Location
Suwanee, GA
Start Date
11-5-2023 1:00 PM
End Date
11-5-2023 4:00 PM
Description
Introduction: Traumatic brain injury (TBI) can be caused by exposure to blast pressure waves (i.e., bombs). Individuals in contact with blast pressure waves have been shown to experience various mental and physical symptoms, including tinnitus and depression. Blast-related damage causes micro-tears in the central nervous system that is caused by shearing, stretching, and rotational forces on neurons. This type of damage is too small to see in conventional imaging such as MRI or CT scans. Secondary damage can occur days or weeks after the blast-exposure. We hypothesize that this secondary damage is caused by hyper-excitation leading to excitotoxicity and cell death via a cascade of cytological events.
Objective: The purpose of this experiment was to examine whether a neural depressant (ethanol) can be used as an effective treatment for the secondary hyper-excitatory events after TBI exposure. We hypothesize that the long-term symptoms of depression and tinnitus may be alleviated by this type of therapy.
Methods: Mice were then split into two categories: control and ethanol treatment groups. Both groups were tested for motor function, tinnitus, and depression before and after exposure to a single blast-pressure wave. The ethanol group were orally gavaged 95% ethanol 2 days after blast exposure. The behavioral responses of animals were compared for each individual animal. Changes in animal behavior across the control and treatment group were then compared.
Results:Mice in the control group exhibited signs of tinnitus and depression after blast-exposure. Compared to the control group, animals treated with ethanol showed significant improvements. None of the treated animals developed tinnitus. Additionally, there was a highly significant decrease in the number of animals that showed depressive behaviors (p
Conclusions: The results help to validate the hypothesis that the hyper-excitation exhibited after a blast-induced TBI may be the cause of secondary symptoms. Creating this new sense of neuronal homeostasis (with neuronal depressants) can allows for further possibilities of improvement in the long-term prognosis of patients with TBI caused by blast pressure waves.
Embargo Period
7-26-2024
Included in
The effects of alcohol treatment after getting blasted
Suwanee, GA
Introduction: Traumatic brain injury (TBI) can be caused by exposure to blast pressure waves (i.e., bombs). Individuals in contact with blast pressure waves have been shown to experience various mental and physical symptoms, including tinnitus and depression. Blast-related damage causes micro-tears in the central nervous system that is caused by shearing, stretching, and rotational forces on neurons. This type of damage is too small to see in conventional imaging such as MRI or CT scans. Secondary damage can occur days or weeks after the blast-exposure. We hypothesize that this secondary damage is caused by hyper-excitation leading to excitotoxicity and cell death via a cascade of cytological events.
Objective: The purpose of this experiment was to examine whether a neural depressant (ethanol) can be used as an effective treatment for the secondary hyper-excitatory events after TBI exposure. We hypothesize that the long-term symptoms of depression and tinnitus may be alleviated by this type of therapy.
Methods: Mice were then split into two categories: control and ethanol treatment groups. Both groups were tested for motor function, tinnitus, and depression before and after exposure to a single blast-pressure wave. The ethanol group were orally gavaged 95% ethanol 2 days after blast exposure. The behavioral responses of animals were compared for each individual animal. Changes in animal behavior across the control and treatment group were then compared.
Results:Mice in the control group exhibited signs of tinnitus and depression after blast-exposure. Compared to the control group, animals treated with ethanol showed significant improvements. None of the treated animals developed tinnitus. Additionally, there was a highly significant decrease in the number of animals that showed depressive behaviors (p
Conclusions: The results help to validate the hypothesis that the hyper-excitation exhibited after a blast-induced TBI may be the cause of secondary symptoms. Creating this new sense of neuronal homeostasis (with neuronal depressants) can allows for further possibilities of improvement in the long-term prognosis of patients with TBI caused by blast pressure waves.