ABSTRACT
Atherosclerotic plaques are the most commonly encountered cerebral circulatory lesions associated with ischemic stokes, and they cause an even higher incidence of transient cerebral ischemic symptoms.[1-3] Atherosclerotic cerebral plaques are frequently associated with atherosclerotic lesions in other regions of the body; therefore a decision is often required as to whether a single therapeutic modality will suffice to treat the underlying vascular disorder or whether individual organ systems threatened by ischemia must be dealt with individually, combining medical with surgical therapies. Where surgical intervention is contemplated, the question is in what order the multiple surgeries should be done.[4-10] The problem is further complicated by the fact that lesions of the carotid bifurcation differ markedly from patient to patient. In some, morphologic components of the plaques suggest that there is marked instability of the pathologic process, indicating possibly imminent cerebral ischemia either through embolization, progression to total occlusion, or even propagation of thrombus to occlude collateral arteries. Even seemingly identical and advanced lesions may be markedly different in their ability to cause cerebral ischemia.[11,12]
Carotid lesions are often associated with other lesions of intra-and extracranial cerebral arteries, which significantly influence the effects of individual arterial occlusions.[13,14]
Clinically, there are marked variations in syndromes resulting from carotid bifurcation lesions, and “the precise mechanism of cerebral infarction may be uncertain clinically.”[15] Symptoms may vary markedly and may be easily characterized as cerebral hemispheric or, less obviously, as vertebrobasilar. They may be as difficult to define as transient global amnesia.[16] Indeed, advanced lesions and even total occlusions of carotid arteries are encountered in asymptomatic individuals, some of whom, nevertheless, at postmortem examination, are found to have cerebral infarcts.
