Location

Suwanee, GA

Start Date

11-5-2023 1:00 PM

End Date

11-5-2023 4:00 PM

Description

Introduction: Exposure from blast-pressure waves caused by explosive devices have resulted in traumatic brain injuries (TBI) with a variety of symptoms (e.g., tinnitus, depression, coordination, and impaired motor abilities). Blast exposure causes tearing, shredding, and rotational forces on brain structures. This pathology is more prominent in cells at the edge of structures with varying density or in neurons with extensive physical volume or dendritic processes. Understanding the unique pathophysiology of TBI may be critical for appropriate treatment of these injuries. Our lab developed a blast-pressure wave device to produce a supersonic energy wave at 20 psi. This wave is identical to a mild exposure to an explosive device without the secondary effects of shrapnel or heat.

Objectives: Animals were tested with a novel blast-pressure wave device to determine whether the method would produce symptoms similar to other animal TBI experiments or human TBI patients.

Methods: Animal behavior was tested for tinnitus with acoustic startle tests, depression with forced swim tests, and motor function with free-field tests before and after blast-pressure wave exposure. For each behavioral test, the behavior for each animal was compared to its own normal (pre-blast exposure) measures to determine if alterations in behavior (symptoms) developed due to the blast-exposure. Behavioral measures and the rate of symptom development were compared for the blast-exposed animal group versus a control group that were exposed to the sound but not the energy of the blast-pressure wave.

Results: The results indicate that the blast-pressure wave device is able to provide consistent supersonic blast pressure-waves that can inflict TBI in a rodent model. Blast-exposed animals exhibited long-term symptoms of depression and tinnitus that were not expressed in control animals. These symptoms persisted for over 3 months. No motor impairments were observed in either the control or blast-exposed groups.

Conclusions: The developed blast-pressure wave device is a reliable method for induction of a mild traumatic brain injury for TBI experiments. Induced TBI symptoms in our rodent populations were similar to human symptoms associated with mild blast-pressure wave exposure. Therefore, these methods provide a valid experimental model for examining both pathology and potential therapies for TBI.

Embargo Period

8-30-2023

COinS
 
May 11th, 1:00 PM May 11th, 4:00 PM

Exploring the mysteries of blast induced traumatic brain injury with a custom device

Suwanee, GA

Introduction: Exposure from blast-pressure waves caused by explosive devices have resulted in traumatic brain injuries (TBI) with a variety of symptoms (e.g., tinnitus, depression, coordination, and impaired motor abilities). Blast exposure causes tearing, shredding, and rotational forces on brain structures. This pathology is more prominent in cells at the edge of structures with varying density or in neurons with extensive physical volume or dendritic processes. Understanding the unique pathophysiology of TBI may be critical for appropriate treatment of these injuries. Our lab developed a blast-pressure wave device to produce a supersonic energy wave at 20 psi. This wave is identical to a mild exposure to an explosive device without the secondary effects of shrapnel or heat.

Objectives: Animals were tested with a novel blast-pressure wave device to determine whether the method would produce symptoms similar to other animal TBI experiments or human TBI patients.

Methods: Animal behavior was tested for tinnitus with acoustic startle tests, depression with forced swim tests, and motor function with free-field tests before and after blast-pressure wave exposure. For each behavioral test, the behavior for each animal was compared to its own normal (pre-blast exposure) measures to determine if alterations in behavior (symptoms) developed due to the blast-exposure. Behavioral measures and the rate of symptom development were compared for the blast-exposed animal group versus a control group that were exposed to the sound but not the energy of the blast-pressure wave.

Results: The results indicate that the blast-pressure wave device is able to provide consistent supersonic blast pressure-waves that can inflict TBI in a rodent model. Blast-exposed animals exhibited long-term symptoms of depression and tinnitus that were not expressed in control animals. These symptoms persisted for over 3 months. No motor impairments were observed in either the control or blast-exposed groups.

Conclusions: The developed blast-pressure wave device is a reliable method for induction of a mild traumatic brain injury for TBI experiments. Induced TBI symptoms in our rodent populations were similar to human symptoms associated with mild blast-pressure wave exposure. Therefore, these methods provide a valid experimental model for examining both pathology and potential therapies for TBI.