Posterior Ischemic Optic Neuropathy Research Articles

The Relationship between Ischemic Optic Neuropathy and Internal Carotid Artery Dissection: A Systematic Review.

Background: To evaluate and review the current evidence regarding the association between ischemic optic neuropathy (ION) and internal carotid artery dissection (ICAD). Methods: We systematically reviewed studies according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines (PRISMA), searching three databases (Scopus, Pubmed, and Embase) for relevant articles that clearly described the correlation between ION and ICAD. All studies that examined the association between ICAD and the development of ION were synthesized. Quality assessment using the Newcastle-Ottawa Scale (NOS) and Joanna Briggs Institute (JBI) Critical Appraisal Checklist for Case Reports and Case Series were conducted. Results: Our search yielded 198 manuscripts published in the English language. Following study screening, fourteen studies were selected. The number of participants with ION following ICAD ranged from one to four, with sixteen patients experiencing either anterior ION, posterior ION, or a combination of both. The anterior or posterior ischemic optic neuropathy (AION and PION) patients' ages were 48.75 ± 11.75 and 49.62 ± 12.85, respectively. Fourteen out of sixteen patients experienced spontaneous ICAD, whereas the traumatic etiology was ascertained in two patients. Conclusions: Hence, albeit rare, ophthalmologists should consider ICAD a potential cause of ION, especially in young adults with concomitant cephalic pain and vision reduction.

Ophthalmic vascular manifestations in eosinophil-associated diseases: a comprehensive analysis of 57 patients from the CEREO and EESG networks and a literature review.

Eosinophils have widespread procoagulant effects. In daily practice, eosinophil-related cardiovascular toxicity consists of endomyocardial damage, eosinophilic vasculitis and arterial or venous thrombosis. Here we aim to report on the clinical features and treatment outcomes of patients with unexplained ophthalmic vascular manifestations and eosinophilia. We conducted a retrospective, multicenter, observational study and a literature review of patients with eosinophilia (≥0.5 x109/L) and concomitant ophthalmic vascular manifestations independent of the underlying eosinophilic disease but with no alternative cause for ophthalmic manifestations. Fifty-seven patients were included (20 from the observational study and 37 from the literature review). Ophthalmic vascular features were the initial manifestation of eosinophil-related disease in 34 (59%) patients and consisted of 29 central retinal artery occlusions, six branch retinal artery occlusions, five central retinal vein occlusions, two branch retinal vein occlusions, seven retinal vasculitides, two retinal vasospasms, 12 Purtscher's retinopathies, 13 anterior ischemic optic neuropathies and two posterior ischemic optic neuropathies. The median [IQR] absolute eosinophil count at onset of ophthalmic vascular manifestations was 3.5 [1.7-7.8] x109/L. Underlying eosinophil-related diseases included eosinophilic granulomatosis with polyangiitis (n=32), clonal hypereosinophilic syndrome (HES) (n=1), idiopathic HES (n=13), lymphocytic HES (n=2), adverse drug reactions (n=3), parasitosis (n=2), polyarteritis nodosa (n=1), IgG4-related disease (n=1), eosinophilic fasciitis (n=1) and primary sclerosing cholangitis (n=1). Other extra-ophthalmologic arterial or venous thromboses related to eosinophilia were reported in four (7%) and nine (16%) patients, respectively. Visual prognosis was poor: only eight (10%) patients achieved full recovery of ophthalmologic symptoms. After a median follow-up of 10.5 [1-18] months, one patient (3%) had a recurrence of an ophthalmic vascular manifestation, and three patients (10%) had a recurrence of other vascular symptoms (deep vein thrombosis in two and pulmonary embolism in one patient). At the time of recurrence, absolute eosinophil counts were above 0.5 x109/L in all cases (n=4). This study broadens the spectrum of vascular manifestations associated with hypereosinophilia by adding ophthalmic vascular manifestations. In patients with ophthalmological vascular manifestations and hypereosinophilia, aggressive treatment of the underlying pathology (and normalization of blood count) should be implemented.

RWC Update: Severe Ocular Trauma; Managing Large Macular Hole; Retinal Venous Malformation With Post-COVID Bilateral Posterior Ischemic Optic Neuropathy.

RWC Update: Severe Ocular Trauma; Managing Large Macular Hole; Retinal Venous Malformation With Post-COVID Bilateral Posterior Ischemic Optic Neuropathy.

