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Arteritic and idiopathic ischemic optic neuropathy.

Ischemic optic neuropathy is a frequent cause of sudden visual loss in the older patient. There are two major causes of ischemic optic neuropathy; one, arteritic, due to an inflammatory process, and the other, idiopathic, possibly linked to hypertension. This paper presents four illustrative cases of ischemic optic neuropathy, one with an associated serous retinal detachment. The clinical appearance of the disorder, differential diagnosis of the two major types of ischemic optic neuropathy, and the pathogenesis and prognosis for vision are discussed. Currently accepted modes of treatment are also included.

Aged↗

Neuroprotective effects of brimonidine treatment in a rodent model of ischemic optic neuropathy.

Ischemic optic neuropathy (ION) is a common disorder caused by disruption of the arterial blood supply to the optic nerve. It can result in significant loss of visual acuity and/or visual field. An ischemic optic nerve injury was produced in rats by intravenous injection of Rose Bengal dye followed by argon green laser application to the retinal arteries overlying the optic nerve, causing a coagulopathy within the blood vessels and disruption of optic nerve and retinal perfusion. The effect of brimonidine tartrate eye drops on survival of retinal ganglion cell axons in this experimental paradigm was studied. One eye was treated and the contralateral eye served as a control. Four groups of animals were used for this study. Group 1 received 7 days of treatment with 0.15% brimonidine tartrate eye drops twice a day prior to the ischemic injury. Group 2 animals received 0.15% brimonidine tartrate eye drops twice a day for 14 days after photocoagulation injury. Animal groups 3 and 4 received eye drops of 0.9% NaCl twice a day either daily for 7 days before injury or daily for 14 days, respectively. All rats were sacrificed 5 months after the injury to ascertain long-term optic axon survival. Coagulopathy-induced optic nerve ischemia resulted in a 71% loss of optic axons. Treatment with brimonidine daily for the 7 days prior to the injury resulted in a greater survival of optic axons, with only a 56.1% loss compared to control. Brimonidine treatment every day for 14 days after the ischemic injury did not result in a significant rescue of optic axons compared to injury alone. In summary, the application of brimonidine eye drops for one week prior to an ischemic injury resulted in a statistically significant increase in survival of optic axons within the injured optic nerves. Brimonidine treatment of the eye after the ischemic injury did not result in axon rescue, and axon loss was similar to the injured optic nerves treated with saline only. These results suggest that brimonidine may have potential use for prevention of ION in at-risk patients.

Adrenergic alpha-Agonists↗

Ischemic optic neuropathy.

Ischemic optic neuropathy (ION), based on vascular anatomy of the optic nerve, pathogenesis and clinical picture, consists of two distinct entities: anterior (AION) and posterior (PION) ischemic optic neuropathies. AION is due to interference with posterior ciliary artery supply to the optic nerve head and retrolaminar part of the optic nerve; it initially presents with visual loss and optic disc edema which progresses to optic atrophy in a month or two. PION is due to occlusion of nutrient arteries to the posterior part of the optic nerve; in this condition during the initial stages the optic disc is normal in spite of marked visual loss, but the atrophy develops later on. Their pathogeneses, causes, clinical pictures, diagnosis and management are discussed briefly.

Adrenal Cortex Hormones↗

[Acute anterior, ischemic optic neuropathy].

Ischemic optic neuropathy (ION) is the most frequent optic neuropathy in patients older than 50. Anterior ION is classified as nonarteritic, especially in patients with vasculopathic risk factors and/or small optic disc, or arteritic. Monocular visual loss is usually sudden. Typical exam findings are optic nerve swelling and altitudinal visual field defect. Clinical profile, sedimentation rate, and especially fluorescein angiography are very useful to make the distinction between nonarteritic and arteritic ION. Treatment of temporal arteritis with steroids is an emergency but there is no effective therapy of the nonarteritic form.

Acute Disease↗

The effects of stellate ganglion block on visual evoked potential and blood flow of the ophthalmic and internal carotid arteries in patients with ischemic optic neuropathy.

