Optic Nerve Edema Research Articles

Bilateral optic disc oedema and associated optic neuropathy in the setting of FOLFOX chemotherapy

BackgroundTo report a case of bilateral optic disc oedema and associated optic neuropathy in the setting of FOLFOX chemotherapy.Case presentationA case of a 57-year-old male being treated with FOLFOX chemotherapy for stage 3B colorectal cancer, who developed bilateral optic disc oedema and associated left sided optic neuropathy is described. The patient presented following cycles 7, 8 and 9 of chemotherapy with a history of bilateral simultaneous intermittent inferior altitudinal field defects. These episodes progressed to bilateral optic nerve oedema and a subsequent left sided optic neuropathy. The patient’s symptoms and oedema regressed with discontinuation of chemotherapy.ConclusionThis is the first report suggesting a vasospastic role of 5-fluoruracil in 5-FU associated optic neuropathy. It highlights that 5-FU may have the potential to cause arterial vasospasm outside the cardiac vasculature, resulting in end-organ optic nerve ischaemia.

SAT0128 Efficacy and safety of adalimumab treatment for refractory juvenile idiopathic arthritis-associated uveitis

BackgroundThe treatment of juvenile idiopathic arthritis (JIA)–associated uveitis is one of the serious problem of paediatric rheumatology, therefore development and implementation of new methods of treatment is relevant. Humanised anti-TNFα...

Quantitative analysis of optic nerve damage in idiopathic intracranial hypertension (IIH) at diagnosis

Optic neuropathy secondary to idiopathic intracranial hypertension (IIH) may be a severe complication which must be early identified, adequately monitored and treated to avoid blindness. The aim of this study was to quantify optic nerve involvement at time of diagnosis in a prospectively series of IIH investigated at a single Institution and to identify objective parameters for early diagnosis and follow-up. 38 consecutive patients (9 men, 29 females, mean age 39.8 years) with IIH underwent a complete neuro-ophthalmological evaluation including standardized automated perimetry as functional measurement of optic neuropathy and spectral domain optical coherence tomography (SD-OCT) measurements to grade papilledema or optic nerve atrophy. An overall diagnosis of optic nerve involvement was made in 50 out of 76 eyes (66 %); ophthalmoscopic signs of papilledema were identified in 35 eyes (46 %) while optic disc pallor was found in 13 (17 %). In all patients mean visual field deviation (MD, dB) was -7.2 (range 5.3-33.2). SD-OCT measurements of peripapillary retinal nerve fiber layer thickness (PRNFLT) and of macular ganglion cell complex thickness (MGCCT) obtained in 40 eyes (20 subjects) showed normal PRNFLT in 12 eyes (30 %), increased in 16 (40 %) and reduced in 12 eyes (30 %); normal MGCCT in 26 eyes (65 %), reduced in 14 (35 %). In all eyes average RNFLT was increased (mean 130 μm, range 219-59) and average MGCCT was decreased compared to normal values (mean 89.5 μm, range 198-65). Increased PRNFLT was associated with reduced MGCCT in 4 eyes (10 %) indicating early retrograde optic nerve damage. Decreased PRNFLT was associated with decreased MGCCT in 10 eyes (83 %). These results indicate that, in IIH patients, signs of optic neuropathy can be identified in more than half of cases, even without papilledema evidenced on ophthalmoscopic examination. Moreover, an SD-OCT analysis, which can be definitively useful to quantify optic nerve edema or atrophy, can show damage of retinal ganglion cells in an early phase of the disease.

A Novel Rodent Model of Posterior Ischemic Optic Neuropathy

To develop a reliable, reproducible rat model of posterior ischemic optic neuropathy (PION) and study the cellular responses in the optic nerve and retina. Posterior ischemic optic neuropathy was induced in adult rats by photochemically induced ischemia. Retinal and optic nerve vasculature was examined by fluorescein isothiocyanate–dextran extravasation. Tissue sectioning and immunohistochemistry were used to investigate the pathologic changes. Retinal ganglion cell survival at different times after PION induction, with or without neurotrophic application, was quantified by fluorogold retrograde labeling. Optic nerve injury was confirmed after PION induction, including local vascular leakage, optic nerve edema, and cavernous degeneration. Immunostaining data revealed microglial activation and focal loss of astrocytes, with adjacent astrocytic hypertrophy. Up to 23%, 50%, and 70% retinal ganglion cell loss was observed at 1 week, 2 weeks, and 3 weeks, respectively, after injury compared with a sham control group. Experimental treatment by brain-derived neurotrophic factor and ciliary neurotrophic factor remarkably prevented retinal ganglion cell loss in PION rats. At 3 weeks after injury, more than 40% of retinal ganglion cells were saved by the application of neurotrophic factors. Rat PION created by photochemically induced ischemia is a reproducible and reliable animal model for mimicking the key features of human PION. The correspondence between the features of this rat PION model to those of human PION makes it an ideal model to study the pathophysiologic course of the disease, most of which remains to be elucidated. Furthermore, it provides an optimal model for testing therapeutic approaches for optic neuropathies.

