CEREBRAL vascular insufficiency caused by extracranial arterial disease is now a well-known entity. When an occlusive brachiocephalic lesion is located in a strategic place, the direction of vertebral or carotid flow is reversed, thereby adding to the degree of cerebral ischemia. This siphoning effect on the cerebral circulation can cause symptoms of vertebral basilar insufficiency or carotid insufficiency, depending on the location of the lesion.
Broadbent,2 in 1875, described arteriosclerotic occlusion of the aortic arch branches and noted its segmental nature. His interest in the patient presented was primarily that of explaining the bilateral absence of radial pulsations in the presence of normal pulses in the lower extremity. Hunt,10 in 1914, emphasized the importance of proximal occlusion of the aortic arch branches in the production of cerebral symptoms. During the past decade volumes have been written on the subject of extracranial occlusive disease.4,6,7,11,13 Cerebral ischemia was considered