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September 1969

Polyneuritis, Papilledema, and Lumbo peritoneal Shunt

Author Affiliations

Tucson, Ariz; Portland, Ore
From the Neurology Section, Veterans Administration Hospital, and the Division of Neurology, Department of Medicine, University of Arizona, Tucson, Ariz (Dr. Buchsbaum), and the Division of Neurosurgery, University of Oregon, Portland, Ore (Dr. Gallo).

Arch Neurol. 1969;21(3):253-257. doi:10.1001/archneur.1969.00480150043005

SINCE the original report of papilledema and polyneuritis by Gilpin et al,1 there have been two theories offered for the causation of the papilledema. The first proposed was that protein interfered with absorption of cerebrospinal fluid (CSF) because of its deposition in the arachnoidal villi.2 The second stated that there was chronic swelling of the brain in the absence of inflammation or demyelination, especially in neurons, demonstrable by histological examination of a biopsy specimen.3 The concept of CSF absorption block has been recently questioned because of the poor correlation between CSF protein levels and the development of papilledema.4 It has been suggested that the alternate concept is not established because the white matter water content was not measured in the case report.4,5 The purpose of this paper is to report a case of chronic polyneuritis developing papilledema two years after onset, who then was

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