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July 24, 1948


Author Affiliations

Director of Cardiovascular Research, U. S. Public Health Service, Staten Island, N. Y.

JAMA. 1948;137(13):1151. doi:10.1001/jama.1948.02890470051022

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To the Editor:—  In a recent report in The Journal entitled "Transient Cerebral Paralysis in Hypertension and in Cerebral Embolism" (J. A. M. A. 137:423 [May 29] 1948), Pickering challenged the hypothesis that cerebral angiospasm is responsible for hypertensive encephalopathy, pointing out that cerebral vessels have relatively thin walls and that they react poorly to vasoconstrictor agents. This author furthermore expressed the view that sudden organic arterial obstruction, for example by a thrombus, and not vasospasm is the cause of the transient paralyses observed in hypertensive disease. This concept is based on his observation that embolic occlusion of cerebral arteries produces attacks that are "precisely similar in kind and range to those occurring in hypertension." Thus in either condition, according to this author, paralyses may be transient or permanent depending entirely on the establishment of a collateral circulation.What Pickering failed to consider, however, is that the similarity between

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