LONG-TERM FOLLOW-UP ON A RARE CASE OF PERIOPERATIVE POSTERIOR ISCHEMIC OPTIC NEUROPATHY: FINDING HOPE IN THE DARKNESS

Abstract
 Introduction : Perioperative posterior ischemic optic neuropathy (PION) following maxillectomy is a rare and devastating condition that leads to permanent vision loss in most reported cases. This case report offers a different perspective through long-term follow-up, providing valuable insights into the prognosis and potential treatments for PION.
 Case Illustration : Following a left maxillectomy for ameloblastoma, a 28-year-old female experienced sudden vision loss in her left eye. The visual acuity was 5/60, and an altitudinal inferior visual field defect with a superior extension was present. Ishihara's color vision examination revealed 15/38. The patient was diagnosed with perioperative PION and treated with neurotropic and folic acid. After 16 months, optic atrophy was observed. However, there are complete recovery in visual acuity to 5/5 and Ishihara score to 38/38, along with a significant improvement in the visual field defect.
 Discussion : The current management of perioperative PION is focused on prevention, because once vision loss occurs, it is usually severe and irreversible. In our case, the patient exhibited a favorable outcome after a long follow-up period, suggesting that there is still potential for improvement in PION patients. The finding is consistent with previous study, which reported that a small percentage of patients may still experience improved vision during follow-up. The role of neurotropics in improving patient outcomes is further supported by in vitro studies that demonstrate early neurotropic treatment significantly prevents loss of retinal ganglion cells in PION.
 Conclusion : Visual improvement is still possible in perioperative PION and early neurotropic administration may be considered in therapy

Simultaneous bilateral application of the Scepter mini balloon microcatheter for occlusion of ethmoidal dural arteriovenous fistulas

Ethmoidal dural arteriovenous fistulas are a rare entity accounting for 10 % of all dAVFs.3-6 Haemorrhage occurs in up to 91 % of cases, which is a particularly high risk and warrants therapeutic intervention.8-9 Endovascular treatment for these fistulas using the conventional detachable microcatheter technique is associated with certain limitations and risks; 8.3 % rate of incomplete obliteration and an 8.3 % rate of complications. Complications include reflux of liquid embolic agent, posterior ischaemic optic neuropathy, acute visual loss, and small subdural haematoma secondary to a micro-perforation.8,10-12 We present our recent experience with the Scepter Mini Balloon Microcatheter for the endovascular treatment of ethmoidal dural arteriovenous fistulas in 3 patients, involving bilateral simultaneous inflation of the balloon. It demonstrates a novel application of this technology with good outcomes. It supports the use of this microcatheter in treating ethmoidal dural arteriovenous fistulas endovascularly, either as a first-line option or as an adjunct to surgery.

Carotid Cavernous Sinus Fistula Supplied by an Embryological Variant of the Ophthalmic Artery Causing Posterior Ischemic Optic Neuropathy and Ophthalmoplegia.

Carotid Cavernous Sinus Fistula Supplied by an Embryological Variant of the Ophthalmic Artery Causing Posterior Ischemic Optic Neuropathy and Ophthalmoplegia.

Impact of coronary artery bypass grafting surgery on the chorioretinal biomicroscopic characteristics.

Most patients with cardiovascular disorders suffer from coronary artery diseases, which can be treated successfully using coronary artery bypass grafting (CABG). One of the unpleasant events following CABG is postoperative vision loss (POVL). Vulnerability of retinal vessels to hemodynamic changes, an expectable event following CABG, may contribute to the development of POVL, which might be associated with the changes in the choroidal and retinal structures. To investigate postoperative changes in chorioretinal and peripapillary nerve fiber layer (NFL) thickness, and progression of diabetic and hypertensive retinopathy after CABG. In this prospective, cross-sectional study, 49 eyes in 25 candidates for CABG underwent both ophthalmic and cardiovascular examinations within 6 mo prior to and 9 mo after surgery. Among the study participants, 56% were male with a mean age of 62.84 years ± 10.49 years (range 33-80 years). Diabetes mellitus was observed in eight participants (32%). None of the patients suffered from postoperative anterior or posterior ischemic optic neuropathy, central retinal artery occlusion, and cortical blindness. The mean value of the preoperative best corrected visual acuity was 0.11 ± 0.10 logMAR (range, 0-0.4), which worsened to 0.15 ± 0.08 logMAR (range, 0-0.4) after CABG (P = 0.031). No significant difference was observed between the pre- and postsurgical choroidal (P = 0.853) and macular (P = 0.507) thickness, NFL thickness in the subfoveal (P > 0.999) and peripapillary areas (P = 0.659), as well as the severity of diabetic and hypertensive retinopathy. CABG may reduce visual acuity without affecting ocular structures. Postoperative vision reduction might be attributable to molecular or cellular variations, changes in visual pathway function, or central nervous system.

