THE NATURAL HISTORY OF AMAUROSIS FUGAX

Abstract

IN 1952 Fisher called attention to the association of transient monocular visual loss (amaurosis fugax) and contralateral hemiplegia in patients with stenosis or occlusion of the internal carotid artery and described seven personal cases. He also made an exhaustive survey of the literature of the preceding one hundred years and found 150 cases of transient monocular blindness. In this material he discerned seven groups of cases: amaurosis fugax occurring in older patients with atherosclerosis; in younger people without apparent cause; in association with migraine, Raynaud's pheno-menon and heart disease; reflex amaurosis fugax and finally a miscel-laneous group. The majority of cases appeared to be due to retinal ischsemia and, on the basis of the then available evidence, Fisher formed the opinion that the intermittent ischaemia was the result of vasospasm. Seven years later Fisher (1959) was able to examine the retina of a patient during a transient attack of monocular blindness and observed the passage of white bodies through the retinal arteries. These bodies impacted for a time at arterial bifurcations, then fragmented and moved on, their disappearance coinciding with the recovery of vision. Fisher formed the conclusion that they were emboli and that amaurosis fugax could be due to the temporary interruption of the retinal circulation during the passage of emboli through the vessels. Hollenhorst (1960) found that amaurosis fugax was a symptom in no less than 50 of 124 cases of carotid artery disease that he examined. He also reported (1961) seeing bright, refractile, yellow plaques in the retinal arterioles of 27 in a series of 235 patients described as having disease of the carotid arterial system; some of the plaques were observed to move by guest on Septem