Funding Agency:

University of Cincinnati

Total Project Period:

9/1/08 - 8/31/12

Total Project Award:

$192,000

Principal Investigator:

David O. Okonkwo, MD, PhD

Co-Investigators:

None

Project Summary:

The objective of this application is to determine whether SDs are secondary insults that adversely affect recovery from TBI, and therefore represent an acute target for treatment.

We hypothesize that SD exacerbates cerebral metabolic crisis, particularly under existing conditions of tissue hypoxia, and contributes to worse neurologic outcome of patients. We further hypothesize that SD is triggered in the brain by hypotension, hyperthermia, and high intracranial pressure, and that monitoring of SD will enable identification of target thresholds for these variables to prevent deterioration of damaged brain tissue.

The Specific Aims of the study are to determine the extent to which SD is correlated with worse neurologic outcome (6 mo. GOS-E), cortical tissue hypoxia (PtiO2), and secondary physiologic insults (hypotension, high intracranial pressure, and fever).

We hypothesize that 1) the incidence of SD is an independent predictor of poor outcome, 2) hyperthermia, hypotension, and brain swelling are risk factors for SD occurrence, and 3) the severities of hypoxia and SD activity are correlated.