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ROBERT D. TAYLOR, M.D.; A. C. CORCORAN, M.D.; IRVINE H. PAGE, M.D.

AMA Arch Intern Med. 1954;93(6):818-824.

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

CUSHING and Bordley,¹ in 1908, observed a patient with high diastolic blood pressure, elevated cerebrospinal fluid pressure, and bilateral papilledema, whose papilledema was relieved by subtemporal decompression. Larsson, in 1923,² described 11 patients with hypertension, mostly secondary to renal disease, all of whom had papilledema and elevated cerebrospinal fluid pressure. Shelburne, Blain, and O'Hare³ surveyed 50 hypertensives and found that 19 of 21 with papilledema had elevated cerebrospinal fluid pressure. Pickering,⁴ after studying 34 hypertensives, in 1934, stated that any individual patient's cerebrospinal fluid pressure is relatively constant and that there is a close correlation between increased cerebrospinal fluid pressure and papilledema. He reaffirmed the latter view in 1952⁵ and suggested that high diastolic blood pressure causes high intrathecal pressure and this in turn, the papilledema, which characterizes the syndrome of malignant hypertension.

This explanation of the papilledema of hypertensive disease is not universally accepted. Fishberg and Oppenheimer,⁶ in 1930, . . . [Full Text PDF of this Article]

Author Affiliations
CLEVELAND

From the Research Division of the Cleveland Clinic Foundation and the Frank E. Bunts Educational Institute.

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