Ischemic optic neuropathy (ION) is a common disease that can cause a loss of visual acuity in the elderly. We treated ION patients with stellate ganglion block (SGB) and investigated its effects on picture visual evoked potential (P-VEP) and blood flow in the ophthalmic artery (OA) and internal carotid artery (ICA). Twelve ischemic eyes in 12 patients diagnosed by the same ophthalmologist were investigated in this study. All patients were treated with daily SGB on the affected side with 2-3 mL of 2% lidocaine for a treatment period of 10-15 days. In ION eyes before SGB, compared with healthy eyes, the latency of P-VEP P(100) was delayed (123 +/- 14 ms versus 98 +/- 3 ms; P < 0.05), and the amplitude was reduced (4.24 +/- 1.76 microV versus 10.26 +/- 4.09 microV; P < 0.05). After SGB, the latency and amplitude returned to normal (103 +/- 6 ms versus 98 +/- 3 ms; 10.43 +/- 4.88 microV versus 10.26 +/- 4.09 microV; P > 0.05). Before treatment, the blood flow velocities of the OA and the ICA on the ischemic side were slow and the resistance indexes were high, but SGB reduced these changes. SGB did not affect the OA and the ICA on the healthy side. We conclude that SGB improves P-VEP and OA and ICA blood flow in ION eyes. Further studies are needed to confirm that this is an effective method for the treatment of ION.

Adult↗

Characteristics of patients with nonarteritic anterior ischemic optic neuropathy eligible for the Ischemic Optic Neuropathy Decompression Trial.

OBJECTIVE: To describe the baseline clinical characteristics of patients in the Ischemic Optic Neuropathy Decompression Trial (IONDT). DESIGN: The IONDT is a single-masked, multicenter, randomized clinical trial. SETTINGS: Twenty-five US clinical centers. PATIENTS: Eligibility criteria for randomization to either optic nerve sheath decompression surgery or careful follow-up included a diagnosis of acute unilateral nonarteritic anterior ischemic optic neuropathy (NAION), a visual acuity of 20/64 or worse and better than no light perception, and an age of 50 years or older. Patients who were eligible except for having visual acuity better than 20/64 were not randomized, but were followed up. METHODS: Each patient underwent a standardized history and examination by certified study personnel within 14 days of the onset of symptoms. Masked personnel performed outcome measurements. RESULTS: Of 420 patients with NAION, 258 were randomized, and 162 were not randomized and are being followed up. Sixty-two percent of the patients were men and 95% were white. The mean +/- SD age at onset was 66.0 +/- 8.7 years. Hypertension was reported in 47% of the patients in the IONDT, and 24% of the patients had diabetes mellitus. Forty-two percent of the patients recalled the onset of visual symptoms to be within 2 hours of awakening. Initial visual acuities in the study eye ranged from 20/20 or better to light perception, with 49% of the patients seeing better than 20/64 and 34% of the patients seeing 20/200 or worse. The mean Westergren sedimentation rate was 18.4 mm/h, with 9% of the patients having a rate greater than 40 mm/h. The nonrandomized patients (visual acuity better than 20/64) were younger, 72% were male, and they had a lower prevalence of hypertension and diabetes mellitus. CONCLUSION: Although our baseline findings are derived from a selected population of patients with NAION who were eligible for the IONDT, they provide the first description of NAION from a large prospective study that used a standard definition of NAION and only included patients who were identified within 2 weeks of the onset of symptoms.

Aged↗

Treatment of ischemic optic neuropathy.

Ischemic damage of the optic nerve has no proven effective treatment. While ischemia related to vasculitis (arteritic) is treated with systemic corticosteroids, the primary goal is to prevent further damage, either in the affected or fellow eye. Thrombolytic or anticoagulation supplementive therapy may be considerations for the future. In the more common idiopathic (nonarteritic) form (NAION), multiple attempts at therapy, including systemic corticosteroids, anticoagulants and antiplatelet agents, diphenylhydantoin, hyperbaric oxygen, and optic nerve sheath decompression have been unsuccessful. The use of levodopa has been proposed but is unproven. Megadose intravenous corticosteroid therapy has not been studied in a systematic way. Neuroprotective strategies are under intense investigation for optic neuropathies including NAION, and clinical trials in humans are in progress. Optic nerve regeneration studies are ongoing in animals. Prophylaxis in NAION is unproven.

Adrenal Cortex Hormones↗

Hypovolemic ischemic optic neuropathy.

