The goal of this project is to describe neurological and electrophysiological responses to different levels of concussive brain injury and to characterize the neurophysiological mechanisms mediating these responses. A central hypothesis of this research is that some consequences of concussion may be attributable to changes in ongoing activity within specifiable endogenous neural systems located in the brain stem and capable of suppressing organisms' responsiveness both supraspinally and at the level of the spinal cord. Studies will describe neurological consequences of brain injury including functions reflecting spinal cord activity (e.g., flexion reflex, muscle tone) as well as supraspinal functions (e.g., orienting, arousal). Electrophysiological studies will examine spinal cord potentials and cortical and subcortical components of multimodality evoked potentials. Experiments will study the effects of spinal and supraspinal lesions on electrophysiological and neurological changes produced by concussion or pharmacological activation of an inhibitory brain stem region. Other autoradiographic studies will examine changes in regional rates of glucose metabolism to make inferences about changes in neural activity following concussion or activation of this brain stem site and the relationship of the changes to changes in electrophysiological measures. A third series of experiments will examine effects of activation of this brain stem site on regional changes in cerebral blood flow and blood volume. Data from concussion experiments will be compared to data from experimental activation of brain stem sites to determine if similar mechanisms mediate electrophysiological and neurological alterations produced by both of these manipulations. These studies could provide insights into mechanisms mediating a reversible, flaccid comatose state following lower levels of concussive injury and determine if such mechanisms contribute to changes seen after more severe brain injury. These studies could also provide information on whether neural processes mediating coma contribute to changes in cerebral blood flow, blood volume or glucose metabolism following injury. These data may provide information on neural processes regulating other states of consciousness (e.g. sleep and arousal).

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS021458-03
Application #
3402578
Study Section
Neurology A Study Section (NEUA)
Project Start
1985-07-01
Project End
1988-06-30
Budget Start
1987-07-01
Budget End
1988-06-30
Support Year
3
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Virginia Commonwealth University
Department
Type
Schools of Medicine
DUNS #
City
Richmond
State
VA
Country
United States
Zip Code
23298
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Newcomb, J K; Zhao, X; Pike, B R et al. (1999) Temporal profile of apoptotic-like changes in neurons and astrocytes following controlled cortical impact injury in the rat. Exp Neurol 158:76-88
Newcomb, J K; Pike, B R; Zhao, X et al. (1999) Altered calpastatin protein levels following traumatic brain injury in rat. J Neurotrauma 16:1-11
Zhao, X; Posmantur, R; Kampfl, A et al. (1998) Subcellular localization and duration of mu-calpain and m-calpain activity after traumatic brain injury in the rat: a casein zymography study. J Cereb Blood Flow Metab 18:161-7

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