Investigation of the cerebral circulation during periods of increased intracranial pressure was given renewed impetus by Cushing.1 He demonstrated the existence of a hindbrain regulatory mechanism and showed that partial anemia of the vasomotor center might bring about a rise in systemic blood pressure great enough to maintain cerebral circulation during excessive elevations of intracranial pressure. In addition to his manometric studies, Cushing made observations of the pial vessels through a window placed in a trephine-sawed hole in the skull in dogs. During the period of increased pressure within the skull, he noted collapse of the sagittal sinus, distention and stasis in the tributary veins, and obliteration of the arteries and arterioles, with blanching of the cortex.
Making use of a recently developed technic we have reinvestigated the effect on the pial blood vessels of large rises in intracranial pressure. Our object has been to learn by actual measurements