Intravitreal bevacizumab for the treatment of nonarteritic anterior ischemic optic neuropathy: a prospective trial

There is currently no accepted treatment for Nonarteritic Anterior Ischemic Optic Neuropathy (NAION). One new therapeutic approach involves decreasing optic nerve edema with intravitreal bevacizumab in order to resolve a proposed compartment syndrome. In this non-randomized controlled clinical trial, 1.25 mg intravitreal bevacizumab was compared with natural history. Patients were examined at baseline, 1, 3, and 6 months with a full neuro-ophthalmic exam, automated perimetry, and optic nerve optical coherence tomography (OCT) measurements. The primary outcome measure was change in mean deviation on Humphrey visual field testing. Secondary outcome measures were change in visual acuity and optic nerve OCT thickness. Incidence and type of complications were also recorded. Twenty-five patients were enrolled (17 treatment and 8 control). There was no significant effect of treatment on the primary outcome measure of mean deviation score (P=0.4). There was similarly no effect of group assignment on the secondary outcome measures of change in mean Early Treatment Diabetic Retinopathy Study letters (P=0.33) or nerve fiber layer thickness on OCT (P=0.11). In the bevacizumab group, there was one case of a corneal abrasion and two cases of recurrent NAION. No other complications were noted. We found no difference between bevacizumab and natural history for change in visual field, visual acuity, or optic nerve OCT thickness. Based on the current evidence we would not recommend the use of intravitreal bevacizumab to treat patients with the new onset of NAION.

Acute Retinal Necrosis Secondary to Varicella Zoster Virus in an Immunosuppressed Post-Kidney Transplant Patient

A woman, aged 42 years, presented to the ophthalmologist complaining of right eye redness, tearing, photosensitivity, and blurred vision of a 1-month duration. Her past medical history was significant for a kidney transplant for which she was immunosuppressed with mycophenolate mofetil 750 mg twice a day and prednisone 10 mg daily. Ophthalmologic examination of the right eye revealed visual acuity of 20/60, intraocular pressure of 16 mmHg, scleral injection, and a significant inflammatory reaction in the anterior chamber. Funduscopy revealed vitreous haze, optic nerve edema, arteriolar sheathing and attenuation, and peripheral 360° of retinal whitening – a clinical picture consistent with retinitis (figure 1). The left eye examination was entirely normal. Figure 1 (A) Examination of the fundus on day of presentation shows peripheral whitening and vasculitis as evidenced by optic nerve edema, vitreous haze, and retinal arteriolar narrowing. The decrease in clarity of the photograph is secondary to the vitreous haze, ... The differential diagnosis for retinitis in an immunocompromised host includes acute retinal necrosis (ARN), progressive outer retinal necrosis, cytomegalovirus (CMV) retinitis, and toxoplasmosis. Less common causes of acute retinitis include syphilis,1 Bechet's disease, and lymphoma. Aqueous fluid obtained from the anterior chamber was sent for polymerase chain reaction (PCR) viral DNA analysis, and the patient was treated with 2 mg of ganciclovir injected intravitreally on the day of presentation. A 2-week course of renal-dose adjusted intravenous (IV) acyclovir was started with subsequent regression of the retinal whitening (figure 2). Varicella zoster virus (VZV) infection with a viral load of 6.5 × 107 IU was later confirmed with PCR of the aqueous fluid. The vision initially improved to 20/40 in the right eye. She was transitioned from IV acyclovir to oral valacyclovir. Figure 2 (A) After treatment with anti-viral medication, there is regression of retinal whitening and atrophic retinal tissue. (B) Areas of regression are indicated by white asterisks. The arterioles that previously were narrowed, indicated by the white arrows, ... Seven weeks later, the patient developed a rhegmatogenous retinal detachment that was diagnosed after she complained of an abrupt decrease in vision. Despite successful surgical reattachment of the retina with pars plana vitrectomy, scleral buckle, and silicon oil, the patient's vision remained at light perception level only. Necrotizing herpetic retinopathies are caused by VZV, herpes simplex virus 1 and 2, CMV, and rarely, Epstein Barr virus. A spectrum of clinical presentations may occur depending on the virus and the host's immunity.2 Immunosuppressed patients are at risk for development of necrotizing retinopathies typically associated with immunocompromised states, such as CMV retinitis and progressive outer retinal necrosis. They may also develop syndromes that are typically seen in immunocompetent hosts, such as ARN. Acute unilateral decrease in vision, photophobia, and eye pain are the usual presentations of ARN.3 The key feature seen on examination is white-yellow, multifocal, peripheral patches that later coalesce into diffuse areas of full-thickness, peripheral retinal necrosis.4 Other signs of ocular inflammation including vitritis, vasculitis, optic disc edema, keratic precipitates, and posterior synechiae may also be seen. Untreated ARN results in blindness from retinal scarring, retinal detachment, or optic atrophy; therefore, ARN is an ophthalmic emergency. One-third of patients develop the disease in the fellow eye within one month of presentation, if left untreated.5 The diagnosis of ARN is made on the basis of clinical appearance, and antiviral treatment should be initiated promptly. Timely referral to a uveitis or retina specialist experienced in the care of such patients and collaboration with an infectious disease specialist are essential.