BACKGROUND: Ischemic optic neuropathy refers to an acute event of ischemia, or decreased blood flow, to the optic nerve resulting in varying degrees of vision loss and visual field defects. Typically this disease affects the elderly population who experience systemic diseases that compromise the blood flow efficiency of the optic nerve head (e.g., giant-cell arteritis, hypertension, diabetes, etc.). However, cases of blood loss to the optic nerve, secondary to traumatic injuries or surgeries, have also been shown to result in ischemic optic neuropathy, regardless of age. It seems that in these cases, the resulting anemia and hypotension play contributing roles in the development of ischemic optic neuropathy. METHODS: A 41-year-old black man came to us with optic nerve head pallor O.S., count-fingers vision O.S., positive afferent pupillary defect O.S., and a central scotoma O.S. after being hospitalized and treated for a stab wound to his left neck that severed his left carotid artery at the bifurcation. RESULTS: This patient had been seen in the Optometry Clinic two years before the stab-wound incident. At that time, he had 20/20 vision in his left eye and no remarkable neurological deficits. His ocular presentation after the traumatic hypovolemic event was probably a direct result of the hypoperfusion to the left optic nerve head. This patient was diagnosed with a hypovolemic, or blood loss-related, ischemic optic neuropathy (O.S.). CONCLUSIONS: Patients who experience large amounts of blood loss due to trauma, surgery, internal bleeding, etc. and report vision loss should be screened for possible optic nerve ischemia. As eye care providers, when we are presented with patients who have optic nerve head atrophy, we should inquire about events that may have precipitated blood loss, potentially triggering ischemic optic neuropathy.

Adult↗

Interaction of heritable and estrogen-induced thrombophilia: possible etiologies for ischemic optic neuropathy and ischemic stroke.

Our specific aim was to assess how thrombophilic exogenous estrogens interacted with heritable thrombophilias leading to non-arteritic ischemic optic neuropathy (NAION) and ischemic stroke. Coagulation measures were performed in a 74 year old patient and her immediate family. The proband had a 47 year history of 9 previous thrombotic episodes, and developed unilateral NAION 4 years after starting estrogen replacement therapy (ERT). The proband was heterozygous for two thrombophilic gene mutations (G20210A prothrombin gene, platelet glycoprotein IIIa P1A1/A2 polymorphism), and homozygous for the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene. Of 238 normal controls, none had these 3 gene mutations together. The proband's mother and brother had deep venous thrombosis (DVT). The proband's brother, sister, nephew, daughter, and two granddaughters were homozygous for the C677T MTHFR mutation. The proband's brother was heterozygous for the G20210A prothrombin gene mutation. The proband's niece was heterozygous for the G20210A prothrombin gene mutation, homozygous for the C677T MTHFR mutation, homozygous for the hypofibrinolytic 4G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene, and heterozygous for the platelet glycoprotein IIIa P1A1/A2 polymorphism. Of 238 normal controls, none had the niece's combination of 4 gene mutations. When ERT-mediated thrombophilia was superimposed on the proband's heritable thrombophilias, unilateral ischemic optic neuropathy developed, her tenth thrombotic event over a 5 decade period. When estrogen-progestin oral contraceptives were given to the proband's niece, she had an ischemic stroke at age 22. Exogenous estrogen-mediated thrombophilia superimposed on heritable thrombophilia and hypofibrinolysis is associated with arterial and venous thrombi, and appears to be a preventable, and potentially reversible etiology for ischemic optic neuropathy and ischemic stroke.

Adult↗

Fluorescein angiographic features of choroidal insufficiency in anterior ischemic optic neuropathy.

Anterior ischemic optic neuropathy(AION) is known to be caused by circulatory disturbance in the anterior optic nerve(AON). Because the AON shares blood supply from the paraoptic short posterior ciliary artery with peripapillary choroid, the authors investigated the angiographic evidences of combined choroidal insufficiency in patients with acute AION. Fundus fluorescein angiograms from 30 eyes from 28 patients with acute AION were enrolled in this study. The diagnosis of acute AION was based primarily on angiographic evidences of filling delay of optic nerve head and the various clinical features, such as decreased visual acuity, visual field defects, afferent pupillary defect, and optic disc swelling. Angiographic evidences of combined choroidal filling delay were as follows: 1) circular or localized filling delay of peripapillary choroid in 15 eyes (50%), 2) generalized filling delay of posterior pole in 11 eyes (36.7%), 3) filling delay of unilateral choroid divided by watershed zone in 5 eyes (16.7%), and 4) choriocapillary filling delay in 10 eyes (33.3%). In this study, various types of choroidal insufficiency in patients with AION were observed, which helped us to differentiate AION from the other various diseases of the anterior optic nerve.

Acute Disease↗

Anterior ischemic optic neuropathy.

