During the routine neurosurgical intensive care of the patient with closed head-injury, bedside physiologic monitoring of the arterial and intracranial pressure signals is accomplished. The long term goals of this work are to develop: 1) a further understanding of the causal factors which produce rhythmic changes in the baseline of the intracranial pressure signals; and 2) techniques to extract additional pathophysiologic information from the intracranial pressure signal used in the intensive care of the patient with closed head-injury. The results of this study may produce methods which could enhance the use of bedside physiological monitoring to include the detection of loss of regulation of cerebral blood flow and lead to an improvement in the management strategies designed for the patient with severe head-injury. From our preliminary clinical and laboratory findings the following hypothesis has been developed: During intact cerebral vascular tone, the low frequency variation in the baseline of intracranial pressure is produced by a corresponding change of cerebral venous blood volume caused by restricted venous flow during positive pressure inhalation. During loss of vascular tone, unrestricted venous flow occurs during positive pressure inhalation. To test his hypothesis two specific aims will be addressed using physiological recordings and determination of cerebral blood flow obtained from a laboratory model. First, with the use of a cranial window proportional changes of cerebral venous blood volume by measurement of the following time-varying parameters of the anterior and posterior parietal veins at a site near to their connection to the sagittal sinus will be made: 1) diameter by video micrometer technique; 2) flow by laser doppler velocimetery; and 3) volume by infrared technique. Second, a hemodynamic model of cerebral blood flow will be developed. comparison of experimental measures with those predicted by the model will be made in order to evaluate its validity.