Four-dimensional ultrasound imaging in neuro-ophthalmology

Summary Purpose To demonstrate diagnostic abilities of space–time (4D) ultrasound imaging in patients with eye pathology and some neuro-ophthalmic syndromes. Methods Fifteen healthy controls and 15 patients with eye pathology (papilledema, retinal detachment, macular degeneration and intraocular metastasis) were studied by multimodal (color duplex, B-flow and 3D/4D imaging) sonography. Results Normal optic disc resulted in a smooth and sharp contour without swelling. Papilledema was presented as a hyperechoic prominence into the vitreous. On its side the optic sheath diameter was increased in association with the degree of optic disc swelling. The retinal detachment was imaged as a hyperechoic undulating membrane, the neovascular macular degeneration – as a hyperechoic membrane behind the retina, and the intraocular metastasis – as irregular unifocal formation into the vitreous. Conclusions The 4D neuro-ophthalmo-sonology helps for the quick and non-invasive volume imaging of the type, size, location and severity of optic disc and optic nerve edema and its differentiation from other types of eye lesions.

An inherited disorder with splenomegaly, cytopenias, and vision loss

We describe a novel inherited disorder consisting of idiopathic massive splenomegaly, cytopenias, anhidrosis, chronic optic nerve edema, and vision loss. This disorder involves three affected patients in a single non-consanguineous Caucasian family, a mother and two daughters, who are half-sisters. All three patients have had splenectomies; histopathology revealed congestion of the red pulp, but otherwise no abnormalities. Electron microscopic studies of splenic tissue showed no evidence for a storage disorder or other ultrastructural abnormality. Two of the three patients had bone marrow examinations that were non-diagnostic. All three patients developed progressive vision loss such that the two oldest patients are now blind, possibly due to a cone-rod dystrophy. Characteristics of vision loss in this family include early chronic optic nerve edema, and progressive vision loss, particularly central and color vision. Despite numerous medical and ophthalmic evaluations, no diagnosis has been discovered.

Clinical guidelines for diagnosing and managing ocular manifestations in children with mucopolysaccharidosis

The mucopolysaccharidoses (MPS) are a group of rare lysosomal storage disorders characterized by the accumulation of glycosaminoglycans in several tissues and organs. This accumulation results in an array of clinical manifestations and premature death in severe cases. Ocular problems are very common in children with MPS and may involve the cornea, sclera, trabecular meshwork, retina, optic nerve and also the posterior visual pathways. The aims of this study are to give an overview of ocular problems in MPS and to provide clinical guidelines for paediatric ophthalmologists for early diagnosis and management of ocular manifestations in children with MPS. Diagnostic problems may arise in children with severe corneal clouding, hampering visualization of the fundus. Intraocular pressures may be falsely high, even leading to suspicion and unnecessary pressure-lowering treatment. Simple interventions such as the use of prescription glasses or photochromatic glasses can considerably improve quality of life in children with MPS.

