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The purpose of this study is to determine whether there are radiographic and systemic clinical characteristics that can predict final visual outcomes in patients with indirect traumatic optic neuropathy (iTON).This study is a retrospective, multicenter case series of adult patients with iTON treated initially at large, urban, and/or academic trauma centers with follow-up at an affiliated ophthalmology clinic. In addition to detailed cranial computed tomography characteristics, demographics, systemic comorbidities, coinjuries, blood products administered, and intracranial pressure, along with other factors, were gathered. LogMAR visual acuity (VA) at the initial presentation to the hospital and up to 12 months follow-up was collected.Twenty patients met inclusion criteria; 16 (80%) were men with a mean age of 40.9 years (±20.9). Mean initial VA was 1.61 logMAR (∼20/800, ± 0.95), and final VA was 1.31 logMAR (∼20/400, ± 1.06). Three patients (4 eyes) had no light perception (NLP) VA at presentation and remained NLP at final follow-up. Of the predictors analyzed, only the initial VA was found to be a significant predictor of visual outcome. The presence of orbital fractures, intraconal and/or extraconal hemorrhage, as well as systemic comorbidities, were not found to significantly affect visual outcome.After evaluating multiple factors, initial VA was the only factor associated with visual prognosis in iTON. This knowledge may better enable clinicians to predict visual prognosis and set reasonable expectations with patients and families at the time of injury.

A 58-year-old man presented with a complaint of subjective visual field loss on the right side and hypertensive emergency. Examination revealed a right homonymous hemianopia. Computed tomography imaging revealed an acute stroke of the left lateral geniculate body. A few months later, automated perimetry revealed characteristic visual field changes associated with this lesion. In this report, the anatomy, pathophysiology, clinical findings, and previously reported etiologies of lateral geniculate body lesions are reviewed.

Background: Oscillopsia is a visual phenomenon in which an individual perceives that their environment is moving when it is in fact stationary. In this report, we describe two patients with pulsatile oscillopsia following orbitocranial approaches for skull base meningioma resection. Case Description: Two patients, both 42-year-old women, underwent orbitocranial approaches for resection of a right sphenoid wing (Patient 1) and left cavernous sinus (Patient 2) meningioma. Patient 1 underwent uncomplicated resection and was discharged home without neurologic or visual complaints; she presented 8 days later with pulsatile oscillopsia. This was managed expectantly, and MRA revealed no evidence of vascular pathology. She has not required intervention as of most recent follow-up. Patient 2 developed trochlear and trigeminal nerve palsies following resection and developed pulsatile oscillopsia 4 months postoperatively. After patching and corrective lens application, the patient’s symptoms had improved by 26 months postoperatively. Conclusion: Oscillopsia is a potential complication following skull base tumor resection about which patients should be aware. Patients may improve with conservative management alone, although the literature describes repair of orbital defects for ocular pulsations in traumatic and with some developmental conditions.

While often idiopathic, anterior ischemic optic neuropathy occasionally may occur from an identifiable cause.Observational case report.A 19-year-old woman with unremarkable medical and ophthalmic histories developed visual loss from nonarteritic anterior ischemic optic neuropathy in her right eye after otherwise uneventful dental extraction of the inferior third molars.Anterior ischemic optic neuropathy may rarely occur after dental extraction. Potential pathophysiologic mechanisms of this rare occurrence are discussed.

Vigabatrin was introduced as an antiseizure medication in the United Kingdom in 1989 and was extensively used until 1997 when concerns arose regarding peripheral visual field loss. When the drug was approved in the United States in 2009, it carried a black box warning for the risk of permanent visual loss, and the pharmaceutical company was mandated to create a drug registry to assess for visual deficits. The vigabatrin drug registry has documented a relatively large percentage (37%) of preexisting, baseline visual deficits and a paucity (2%) of potential new visual findings. The vigabatrin vision study, a prospective, longitudinal, single-arm, open-label study, confirmed that adult patients with refractory complex partial seizures had a large number of visual deficits at baseline. An unexpected finding during the first year of therapy with vigabatrin was an increase in retinal thickness on optical coherence tomography. The experience from vigabatrin in the United States emphasizes the importance of baseline eye findings when considering the potential of drug toxicity involving the visual pathways.

