A, Dynamic fundus changes over time during the attack in the images captured from the video. The times indicate when the images were obtained after the onset of the attack. B, A control image obtained 1 month after the attack.
Images of the right eye obtained with a regular fundus camera taken immediately after the attack (A) and 1 month after the attack under normal conditions (B).
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Ota I, Kuroshima K, Nagaoka T. Fundus Video of Retinal Migraine. JAMA Ophthalmol. 2013;131(11):1481–1482. doi:10.1001/jamaophthalmol.2013.4686
Retinal migraines are characterized by attacks of fully reversible monocular vision loss associated with migraine headaches, and these phenomena are rare. Furthermore, because it is difficult to observe dynamic changes in fundus images during transient vision loss, retinal vasospasm rarely has been documented photographically.1-4 Using videos, we documented a case of retinal vasospasm during a transient episode of monocular vision loss in a patient with a history of migraine.
A 29-year-old healthy woman described a 10-year history of migraine with aura; her mother had also had migraines. The patient described a visual aura of twinkling stars that preceded the headaches by several hours. The recurrent monocular vision loss (whiteout) resolved in 2 to 5 minutes in the right eye. She visited us after the third episode. Visual acuity measured during the ophthalmologic examination was 20/15 OU. During the slitlamp examination, visual acuity decreased to light perception OD during the fourth, fifth, and sixth attacks. Four attacks occurred over several hours after the examination.
We recorded the fundus for 1 minute 55 seconds during the sixth attack (Video 1); the video shows the dynamic changes in the retinal arteries and veins (narrowing, reperfusion, and dilation) and alterations in the color of the optic disc and choroid. The images captured from the video show dynamic fundus changes over time (Figure 1). The retinal arteries and veins were extremely narrow compared with those in the control image. The blood columns in the veins were interrupted and had a rouleaux formation. The optic disc was pale and the choroid seemed to be dark. The narrowing of the retinal vessels and disc pallor diminished gradually over time. In the late phase of the attack (after 1 minute 28 seconds), the retinal vessels were dilated and the disc was hyperemic. Video 2 and Video 3 show the reperfusion of the retinal circulation in the late phase. The images obtained immediately after the attack (Figure 2) show the dilated retinal vessels in the right eye. The images show that the retinal veins and arteries in the right eye were more dilated than those in the left eye (not shown) or those obtained under normal conditions 1 month after the attack.
No hypercoagulability was identified with hematologic and serologic testing. Findings on neurologic tests and magnetic resonance imaging of the brain were normal. The patient was treated with propranolol hydrochloride because of an allergy to lomerizine hydrochloride, and the retinal migraines have not recurred.
Most cases of previously documented retinal vasospasms have been associated with emboli or systemic diseases.1,3,4 Most cases reported to be retinal migraine were cases of presumed retinal vasospasm, and this disorder is exceedingly rare.5 Because our patient had no systemic disease except migraine and no embolus, the attacks were likely to have been primary vasospasms. The images clearly show vasospasm in a patient with a history of migraine with aura, which supports the belief that retinal migraine is a distinct entity. Individual cases of transient monocular vision loss have varied in the main component of vasoconstriction.6 In our case, diffuse narrowing of the retinal vessels may have represented decreased blood flow in the central retinal artery, and disc pallor and a dark choroid may have indicated decreased posterior ciliary circulation. Therefore, we speculated that the main component of the vasoconstriction may be the ophthalmic artery and that marked retinal vasodilation at the end and immediately after the attack may represent compensation for hypoxia of the retinal tissues.
Corresponding Author: Isao Ota, MD, PhD, Department of Ophthalmology, Asahikawa Red Cross Hospital, 1-1 Akebono, Asahikawa, 070-8530, Japan (email@example.com).
Published Online: September 5, 2013. doi:10.1001/jamaophthalmol.2013.4686.
Author Contributions:Study concept and design: All authors.
Acquisition of data: Ota, Kuroshima.
Analysis and interpretation of data: Ota, Kuroshima.
Drafting of the manuscript: All authors.
Critical revision of the manuscript for important intellectual content: Ota.
Obtained funding: Ota.
Administrative, technical, or material support: Ota, Kuroshima.
Study supervision: Nagaoka.
Conflict of Interest Disclosures: None reported.
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