Location
Philadelphia, PA
Start Date
10-5-2021 12:00 AM
End Date
13-5-2021 12:00 AM
Description
Objective: The objective of this review is to explore the relationship between traumatic brain injury and the development of post-traumatic epilepsy.
Background: According to the Centers for Disease Control and Prevention, traumatic brain injury (TBI) is considered a major public health problem in the United States. Each year, 2.53 million Americans, including 812,000 children, document a TBI-related emergency room visit. TBI is a disruption in the brain’s normal function, caused by a bump or blow to the head or by penetrating head injury. These injuries range in severity and can cause damage to one area of the brain, as in focal injuries, or multiple areas of the brain, as in diffuse injury. Mild TBI is often used synonymously with concussion, and these injuries comprise more than 90% of TBI cases. It has also been estimated that more than 40% of TBI-related hospitalizations result in long-term disability. Post-Traumatic Epilepsy (PTE) is defined as a recurrent seizure disorder secondary to trauma to the brain and has been described as one of the most devastating complications associated with TBI, as it can lead to neurodegenerative and neurocognitive symptoms. Most cases of PTE are resistant to existing anti-epileptic drugs, making treatment extremely difficult.
Methods: The search engine PubMed was used. Search criteria included terms such as traumatic brain injury, epidemiology, post-traumatic epilepsy, mild TBI, sport-related concussion, neuroinflammation, astrocytes, gliosis, and biomarkers. Information from the Centers for Disease Control and Prevention and the American Association of Neurological Surgeons was also examined. Results were narrowed down to include literature from the years 2015-2021 and relevant literature from peer-reviewed journals was evaluated.
Conclusions: Several pathophysiological mechanisms may be involved in the development of PTE. Elements of the neuroinflammatory response, including reactive astrogliosis and production of inflammatory compounds, may offer valuable insight into the development of PTE. Further research is needed to establish causal relationships, identify targets for therapeutic intervention, and ultimately prevent, manage, and treat PTE. Additionally, biomarkers may offer insight into secondary injury processes and provide a preventative advantage. Future studies should aim to qualitatively and quantitatively identify biomarkers specific to PTE development.
Embargo Period
6-7-2021
Exploring the relationship between mild, repetitive traumatic brain injury and post-traumatic epilepsy: a review
Philadelphia, PA
Objective: The objective of this review is to explore the relationship between traumatic brain injury and the development of post-traumatic epilepsy.
Background: According to the Centers for Disease Control and Prevention, traumatic brain injury (TBI) is considered a major public health problem in the United States. Each year, 2.53 million Americans, including 812,000 children, document a TBI-related emergency room visit. TBI is a disruption in the brain’s normal function, caused by a bump or blow to the head or by penetrating head injury. These injuries range in severity and can cause damage to one area of the brain, as in focal injuries, or multiple areas of the brain, as in diffuse injury. Mild TBI is often used synonymously with concussion, and these injuries comprise more than 90% of TBI cases. It has also been estimated that more than 40% of TBI-related hospitalizations result in long-term disability. Post-Traumatic Epilepsy (PTE) is defined as a recurrent seizure disorder secondary to trauma to the brain and has been described as one of the most devastating complications associated with TBI, as it can lead to neurodegenerative and neurocognitive symptoms. Most cases of PTE are resistant to existing anti-epileptic drugs, making treatment extremely difficult.
Methods: The search engine PubMed was used. Search criteria included terms such as traumatic brain injury, epidemiology, post-traumatic epilepsy, mild TBI, sport-related concussion, neuroinflammation, astrocytes, gliosis, and biomarkers. Information from the Centers for Disease Control and Prevention and the American Association of Neurological Surgeons was also examined. Results were narrowed down to include literature from the years 2015-2021 and relevant literature from peer-reviewed journals was evaluated.
Conclusions: Several pathophysiological mechanisms may be involved in the development of PTE. Elements of the neuroinflammatory response, including reactive astrogliosis and production of inflammatory compounds, may offer valuable insight into the development of PTE. Further research is needed to establish causal relationships, identify targets for therapeutic intervention, and ultimately prevent, manage, and treat PTE. Additionally, biomarkers may offer insight into secondary injury processes and provide a preventative advantage. Future studies should aim to qualitatively and quantitatively identify biomarkers specific to PTE development.