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Stroke patients often have visual symptoms and signs, the characteristics of which vary mostly depending on the type of vessel involved (arteries versus veins), the type of stroke (ischemic or hemorrhagic), and the size of the arteries involved (large versus small artery disease). Because the blood supply to the eye is mostly provided by branches of the ophthalmic artery, the first intracranial branch of the internal carotid artery (ICA), patients with anterior circulation cerebral ischemia may present with ipsilateral visual changes. Binocular visual loss or abnormal extraocular movements are common with vascular diseases affecting the posterior circulation, which provides the blood supply to the occipital lobes and posterior fossa. In addition, a number of ocular vascular disorders are associated with numerous systemic diseases affecting the eyes and the brain simultaneously .
Monocular (ipsilateral to the affected ICA) transient and permanent visual symptoms and signs may develop in patients with carotid artery disease or those with emboli from the aortic arch or the heart. Contralateral homonymous visual field defects, bitemporal visual field defects, and bilateral simultaneous visual loss may also result from anterior circulation ischemia, particularly when the disease is bilateral .
Although transient monocular visual loss may result from retinal transient ischemic attack (TIA), it is important to emphasize that there are numerous nonvascular causes of transient monocular visual loss, which require an emergent detailed ocular examination; therefore, an ophthalmic consultation should be obtained before obtaining an extensive workup for presumed vascular transient monocular visual loss (so-called “amaurosis fugax”). Retinal TIAs classically present as sudden, complete blackout of vision in one eye, lasting few minutes without residual visual loss. Ocular examination may show retinal emboli or may be normal. The workup is similar to that of a cerebral TIA, including stroke protocol brain imaging, since about 25% of patients with acute retinal ischemia have concomitant acute cerebral ischemia . Multiple episodes of transient visual loss or painful transient visual loss in the elderly should raise the possibility of giant cell arteritis .
Partial or complete monocular loss of vision may occur in patients with ipsilateral carotid artery disease, or emboli in the anterior circulation. This results most often from a central retinal artery occlusion (CRAO) ( Fig. 88.1 ) or from one or multiple branch retinal artery occlusions (BRAOs) ( Fig. 88.2 ). In such cases, emboli may be seen in the affected vessels. The most common emboli that occlude retinal arterioles are made of cholesterol, fibrin platelets, and calcium fragments ( Table 88.1 ). Acute retinal ischemia should be evaluated emergently, in a similar manner as with acute cerebral infarctions .
Type of Retinal Emboli | Source of Emboli | Funduscopic Appearance |
---|---|---|
Cholesterol (Hollenhorst plaque) | Ipsilateral internal carotid artery Aortic arch |
Yellow, refractile |
Multiple in 70% of cases | ||
Appear wider than the arteriole | ||
Often at an arteriole bifurcation | ||
Platelet fibrin | Carotid thrombus Aortic arch thrombus Cardiac thrombus Cardiac prosthesis |
White–gray, pale, not refractile |
Often multiple | ||
Within small retinal arterioles | ||
Calcium | Calcified atheromatous plaque Calcified cardiac valve |
White and large |
Usually isolated | ||
In the proximal segment of the central retinal artery or its branches | ||
Infectious | Infective endocarditis | White spots (Roth’s spots) |
Candidemia | Multiple | |
Talc | Intravenous drugs | Yellow, refractile |
Multiple | ||
Neoplasm | Cardiac myxoma | White, gray |
Often multiple | ||
Fat | Fat emboli in the setting of leg facture | Whitish spots with hemorrhages and cotton wool spots |
Multiple |
Venous stasis retinopathy and ocular ischemic syndrome are caused by severe carotid obstructive disease and poor collateral circulation. The retinopathy is characterized by insidious onset, dilated and tortuous retinal veins, peripheral microaneurysms, and dot-blot hemorrhages in the mid-peripheral retina, associated with neovascularization when ocular ischemic syndrome develops ( Fig. 88.3 ). Patients with this condition develop progressive and often irreversible visual loss, sometimes associated with cerebral hypoperfusion, and the prognosis is poor .
Ischemic optic neuropathy, anterior or posterior, results from small vessel disease and is usually not associated with large artery disease, explaining why carotid artery evaluation is not usually indicated in patients with classic anterior ischemic optic neuropathy .
Partial or complete contralateral homonymous hemianopic visual field defects may result from cerebral ischemia in the anterior circulation. This is most often caused by occlusion of branches of the middle cerebral artery, but it may result from occlusion of the anterior choroidal artery or some of its branches to the optic tract and lateral geniculate body .
Horner syndrome is a classic sign of carotid dissection and may also occur in patients with atherosclerotic carotid artery disease. The Horner syndrome may be isolated (often with ipsilateral facial pain) or may be associated with other neurological symptoms and signs of carotid artery disease .
Isolated facial pain (often periocular) may be a symptom of carotid occlusive disease, even without other symptoms and signs of vascular disease. It is usually a referred pain resulting from ischemia or compression of the trigeminal branches. It may also be part of the ocular ischemic syndrome .
Exceptionally, patients with acute occlusion or severe ICA stenosis may develop one or more ocular motor nerve pareses on the side of the occlusion, either in isolation or with signs of ocular ischemia .
The vertebrobasilar system supplies the entire brain stem ocular motor system as well as the posterior visual sensory pathways and visual cortex. For this reason, ocular motor and visual symptoms and signs play a major role in the diagnosis of vascular disease in the vertebrobasilar system .
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