PATHOGENESIS OF SUBCORTICAL HYPERINTENSE LESIONS ON MAGNETIC-RESONANCE-IMAGING OF THE BRAIN - OBSERVATIONS IN PATIENTS UNDERGOING CONTROLLED THERAPEUTIC INTERNAL CAROTID-ARTERY OCCLUSION

Background and Purpose: Factors associated with the pathogenesis of subcortical hyperintense lesions on magnetic resonance imaging of the brain are not known. We describe four cases of de novo genesis of subcortical hyperintense lesions in patients undergoing controlled therapeutic internal carotid artery occlusion, and we speculate on associated pathophysiological mechanisms. Methods: Twelve consecutive patients underwent controlled therapeutic internal carotid artery occlusion for symptomatic giant cerebral aneurysm using the detachable balloon technique under full anticoagulation. Preocclusion (within 2 weeks) and postocclusion (within 6 weeks) magnetic resonance imaging of the brain was performed in eight cases and evaluated for preexisting and new appearance of subcortical hyperintense lesions. Results: There were four instances of de novo genesis of subcortical hyperintense lesions after carotid occlusion. New subcortical hyperintense lesions were ipsilateral to carotid occlusion in every instance and in two cases were associated with ipsilateral hemispheric ischemic symptoms despite anticoagulant therapy. In one instance, there were transient hemispheric symptoms without the appearance of new subcortical hyperintense lesions. Age, vascular risk factors, and preexisting subcortical hyperintense lesions did not appear to predispose patients to de novo genesis of new hyperintensities. Conclusions: This is the first documentation of de novo genesis of subcortical hyperintense lesions in a controlled setting of hemodynamic ischemic insult. Symptomatic and asymptomatic lesions can be detected in this setting. Anticoagulation does not appear to provide protection from this phenomenon. Careful prospective studies are required to further evaluate risk factors and possible clinical consequences associated with the genesis of new subcortical hyperintense lesions.