An unusual case of bilateral retinal haemorrhage following snakebite

Snakebite is a serious community health problem in India. On an average, there are 200,000 people bitten by snakes annually and 30,000–40,000 of them die because of the ensuing complications [1]. In India 20,000 people die every year due to the same reason. Snake venoms are complex heterogeneous poisons with multiple effects. Venomous snakebites may result in haemostatic or neurological dysfunction. Ocular complications are very rare, but common ocular involvements are generally connected with neurological ones. The varied ophthalmic effects of envenomation are blepharoptosis, muscle palsies, haemorrhages into the conjunctiva, anterior chamber, vitreous or retina, lid oedema, conjunctival chemosis, retinal and optic nerve oedema, pupillary changes, optic neuritis and optic atrophy [2]. Bilateral retinal haemorrhage is an infrequent ocular effect caused by snakebite. In the current study, we describe a case that developed bilateral retinal haemorrhage following Indian Russell viper (Daboia russelii) snakebite.

Proptosis, Congestion, and Secondary Glaucoma Due to Carotid-Cavernous Fistula After Embolization

Carotid-cavernous fistulas (CCFs) are traumatic or spontaneously occurring communications between the carotid artery and the cavernous sinus. Carotid-cavernous fistulas can be due to a direct connection or indirect connections between the carotid artery system and the cavernous sinus. According to the etiologic classification, they may be of traumatic or spontaneous origin, and according to the angiography classification, they may be of direct or dural. Most CCFs are of spontaneous origin, and these are reported as frequently self-healing lesions. Spontaneous CCFs are mostly secondary to arteriosclerotic changes, which explains the increased ratio of elderly patients. Traumatic CCFs are usually of high-flow type and need intervention. The symptoms are various usually correlated to the size and type of venous drainage. The most frequent symptoms on presentation are proptosis, conjunctivitis, and chemosis; however, this picture may be complicated by optic nerve edema, cranial nerve palsies, and intracranial hemorrhage. We report a case with right low-flow dural CCF, which has worsened after angiography and recovered totally soon after endovascular embolization process.

MR Imaging Findings in Patients with Secondary Intracranial Hypertension

IH can alter the configuration of anatomic structures of the central nervous system. We determined the sensitivity and specificity of MR imaging to detect these changes in patients with secondary IH. Patients (n = 36) with IH were prospectively investigated with MR imaging and were matched to 36 controls. MR images were evaluated for elongation and edema of the optic nerves, protrusion of the optic disc, flattening of the posterior sclera, height of the pituitary gland, and width of the optic nerve sheath. On MRV, we recorded venous sinus abnormalities and measured the luminal width of the superior ophthalmic veins. A grading score was introduced to define cranial venous outflow obstruction. Cranial venous outflow obstruction and ONS hydrops were the most valid signs indicating IH with a sensitivity of 94% and 92% and a specificity of 100% and 89%, respectively. Sensitivities and specificities were 56% and 97% for reduced pituitary height, 64% and 78% for flattening of the posterior sclera, 31% and 97% for widening of the superior ophthalmic veins, 33% and 100% for optic disc protrusion, 14% and 100% for optic nerve edema, and 6% and 100% for elongation of the optic nerve. At least 2 MR imaging findings could be demonstrated in each patient but in none of the controls. The number of positive MR imaging findings correlated with CSF pressure (r = 0.62, P = .01). The combination of cranial and orbital MR imaging and MRV can be highly sensitive and specific in the diagnosis of patients with IH.

Use of Optical Coherence Tomography to Evaluate Papilledema and Pseudopapilledema

Idiopathic intracranial hypertension (IIH), or pseudotumor cerebri, describes a condition of elevated intracranial pressure (ICP) that typically presents in obese women of childbearing age with symptoms and signs of posture-dependent headaches, pulsatile tinnitus, visual changes, and papilledema. Optical coherence tomography (OCT) has begun to be utilized as an adjunctive, quantitative tool in the evaluation of patients with IIH to help distinguish between true optic nerve head edema and pseudopapilledema, and to contribute to our understanding of the consequences of prolonged optic nerve edema. Although few longitudinal studies of patients with IIH have been published to date, it appears that there may be a correlation between retinal nerve fiber layer (RNFL) thickness and visual function. With the new spectral domain OCT, additional parameters of the optic nerve imaging, including volume and height measurements, might provide greater sensitivity of the response to treatment and the long-term visual outcome in patients with IIH.

