bubble_chart Overview

Ischemic optic neuropathy refers to an acute nutritional disorder caused by circulatory disturbances in the nutrient vessels of the optic nerve. Generally, it is divided into anterior and posterior ischemic optic neuropathy based on the boundary where the central retinal artery enters the optic nerve approximately 9–11 mm behind the globe. Circulatory disturbances in the posterior ciliary arteries supplying the optic disc lead to acute ischemia and hypoxia, resulting in optic disc edema. Not only the optic disc but also the lamina cribrosa and the nerve fibers behind it can be affected, known as anterior ischemic optic neuropathy (AION). Ischemic changes occurring from the intraorbital segment of the optic nerve to the optic chiasm are referred to as posterior ischemic optic neuropathy (PION), which does not involve optic disc edema.

bubble_chart Etiology

It is more common in the elderly, over 60 years old, and the onset age in domestic statistics is earlier than that abroad. It is more common in women than in men, and may occur in one eye or both eyes sequentially. Any systemic or {|###|}eye disease{|###|} that can lead to insufficient blood supply to the optic disc may cause this condition. Systemic diseases include hypertension, {|###|}stirred pulse{|###|} sclerosis, temporal {|###|}stirred pulse{|###|} inflammation, carotid {|###|}stirred pulse{|###|} obstruction, diabetes, leukemia, and polycythemia. Either excessively low or high intraocular pressure disrupting the balance between perfusion pressure in the optic disc capillaries and intraocular pressure can also be a cause. Changes in blood composition and increased blood viscosity slow circulation and reduce oxygen-carrying capacity, leading to optic disc hypoxia.

The causes of anterior ischemic optic neuropathy are as follows:

1. Vasculitis types: Giant cell {|###|}stirred pulse{|###|} inflammation, nodular poly {|###|}stirred pulse{|###|} inflammation, systemic lupus erythematosus, Buerger's disease, allergic vasculitis, post-viral vasculitis, post-vaccination immune response, syphilis, radiation necrosis.

2. Systemic vascular diseases: Hypertension, {|###|}stirred pulse{|###|} atherosclerosis, diabetes, migraine, large {|###|}stirred pulse{|###|} inflammation, carotid {|###|}stirred pulse{|###|} obstruction, sexually transmitted disease changes.

3. Hematological diseases: Polycythemia vera, sickle cell disease, acute hypotension (shock), G-6-P-D deficiency.

4. Ocular: Post-cataract surgery, low intraocular pressure, glaucoma.

bubble_chart Clinical Manifestations

Generally, the decline in vision is not severe, but it can be more significant or even result in no light perception if caused by temporal arteritis. The onset is often sudden. In the early stages, the optic disc shows grade I swelling with a pale red color due to capillary dilation on its surface, though a grayish-white appearance is more common, usually confined to a specific quadrant of the optic disc and corresponding to visual field defects. Bilateral cases are rare. If located around the optic disc, there may be small hemorrhages in the nerve fiber layer, which resolve spontaneously within 1–2 weeks, and cotton-wool exudates may also be observed. After 1–2 months, optic nerve atrophy may develop, sometimes appearing cupped, similar to glaucoma-induced optic atrophy. When secondary to conditions like giant cell arteritis or arteriosclerosis, the retinal vessels generally remain normal. Patients with hypertension or arteriosclerosis may exhibit corresponding retinal arteriosclerotic changes. If both eyes are affected sequentially—where optic disc edema in one eye leads to secondary optic atrophy while the other eye develops optic disc edema—this may present as a global Foster-Kennedy syndrome, often suggesting an intracranial tumor. Due to the segmental blood supply of the optic disc by branches of the posterior ciliary artery, visual field defects in this condition often feature a short bundle-shaped scotoma connected to the physiological blind spot. This indicates that the damaged optic nerve originates from the optic disc, unlike lesions along the visual pathway, where quadrantanopia or hemianopia does not connect to the blind spot. These scotomas may extend and merge with larger defects, typically occurring in the inferonasal or inferior visual field, often occupying roughly a "quadrant." They may also appear sequentially or simultaneously in multiple quadrants, presenting as horizontal or vertical hemianopia or quadrantanopia, though these changes do not strictly follow horizontal or vertical boundaries, distinguishing them from visual pathway lesions that produce quadrantanopia or hemianopia strictly aligned with the midline. Visual field defects in this condition usually spare the macular fixation area, so central scotomas are absent. Early fluorescein angiography reveals a common feature: asymmetry in fluorescence intensity between obstructed and unobstructed small areas on the same optic disc, showing delayed or deficient fluorescence filling. This asymmetry roughly corresponds to the location of the visual field defect, with localized hypofluorescence near the affected optic disc area and delayed choroidal fluorescence filling in the same region.

