This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Lack of Association

Teresa A. Timmons, MD; Geoffrey A. Donnan, MD; Jack P. Whisnant, MD; Celia D. Shelley, MT(HEW); Thomas F. Smith, PhD

Arch Neurol. 1986;43(4):376-378.

Abstract
• We tested the hypothesis that intracranial aneurysm develops because of viral infection that produces arterial damage, and that aneurysmal rupture is related to viral infection. The following viral agents were studied: influenza A, influenza B, and respiratory syncytial viral titers, by the indirect immunofluorescence method, in 29 patients and 29 controls; herpes simplex virus titers, by immunofluorescence, in 31 patients and 31 controls; rubella viral titers (Rubazyme test), in 34 patients and 34 controls; and influenza A and B viral titers, by the complement fixation method, in 54 patients and 54 controls. Patients were selected on the basis of documented aneurysmal subarachnoid hemorrhage. Analysis, with derivation of the ² method, to compare titer levels in patients and controls for each specific viral titer did not reveal positive correlations between the viral titers and aneurysmal subarachnoid hemorrhage.

Author Affiliations
From the Departments of Neurology (Drs Timmons, Donnan, and Whisnant) and Laboratory Medicine (Ms Shelley and Dr Smith), Mayo Clinic and Mayo Foundation, Rochester, Minn.

Footnotes
Accepted for publication Oct 22, 1985.

Reprint requests to Mayo Clinic, 200 First St SW, Rochester, MN 55905 (Dr Whisnant).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?