Choroidal Lymphoma Masquerading as Anterior Ischemic Optic Neuropathy

To report a patient with presumed nonarteritic anterior ischemic optic neuropathy (NAION) found on our evaluation to have bilateral uveal lymphoma. The clinical history and physical examination, Humphrey visual field testing, ultrasonography, magnetic resonance imaging (MRI), and fine needle aspiration biopsy specimen of a 60-year-old man with presumed NAION were evaluated. The patient initially presented with painless blurred vision OD and foreign body sensation OS. Upon examination, he was found to have optic nerve edema OD suspicious for NAION and oral steroids were employed with no improvement. Later, an abnormality in the left eye raised suspicion for choroidal metastasis. By ultrasound, the tumor in the left choroid was acoustically hollow. MRI of the orbits revealed a choroidal infiltrative process OU. Fine needle aspiration biopsy of OS confirmed atypical lymphocytes, predominantly small to intermediate sized, without necrosis. The patient was treated with external beam radiation therapy to both eyes. Choroidal lymphoma may present with clinical features of anterior ischemic optic neuropathy or choroidal metastasis.

Systemic therapies for mucopolysaccharidosis: ocular changes following haematopoietic stem cell transplantation or enzyme replacement therapy – a review

AbstractThe management of mucopolysaccharidosis (MPS) is focused on the multi‐organ, sometimes life‐threatening, clinical manifestations that occur over time. In the past, the limited, symptom‐based treatment options led physicians to adopt a palliative approach towards individual disease‐associated complications. The availability of systemic treatments such as haematopoietic stem cell transplantation (HSCT) and enzyme replacement therapy (ERT) has created a better prognosis for MPS patients, particularly when initiated early in life. As part of an integrated management approach, these therapies could be valuable in managing the ocular features that are present in many children with MPS. HSCT has been shown to stabilize or improve corneal clouding and optic nerve oedema for the majority of patients. Retinal degeneration, in contrast, seems not to be permanently arrested. ERT was more recently introduced and has therefore been less well examined than HSCT; with respect to ocular problems in MPS, the majority of reports indicate stabilization of corneal clouding or visual acuity. However, controversy remains about its effect on other ocular pathologies. Despite the lack of consistent ophthalmic improvement for all patients, both treatment modalities deserve consideration, because even reducing MPS‐related eye disease progression is worthwhile.

Bilateral Panuveitis following Intravesical BCG Immunotherapy for Bladder Carcinoma

Purpose: To report a case of bilateral panuveitis following local treatment with Bacille Calmette-Guérin (BCG) immunotherapy for superficial bladder carcinoma.Design: Case report and literature review.Methods: A 70-year-old female presented with severe bilateral anterior chamber inflammation 5 days after intravesical BCG instillation. Despite topical steroids and mydriatics, inflammation worsened and bilateral optic nerve swelling developed.Results: Oral corticosteroids settled the ocular inflammation, and optic nerve function recovered. A trial of steroid cessation caused rebound uveitis, so she remains on maintenance doses of oral corticosteroid.Conclusions: Ocular inflammations following BCG therapy for bladder cancer are rare, and little is known about the management of such cases. This is the first report of bilateral panuveitis with optic nerve edema following such treatment.