Background: Although QuantiFERON-TB Gold In-Tube (QFT-GIT) testing is regularly used to detect infection with Mycobacterium tuberculosis, its utility in a patient population with a low risk for tuberculosis (TB) has been questioned. The following is a cohort study analyzing the efficacy of QFT-GIT testing as a method for detection of active TB disease in low-risk individuals in a neuro-ophthalmologic setting. Methods: Ninety-nine patients from 2 neuro-ophthalmology centers were identified as having undergone QFT-GIT testing between January 2012 and February 2016. Patients were divided into groups of negative, indeterminate, and positive QFT-GIT results. Records of patients with positive QFT-GIT results were reviewed for development of latent or active TB, as determined by clinical, bacteriologic, and/or radiographic evidence. Results: Of the 99 cases reviewed, 18 patients had positive QFT-GIT tests. Of these 18 cases, 12 had documentation of chest radiographs or computed tomography which showed no evidence for either active TB or pulmonary latent TB infection (LTBI). Four had chest imaging which was indicative of possible LTBI. None of these 18 patients had symptoms of active TB and none developed active TB within the follow-up period. Conclusions: Based on our results, we conclude that routine testing with QFT-GIT in a low-risk cohort did not diagnose active TB infection. We do not recommend routine QFT-GIT testing for TB low-risk individuals, as discerned through patient and exposure history, ocular examination, and clinical judgment, in neuro-ophthalmology practice.

A 25-year-old woman with dermatomyositis suffered a right central retinal vein occlusion (CRVO) with visual acuity of 20/40. Examination of the right eye showed vitreous cells, suggesting inflammation of the central retinal vein leading to a CRVO as the presumed mechanism. She was admitted to hospital, and extensive evaluation was negative. She was maintained on corticosteroids to manage her dermatomyositis. One month later, she had macular edema and elevated intraocular pressure. Both resolved with dorzolamide, timolol, and intravitreal bevacizumab, and vision returned to 20/20 in the right eye.

A 39-year-old woman with a history of Behçet disease presented for evaluation of oscillopsia that began postpartum. Examination showed oculopalatal tremor (OPT), documented videographically. Brain magnetic resonance imaging revealed bilateral pseudohypertrophy of the inferior olivary nuclei. Treatment with gabapentin was initiated for OPT presumed secondary to neuro-Behçet disease.

Two patients undergoing long-term treatment with linezolid for pneumonia had decreased visual acuity, dyschromatopsia, and cecocentral scotomas characteristic of toxic optic neuropathy. Visual function slowly recovered 3 to 4 months after discontinuation of the antibiotic treatment in both patients. Toxic optic neuropathy may occur from linezolid. Early withdrawal of the antibiotic may be associated with visual recovery.

Giant cell arteritis (GCA) is a systemic vasculitis that affects large and medium sized arteries. Visual loss is one of the most devastating complications of GCA and usually occurs from occlusion of the posterior ciliary arteries (PCA) leading to anterior ischaemic optic neuropathy (AION). Visual loss can also occur from occlusion of other arteries that supply the visual pathway, such as the central retinal and ophthalmic arteries. Corticosteroid therapy, given orally or intravenously, is the standard treatment for GCA associated visual loss.1 The optimal route of administration and dosage to prevent further visual loss are not known; however, most clinicians advocate higher doses in patients who already have experienced visual loss. Treatment with corticosteroids usually results in stabilisation of visual loss and some patients may have some degree of visual recovery.2,3 However, despite treatment with high dose intravenous corticosteroids, visual loss may progress.1 The reported use of adjunctive agents under these circumstances has been limited. We report a patient who had progressive visual loss while on high dose intravenous corticosteroids and who markedly improved after treatment with heparin. An 85 year old man presented to his optometrist for a routine eye examination. His visual acuity was 20/40 both eyes and his optic discs were normal. Three weeks later (day 1), he lost vision in his right eye. His visual acuity was now 20/100 right eye and 20/40 left eye. On visual field testing with static perimetry he had an inferior altitudinal defect in the right eye and his visual field was normal in the left. His right optic disc was pale and oedematous and his left optic disc was normal. He was suspected of having GCA and was admitted for treatment with intravenous methylprednisolone (IVMP) 250 mg every 6 hours. On day 2, the visual field …