Acute Retinal Necrosis due to Varicella Zoster Virus Presenting Initially as Central Retinal Artery Occlusion and Posterior Ischemic Optic Neuropathy.

Acute Retinal Necrosis due to Varicella Zoster Virus Presenting Initially as Central Retinal Artery Occlusion and Posterior Ischemic Optic Neuropathy.

Probable Posterior Ischemic Optic Neuropathy Associated with Acute Fungal Sinusitis

Purpose: We report a case of probable posterior ischemic optic neuropathy in a patient with acute fungal sinusitis.Case Summary: An 81-year-old male patient presented with sudden-onset visual loss in his left eye 3 weeks prior to presentation. His best corrected visual acuity was 0.6 in his right eye and light perception in his left eye. Pupillary size was 3 mm in both eyes, and a relative afferent pupillary defect was detected in his left eye. In fundus examination, diabetic retinopathy was found, and cup/disc ratios were increased in both eyes, but disc swelling and hemorrhage were not observed. Fluorescein angiography did not indicate filling delay, defects, or leakage of discs in either eye. Magnetic resonance imaging of the brain revealed multi-sinusitis in the sphenoid, ethmoid, and frontal sinuses. No bony defects or erosion were found around the optic canal or orbital apex during endoscopic surgery; however, histological examination revealed aspergillosis. The patient was diagnosed with posterior ischemic optic neuropathy caused by acute fungal sinusitis.Conclusions: When elderly patients with uncontrolled diabetes experience sudden visual disturbances without ocular pain, posterior ischemic optic neuropathy with fungal sinusitis should be considered as a differential diagnosis. Immediate imaging studies and appropriate treatment should be performed.

Orbital magnetic resonance imaging of giant cell arteritis with ocular manifestations: a systematic review and individual participant data meta-analysis.

We conducted a systematic review and individual participant data meta-analysis of publications reporting the ophthalmologic presentation, clinical exam, and orbital MRI findings in patients withgiant cell arteritisand ocular manifestations. PubMed and Cochrane databases were searched up to January 16, 2022. Publications reporting patient-level data on patients with ophthalmologic symptoms, imaged with orbital MRI, and diagnosed with biopsy-proven giant cell arteritis were included. Demographics, clinical symptoms, exam, lab, imaging, and outcomes data were extracted. The methodological quality and completeness of reporting of case reports were assessed. Thirty-two studies were included comprising 51 patients (females = 24; median age, 76years). Vision loss (78%) and headache (45%) were commonly reported visual and cranial symptoms. Ophthalmologic presentation was unilateral (41%) or bilateral (59%). Fundus examination most commonly showed disc edema (64%) and pallor (49%). Average visual acuity was very poor (2.28 logMAR ± 2.18). Diagnoses included anterior (61%) and posterior (16%) ischemic optic neuropathy, central retinal artery occlusion (8%), and orbital infarction syndrome (2%). On MRI, enhancement of the optic nerve sheath (53%), intraconal fat (25%), and optic nerve/chiasm (14%) was most prevalent. Among patients with monocular visual symptoms, 38% showed pathologic enhancement in the asymptomatic orbit. Six of seven cases reported imaging resolution after treatment on follow-up MRIs. Vision loss, pallid disc edema, and optic nerve sheath enhancement are the most common clinical, fundoscopic, and imaging findings reported in patients diagnosed with giant cell arteritiswith ocular manifestations, respectively. MRI may detect subclinical inflammationand ischemia in the asymptomatic eye and may be an adjunct diagnostic tool. Brain and orbital MRIs may have diagnostic and prognostic roles in patients with suspected giant cell arteritis who present with ophthalmic symptoms.

