Abstract
The ocular fundus allows direct visualization of the retinal vasculature, blood vessels that are part of the cerebral circulation. Unraveling the causes of retinal ischemia may provide further insight in the pathophysiological processes that underlie cerebral ischemia. The primary aim of the studies described in this thesis was to elucidate
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the causes, pathophysiology, and prognostic implications of symptoms of retinal ischemia (transient monocular blindness and retinal infarction) and the presence of asymptomatic retinal emboli in several patient populations. In addition to a retrospective cohort of patients with retinal ischemia, we prospectively studied a cohort of 77 patients with retinal ischemia or with documented retinal embolism (or both). We also studied the outcome of symptoms of retinal ischemia in a cohort of patients with systemic lupus erythematosus and of migraine equivalents in the general population.
We found that the most important cause of retinal ischemia is atherosclerotic vascular disease and that the predominant pathophysiologic mechanism is embolism from a proximal vascular lesion. However, there are many other causes and mechanisms of retinal ischemia that need to be considered in the differential diagnosis of an individual patient. The presence of cerebral microemboli in a patient with symptoms of retinal ischemia increases the likelihood of finding an underlying athero-embolic lesion. We hypothesize that some of the pathophysiological vascular processes that play a role in retinal ischemia may also be important in cerebral ischemia. Examples are: in situ formation of platelet-fibrin emboli, vasospasm, and secondary microembolization from a cardiac embolus lodged in a proximal blood vessel.
Retinal emboli, visualized on funduscopic examination, can be found in patients with symptoms of retinal ischemia, but more often are detected in asymptomatic individuals during routine ophthalmologic examination. In patients with symptomatic retinal embolism, ipsilateral carotid artery stenosis, cerebral microemboli, and early recurrent vascular events are more common than in patients with asymptomatic retinal emboli, suggesting that there are pathophysiological differences.
Patients who present with retinal ischemia or asymptomatic retinal emboli are at an increased risk for recurrent vascular events. Therefore, a timely and meticulous work-up for an underlying cardio-vascular source of embolism is indicated and modifiable vascular risk factors should be carefully monitored and treated in these patients.
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