Location
Suwaneee, GA
Start Date
11-5-2023 1:00 PM
End Date
11-5-2023 4:00 PM
Description
INTRODUCTION: Blast-induced traumatic brain injury (TBI) is characterized by both immediate and long term symptoms that are hypothesized to result from hyper-excitation. The use of a neural depressant as a prophylactic protective measure in mice exposed to blast-induced TBI was evaluated.
OBJECTIVES: The primary objective of this study was to determine if ethanol can decrease the long-term symptoms associated with TBI.
METHODS: Mice were either orally gavaged 95% ethanol or saline prior to blast-pressure wave exposure. Animals were exposed to a blast-pressure wave at 20 psi. Pre and post-blast exposure, animals were assessed for tinnitus, depression, and motor abilities via behavioral experiments.
RESULTS: Motor function was not affected in any of the experimental animals (control and treatment groups). Blast-exposed animals showed signs of depression and tinnitus. The ethanol treated group showed a significant decrease in symptom formation.
CONCLUSION: Ethanol has a prophylactic protective effect if administered immediately prior to a blast-pressure wave exposure. It is plausible the protective effect is caused by decreasing the influence of the cortical hyperexcitation symptoms thus decreasing secondary damage associated with blast induced TBI.
Embargo Period
8-30-2023
Included in
Alcohol and TBI - prophylactic treatment of long-term symptoms of blast-induced traumatic brain injury
Suwaneee, GA
INTRODUCTION: Blast-induced traumatic brain injury (TBI) is characterized by both immediate and long term symptoms that are hypothesized to result from hyper-excitation. The use of a neural depressant as a prophylactic protective measure in mice exposed to blast-induced TBI was evaluated.
OBJECTIVES: The primary objective of this study was to determine if ethanol can decrease the long-term symptoms associated with TBI.
METHODS: Mice were either orally gavaged 95% ethanol or saline prior to blast-pressure wave exposure. Animals were exposed to a blast-pressure wave at 20 psi. Pre and post-blast exposure, animals were assessed for tinnitus, depression, and motor abilities via behavioral experiments.
RESULTS: Motor function was not affected in any of the experimental animals (control and treatment groups). Blast-exposed animals showed signs of depression and tinnitus. The ethanol treated group showed a significant decrease in symptom formation.
CONCLUSION: Ethanol has a prophylactic protective effect if administered immediately prior to a blast-pressure wave exposure. It is plausible the protective effect is caused by decreasing the influence of the cortical hyperexcitation symptoms thus decreasing secondary damage associated with blast induced TBI.