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Management of ischemic optic neuropathies.

Hayreh SS - Indian J Ophthalmol (2011 Mar-Apr)

Bottom Line: Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones.NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes.There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology and Visual Sciences, College of Medicine, University of Iowa, Iowa City, IA, USA. sohan-hayreh@uiowa.edu

ABSTRACT
Ischemic optic neuropathies (IONs) consist primarily of two types: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION comprises arteritic AION (A-AION: due to giant cell arteritis) and non-arteritic AION (NA-AION: due to other causes). PION consists of arteritic PION (A-PION: due to giant cell arteritis), non-arteritic PION (NA-PION: due to other causes), and surgical PION (a complication of several systemic surgical procedures). These five types of ION are distinct clinical entities etiologically, pathogenetically, clinically and from the management point of view. In the management of AION, the first crucial step with patients aged 50 and over is to identify immediately whether it is arteritic or not because A-AION is an ophthalmic emergency and requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones. Systemic risk factors, particularly nocturnal arterial hypotension, play major roles in the development of NA-AION; management of them is essential in its prevention and management. NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes. A-PION, like A-AION, requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.

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Related in: MedlinePlus

Schematic representation of blood supply of the optic nerve (A = arachnoid; C = choroid; CRA = central retinal artery; Col. Br. = collateral branches; CRV = central retinal vein; D = dura; LC = lamina cribrosa; ON = optic nerve; P = pia; PCA = posterior ciliary artery; PR = prelaminar region; R = retina, S = sclera; SAS = subarachnoid space)
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Figure 0001: Schematic representation of blood supply of the optic nerve (A = arachnoid; C = choroid; CRA = central retinal artery; Col. Br. = collateral branches; CRV = central retinal vein; D = dura; LC = lamina cribrosa; ON = optic nerve; P = pia; PCA = posterior ciliary artery; PR = prelaminar region; R = retina, S = sclera; SAS = subarachnoid space)

Mentions: A scientifically valid term is essential in describing a clinical entity. It should reflect true nature of the disease. Before 1974, IONs were described under multiple eponyms.[1] The generic term “ischemic optic neuropathy”, which is widely used, is inadequate, as is evident from the following discussion. On the basis of blood supply, the optic nerve can be divided into two distinct regions: (1) the anterior part of optic nerve head (ONH), which is supplied primarily by the posterior ciliary artery (PCA) circulation and (2) the rest of the optic nerve, which is not supplied by the PCAs but from multiple sources [Fig. 1].[2–7] In the early 1970s, I found from my studies on the blood supply of the optic nerve[2–4] and experimental[8] and clinical[910] studies that interference with the PCA circulation resulted in the clinical picture for which I coined the term “anterior ischemic optic neuropathy” (AION).[11] This term represents the exact site and ischemic nature of the lesion in the optic nerve. Later, in 1981, I first described the clinical entity “posterior ischemic optic neuropathy” (PION)[12] which is due to ischemia of a segment of the posterior part of the optic nerve, not supplied by the PCA [Figs. 1b2].


Management of ischemic optic neuropathies.

Hayreh SS - Indian J Ophthalmol (2011 Mar-Apr)

Schematic representation of blood supply of the optic nerve (A = arachnoid; C = choroid; CRA = central retinal artery; Col. Br. = collateral branches; CRV = central retinal vein; D = dura; LC = lamina cribrosa; ON = optic nerve; P = pia; PCA = posterior ciliary artery; PR = prelaminar region; R = retina, S = sclera; SAS = subarachnoid space)
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3116541&req=5

Figure 0001: Schematic representation of blood supply of the optic nerve (A = arachnoid; C = choroid; CRA = central retinal artery; Col. Br. = collateral branches; CRV = central retinal vein; D = dura; LC = lamina cribrosa; ON = optic nerve; P = pia; PCA = posterior ciliary artery; PR = prelaminar region; R = retina, S = sclera; SAS = subarachnoid space)
Mentions: A scientifically valid term is essential in describing a clinical entity. It should reflect true nature of the disease. Before 1974, IONs were described under multiple eponyms.[1] The generic term “ischemic optic neuropathy”, which is widely used, is inadequate, as is evident from the following discussion. On the basis of blood supply, the optic nerve can be divided into two distinct regions: (1) the anterior part of optic nerve head (ONH), which is supplied primarily by the posterior ciliary artery (PCA) circulation and (2) the rest of the optic nerve, which is not supplied by the PCAs but from multiple sources [Fig. 1].[2–7] In the early 1970s, I found from my studies on the blood supply of the optic nerve[2–4] and experimental[8] and clinical[910] studies that interference with the PCA circulation resulted in the clinical picture for which I coined the term “anterior ischemic optic neuropathy” (AION).[11] This term represents the exact site and ischemic nature of the lesion in the optic nerve. Later, in 1981, I first described the clinical entity “posterior ischemic optic neuropathy” (PION)[12] which is due to ischemia of a segment of the posterior part of the optic nerve, not supplied by the PCA [Figs. 1b2].

Bottom Line: Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones.NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes.There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology and Visual Sciences, College of Medicine, University of Iowa, Iowa City, IA, USA. sohan-hayreh@uiowa.edu

ABSTRACT
Ischemic optic neuropathies (IONs) consist primarily of two types: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION comprises arteritic AION (A-AION: due to giant cell arteritis) and non-arteritic AION (NA-AION: due to other causes). PION consists of arteritic PION (A-PION: due to giant cell arteritis), non-arteritic PION (NA-PION: due to other causes), and surgical PION (a complication of several systemic surgical procedures). These five types of ION are distinct clinical entities etiologically, pathogenetically, clinically and from the management point of view. In the management of AION, the first crucial step with patients aged 50 and over is to identify immediately whether it is arteritic or not because A-AION is an ophthalmic emergency and requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones. Systemic risk factors, particularly nocturnal arterial hypotension, play major roles in the development of NA-AION; management of them is essential in its prevention and management. NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes. A-PION, like A-AION, requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.

Show MeSH
Related in: MedlinePlus