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 signal; and 2) techniques to extract additional pathophysiologic information from the intracranial pressure signal used in the intensive care of the patient with traumatic brain injury. The results of this study may produce methods that could enhance the use of bedside physiological monitoring to include the recognition of progressive loss of vascular tone and impaired regulation of cerebral blood flow and lead to an improvement in the management strategies designed for the patient with severe head-injury. From their laboratory and clinical findings in the previous award period the following hypothesis has been developed: When cerebrovascular tone is intact, compression of the cerebral capillary bed and venules occurs during positive pressure inhalation. The compressional effect progressively reduces as tone is lost. To test this hypothesis three Specific Aims will be addressed using physiologic recordings and determinations of cerebral venous blood flow obtained from a laboratory model. First, with the use of a cranial window, time-varying changes of cerebral venous flow and characteristics of pial vasculature induced by mechanical ventilation will be made using digital image analysis and laser doppler flow measures. Second, with the use of dual optode near infrared reflectometry regional hemispheric changes of cerebral blood volume will be compared to changes of arterial pressure recordings. Third, 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.
