| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on February 20, 2007
From the Department of Academic Neurosurgery (C.H., Z.C., A.L., P.S., J.D.P., M.C.), Addenbrooke’s Hospital, Cambridge, UK; the Department of Neurology (C.H.), University Hospital Aachen, Aachen, Germany; the Institute of Anaesthesiology and Intensive Care Medicine (A.L.), University of Brescia, Italy; and the Department of Neurology (R.R.D.), Alfried-Krupp-Krankenhaus, Essen, Germany. * To whom correspondence should be addressed. E-mail: Mc141{at}medschl.cam.ac.uk.
Background and Purpose—Cerebral blood flow is coupled to brain metabolism by means of active modulation of cerebrovascular resistance. This homeostatic vasogenic activity is reflected in slow waves of cerebral blood flow velocities (FV) which can also be detected in intracranial pressure (ICP). However, effects of increased ICP on the modulation of cerebral blood flow are still poorly understood. This study focused on the question whether ICP has an independent impact on slow waves of FV within the normal cerebral perfusion pressures range. Methods—Twenty patients presenting with communicating hydrocephalus underwent a diagnostic intraventricular constant-flow infusion test. Blood flow velocities in the middle cerebral artery and posterior cerebral arteries were measured using Transcranial Doppler. Pulsatility index, FV variability of slow vasogenic waves (3 to 9 bpm), ICP, and arterial blood pressure were simultaneously monitored. Results—During the test, ICP increased from a baseline of 11 (6) mm Hg to a plateau value of 21 (6) mm Hg (P=0.00005). Although the infusion did not induce significant changes in cerebral perfusion pressures, FV, pulsatility index, or index of autoregulation, the magnitude of FV vasogenic waves at plateau became inversely correlated to ICP (middle cerebral artery: r=-0.58, P<0.01; posterior cerebral arteries: r=-0.54, P<0.01). Conclusions—This study shows that even moderately increased ICP can limit the modulation of cerebral blood flow in both vascular territories within the autoregulatory range of cerebral perfusion pressures. The exhaustion of cerebrospinal fluid volume buffering reserve during infusion studies elicits a direct interaction between the cerebrospinal fluid space and the cerebrovascular compartment.
Revised on March 27, 2007
Accepted on April 12, 2007
Is There a Direct Link Between Cerebrovascular Activity and Cerebrospinal Fluid Pressure-Volume Compensation?
Christina Haubrich MD;
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |