Transient Visual Loss

Educational Objectives

The goal of this program is to improve the management of neuro-ophthalmologic disorders. After hearing and assimilating this program, the clinician will be better able to:

1. Recognize the role of ischemia and the need for prompt evaluation and treatment in patients with transient visual loss.

 

Summary

Visual pathway: prechiasmal lesions or structural problems cause monocular visual field defects; chiasmal lesions cause visual field defects in both eyes; patient history — patients not always certain whether loss monocular or binocular (homonymous hemianopia); history, examination, and knowledge of anterior and posterior visual pathways essential for localization; examination often unremarkable by time patient presents

Circulation: posterior cerebral artery supplies posterior visual pathways and occipital lobe (striate cortex); isolated transient ischemic attack (TIA) of posterior cerebral artery may cause isolated homonymous hemianopia; anterior circulation includes internal carotid artery and ophthalmic artery (first branch; supplies entire orbit); ophthalmic artery gives rise to central retinal artery that supplies inner layers of retina

Ischemic causes of transient visual loss: atherosclerosis; carotid emboli (especially central retinal artery occlusion [CRAO]); retinal TIA; valvular disease; dissection; atrial fibrillation; hypercoagulability; patent foramen ovale; aortic arch emboli; hemodynamic causes — marked hypotension or HTN; high blood viscosity (eg, polycythemia); reduced ocular perfusion (eg, ocular ischemic syndrome); vascular causes — vasculitis (including GCA); fistula; vasospasm; vertebrobasilar insufficiency

Ischemic monocular vision loss: sudden, painless, and persists 1 to 5 min; often described as curtain or shade descending or ascending over visual field; however, 48% of patients experience complete, diffuse, and instantaneous vision loss; sparing of central vision possible if cilioretinal artery supplies fovea (as in 20% of population); always include GCA in review of systems

Retinal TIA: TIA currently defined as transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction; implies use of diffusion-weighted imaging/magnetic resonance imaging (DWI/MRI); treatment of retinal TIA same as that for cerebral TIA; short-term risk for stroke or cardiac events very high with both types of TIA; triage, appropriate workup, and early determination of etiology can prevent progression to stroke

Imaging: anoxia in brain tissue leads to accumulation of intracellular sodium and water; seen on DWI/MRI as hyperintense, bright signal; case 1 — 66-yr-old woman with HTN and hyperlipidemia developed abrupt loss of vision in right eye; negative review of systems for GCA and transient neurologic symptoms; neurologic and neuro-ophthalmic examinations normal; DWI/MRI showed small lesion, with corresponding hypointense area on apparent diffusion coefficient mapping of left hemisphere; DWI/MRI indicated patient experienced stroke, despite presenting with right retinal TIA; atrial fibrillation possible cause; case 2 — 75-yr-old woman with same history and presentation as in case 1; DWI/MRI normal, indicating TIA

Workup: may be required for stroke or TIA based on results of DWI/MRI; includes vascular imaging (computed tomography [CT] or magnetic resonance [MR] angiography) and carotid Doppler ultrasonography; 25% of patients with acute retinal ischemia or CRAO, and 18% of patients with retinal TIA have brain infarctions (often visible only on DWI/MRI); risk for stroke or cardiac event after TIA high, especially in first 48 hr (risk higher after stroke); North American Symptomatic Carotid Endarterectomy Trial indicated risk for stroke after retinal TIA significant (24.2% in 3 yr), but not as high as after cerebral TIA

Monocular vs binocular vision loss: more important to differentiate vascular vs nonvascular vision loss; homonymous hemianopia receives same workup (DWI/MRI; CT or MR angiography of head and neck; cardiac workup with electrocardiography and echocardiography)

Vasospasm: case 3 — 76-yr-old woman with history of HTN reported several weekly episodes of abrupt loss of vision in left eye upon bending neck and looking up; neuro-ophthalmic examination normal; episode in office revealed change in acuity from 20/20 to hand motions only and large APD in affected eye; MRI and MR and CT angiography negative; symptoms resolved with nifedipine for presumed stenosis at origin of central retinal artery; vasospasm underrecognized but treatable cause of transient vision loss

Other causes of transient visual loss: epilepsy — homonymous visual loss can occur during or after episode; Uhthoff phenomenon — seen with chronic optic neuritis or demyelination; vision loss occurs in affected eye when body temperature increased; transient visual obscurations — monocular or binocular vision loss after bending over and standing; often seen with pseudotumor cerebri (edema may cause relative hypoperfusion of optic nerve head) or pseudopapilledema (especially drusen); gaze-evoked amaurosis — usually monocular; obtain imaging to rule out impingement on optic nerve; migraine — gradual onset over minutes; should last <1 hr; visual phenomenon (eg, scintillating scotoma) may precede loss of vision, usually followed by headache; ask about history of migrainous features (eg, photophobia), personal or family history of migraine, and triggers (eg, caffeine)

Readings

Suggested Reading

Antonio-Santos AA et al: Pharmacological testing of anisocoria. Expert Opin Phamacother 6(12):2007-13, 2005; Biousse V, Trobe JD: Transient monocular vision loss. Am J Opthalmol 140(4):717-21, 2005; Davagnanam I et al: Adult Horner’s syndrome: a combined clinical, pharmacological, and imaging algorithm. Eye (Lond) 27(3):291-8, 2013; Easton JD et al: Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council. Stroke 40(6):2276-93, 2009; Ferguson GG et al: The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke 30(9):1751-8, 1999; Glazer-Hockstein C, Volpe NJ: Transient Vision Loss. Curr Treat Options Neurol 6(1):37-43, 2004; Hayreh SS: Anterior ischaemic optic neuropathy. 1. Terminology and pathogenesis. Br J Ophthalmol 58(12):955-93, 1974; Kaufman D et al: Ischemic optic neuropathy decompression trial twenty-four-month update. Arch Ophthalmol 118(6):793-8, 2000; Lam BL et al: Risk of non-arteritic anterior ischaemic optic neuropathy (NAION) after cataract extraction in the fellow eye of patients with prior unilateral NAION. Br J Ophthalmol 91(5):585-7, 2007; Patel R et al: Anisocoria — not always cause for alarm. J Pediatr 164(6):1497, 2014; Vortmann M, Schneider JI: Acute monocular visual loss. Emerg Med Clin North Am 26(1):73-96, 2008; Warner JEA et al: Does optic disc appearance distinguish ischemic optic neuropathy from optic neuritis? Arch Ophthalmol 115(11):1408-10, 1997; Wilhelm H: Disorders of the pupil. Handb Clin Neurol 102:427-66, 2011; Winterkorn JM, Teman AJ: Recurrent attacks of amaurosis fugax treated with calcium channel blocker. Ann Neurol 30(3):423-5, 1991.

Disclosures

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, members of  the faculty and planning committee reported nothing to disclose.

Acknowledgements

Dr. Gold was recorded at Neuro-ophthalmology for the Clinician: A Practical Approach, held April 25, 2014, in Baltimore MD, and presented by the Wilmer Eye Institute at Johns Hopkins University School of Medicine. For details on continuing medical education from the Wilmer Eye Institute at Johns Hopkins University School of Medicine, please visit wilmer.org. The Audio-Digest Foundation thanks Dr. Gold and the Wilmer Eye Institute for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

OP521502

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.

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