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J. P. EVANS, M.D.; F. F. ESPEY, M.D.; F. V. KRISTOFF, M.D.; F. D. KIMBELL, M.D.; H. W. RYDER, M.D.; D. H. LAMB, B.S.; E. B. BARNES, B.A.; D. J. YOUNG, R.N.
AMA Arch Surg. 1951;63(1):107-114. doi:10.1001/archsurg.1951.01250040110016.
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CUSHING in 1901 stated: "The fact that cerebral compression occasions a rise in blood pressure is universally known but it does not seem to have been recognized that the degree of this elevation occurs pari passu with the degree of compression to which medullary centers are subjected."1 He later elaborated clinically on this concept.2 Although his experimental work demonstrated clearly that blood pressure elevation did not occur until high degrees of compression had developed, the application of the experimental concept to clinical problems inexplicably lost sight of this fact. In the next four decades it became widely accepted teaching that the clinical state produced by expanding intracranial lesions is characterized by a concomitant association among increased intracranial pressure, vascular hypertension and bradycardia, a triad of responses that has been termed the Cushing phenomenon. These changes in the vital signs are seen together so rarely in subjects with high


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