Anterior ischemic optic neuropathy (AION), one of the most prevalent and visually crippling diseases in the middle-aged and elderly, potentially bilateral, is due to acute ischemia of the optic nerve head. For a logical understanding of its pathogenesis, underlying causes, clinical features, and management, it is essential to comprehend the basic scientific issues involved; these are discussed briefly in this paper. Clinically, AION is of two types: (1) arteritic AION (due to giant cell arteritis) and (2) nonarteritic AION (due to other causes). Arteritic AION is an ophthalmic emergency because of its potential of causing rapid, bilateral complete blindness which is almost always preventable if treated immediately with large doses of systemic corticosteroids. Clinical parameters which help to differentiate the two type of AION, and their management are discussed.

Arteritis↗

Migrainous ischemic optic neuropathy.

Anterior ischemic optic neuropathy (AION) is a stroke syndrome of the eye seen in isolation or as a manifestation of underlying disease. A case of migrainous AION is reported, and the implications of anterior visual pathway migraine discussed.

Adult↗

Anterior ischemic optic neuropathy.

Anterior ischemic optic neuropathy (AION) occurs when there is compromised blood supply to the optic nerve and can result in visual loss. Ophthalmic nurses are key health professionals to recognize this entity and triage the patient accordingly. A case study of a patient with non-arteritic AION is presented.

Female↗

[Anterior ischemic optic neuropathy].

Anterior ischemic optic neuropathy is based on the lesion of blood supply to the optic nerve head. The disease presents decrease of visual acuity and altitudinal field defects with optic dics oedema in ophthalmoscopic view, which progresses in optic atrophy. Anatomy, pathogenesis, causes, clinical picture and management are discussed. 20% of patients from the group treated with vasodilatants and 50% of those treated with corticosteroids improved their visual acuity.

Female↗

Surgery for nonarteritic anterior ischemic optic neuropathy.

BACKGROUND: Nonarteritic ischemic optic neuropathy is characterized by sudden and painless loss of vision in one eye, accompanied by pallid swelling of the optic disc. Although various medical interventions, such as corticosteroids and phenytoin sodium, have been used to treat nonarteritic ischemic optic neuropathy, no therapy has been proven effective. OBJECTIVES: The objective of this review is to assess the safety and efficacy of surgical treatment compared with other treatment or usual care in people with nonarteritic ischemic optic neuropathy. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register - Central and MEDLINE. The most recent searches were performed in December 1997. SELECTION CRITERIA: We included randomized trials comparing surgery to no surgery in people with nonarteritic ischemic optic neuropathy. DATA COLLECTION AND ANALYSIS: We obtained full copies of all potentially relevant articles. Only one article described a randomized trial of surgery and it was eligible for inclusion. No formal assessment of quality was done. One reviewer extracted data. No synthesis was required, as there was only one trial. MAIN RESULTS: The one trial identified randomized 258 patients. The only published report with outcomes data for that trial presents preliminary results from 244 patients who had achieved six months of follow-up at the time of the report. Participants assigned to surgery did no better than participants assigned to careful follow-up regarding improved visual acuity of three or more lines of vision at six months: 32.6% of the surgery group improved compared with 42.7% of the careful follow-up group. The adjusted odds ratio (OR), adjusted for baseline visual acuity and diabetes, comparing the two groups for three or more lines improvement was 0.74 (95% confidence interval (CI) 0.39 to 1. 38) (surgery group improvement was worse than careful follow-up). In addition, participants receiving surgery had a significantly greater risk of losing three or more lines of vision at six months: 23.9% in the surgery group worsened compared with 12.4% in the careful follow-up group. The six-month adjusted OR comparing the two groups for loss of three or more lines of vision was 1.96 (95% CI 0.87 to 4.41). Spontaneous improvement of three or more lines of vision was observed in 42.7% of participants in the careful follow-up group. REVIEWER'S CONCLUSIONS: Results from the Ischemic Optic Neuropathy Decompression Trial indicate that optic nerve decompression surgery for nonarteritic ischemic optic neuropathy is not effective.

Humans↗

Surgery for nonarteritic anterior ischemic optic neuropathy.

