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Fred P. Handler, M.D.; Herman T. Blumenthal, M.D., Ph.D.
JAMA. 1954;155(17):1479-1483. doi:10.1001/jama.1954.03690350021007.
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The formation of intracranial aneurysms with rupture that results in massive subarachnoid hemorrhage has been variously attributed to inflammation, trauma, congenital defects of the arterial wall, and arteriosclerosis.1 Except for reports of syphilis and septic emboli, we have been unable to find reports indicating an inflammatory basis for the origin of these lesions, and traumatic causes are obvious and rare. A controversy has continued for many years as to whether the great majority of intracranial aneurysms develop on the basis of a congenital defect of the medial muscle at points of bifurcation or as the result of arteriosclerosis. While many investigators have observed medial defects in cerebral arteries, few have been willing to accept these as the sole or even major causative factor because of the following considerations. 1. Medial defects are found as often in cerebral arteries of persons without aneurysms as in persons with these lesions.2


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