A Neuropathology Approach to Understanding of Explosive Blast TBI Seizure Risk

It is recognized that explosive blast Traumatic Brain Injury (TBI) may be a significant risk factor for seizure and consequently Post-Traumatic Epilepsy (PTE). This has importance clinically as the manifestation of seizures following a blast exposure may be the only objective clinical sign that a victim may have suffered cellular and structural brain injury. The mechanisms by which explosive blast damages brain remain unclear. Characterizing blast TBI neuropathology will provide the basis for a deeper understanding of this condition thereby facilitating development of meaningful therapies. The evidence to date reveals that explosive blast TBI leads to the neuropathological features of axonal injury as evidenced by focal and diffuse axonal degeneration and axonal swelling detected by silver staining and beta-Amyloid Precursor Protein (APP). Silver stained and immunfluorescent Fluoro-jade reactive neurons consistent with neuronal degeneration and apoptotic bodies of cell death are also observed. Electron microscopy reveals neuron cell body chromatolysis and pycnosis as evidences of neuronal cell degeneration as well as swollen degenerating nerve fibers. These findings are mainly distributed in long fiber tracts, such as the corticospinal tract and visual pathways (including the optic tract and its deep nuclear structures such as the lateral geniculate body and superior colliculus), cerebellar white matter structures, the hippocampus and the brainstem. The neuropathological features of neuronal cell degeneration and cell loss and astrogliosis, particularly in hippocampal structures, have been shown in other clinical conditions with seizures and PTE, which supports the risk of this disorder following explosive blast TBI.