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Knut Naess, M.D.
JAMA. 1958;166(5):525-526. doi:10.1001/jama.1958.02990050095018.
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To the Editor:—  Rothenberg and Corday (J. A. M. A.164:2005 [Aug. 31] 1957) have recently discussed the question of the etiology of transient stroke on the basis of careful investigations of the pial vessels of monkeys after different types of mechanical and chemical stimulation. As no sign of active contraction could be demonstrated in these vessels and as they only altered their diameter passively in relation to the peripheral blood pressure, the authors drew the natural conclusion that these vessels were not able to contract actively.In their paper they conclude: "In view of the absence of vasoconstrictor innervation of musculature in the pial vessels, as demonstrated by Pickering, and the results of the experiments described in this paper, it appears unlikely that primary cerebral angiospasm can occur."Although these authors' results are convincing, their discussion and conclusion is nevertheless surprising when other recent investigations are taken into


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