Dynamic Axial Brain-Stem Distortion as a Mechanism Explaining the Cardiorespiratory Changes in Increased Intracranial Pressure

OR the past half centm'y the generally accepted theory of the mode of action of increased intracranial pressure on cardiorespirat!)ry mechanisms has been based on the experimental work of Harvey Cushing. s-n As a result of his and other experimental studies it has been conceded that the mechanism whereby increased intracranial pressure produces cardiorespiratory changes was that of anemia of the medullary centers. Bailey 1 in his book on intracranial tumors illustrates this theory (Fig. 1). It was Cushing's contention that in order for medullary anemia to exist there must be a suppression of blood flow into the medulla. This occurred at an intracranial pressure in excess of the systolic pressure of blood. These cardiorespiratory changes consist of slowing of the pulse, increase in pulse pressure, elevation of blood pressure, and slowing of respiration with terminal respiratory arrest and final cardiovascular failure. In applying Cushing's experimental findings to increased intracranial pressure in the human being, most students and investigators have had difficulty in accepting increased intracranial pressure as high as the systolic pressure of blood in the clinical patient. For it is the clinical observation of most investigators that these cardiorespiratory changes usually attributed to increased intracranial pressure occur at levels of intracranial pressure below that of the systolic pressure of blood. Therefore, a search has been underway to find a mechanism whereby these cardiorespiratory changes can be explained at lower levels of intracranial pressure more compatible with those levels found in clinical cases. It is our feeling that this mechanism responsible for cardiorespiratory changes in increased intracranial pressure is an acute dynamic axial distortion of the brain stem affecting the conductivity of the ponto