Transient Loss of Vision 

  • Author: Andrew J Tatham, MBChB, FRCOphth; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jul 13, 2011
 

Background

Transient visual loss in adults is a frequently encountered complaint and, in most cases, has an identifiable cause. Visual loss may be monocular or bilateral and last from seconds to hours. Episodes are usually ischemic in origin. Causes of ischemic transient visual loss include cerebrovascular ischemia, retinal arteriolar emboli, and amaurosis fugax syndrome.

Transient visual loss in children is less common but is more likely to have a benign origin. Causes of transient visual loss in children include migraine and epileptic seizure.[1, 2]

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Pathophysiology

Transient visual loss may be due to a variety of ophthalmic and systemic conditions. Transient hypoxia of any part of the visual system can result in a temporary disturbance of vision. Compromised perfusion of the occipital lobe, the visual pathways, or the eye may be secondary to thromboembolism, hypoperfusion, or angiospasm.

Embolic occlusions of the arteries supplying the eye are a common cause of transient visual loss in adults. Emboli causing circulatory disturbances may originate in the heart or the carotid arteries. Embolic events are usually isolated, so if the visual disturbance occurs frequently, emboli are less likely to be responsible.

Hypoperfusion may be due to hypotension, cardiac arrhythmias, anemia, heart failure, or atherosclerotic and arteritic cerebrovascular disease. Arteritic and nonarteritic anterior ischemic optic neuropathy may also present with transient visual loss.

Angiospasm may cause a temporary reduction in blood flow to the visual system and transient visual disturbance.

Children with transient visual loss are less likely to have an ischemic cause for their symptoms and are more likely to have a benign disorder. In some children, a cause for the visual disturbance cannot be identified and the symptoms are medically unexplained.[1]

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Epidemiology

Frequency

United States

The frequency of transient visual disturbance in children is not known but is uncommon.

International

Uncommon

Mortality/Morbidity

When a patient presents with transient visual disturbance, the underlying cause must be ascertained and any serious treatable disorder must be excluded. In adults, identifying risk factors, such as hypertension, hypercholesterolemia, and carotid artery disease, and treating systemic disease are important. For example, if retinal emboli are found, the patient needs to be promptly referred for evaluation and management of cardiovascular risk factors. The Beaver Dam Eye Study found that participants with retinal emboli who present at baseline had a 3-fold higher risk of 8-year mortality from stroke than persons without emboli (age- and sex-adjusted relative risk 2.9, 95% CI 1.3, 6.7).[3]

Although children are more likely to have a benign cause for their symptoms, some may have a serious underlying problem. For example, cases of central retinal artery occlusion and central retinal vein occlusion have been reported in children associated with trauma, vasculitis, antiphospholipid antibody syndrome, sickle cell disease, and leukemia.[4, 5]

Sex

The sex distribution of transient visual loss in children is not known.

Migraine, a common cause of transient visual loss at all ages, is more common in females than in males. In the United States, the 1-year prevalence of migraine is 14-18% in females and 6% in males. However, the female predominance is not seen until after menarche.[6] In children younger than 7 years, boys are affected by migraine equally or slightly more than girls.[7]

Medically unexplained visual symptoms are more common in women than in men. According to Griffiths et al, of those affected with medically unexplained visual loss, 79% are female and 21% are male.[8]

Age

Transient visual disturbance is more common in adults than in children.

Transient visual disturbance in children also has a different etiological profile than transient visual disturbance in adults.

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Contributor Information and Disclosures
Author

Andrew J Tatham, MBChB, FRCOphth  Fellow in Glaucoma, Department of Ophthalmology, University Hospitals of Leicester, UK

Andrew J Tatham, MBChB, FRCOphth is a member of the following medical societies: American Academy of Ophthalmology, British Medical Association, and Royal College of Ophthalmologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Andrew W Lawton, MD  Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor 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, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

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, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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