The Interrelations between Increased Intracranial Pressure, Cerebral Ischemia, Cerebral Hypoxia, and Cerebral Hypercapnia on the Cushing Response

Abstract

The rise in systemic blood pressure (BP) following an increase in intracranial pressure (ICP) has been known for many years (1). CUSHING first noted that it was a graded response related to the difference between BP and ICP (2). He postulated that the response was due to ischemia of the medullary centers. Until recently this hypothesis was accepted. Doubt was cast by BROWDER and MEYERS (3) when they noted that elevated BP was produced during states of intracranial hypertension where the level of ICP was well below the BP. Recently the emphasis has shifted to the pressure-stretch effect on (4), or distortion of (5), brain stem structures. Discrete areas in the floow of the 4th ventricle closely corresponding to the classical “vasomotor area” have been found to produce a rapid hypertensive response when subjected to localized pressures. Local pressures on the cervical and thoracic spinal cord also have been noted to produce a hypertensive response. Consequently, the role of ischemia, with hypoxia and hypercapnia, in the production of the Cushing response has been downgraded.

This project was supported in part by the National Institute of Neurological Disease and Stroke research grant NS 111 03–01.