Posterior Ischemic Optic Neuropathy after Surgery: A Case Report and Review of Literature

We propose in this work to report a case of perioperative posterior ischemic optic neuropathy, after a cardiac surgery. This is a 45-year-old patient, operated for Coronary Angioplasty and Stenting. 24h after the surgery he noticed a bilateral loss of vision. Examination of the both eyes revealed visual acuity decreased to no light perception, absent pupillary light reflexes and normal fundus. The neurological examinationis normal, macular OCT and cerebral magnetic imaging were normal. Visual evoked potentials were absent confirming the diagnosis of right retrobulbar optic neuropathy. The evolution was marked by no improvement of vision and the development of optic nerve atrophy. Perioperative posterior ischemic optic neuropathy during cataract surgery is an extremely rare incident. Posterior ischemic optic neuropathy is an uncommon complication Its physiopathology is multifactorial and dominated by hypotension and anemia. Its prognosis is bad and visual recovery is generally poor.

Acute zonal occult outer retinopathy misdiagnosed as giant cell arteritis: a challenging case

Background: Acute zonal occult outer retinopathy (AZOOR) is a rare autoimmune retinopathy that is challenging to diagnose and treat. It usually presents with subtle fundus changes and severe visual symptoms. Herein, we report a challenging case of AZOOR, emphasizing that multimodal imaging could be valuable in diagnosis and monitoring of treatment response.
 Case Presentation: A 53-year-old woman presented to the emergency department with a one-week history of subacute, severe, painless vision loss without photopsia in her right eye. Her best-corrected distance visual acuity was 20/800 in the right eye and 20/20 in the left eye. Slit-lamp examination findings were unremarkable, and intraocular pressure was normal in both eyes. Initially, fundus examination findings appeared normal; however, serum levels of inflammatory markers were elevated. Brain and orbital magnetic resonance imaging results were unremarkable. A relative afferent pupillary defect was present in subsequent follow-up examinations at the hospital. The patient initially received a diagnosis of posterior ischemic optic neuropathy secondary to occult giant cell arteritis, underwent steroid treatment, and was evaluated by rheumatology and neurology consultants. Both consultants concurred with the presumed diagnosis. Subsequent multimodal imaging in the ophthalmology clinic revealed a trizonal pattern of fundus autofluorescence. Corresponding to these areas, we noted a loss of the ellipsoid zone on optical coherence tomography, depression on multifocal electroretinogram, and scotoma on visual field testing. Accordingly, the diagnosis of AZOOR was made. The patient was referred back to the rheumatologist for initiation of steroid-sparing treatment, and methotrexate was administered. Five months after the initial presentation, the patient showed significant visual field improvement in both eyes.
 Conclusions: Eye care practitioners should consider AZOOR in the differential diagnosis of patients with subacute painless severe unilateral vision loss and unremarkable findings on fundus examination. Multimodal imaging could be valuable in diagnosis and monitoring of treatment response, as observed in the current case. Further studies with larger sample sizes are needed to confirm the value of multimodal imaging and the available management options for AZOOR.

A Rare Case of Posterior Ischemic Optic Neuropathy after Appendicectomy

Ischemic optic neuropathy is classified into anterior and posterior ischemic optic neuropathy depending upon the part of optic nerve involved. In anterior optic neuropathy, optic nerve head is involved and in posterior ischemic optic neuropathy(PION) retrobulbar portion is involved. There is sudden loss of vision in both the entities but there are optic disc changes in anterior optic neuropathy while in posterior ischemic optic neuropathy optic disc is normal initially. Etiologically, posterior ischemic optic neuropathy is divided into non arteritic non-surgical, arteritic and perioperative non arteritic posterior ischemic optic neuropathy.

Bilateral Posterior Ischemic Optic Neuropathy Due to Bilateral Anterior-Drainage Dural Carotid-Cavernous Fistulas: A Case Report

