Imaging of Glial Activation and Risk for Post-Traumatic Epilepsy
Abstract
The development of post-traumatic epilepsy (PTE) is associated with significant disability. Despite our keen awareness of this significant public health issue, little is known regarding the biological mechanism leading to PTE. One plausible mechanism is that unchecked neuroinflammation, a process that occurs in animal and human models of both traumatic brain injury (TBI) and epilepsy, leads to altered synaptic transmission and neuronal excitability. Positron emission tomography (PET) can be used to measure the degree of in vivo neuroinflammation in the central nervous system through radiotracer binding of the translocator protein (TSPO), which co-localizes to neuro-inflammatory cells. Currently, no preclinical or clinical study has analyzed the relationship between neuroinflammation, as measured by TSPO PET, and the risk for developing PTE. We hypothesize that persistent neuroinflammation following moderate-to severe TBI will be associated with an increased risk for developing PTE, and with this current proposal, set out to discover a mechanistic link between persistent trauma-induced glial activation and epilepsy. To investigate this hypothesis, we are enrolling patients with moderate-to-severe TBI to undergo two TSPO PET scans at 2 weeks and 2 months following injury to determine the degree of in vivo neuroinflammation and its relationship with the risk for PTE. These patients will be followed longitudinally for up to one -year with regular assessments for the develop of PTE and assessment for cognitive outcome.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2020
- Accession Number
- AD1110688
Entities
People
- Ryan Martin
Organizations
- University of California