Intraocular pressure (IOP) is dependent on the rate of aqueous production, facility of outflow, and episcleral venous pressure. Increased IOP and visual field loss may result from an elevation of episcleral venous pressure, the causes of which include large vessel venous obstruction (venous sinus thrombosis and superior vena cava syndrome), arteriovenous shunts or fistulas, Sturge-Weber syndrome, scleritis, thyroid related orbitopathy, and orbital tumours.1 Increased episcleral venous pressure may result in elevated IOP and optic neuropathy, even in the absence of these entities. We report a 34 year old man with idiopathic dilated episcleral veins (IDEV) and increased IOP, with visual field loss. A 34 year old man presented for neuro-ophthalmic evaluation because of decreased vision in the right eye and injection of both eyes. His intraocular pressure (IOP) had been elevated in the right eye more than the left for the past 13 years, reaching 32 mm Hg in the right eye. His eyes appeared red for as long as he could remember, but details of his previous ophthalmic examinations were unavailable. Because of the bilateral injection he saw two other neuro-ophthalmologists, who suspected an arteriovenous fistula. One year before presentation he underwent magnetic resonance imaging (MRI) of the head and orbits and catheter arteriography on two occasions, which were both normal. He had no other previous medical problems, was taking …

This report describes the case of a 48-year-old white woman who was found to have an entirely pigmented optic disc in an otherwise normal eye. Pigmentation of the optic disc is an uncommon finding. The possible explanations of this physiologic variant are discussed.

A 62-year-old woman presented with a chronic left homonymous visual field defect because of a right occipital cyst. Serial visual field examination documented stable visual fields for 12 months, after which there was worsening of visual fields associated with enlargement of the cyst. Surgical decompression of the occipital cyst resulted in marked improvement of the visual field defect over 9 months. This case demonstrates that surgical decompression of cystic lesions adjacent to posterior visual pathways can result in recovery of chronic visual field loss.

Assessing pupil reactivity using the swinging flashlight technique in patients with miotic pupils or heavily pigmented irides can be difficult due to the reflection of the examination light off the cornea. We describe a modification of the standard method of detecting pupil reactivity in these difficult-to-see pupils. With the patient facing forward and eyes looking in maximal upgaze, fixed at distance, the examiner shines the light at the limbus in the straight ahead direction. Improved view of the pupil in upgaze results from reduction of the blink reflex and elimination of the Purkinje-1 image with minimal refractive distortion by the cornea. Optical calculations and multimedia demonstrations are provided to document these findings.

A 55-year-old man developed bilateral posterior ischemic optic neuropathy after prolonged prone position lumbar laminectomy. Brain MRI performed 19 hours after the procedure revealed markedly dilated superior ophthalmic veins, a finding that had disappeared on a comparable study performed 5 months later. This first report of dilated superior ophthalmic veins present in the immediate postoperative period but not later may be important in suggesting that an increase in orbital venous pressure during surgery contributes to the development of postoperative posterior ischemic optic neuropathy (PION).

Background: It is difficult to assess the degree of optic nerve damage in patients with ethambutol-induced optic neuropathy, especially just after the onset of visual loss, when the optic disc typically looks normal. Aim: To evaluate changes in retinal nerve fibre layer thickness (RNFLT) using optical coherence tomography (OCT) in patients with optic neuropathy within 3 months of cessation of ethambutol treatment. Design: A retrospective observational case series from a single neuro-ophthalmology practice. Methods: 8 patients with a history of ethambutol-induced optic neuropathy were examined within 3 months after stopping ethambutol treatment. All patients underwent a neuro-ophthalmologic examination, including visual acuity, colour vision, visual fields and funduscopy. OCT was performed on both eyes of each patient using the retinal nerve fibre layer analysis protocol. Results: The interval between cessation of ethambutol treatment and the initial visit ranged from 1 week to 3 months. All patients had visual deficits characteristic of ethambutol-induced optic neuropathy at their initial visit, and the follow-up examination was performed within 12 months. Compared with the initial RNFLT, there was a statistically significant decrease in the mean RNFLT of the temporal, superior and nasal quadrants (p = 0.009, 0.019 and 0.025, respectively), with the greatest decrease in the temporal quadrant (mean decrease 26.5 μm). Conclusions: A decrease in RNFLT is observed in all quadrants in patients with ethambutol-induced optic neuropathy who have recently discontinued the medication. This decrease is most pronounced in the temporal quadrant of the optic disc.

Background/aims: Vitamin A deficiency, often presenting with nyctalopia, has been described in a number of patients with malabsorption as a result of intestinal bypass surgery and, more recently, bariatric surgery. In these reports vitamin A deficiency developed within several years of gastric or intestinal surgery. Three patients who developed decreased vision from vitamin A deficiency more than 18 years after their intestinal surgery are reported. Methods: A retrospective review of the clinical findings of all patients diagnosed with vitamin A deficiency, as confirmed by serological testing, over the past year in a single neuro-ophthalmic practice. Results: Four patients with vitamin A deficiency were seen, three of whom had intestinal surgery more than 18 years before the development of visual symptoms. Conclusion: The authors suggest that vitamin A deficiency should be suspected in patients with unexplained decreased vision and a history of intestinal surgery, regardless of the timing of the surgical procedure.