bubble_chart Diagnosis

For individuals over the age of 40 who experience sudden vision loss with non-tangential visual field defects, the possibility of ischemic optic neuropathy should be considered. However, compressive optic neuropathy, demyelinating diseases, and hereditary disorders must be ruled out.

The diagnosis of anterior ischemic optic neuropathy can be based on: ① sudden vision loss with typical visual field defects; ② headache, eye pain, especially caused by temporal arteritis; ③ grayish-white edema of the optic disc; ④ fundus fluorescein angiography showing hypofluorescence or delayed or absent filling of the optic disc; ⑤ presence of Raynaud's phenomenon in the extremities; ⑥ significantly reduced intraocular pressure recovery rate in the ocular compression test.

The diagnosis of posterior ischemic optic neuropathy can be based on: ① sudden vision loss with visual field defects; ② absence of headache or eye pain; ③ normal fundus or slightly pale nasal optic disc with clear margins; ④ age over 40, often with hypertension, hypotension, arteriosclerosis, or changes in blood composition; those under 40 often have Raynaud's phenomenon or a history of trauma or shock.

It should be noted that clinically diagnosing posterior ischemic optic neuropathy is often challenging and mostly speculative, making it difficult to differentiate from retrobulbar optic neuritis. Some suggest that abnormal ocular blood flow or evidence of cerebral infarction on cranial CT may serve as reference points.

bubble_chart Treatment Measures

First, treatment should target the disease cause. Systemic or retrobulbar/parabulbar corticosteroid therapy can reduce ischemia-induced edema, improve blood circulation disorders, and break the vicious cycle. Oral vinegar carbonic anhydrase inhibitors can lower intraocular pressure and improve the imbalance of blood supply to the optic disc. At the same time, neurotrophic drugs such as vitamin B₁

, B₁₂, ATP, and coenzyme A can be administered. Low-molecular-weight dextran, compound formula Salvia, Venoruton, and Sichuan Lovage Rhizome can also be appropriately used. External counterpulsation therapy can increase the diastolic pressure of the main stirred pulse, thereby increasing the blood flow of the common carotid stirred pulse. The ophthalmic stirred pulse is a branch of the internal carotid stirred pulse, supplying blood to the posterior ciliary stirred pulse and the retinal membrane stirred pulse of the optic disc. It can enhance the blood supply to the posterior ciliary stirred pulse and the central retinal membrane stirred pulse, ensuring sufficient blood for the optic nerve, boosting tissue metabolism, and activating microcirculation, thereby improving the ischemic and hypoxic state of the optic nerve. Song Chen believes that corticosteroids are generally unnecessary unless caused by temporal stirred pulse inflammation and strongly advocates the use of compound formula anisodine for treatment. Its mechanism may involve central regulation of vascular tone, relieving vasospasm, and improving ocular microcirculation, including the blood supply to the optic nerve. Compound formula anisodine can be divided into Type I (0.05% anisodine 0.5–1.0ml plus 4% procaine 1.5ml) for injection at bilateral Shenshu acupoints; and Type II (0.05% anisodine 0.5ml plus vitamin B₁₂ 100μg plus 2% procaine 0.3ml) for subcutaneous injection near the affected superficial temporal stirred pulse, parabulbar, or retrobulbar injection, administered once daily or three times weekly depending on the condition, with 10 sessions as one course, up to a maximum of 4 courses before gradual discontinuation. Hayreh believes that as long as optic disc swelling persists in non-stirred pulse sclerotic ischemic optic neuropathy, prednisone treatment should be administered.