Regional cerebral blood flow and CSF pressures during the Cushing response induced by an infratentorial expanding mass.

An experimental study was carried out in eight dogs to investigate whether the Cushing response (CR) during intracranial hypertension is due to pressure per se, tissue distortion, or ischemia in the brain stem. To minimize the effects of rostrocaudal displacement, intracranial pressure was raised by an expanding mass lesion located in the posterior fossa. Regional cerebral blood flow (rCBF) was measured with radioactive microspheres and compartmental cerebrospinal fluid (CSF) pressures were recorded during the CR which was induced by the continuous inflation at a constant rate of an infratentorial epidural rubber balloon in two groups of four dogs. In one group (A) rCBF was measured at the onset of the CR and in the other group (B) at the peak of the systemic blood pressure rise. In the animals of group A blood flow in the mesencephalon, pons and upper medulla oblongata was reduced from control values by 32%, 57% and 85% respectively. In group B blood flow in the same areas did not differ significantly from pre-inflation values. In contrast, the recorded balloon volume, which was assumed to be an index of mechanical distortion of the brain stem, varied considerably at the beginning of the blood pressure rise (from 2.5 to 4.7% of the calculated intracranial space). Similarly, CSF pressure in the posterior fossa at the onset of the CR also varied considerably (from 52 to 117 mmHg). Thus, the large quantitative variations meant that both absolute pressure and tissue distortion were poor predictors of the onset of the CR. The findings suggest that ischemia, rather than brain stem distortion per se or pressure by itself, is responsible for the initiation of the CR. The rise in blood pressure elicited during the CR seems capable of restoring blood flow in the brain stem back to control values.