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July 1959

Acute Intracranial Hypertension: Experimental-Clinical Correlations

Author Affiliations

New York
From the Department of Neurology and Neurosurgery, New York Medical College.

AMA Arch Neurol. 1959;1(1):3-18. doi:10.1001/archneur.1959.03840010005002

It is known that even in expanding lesions that cause fatal rises in intracranial pressure, the Kocher-Cushing guides6,7,14 for diagnosing severely high intracranial pressure are often absent. These guides are slowing pulse and respirations and steadily rising blood pressure. If the high intracranial tension is not relieved, the pulse begins to rise, blood pressure falls, and respiration stops.

Our purpose was to determine the circumstances under which alterations of these signs may prove helpful in the diagnosis of rapidly expanding brain lesions and in the management of patients suffering from them. We attempted also to clarify the mechanism by which the Kocher-Cushing changes occur.

We used new techniques21,22 to produce gradually increasing intracranial pressure and to measure pressure within and around the animal brain tissue. To test the results of these experiments, they were correlated with a study of 43 patients suffering from acutely high intracranial pressure.

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