alone. KML29′s failure to suppress PGE2 ocular synthesis, despite its purported effects in other CNS tissues may result from alternative PG synthesis pathways. Neither KML29 nor meloxicam treatment significantly improved RGC survival compared with vehicle. While exogenous PGJ2 has been shown to be neuroprotective, treatments combining PGJ2 with these PG synthesis inhibitors do not enhance PGJ2’s neuroprotection.

Biomarkers of lesion severity in a rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION).

The rodent model of nonarteritic anterior ischemic optic neuropathy (rNAION) is similar in many of its pathophysiological responses to clinical NAION. Like human NAION, there is significant variability in the severity of the lesion produced, and little is known of the parameters associated with rNAION induction severity or if pre- or early post-induction biomarkers can be identified that enable prediction of lesion severity and ultimate loss of retinal ganglion cells (RGCs). Adult male Sprague-Dawley outbred rats were evaluated for various parameters including physiological characteristics (heart rate, respiratory rate, temperature, hematocrit [Hct]), optic nerve head (ONH) appearance, pre- and post-induction mean diameter, and intravenous fluorescein and indocyanine green angiographic patterns of vascular leakage at 5 hours post-induction, performed using a spectral domain-optical coherence tomography (SD-OCT) instrument. Early changes were correlated with ultimate RGC loss by Brn3a (+) immunohistology. RGC loss also was correlated with the relative level of laser exposure. The severity of ONH edema 2d, but not 5hr, post induction was most closely associated with the degree of RGC loss, revealing a threshold effect, and consistent with a compartment syndrome where a minimum level of capillary compression within a tight space is responsible for damage. RGC loss increased dramatically as the degree of laser exposure increased. Neither physiological parameters nor the degree of capillary leakage 5hr post induction were informative as to the ultimate degree of RGC loss. Similar to human NAION, the rNAION model exhibits marked variability in lesion severity. Unlike clinical NAION, pre-induction ONH diameter likely does not contribute to ultimate lesion severity; however, cross-sectional ONH edema can be used as a biomarker 2d post-induction to determine randomization of subjects prior to inclusion in specific neuroprotection or neuroregeneration studies.

Papilledema in Space Flight: Pathogenesis, Diagnostics and Monitoring

Some Russian cosmonauts in space flight have revealed swelling of the optic nerve head of varying severity. Four clinical cases presented in this article. A quantitative method for the analysis of OCT images of the optic nerve head and the retina has been developed for the diagnosis and monitoring of the optic nerve’s state. This method is quite informative, regardless of the opinion of each specific medical consultant; diagnosis of optic nerve head edema can be performed according to the generally accepted Frisen’s grading, and thus objectify its diagnostic capabilities. In cases when changes in the optic nerve head are not visualized during ophthalmoscopy, quantitative analysis of OCT images allows one to quantify the presence of optic nerve head edema at the subclinical stage. This objective diagnostic method allows us to establish and quantify the amount of industrial activity, which, with edema of the optic nerve because of intracranial hypertension, mostly pronounced on the nasal side of the nerve disc. Determining the thickness of the retina and head of the optic nerve in the nasal side are paramount for monitoring changes in papilledema in dynamics, especially in the subclinical and 0 stage according to Frisen. Quantitative measurements of the optic nerve head in the temporal side are necessary for the diagnosis, developed papilledema and differential diagnosis of 1-2 stages on the Frisen scale. The use of this diagnostic method has the great importance in assessing the influence of various factors of the space flight on the optic nerve head.

Protective Effects of Intravitreal Injection of the Rho-Kinase Inhibitor Y-27632 in a Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy (rAION).

Purpose We sought to explore the effects of intravitreal injection of the Rho-kinase inhibitor Y-27632 in a rodent model of nonarteritic anterior ischemic optic neuropathy (rAION). Methods The rAION model was established by using laser-induced photoactivation of intravenously administered Rose Bengal in rats. The rats received intravitreal injections of Y-27632 or PBS 1, 3, and 6 days after rAION induction. Optical coherence tomography (OCT) was performed at 2 days and 4 weeks after induction. Visual evoked potential (VEP) was used to evaluate the visual function at 4 weeks. Brn3a immunofluorescence staining of surviving RGCs and apoptosis assays of RGCs were performed at 4 weeks. Results Optic nerve head (ONH) width was significantly reduced in the Y-27632 group compared with that in the PBS group at 2 days after induction (p < 0.05). At 4 weeks, the P1 amplitude of flash-VEP (FVEP) in the Y-27632 group was significantly higher than that of the PBS group (p < 0.05). The RGC densities in the central and midperipheral retinas in the Y-27632 group were significantly higher than those in the PBS group (p < 0.05). Furthermore, there was a significant decrease in apoptotic RGCs in the Y-27632 group than in the PBS group (p < 0.05). Conclusions Intravitreal injection of Y-27632 had neuroprotective effects on ONH edema, RGC survival, and visual function preservation in rAION.