To report a case of bilateral posterior ischemic optic neuropathy (PION) due to bilateral anterior-drainage dural carotid-cavernous fistulas (CCFs). We report on a 62-year-old woman with a history of poorly controlled hypertension who presented with sudden bilateral visual loss and headache for 5 days. She denied a history of head trauma. On examination, her visual acuities were no light perception (NLP) with fixed pupils in both eyes. The ocular motility of both eyes was limited in all directions. Both eyelids were difficult to open. Anterior segment examination revealed bilateral chemosis and episcleral corkscrew vessels. Intraocular pressures were 45 and 48 mmHg in her right and left eyes, respectively. Gonioscopy revealed blood in Schlemm's canal at the nasal angle of the right eye. Fundus examination showed slightly dilated and tortuous retinal veins with normal-appearing optic discs in both eyes. The cup-to-disc ratios were 0.3 bilaterally. Other neurological examinations were unremarkable. Magnetic resonance imaging demonstrated dilation of the bilateral superior ophthalmic veins (SOVs), and marked orbital and periorbital congestion bilaterally. However, there was no compression or stretching of the bilateral optic nerves. Diffusion restriction on diffusion-weighted imaging, with corresponding reduced apparent diffusion coefficient, in the entire bilateral orbital segment of the optic nerves was revealed, consistent with bilateral PION. Magnetic resonance angiography revealed arterialization of the bilateral cavernous sinuses and SOVs. Cerebral angiography confirmed the diagnosis of bilateral anterior-drainage dural CCFs. Treatment with transvenous coil embolization was successful. Three months after embolization, ophthalmic examination demonstrated progressive improvement of aforementioned ophthalmic signs; however, her visual acuities remained NLP in both eyes. To our knowledge, this is the first reported case of bilateral PION due to bilateral anterior-drainage dural CCFs. In spite of its rarity, PION should be considered as a severe, irreversible ophthalmic complication of anterior-drainage dural CCF.

Posterior ischemic optic neuropathy following postoperative bleeding and internal jugular vein compression.

Perioperative blindness, especially posterior ischemic optic neuropathy (PION), is an uncommon but potentially devastating complication. We report a case of a 65-year-old male patient who underwent laryngopharyngectomy, bilateral neck dissection, and free jejunum flap reconstruction, but then experienced PION in his right eye following postoperative bleeding and bilateral internal jugular veins (IJVs) compression. Despite systemic corticosteroid therapy, his visual recovery prognosis was poor. The specific mechanism responsible for PION remains unclear, and no therapy has been shown to improve this condition. As such, prevention of perioperative PION remains the only available strategy. Surgeons should be aware of this rare potential complication and its risk factors and strive to avoid it. As postoperative bleeding and IJV compression are one of important risk factors for PION, avoiding these are critical.

SUDDEN LOSS OF VISION: A RARE PRESENTATION OF DIABETIC KETOACIDOSIS IN THE ICU

SUDDEN LOSS OF VISION: A RARE PRESENTATION OF DIABETIC KETOACIDOSIS IN THE ICU

Diagnosis of giant cell arteritis using clinical, laboratory, and histopathological findings in patients undergoing temporal artery biopsy

ObjectiveTo identify the clinical, laboratory, and histopathological features that may predict the diagnosis of giant cell arteritis (GCA). MethodsA retrospective chart review was performed on patients who underwent temporal artery biopsy (TAB) between January 1, 2011 and March 31, 2019. Patient demographics, clinical characteristics, laboratory features, histopathological features, and biopsy results were collected. GCA status was determined by a neuro-ophthalmologist (OOA). Stepwise logistic regression analysis was performed to identify features that predict GCA status. ResultsOf 101 patients who underwent TAB, 31 (31%) were diagnosed with GCA. Age was found to be statistically significant for the diagnosis of GCA (P = 0.009), with an average age of 74.4 years ( ± 8.1) in those with GCA vs. 68.9 years ( ± 10.0) in those without. The incidence of transient vision loss was higher in GCA than non-GCA patients (P = 0.005). Anterior arteritic ischemic optic neuropathy (n = 3), ophthalmic artery occlusion (n = 2), and posterior ischemic optic neuropathy (n = 1) were seen only in the GCA group. Of the 31 GCA patients, 15 had active GCA (48%), 3 (10%) had healed temporal arteritis (HTA), 8 (26%) had suggested HTA, and 5 (16%) had false negative biopsies. Of the 70 non-GCA patients, 63 (90%) had negative biopsies, 2 (3%) had HTA, and 5 (7%) had suggested HTA. Histopathological analysis revealed that CD68 staining had a sensitivity of 69% and specificity of 86%. Both presence of multinucleated giant cells (MNGC) and transmural inflammation had 100% specificity; however, sensitivity was ≤ 50%. In patients with negative TABs and complete risk factor data available (n = 66), the odds of GCA increased 2.16-fold every 5 years of age, and 1.08-fold every mg/day of oral steroid use. A biopsy result of HTA had an odds ratio of 84.7 and suggested HTA of 49.2 against a negative TAB for diagnosis of GCA. ConclusionAge at time of biopsy, HTA, and suggested HTA are predictive for the diagnosis of GCA. Transient vision loss is more commonly seen in GCA, and anterior arteritic ischemic optic neuropathy, ophthalmic artery occlusion, and posterior ischemic optic neuropathy are important ophthalmic manifestations of GCA. CD68 staining is more sensitive but less specific for diagnosing GCA in comparison to other histopathologic findings such as presence of MNGC and transmural inflammation. Further work is recommended to investigate the importance of the specific histopathologic finding of CD68 staining in the diagnosis of GCA.

