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LEWIS M. WIENER, MD; RICHARD G. BERRY, MD; JACK KUNDIN, MD

Arch Neurol. 1964;11(5):554-561.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

For many years it has been known that neurological deficit and cerebral infarction do not invariably follow occlusion of the carotid artery. It is probable that the development of stroke in patients with carotid occlusion is due to a variety of coexisting abnormalities of the intracranial or systemic circulations. As early as 1914, Hunt¹ suggested that the severity of symptoms following carotid occlusion depended upon the presence of various factors including heart disease, extension of the thrombus into the cerebral vessels, and adequacy of collateral channels especially the communicating arteries of the circle of Willis. To these must be added forward embolization from the carotid thrombus or atherosclerotic lesion,^2-6 independent cerebral artery occlusion,^7-10 and occlusive disease of the remaining extracranial arteries to the brain.^9,11,12 In the present investigation the incidence, type, and significance of each of these abnormalities have been reviewed in a group of 61 . . . [Full Text PDF of this Article]

Author Affiliations
PHILADELPHIA

From the Jefferson Neurology Service (A-1), Philadelphia General Hospital, and the Department of Neurology, Jefferson Medical College, Philadelphia.

Footnotes
Read before the 89th Annual Meeting of the American Neurological Association, Atlantic City, NJ, June 17, 1964.

Present address: Division of Neurology, Maimonides Hospital, Brooklyn, NY (Dr. Wiener).

This work was supported in part by National Institutes of Health grant No. NB-02767.

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