A 30-year-old woman had bilateral anterior ischemic optic neuropathy after undergoing large-volume liposuction. Visual function remained stable over a four-month follow-up, with decreased visual acuity and marked constriction of the visual fields. To our knowledge, this is the second reported case of ischemic optic neuropathy in this setting.

Aim: To determine the clinical features of amiodarone induced optic neuropathy, which may help distinguish it from non-arteritic anterior ischaemic optic neuropathy. Methods: Retrospective observational case series of patients diagnosed with amiodarone induced optic neuropathy at the neuro-ophthalmology service from March 1998 to February 2001. Amiodarone was discontinued after discussion with the patient9s cardiologist. Visual acuity, colour vision, automated perimetry, and funduscopy were performed on initial and follow up examinations. Results: Three patients with amiodarone induced optic neuropathy presented with mildly decreased vision, visual field defects, and bilateral optic disc swelling. Upon discontinuing the medication, visual function and optic disc swelling slowly improved in all three patients. Conclusion: Amiodarone induced optic neuropathy can present with visual dysfunction, and is typically a bilateral process. Upon discontinuation of amiodarone, slow resolution of optic disc swelling occurs and visual function improves in some patients.

The tonic pupil is characterised by poor reactivity to light, a slow tonic constriction and redilation to a near target, and supersensitivity to topical dilute pilocarpine.1 Most instances do not have an identifiable cause; however, a variety of conditions including herpes zoster, orbital trauma including surgery, and paraneoplastic syndromes may result in tonic pupils. The mechanism(s) which produce tonic pupils are not known, although axonal loss within the ciliary ganglion is generally believed to result in supersensitivity of the iris sphincter muscle. Giant cell arteritis (GCA) has been reported as an uncommon cause of tonic pupils.2 Furthermore, the cause of tonic pupils in GCA is unknown and direct evidence for an ischaemic cause is not convincing. We used orbital colour Doppler imaging to study orbital and ocular blood flow in a patient with GCA, unilateral visual loss, and bilateral tonic pupils. A 58 year old woman presented with visual loss of the left eye for 2 days. She had had neck discomfort and intermittent jaw claudication over the previous 2 weeks. She had no past medical or ocular problems. Visual acuity was 20/20 in the right eye and no light perception in the left eye. The right pupil reacted briskly to light, with a normal consensual response, the left was amaurotic. She identified all of the Ishihara pseudoisochromatic colour plates with the right eye, and automated perimetry of the right eye was normal. Extraocular motility was normal. Funduscopy of the right eye (Fig 1A) was normal, and the left optic disc was pale and swollen, with retinal cotton wool infarcts within the retina, chiefly within the left …

Purpose To investigate the spatial relationship between retinal nerve fiber layer (RNFL) thickness measured with optical coherence tomography (OCT) and visual field sensitivity (VFS) measured by standard automated perimetry (SAP) in chiasmal compression. Methods Twenty-six patients with chiasmal compression were enrolled. RNFL thickness was measured with the StratusOCT and VFS with SAP (Humphrey Field Analyzer; both from Carl Zeiss Meditec, Dublin, CA). Relationships between RNFL thickness (in clock hours, hemifields, and sectors) and VFS (zones were divided into hemifields, quadrants, and sectors based on a validated visual field map) expressed in a decibel scale and 1/lambert (L) were evaluated by linear and nonlinear regression. Coefficients of determination (R(2)) were calculated by using a multivariate model. Results Average RNFL thickness correlated strongly with pattern standard deviation (PSD; R = 0.622) and mean deviation (MD; R = 0.413). The four strongest correlations were between the 8 o'clock OCT position (temporal disc), with the temporal hemifield (R = -0.813), the superotemporal quadrant (R = -0.847), the inferotemporal quadrant (R = -0.855), and the field sector representing the papillomacular bundle (R = -0.809). Coefficients of determination improved significantly in all sectors when time since surgery was included in the regression model-most notably, average thickness and 1/L (R(2) = 0.35-0.49), the decibels (R(2) = 0.31-0.47), and the temporal sector (R(2) = 0.44-0.57). Conclusions This is the first study to compare the structure-function correlation of RNFL measured by OCT with SAP in patients with chiasmal compression. RNFL is topographically related globally and sectorally to decreased SAP, with the temporal sectors showing the strongest correlations. The correlation between RNFL and VFS strengthens as the time from surgical intervention increases.