Brain injury resulting from blunt head trauma remains a major medical complication, the sequelae of which are among the most common of neurologic problems. Because of the central role of the sympathetic nervous system in mediating bodily function and stress, it is hypothesized that the magnitude of SNS activation, as assessed by circulating catecholamine levels, will be an indicator of the severity of traumatic brain injury and, thus, will be useful in predicting patient morbitity and mortality. Conversely, hyperstimulation of the adenergic component of the SNS may itself negatively impact on the severity of illness and on patient survival by a variety of mechanisms. While acute ethanol abuse plays a major role in contributing to the trauma, its affect on SNS activation in the setting of traumatic brain injury is unknown. Consequently, catecholamine levels on admission in both intoxicated and non-intoxicated patients will be quantitated with the severity and type of injury as assessed by neurologic examination, neuroradiologic techniques, and CSF markers of brain damage. The efficacy of treatement with adrenergic blockade in both patient populations will be determined in patients in whom catecholamines predict a poor outcome.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Research Project (R01)
Project #
5R01AA007066-04
Application #
3110646
Study Section
Alcohol Biomedical Research Review Committee (ALCB)
Project Start
1986-08-01
Project End
1990-07-31
Budget Start
1989-08-01
Budget End
1990-07-31
Support Year
4
Fiscal Year
1989
Total Cost
Indirect Cost
Name
University of Rochester
Department
Type
School of Medicine & Dentistry
DUNS #
208469486
City
Rochester
State
NY
Country
United States
Zip Code
14627
Kido, D K; Cox, C; Hamill, R W et al. (1992) Traumatic brain injuries: predictive usefulness of CT. Radiology 182:777-81
Woolf, P D; Lee, L A; Hamill, R W et al. (1988) Thyroid test abnormalities in traumatic brain injury: correlation with neurologic impairment and sympathetic nervous system activation. Am J Med 84:201-8
Woolf, P D; Hamill, R W; Lee, L A et al. (1988) Free and total catecholamines in critical illness. Am J Physiol 254:E287-91