Using diffuse weighted image and apparent diffusion coefficient in MRI for diagnosis of posterior ischemic optic neuropathy in a young male: a case report and literature review

BackgroundPosterior ischemic optic neuropathy (PION) is a rare cause of visual loss, especially in young patients who are more prone to inflammatory demyelinating optic neuritis (ON) compared to other types of optic neuropathy. The diagnosis of PION is usually a diagnosis of exclusion; however, the emergence of modern neuroimaging technique with diffuse-weighted image (DWI) and apparent diffusion coefficient (ADC) sequences in Magnetic Resonance Imaging (MRI) provides more evidence for accurate diagnosis and management.Case presentationA 30-year-old man with a history of hypertension and chronic renal failure secondary to glomerulonephritis presented with sudden onset of blurred vision, dyschromatopsia, pain, and positive relative afferent pupillary defect (RAPD) in the left eye for 1 week. He was initially admitted for steroid pulse therapy and was further monitored due to suspicion of optic neuritis oculus sinister (OS). However, his brain MRI revealed a focal high hyperintensity signal at the left optic nerve on the T2 DWI series. The area was corresponded with the hypointensity area in the ADC series, which was a powerful clue for PION. We explained the poor visual prognosis of PION to the patient after finishing steroid pulse therapy and referred him to the Nephrology and Neurology department for hypertension control to prevent additional hypertension related complication.ConclusionsThe diagnosis of PION is usually a diagnosis of exclusion; however, carefully interpreting the DWI and ADC sequence in MRI may give the clinician more evidence for the definite diagnosis and leads to proper management.

Optic nerve neuropathies – causative factors, methods of diagnostics, current and future possibilities of treatment

Introduction: Optic neuropathies are a broad group of diseases in which the dominant disturbance is damage to the optic nerve, often irreversible. Underlying causes of neuropathy are both genetic and environmental. Despite limited treatment options, much research is currently being done on substances that could improve optic nerve function and alleviate the clinical consequences of optic nerve damage.
 Purpose: This article describes current findings in both the optic nerve neuropathy pathophysiology and diagnosis of the disorder, as well as treatment options and future perspectives.
 State of knowledge: The pathogenetic cause of neuropathy is mainly demyelination within the neural sheath, often caused by inflammation. It is characterized by progressive loss of vision. The most common genetic cause of optic neuropathy is mitochondrially inherited Leber hereditary optic neuropathy (LHON) and is characterized by mostly sudden and painless loss of visual acuity. Toxic neuropathies are a group of diseases caused by heavy metals, pharmaceuticals, methanol and carbon monoxide. Nutritional neuropathy is mainly related to vitamin B1, B9 and B12 deficiency, and is a rare example of neuropathy that can be curable at the early stage of the disease. Another group of neuropathies is caused by ischemia and can be divided according to the place of the optic nerve affected – AION (anterior ischemic optic neuropathy) and PION (posterior ischemic optic neuropathy).
 Conclusions: The therapeutic options in the treatment of optic neuropathy strictly depend on the causative factor. Nutritional deficiencies are treated with appropriate supplementation, so it is vital to truly determine the missing vitamins and elements.

Ischemic Optic Neuropathies: Current Concepts.

Ischemic optic neuropathy (ION) is the term ascribed to optic nerve disease that is the result of a transient or permanent interruption of the blood supply to any portion of the optic nerve. Anterior ischemic optic neuropathy (AION) refers to ischemia of the optic nerve head, whereas posterior ischemic optic neuropathy (PION) indicates ischemia of the posterior optic nerve. IONs are primarily classified as arteritic ION and non-arteritic ION. A subset of ION that occurs around the time of surgery is termed peri-operative ION. These phenomena will be discussed as distinct entities.