Analysis of misdiagnosis glomus jugulare tumor

Objective:To analyze the causes of misdiagnosis of patients with glomus jugulare tumor. Method:The clinical data of 116 patients with glomus jugulare tumor were retrospectively analyzed. Result:Among the 116 patients, 65 were misdiagnosed, the average duration of misdiagnosis was 4.90 years. The misdiagnosed diseases were chronic otitis media or cholesteatoma in 25 cases, neurological tinnitus or hearing loss in 16 cases, facial paralysis in 6 cases, external auditory canal masses in 4 cases, secretory otitis media in 3 cases, neck mass in 3 cases, intracranial neoplasma in 2 cases, middle ear cancer in 1 case, vocal cord paralysis in 1 case, stomatitis in 1 case, optic nerve head edema in 1 case, middle ear hemangioma in 1 case and vascular tinnitus in 1 case. Conclusion:The misdiagnosis of glomus jugulare tumor can be summarized as follows: the patients' first symptoms were not specific; lack of auxiliary examination, especially imaging examination; physicians have insufficient understanding of imaging and pathological examination of glomus jugulare tumor.

Topical Trabodenoson Is Neuroprotective in a Rodent Model of Anterior Ischemic Optic Neuropathy (rNAION).

PurposeNonarteritic anterior ischemic optic neuropathy (NAION) is the leading cause of sudden optic nerve–related vision loss currently without effective treatment. We evaluated the neuroprotective potential of ocular (topical) delivery of trabodenoson, a selective A1 receptor mimetic, in a rodent model of NAION (rNAION).MethodsDaily topical delivery of 3% trabodenoson or vehicle administered in both eyes 3 days prior to rNAION induction and for 21 days post induction. Retinal appearance and optic nerve head (ONH) edema was evaluated using spectral-domain optical coherence tomography (SD-OCT). Retinal function was evaluated before and after induction by ganzfeld electroretinography (ERG). Brn3a(+) retinal ganglion cells (RGCs) were quantified by stereology. Axonal ultrastructure was evaluated by electron microscopy.ResultsTrabodenoson-treated eyes had significantly reduced optic nerve (ON) edema compared with vehicle-treated eyes (ANOVA, P < 0.05). Electrophysiologically, there was a nonsignificant trend toward b-wave and oscillatory potential (OP) preservation in the trabodenoson-treated eyes. RGC counts were higher in trabodenoson-treated eyes compared to vehicle (74% versus 47% of the contralateral eye; two-tailed t-test; P = 0.01), as were ON axons. No overt morphologic differences in cell inflammation were observed between vehicle- and trabodenoson-treated ONHs, but trabodenoson-treated ONHs revealed increased expression of astrocyte-related neuroprotective responses.ConclusionsTrabodenoson preserves RGCs in the rodent NAION model. While previous clinical trials focused on trabodenoson's ocular antihypertensive effect, our data suggest trabodenoson's primary target may be both the retina and ONH. Selective adenosine A1 agonists may prove an appropriate neuroprotective adjunctive for ischemia-related ON diseases such as NAION and glaucoma.Translational RelevanceRGC and ON neuroprotection in ischemic neuropathies may be achievable by topical administration of A1 adenosine agonists rather than by simply relying on intraocular pressure reduction.

A Rare Case of Combined Vascular Block

Papillophlebitis or central retinal vein occlusion (CRVO) of the young is a condition affecting healthy adults, less than 50 years of age. We report a case of papillophlebitis with cilioretinal artery occlusion along with its fundus fluorescein angiography (FFA) and Spectral Domain Ocular Coherence Tomography (SD-OCT) features. A 27 year old female with no systemic illness reported with sudden onset diminution of vision for 1 day. Fundus examination revealed optic nerve head edema, dilated tortuous veins and whitening of papillomacular bundle suggestive of cilioretinal artery occlusion. Fundus fluorescein angiography showed normal filling of cilioretinal artery and no rteriovenous delay. OCT showed hyperreflective inner retinal layers with obscuration of external limiting membrane. Prompt therapy with high dose intravenous steroids lead to early resolution and better visual prognosis.