Choroidal Infarction in Fulminant Idiopathic Intracranial Hypertension

We report a unique case of idiopathic intracranial hypertension (IIH) in which vision loss likely occurred from a variety of mechanisms, including an acute choroidal infarction. A 20 year-old white woman complained of severe headaches with nausea, photophobia and pulsatile tinnitus. For the past week, she had noticed rapidly progressive visual loss in both eyes with severe constriction of her peripheral visual field. Review of systems was remarkable only for recent weight gain of 20 pounds over the previous year. On examination, body mass index was 26.6, blood pressure was 110/68 mmHg, and neurologic examination was normal. Visual acuity was 20/20 in the right eye and 20/30 in the left eye. Humphrey and Goldmann visual fields showed bilateral constriction with an inferior nasal defect and enlarged blind spot in the right eye and an inferior altitudinal defect in the left eye. Funduscopic examination (Figure 1) showed bilateral severe optic nerve head edema with peripapillary hemorrhages and white nerve fiber layer infarctions. In the left eye, there was an area of juxtapapillary whitening extending to the macula, which appeared deep in the retina or subretina. A fluorescein angiography (FA) showed normal choroidal, arterial and venous filling 25 seconds after injection of fluorescein and normal retina (no mask effect, no edema), ruling out a branch retinal artery or cilioretinal artery occlusion (Figure 2a). Indocyanine green (ICG) videoangiography (figure 2b) demonstrated a choroidal perfusion defect matching the white patch seen in the left ocular fundus, confirming a choroidal infarction. Figure 1 Fundus photography (the right eye is shown on the left and the left eye is shown on the right) showing bilateral optic nerve edema with white exudates. In the left eye, there is an area of whitening extending to the macula and located deeper than the ... Figure 2 (a) Fluorescein angiography of the left eye 25 seconds after injection of fluorescein showing normal retinal vascular filling (earlier transit times were not shown and choroidal filling could not be evaluated); (b) Indocyanine angiography of the left ... We believed the patient's clinical presentation was highly suggestive of raised intracranial pressure (ICP) with severe papilledema complicated by a choroidal infarction in the left eye, and probably also a superimposed anterior ischemic optic neuropathy (AION) in the left eye, given the inferior altitudinal defect. The diagnosis of IIH was confirmed by normal brain magnetic resonance imaging (MRI) and brain magnetic resonance venography (MRV), and elevated CSF opening pressure (560 mm of water) with normal CSF contents1. Diagnostic lumbar puncture relieved her headaches immediately and she was begun on oral acetazolamide 500mg twice a day. Her visual function, however, remained poor and she underwent bilateral sequential optic nerve sheath fenestrations (ONSF) (left eye first) 8 and 21 days later. The headaches did not recur, and her visual function improved over time, especially in the right eye. The disk edema resolved and she developed secondary optic atrophy. The juxtapapillary whitening resolved within two weeks of the ONSF. Her altitudinal defect remained unchanged in the left eye and her visual field improved in the right eye, but remained constricted (Figure 3). Final visual acuity was 20/20 in both eyes. Figure 3 Humphrey visual fields (24-2 SITA Fast) after ONSF showing persistent constriction and a small paracentral scotoma above fixation in the left eye corresponding to the choroidal infarction.

Optic nerve trauma with unilateral edema as a result of head injury

We encountered a patient who suffered a head injury that translated to the optic nerves, leading to dramatic unilateral right optic nerve edema. The decedent was a 20-year-old unsecured passenger in a convertible. The car collided with a pickup truck. The patient survived for 8 h. At autopsy, a comminuted skull fracture involving the right frontal bone including the right orbital plate was found. The right optic nerve measured 1.2 cm in diameter, compared to only 0.4 cm for the left optic nerve. Microscopically, the right optic nerve was markedly edematous, but the nerve fibers and nuclei were viable and intact. The dramatic difference in size between the right and left optic nerves can be attributed to several mechanisms. The survival interval was essential for the asymmetrical swelling to take place. Optic nerve trauma is relatively rare in head injuries, reported to be present in 0.5% of automobile accidents and assaults. Other causes of optic nerve trauma and edema include tumors, osteopetrosis, or reaction to a peripheral hemodialysis shunt.

Adult nasal glioma presenting with visual loss

We report a rare case of a nasal glioma found incidentally in an adult, presenting with visual loss, optic nerve oedema and proptosis. A 41-year-old woman presented with bilateral proptosis, impairment in visual acuity (6/60 bilaterally) and loss of colour vision. Computed tomography and magnetic resonance imaging showed proptosis, bilateral optic nerve swelling and a heterogeneous mass occupying the left nasal cavity and extending through a skull base defect into the anterior cranial fossa. Biopsy confirmed a nasal glioma. Treatment with intravenous dexamethasone resolved the proptosis, and the patient's visual acuity recovered to 6/9 bilaterally. At the multidisciplinary team meeting, it was felt that the nasal glioma probably represented an incidental finding and was not directly responsible for the patient's proptosis and transient visual loss. To our knowledge, this is the first report in the English language literature of adult nasal glioma presenting with visual loss. The management of nasal gliomas in adults is contentious and the relevant literature is reviewed. This case was managed conservatively with regular follow up.

Optic neuropathy and a reversible splenial lesion after gastric bypass: A shared pathophysiology?

A 22-year-old female presented 2 months after a laparascopic gastic bypass with 3 weeks of progressive painless visual loss. Ophthalmologic exam revealed severely reduced visual acuity, central scotomas, and optic nerve edema bilaterally. She was noted to have a mild encephalopathy. MRI of the brain revealed restricted diffusion in the splenium of the corpus callosum. The patient was treated with 3 days of intravenous methylprednisolone, intravenous fluids, and re-institution of vitamin supplementation. Four weeks later, she had significant improvement in her visual acuity and marked reduction in central scotomas. Her encephalopathy resolved and the splenial abnormality disappeared on repeat brain MRI. This is the first reported case of a bilateral optic neuropathy and a reversible splenial lesion syndrome after gastric bypass. The presentation of both conditions in our patient may suggest a shared pathophysiology.