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Anterior Ischemic Optic Neuropathy Clinical Presentation

  • Author: Andrew A Dahl, MD, FACS; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Jan 05, 2016
 

History

Visual loss is painless in at least 90% of patients with nonarteritic anterior ischemic optic neuropathy (NAION). The vision loss is often noticed upon awakening, perhaps due to nocturnal hypotension. NAION can occur after procedures such as spinal fusion surgery. Risk factors for NAION after spinal fusion surgery include obesity, male sex, Wilson frame use, longer anesthetic duration, greater estimated blood loss, and decreased percent colloid administration.[5]

Patients with arteritic anterior ischemic optic neuropathy (AION) often have symptoms other than visual loss, such as malaise, headache, scalp tenderness and tender temporal arteries, jaw pain on mastication (jaw claudication), generalized muscle aches and swelling.

The earlier manifestations of arteritic AION include malaise, weight loss, fever, vague abdominal or GI pains, and anorexia.

Late manifestations of arteritic AION, often years later, include a much higher incidence of abdominal aortic aneurysm.

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Physical

Nonarteritic anterior ischemic optic neuropathy

Nonarteritic anterior ischemic optic neuropathy (NAION) has typical findings of visual loss and field loss in an otherwise asymptomatic individual.

A small cup disc ratio is usually noted. Initially, the optic disc is swollen and pale, often in a generalized or diffuse manner.

Sectorial disc edema, especially of the superior disc, is classic. Altitudinal visual field loss is common.

Visual loss with NAION is not usually as severe as with arteritic anterior ischemic optic neuropathy (AION), but vision loss as severe as no light perception has been described.

Arteritic anterior ischemic optic neuropathy

In patients with arteritic AION, the disc is classically described as chalky white, pale, and swollen.

Ischemia in multiple vascular territories is not uncommon (eg, central retinal artery occlusion, choroidal infarction, anterior segment ischemia, extraocular muscle ischemia causing diplopia).

The temporal arteries may be quite prominent, ropey, and tender.

Oral, tongue, or even scalp ulcers may rarely be seen.

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Causes

Anterior ischemic optic neuropathy (AION) is an ischemic disease, but the cause is yet to be found definitively. In nonarteritic ischemic optic neuropathy (NAION), atherosclerosis is assumed to be the basis, with its effect on the circulation of the optic nerve head. The posterior ciliary arteries feed the optic nerve head, and, despite variable results in animal primate models with ligation of the posterior ciliary arteries, their susceptibility to atherosclerosis and arteriosclerosis in a widespread manner seems to be the underlying cause. In the arteritic form, the basis for the ischemia is identical in pattern, with a giant cell arteritis (GCA) involving most of the orbital vessels, including the central retinal artery, and the posterior ciliary arteries. Involvement of the branch retinal arterioles is rare presumably because of the lack of internal elastic lamina.

Elucidating the genetic predisposition to GCA has yet to be completed but has promise. Incidence in families of Scandinavian origin is high, and genetically determining persons who are predisposed to this disorder may be possible. Human leukocyte antigen (HLA) haplotypes may also provide some interesting relationships, as there are very rare instances of GCA in patients with true rheumatoid arthritis. The proximity of the gene locus in these 2 diseases seems to preclude the expression of both diseases in the same individual.

According to Miller's edition of Walsh and Hoyt's Clinical Neuro-ophthalmology, the causes and associated conditions of AION are as follows.[6]

Vasculitides include the following:

Systemic vasculopathies include the following:

  • Hypertension
  • Atherosclerosis
  • Diabetes mellitus
  • Migraine
  • Takayasu disease
  • Carotid occlusive disease

Hematologic causes include the following:

  • Sickle cell disease (trait)
  • Acute hypotension (shock)
  • Glucose-6-phosphate dehydrogenase deficiency (G-6-PD)

Ocular causes include the following:

  • Postcataract (possibly)
  • Low-tension glaucoma
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Contributor Information and Disclosures
Author

Andrew A Dahl, MD, FACS Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center

Andrew A Dahl, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Intraocular Lens Society, American Medical Association, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Medical Society of the State of New York, New York State Ophthalmological Society, Outpatient Ophthalmic Surgery Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Brian R Younge, MD Professor of Ophthalmology (Retired), Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Royal College of Physicians and Surgeons of Canada, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, Canadian Society of Oculoplastic Surgery, European Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Medical Association, Ontario Medical Association, Statistical Society of Canada, Chinese Canadian Medical Society

Disclosure: Nothing to disclose.

References
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  2. Ali Ibn Isa. Memorandum Book of a Tenth-Century Oculist. (Translated by CA Wood). Chicago: Northwestern University; 1936.

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  5. The Postoperative Visual Loss Study Group. Risk Factors Associated with Ischemic Optic Neuropathy after Spinal Fusion Surgery. Anesthesiology. 2012 Jan. 116(1):15-24. [Medline].

  6. Miller NR. Anterior ischemic optic neuropathy. Walsh and Hoyt's Clinical Neuro-Ophthalmology. 1982. Vol 1: 212-226.

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Anterior ischemic optic neuropathy of the right eye. Swollen pale disc that can be seen in stereo by converging the eyes and fusing the central image.
Sectorial optic atrophy of the right eye as a late finding resulting from anterior ischemic optic neuropathy. Atrophy has supervened, and the atrophic pale disc with a more pronounced cup can be seen in stereo.
 
 
 
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