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Clinical Pathways in Neuro-ophthalmology : An ... - E-Lib FK UWKS

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172 <strong>Cl<strong>in</strong>ical</strong> <strong>Pathways</strong> <strong>in</strong> <strong>Neuro</strong>-Ophthalmology, second edition<br />

of transient visual loss, but more often attacks of TVL with carotid disease last 2 to 15<br />

m<strong>in</strong>utes (see below).<br />

Patients with transient visual obscurations first require ophthalmologic exam<strong>in</strong>ation.<br />

If papilledema is evident (Chapter 7), these patients must have an MRI scan of the bra<strong>in</strong>.<br />

If this study is normal, a sp<strong>in</strong>al tap is <strong>in</strong>dicated to <strong>in</strong>vestigate the possibility of <strong>in</strong>fection<br />

or pseudotumor cerebri (idiopathic <strong>in</strong>tracranial hypertension). Patients with drusen or<br />

other optic disc anomalies caus<strong>in</strong>g monocular TVL may require no further evaluation. If<br />

there are signs of an optic neuropathy on the side of the TVL (e.g., relative afferent<br />

pupillary defect, ipsilateral swollen or atrophic optic nerve, etc.), then MRI with<br />

attention to the orbit is warranted to evaluate a compressive lesion. Patients without<br />

apparent disc abnormalities should be screened for carotid atherosclerotic disease or<br />

other sources of emboli (see below). In selected cases, MRI should be performed to<br />

<strong>in</strong>vestigate the possibility of a structural bra<strong>in</strong> lesion such as optic nerve sheath<br />

men<strong>in</strong>gioma.<br />

Do the Episodes of Monocular TVL Last<br />

M<strong>in</strong>utes?<br />

Monocular TVL last<strong>in</strong>g 5 to 60 m<strong>in</strong>utes (usually 2 to 30 m<strong>in</strong>utes) is strongly suggestive<br />

of thromboembolic disease. Ret<strong>in</strong>al emboli may arise from the aorta (Romano, 1998), the<br />

carotid artery, or the heart. Patients often describe the TVL as a veil or shade descend<strong>in</strong>g<br />

or ascend<strong>in</strong>g over a portion of their visual field. Other patients compla<strong>in</strong> of patchy<br />

visual loss (‘‘Swiss cheese’’ pattern) or peripheral constriction with central visual<br />

spar<strong>in</strong>g (Bruno, 1990). Some episodes of monocular TVL are accompanied by a<br />

sensation of color or other photopsias. These may superficially be similar to migra<strong>in</strong>e,<br />

consist<strong>in</strong>g of showers of stationary flecks of light that disperse quickly (Bruno, 1990;<br />

Goodw<strong>in</strong>, 1987; Pess<strong>in</strong>, 1977). Most episodes of embolic monocular TVL last 2 to 30<br />

m<strong>in</strong>utes. Marshall and Meadows found that <strong>in</strong> 51 of 67 patients (76%) episodes lasted 30<br />

m<strong>in</strong>utes or less, with 29 patients (43%) experienc<strong>in</strong>g episodes last<strong>in</strong>g 5 m<strong>in</strong>utes or less<br />

(Marshall, 1968). Pess<strong>in</strong> et al noted that attacks lasted less than 15 m<strong>in</strong>utes <strong>in</strong> 30 of 33<br />

patients, and <strong>in</strong> 14 patients (42%) the episodes lasted 5 m<strong>in</strong>utes or less (Pess<strong>in</strong>, 1977).<br />

Among 35 patients evaluated by Goodw<strong>in</strong> et al, 22 patients (63%) had attacks last<strong>in</strong>g 5<br />

m<strong>in</strong>utes or less, 8 (23%) had episodes last<strong>in</strong>g 6 to 15 m<strong>in</strong>utes, and 6 patients (17%) had<br />

episodes last<strong>in</strong>g more than 15 m<strong>in</strong>utes (Goodw<strong>in</strong>, 1987). Episodes of monocular TVL<br />

due to thromboembolic disease rarely last several hours.<br />

Patients with thromboembolic disease may demonstrate emboli with<strong>in</strong> the ret<strong>in</strong>al<br />

vessels. Emboli may be composed of clotted blood, fibr<strong>in</strong>, platelets, atheromatous tissue,<br />

white cells, calcium, <strong>in</strong>fectious organisms (septic emboli), air, fat, tumor cells, amniotic<br />

fluid, or foreign materials (e.g., talc, artificial valve material, catheters, silicone,<br />

cornstarch, mercury, corticosteroids). The most common types of emboli seen <strong>in</strong><br />

atherosclerotic disease of the aorta=carotid arteries or cardiac disease <strong>in</strong>clude the<br />

follow<strong>in</strong>g:<br />

1. Cholesterol emboli (Hollenhorst plaques) are bright, glisten<strong>in</strong>g, yellow or coppercolored<br />

fragments, most often seen <strong>in</strong> peripheral arterioles <strong>in</strong> the temporal fundus.<br />

These emboli most often arise from atheromatous plaques <strong>in</strong> the aorta or carotid<br />

bifurcation.

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