BACKGROUND: Nonarteritic ischemic optic neuropathy is characterized by sudden and painless loss of vision in the eye, accompanied by pallid swelling of the optic disc. No medical therapy has been proven effective in treating this condition. OBJECTIVES: The objective of this review is to assess the safety and efficacy of surgery compared with other treatment or usual care in people with nonarteritic ischemic optic neuropathy. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (CENTRAL), which contains the Cochrane Eyes and Vision Group Trials Register, in The Cochrane Library, MEDLINE, EMBASE and the UK National Research Register (NRR). The last search was on 13 July 2005. SELECTION CRITERIA: We included randomized controlled trials. DATA COLLECTION AND ANALYSIS: We obtained full copies of all potentially relevant articles. One randomized trial was eligible for inclusion. One author extracted data which was verified by another author. No synthesis was required. MAIN RESULTS: The one included trial randomized 258 participants and was stopped early. At the time of the 24-month report the follow-up rate was 95.3% for six months and 67.4% for 24 months (174 participants, 89 careful follow up and 85 surgery). There was no evidence of a benefit of surgery on visual acuity. At six months 32.0% of the surgery group had improved visual acuity by three or more lines compared with 42.6% of the careful follow up group (unadjusted risk ratio (RR) 0.75, 95% confidence interval (CI) 0.54 to 1.04). At 24 months 29.4% of the surgery group had improved compared with 31.0% of the careful follow up group (unadjusted RR 0.95, 95% CI 0.60 to 1.49). Participants who underwent surgery had a greater risk of losing three or more lines of vision. At six months 18.9% in the surgery group had worsened compared with 14.8% in the careful follow up group (RR 1.28; 95% CI 0.73 to 2.24). At 24 months 20.0% in the surgery group had worsened compared with 21.8% in the careful follow up group (RR 0.92; 95% CI 0.51 to 1.64). AUTHORS' CONCLUSIONS: Results from the single trial indicate no evidence of a beneficial effect of optic nerve decompression surgery for nonarteritic ischemic optic neuropathy.

Humans↗

Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. The Ischemic Optic Neuropathy Decompression Trial Research Group.

OBJECTIVE: To assess the safety and efficacy of optic nerve decompression surgery compared with careful follow-up alone in patients with nonarteritic anterior ischemic optic neuropathy (NAION). DESIGN: The Ischemic Optic Neuropathy Decompression Trial (IONDT) is a randomized, single-masked, multicenter trial. SETTING: Twenty-five US clinical centers. PARTICIPANTS: The IONDT ceased recruitment on October 20, 1994, on the recommendation of its Data and Safety Monitoring Committee. The preliminary results presented herein are based on data as of September 8, 1994, from 244 patients with NAION and visual acuity of 20/64 or worse. One hundred twenty-five patients had been randomized to careful follow-up, and 119 had been randomized to surgery, with 91 and 95, respectively, having completed 6 months of follow-up. INTERVENTION: Patients in the surgery group received optic nerve decompression surgery and follow-up ophthalmologic examinations; those in the careful follow-up group received ophthalmologic examinations at the same times as the surgery group. MAIN OUTCOME MEASURES: Gain or loss of three or more lines of visual acuity on the New York Lighthouse chart at 6 months after randomization, as measured by a technician masked to treatment assignment. RESULTS: Patients assigned to surgery did no better when compared with patients assigned to careful follow-up regarding improved visual acuity of three or more lines at 6 months: 32.6% of the surgery group improved compared with 42.7% of the careful follow-up group. The odds ratio (OR) for three or more lines better, adjusted for baseline visual acuity and diabetes, was 0.74 (95% confidence interval [CI], 0.39 to 1.38). Patients receiving surgery had a significantly greater risk of losing three or more lines of vision at 6 months: 23.9% in the surgery group worsened compared with 12.4% in the careful follow-up group. The 6-month adjusted OR for three or more lines worse was 1.96 (95% CI, 0.87 to 4.41). No difference in treatment effect was observed between patients with progressive NAION and all others. CONCLUSION: Results from the IONDT indicate that optic nerve decompression surgery for NAION is not effective, may be harmful, and should be abandoned. The spontaneous improvement rate is better than previously reported.

Aged↗

Nonarteritic anterior ischemic optic neuropathy.

Nonarteritic anterior ischemic optic neuropathy refers to an idiopathic ischemic process of the anterior portion of the optic nerve. The typical presentation is sudden and painless visual loss with examination features of an optic neuropathy. Among the various associated risk factors are optic disc morphology, advanced age, systemic arterial hypertension, diabetes mellitus, and nocturnal hypotension. Currently, there is no proven effective long-term treatment for this disorder.

Decompression, Surgical↗