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I. Experimental Investigations of Role of Hypertension and of Collateral Circulation

AMIN A. FARIS, MD; CREIGHTON A. HARDIN, MD; CHARLES M. POSER, MD

Arch Neurol. 1963;9(5):468-472.

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Introduction

The pathogenic mechanism of the hemorrhagic or red cerebral infarct, as opposed to the pale or ischemic infarct, remains controversial. Clinical and pathologic observations have emphasized the close association that exists between cerebral hemorrhage and systemic arterial hypertension.¹ However, cerebral hemorrhage is a different syndrome from that of hemorrhagic infarction, which frequently cannot be differentiated clinically from ischemic infarction. The demonstration of meningeal cortical anastomoses,² as well as radiologic evidence supporting the functional availability of such anastomotic channels in the presence of clinically obstructive vascular lesions,³ points up the necessity for investigation of the exact role of collateral circulation in acute cerebral infarction.

It is the purpose of this communication to report upon the experimental investigation of two major factors in the pathogenesis of the hemorrhagic cerebral infarct: first, the role of systemic arterial hypertension; and second, the role of meningeal cortical anastomoses in this mechanism. . . . [Full Text PDF of this Article]

Author Affiliations
KANSAS CITY, KAN

From the Section of Neurology, Department of Medicine, and the Department of Surgery, University of Kansas Medical Center.

Footnotes
Submitted for publication June 24, 1963; accepted July 30.

Chief Resident in Neurology (Dr. Faris); Associate Professor of Surgery (Dr. Hardin); Associate Professor of Medicine (Neurology) (Dr. Poser).

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